ROST’S 
PATHOLOGICAL PHYSIOLOGY 
OF SURGICAL DISEASES 
REIMANN THE 
PATHOLOGICAL PHYSIOLOGY 
OF 
SURGICAL DISEASES 
A Basis for Diagnosis and Treatment of Surgical Affectio7is 
BY 
PROFESSOR DR. FRANZ ROST 
<> i 
University of Heidelberg 
Authorized Translation 
by 
STANLEY P. REIMANN M. D. 
Chief of Pathological Department of the Lankenau Hospital and Assistant Professor 
of Experimental Pathology, University of Pennsylvania, Philadelphia, Pennsylvania 
WITH A FOREWORD 
BY 
JOHN B. DEAVER,vM.D., LL. D., Sc. D., F. A. C. S. 
PHILADELPHIA 
P. BLAKISTON’S SON & CO. 
1012 WALNUT STREET Copyright, 1923, by P. Blakiston’s Son & Co. 
PRINTED IN U. S. A. 
BY THE MAPLE PRESS YORK PA AUTHOR’S PREFACE 
This text book has been evolved from teaching. When a teacher 
comes into close relation with his students, he quickly sees the need for an 
exposition of surgical questions from a somewhat generalized pathological 
anatomical viewpoint, as is done, more or less routinely, in internal 
medicine. It is not sufficient for the student to know that a patient may 
live without an organ, that he may tolerate, for example, a total resection 
of the stomach; he also wants to know the manner in which nature balances 
and compensates those defects, often extensive, that are caused by opera- 
tion. In the ordinary text books, there is little information on this 
subject, and the student has no time for special studies. 
But it is not merely the stimulation to thought which makes desirable 
the discussion of such pathological physiological questions. Surgical 
teaching, more than any other, should be a “viewpoint teaching.” The 
student receives an endless number of single isolated impressions, which 
he absorbs, in general, as a feat of memory. Experience, memory pictures, 
must necessarily constitute the greater part of the teaching of external 
diseases, but in the time usually allotted to the study of the wide field of 
surgery, only a superficial amount of knowledge can be acquired. Doubt- 
less this is the principal way to teach surgery, and it must remain so, but 
the thing most often lacking is a comprehension of the peculiarity of 
surgical thought. 
In surgery, as in no other branch of medicine, the pathological changes 
are actually seen daily. The surgeon disturbs the various mechanisms of 
the body by his operative procedures, and in cases operated too late, sees 
the final picture, and thus evolves a personal conception of the causes and 
effects of disease. Herein lies the peculiar specificity of surgical thought 
based on observations of life processes in organisms changed by disease, 
and their reaction to the special methods used in surgery. It is most 
important for the student to be able to follow the mental processes of the 
surgeon; in other words, not only should he be trained “mechanically” 
in the art of surgery, but “intellectually ” as well. Only then will he be able 
to estimate correctly which diseases are amenable to surgical treatment, 
when interference is most useful, and how best to proceed even when he 
sees a case which has not been presented to him in his student days. The 
purpose of this book is to provide a link between the student and physi- 
cian, in the interpretation of diseases of the human body. 
V VI 
PREFACE 
But it is not only the student who finds it difficult to obtain information 
on any pathological physiological question, but also the young assistant; 
indeed even the independent surgeon finds it difficult if there is no complete 
library in his locality. The literature containing this material is scattered 
in the periodicals of the most diverse’ specialties of medicine. A valuable 
treasure house of pathological physiological work is contained in surgical 
literature itself, because much special investigation has been done from 
the surgical standpoint. 
The importance of such questions is continually increasing. Surgical 
technique, which is essentially well standardized and thoroughly treated 
in the ordinary text books, is not especially difficult to master with a 
fairly skilled hand and a keenly observant eye. Technique alone does 
not make a good surgeon; to it must be added the faculty of judging the 
strength of the patient in reference to the severity of the proposed opera- 
tion, the courage and knowledge to deal with unforeseen circumstances, 
the ability to determine swiftly the most suitable treatment, and many 
other things. These all require an extensive knowledge and understand- 
ing of physiology, indeed it is only by a broadening of physiological con- 
ceptions, that progress in surgery may be expected. 
In this book purely technical matters, that is, animal experiments 
covering operative methods, have been discussed only when pathological 
physiological questions were involved. Furthermore, I have omitted or 
merely mentioned subjects which are treated completely in the usual 
text books, for example, transplantations, regenerations, rachitis, etc. 
It was not always easy to draw a boundary line. 
I have worked on this book for seven years, but feel at this time of 
publication, the painful sensation of having perhaps overlooked many 
important works. I shall be grateful for advice on these points. 
I must express my thanks to all those gentlemen in whose institutions 
and clinics I obtained, as assistant, the knowledge which enabled me to 
write this book. These gentlemen are Geh. Rat. Prof. Dr. Knauf and 
Prof. R. O. Neumann (Hygienisch-bacteriologisches Institut, Heidelberg), 
Prof. Dr. Weintraud (Innere Abteilung des Stadt. Krankenhauses, 
Wiesbaden); Geh. Rat. Prof. Dr. Furbinger (Anatomisches Institut 
Heidelberg); Geh. Rat. Prof. Dr. Schmorl (Pathologisch-anatomisches 
Institut, Dresden-Friedrichstadt); Geh. Rat. Prof. Dr. Enderlen (Chirur- 
gische Universitatsklinik, Heidelberg). 
I also thank the publishers for their great kindness during the 
preparation of the work. 
Heidelbekg.’ 
Franz Rost. TRANSLATOR’S PREFACE 
This book has appealed to us for a number of reasons, chief of which is 
the fact that questions such as are discussed in it have confronted us in 
our hospital work, many times. It has been the desire of the staff of the 
pathological department of the Lankenau Hospital to have the depart- 
ment regarded, in addition to its other uses, as a sort of clearing house 
for information . . a place in which the many questions arising in 
daily clinical work, not only on the surgical service, but on the other 
services of the hospital as well, could be discussed and answers found, if 
possible. In other words, we have undertaken the rather difficult task 
of seeking for explanations of phenomena met with in the wards, when 
such explanations were not forthcoming from our previous experience or 
knowledge. To us it seemed that this book filled considerable need, not 
only in its discussion of many of the subjects, but also in its direct reference 
to a rather extended bibliography, a bibliography with which we were not 
as familiar as with the writings in our own language. 
This is not a literal translation, but it is hoped that the spirit of the 
sentences is preserved, especially in reference to the general underlying 
idea of the way the author has expressed himself. I mean particularly 
the style or philosophical system of his expression. It is, of course, 
understood that by “explanation” in science is meant the gathering 
together of a group of facts under the application of more general laws. 
It will be found that the author is very fond of using such expressions as 
indicate the purposefulness of many of the phenomena which he dis- 
cusses. He does not insist on a mechanistic explanation of his facts, but 
recognizes the incompleteness and short-comings of such endeavors. 
This is the spirit which I have attempted to preserve in the English 
translation. Much stress has been laid for many years upon the idea 
that when an explanation for a phenomenon is not immediately forth- 
coming in mechanistic terms, that is, in terms of matter or motion, it is 
highly dangerous, disadvantageous and obstructive to progress to assume 
that there is a “vital” process concerned. It is said that this idea hinders 
further investigative work. It seems forced to me, however, to regard 
this assumption as such a bugaboo, especially when applied to a clinico- 
investigative field in which we may happen to deal with arranged, 
VII VIII 
translator’s preface 
classified and more or less generalized knowledge, but must perforce use 
this knowledge in connection with patients, each one an individual, 
and a problem in himself. At least, that is our idea of the best way of 
treating a sick human being. It is interesting to observe the emphasis 
laid by the author upon the power of the nervous system. It is also 
interesting to consider the emphasis which he so often places upon indi- 
vidual predispositions. In this connection, it is most interesting to read 
Karl Pearson’s well known book, “The Grammar of Science,” as well as 
J. Arthur Thompson’s text, “The System of Animate Nature.” 
It occurred to me while translating this book, that some additions 
might be added, regarding the subjects with which we, in our hospital 
work, have had more experience than certain others. These additions 
by the translator are bracketed. It may well be objected that the litera- 
ture quoted is German almost exclusively, with very few references in other 
languages. An attempt was made in one chapter, that on the stomach, 
to review an extensive bibliography of publications in the English langu- 
age, but it was found after the task had been finished, one which took 
many months, that it was scarcely worth the trouble. The references 
were easily found, and when read, actually it was discovered that the same 
viewpoints were expressed as in the text; in other words, it was thought 
that the object of the book in this particular field, namely, to present 
various viewpoints on any particular problem, was complete enough to 
allow anyone interested in those points to easily work them up in more 
detail by himself. Many of the references are what we may consider old. 
A professor of English, whom I knew very well, often said in reference to 
the use of words, that it is better to use the oldest of the new and the newest 
of the old. This, it appears to me, is important; therefore, in this book, 
we have been conservative regarding the discussion of new work. Just to 
mention an example, the preparation of insulin from the islands of Langer- 
hans of the pancreas might very well have been mentioned, but on the 
other hand, if all, or even a large part, of the very new things had been 
put in, the book could very well have attained enormous proportions, 
not to speak of the great amount of time necessary for the gathering 
together of the data, after which still newer work would be reported, and 
so on, ad infinitum. In the special case of insulin, it was thought better 
to wait for fuller information and more definite conclusions, and this was 
the rule with many other cases. 
I wish to acknowledge my indebtedness to members of the staff of the 
hospital and to certain of my colleagues at the University of Pennsylvania 
for assistance and advice in reference to many of the points. In the translator’s preface 
IX 
hospital, I must mention in particular, Dr. Carl E. Becker and Miss 
Lida Snellbaker for their cheerful and most valuable help throughout the 
entire preparation of the translation. To Miss Maude T. Shutt, I must 
also express gratitude for her tireless help in the stenographic work. 
Finally, the publishers also deserve my thanks for their many courtesies. FOREWORD 
John B. Deaver, M.D., LL.D., Sc.D., F.A.C.S. 
It is a self-evident fact that good surgery demands of the surgeon not 
only nicety of judgment and faultless technique, but also a working knowl- 
edge of physiology, pathology, and bacteriology for purposes of diagnosis 
as well as for the important matter of postoperative results. This princi- 
ple forms the basis of the comprehensive work of Rost now available to 
surgical English readers. 
This systematic treatise makes no attempt to indicate practical tech- 
nique of surgery, but is devoted to a discussion of the principles underly- 
ing diagnosis as well as operative methods. 
As a guide to surgical diagnosis it aims to outline general facts which 
can be applied to specific cases, so that although a practitioner may be 
unacquainted with a given condition, he will find that the general knowl- 
edge of the essential features of that particular group of diseases herein 
presented, will enable him to treat his patients more intelligently and 
consequently more satisfactorily than otherwise. 
As a guide to the proper surgical measures to be applied in a given 
case, it aims to present the physiologic effects of surgery, inasmuch as it 
discusses nature’s method of compensation for and defense against the 
effects of man’s interference. These effects are amply illustrated by 
animal experimentation by the author himself, as well as by examples 
taken from the literature. Observations on the living human subject at 
the operating table have advanced so far that the surgeon is often enough 
now in a position to note the results of surgical treatment at a period more 
or less remote to a previous intervention. The deductions derived from 
such observations are without doubt the most valuable contributions to 
practical medicine and surgery of our times. 
The citations are voluminous and of themselves make available to the 
research worker in collected form the results of experimental and practical 
work in normal and pathologic physiology, that are scattered in journals, 
textbooks, and treatises, which few have either the time or the opportunity 
to collect and digest. 
The scope of the book includes every region'of the body amenable to 
surgery, and will no doubt prove useful to the student, the general practi- 
tioner, the general surgeon as well as to the specialist in surgery. 
XI XII 
FOREWORD 
Only a thorough-going thoughtful scientist, imbued with the sense 
that science knows no geographical or national limitations could so enthusi- 
astically have undertaken the translation of the work at this time and 
carried it to such successful conclusion. He has rendered the thoughts of 
the author in simple illuminating language in this English edition of Rost 
which is herewith presented to the public. 
John B. Deaver. CONTENTS 
CHAPTER I 
Page 
Oral Cavity. Salivary Glands. Tongue and Esophagus i 
Literature 31 
CHAPTER II 
Stomach 36 
Literature 81 
CHAPTER III 
Pancreas 95 
Literature 106 
CHAPTER IV 
Liver and Gall Bladder no 
Literature 141 
CHAPTER V 
Spleen 148 
Literature 158 
CHAPTER VI 
Peritoneum 161 
Literature 186 
CHAPTER VII 
Intestines 190 
Literature .... 269 
CHAPTER VIII 
Kidneys, Bladder, Male Genitalia. Hypophysis 279 
Literature 330 
XIII XIV 
CONTENTS 
CHAPTER IX 
Page 
Thyroid Gland 
Literature 3^6 
CHAPTER X 
Chest Cavity 
Literature 
CHAPTER XI 
Brain and Spinal Cord 
Literature 423 
CHAPTER XII 
Extremities 
Literature 483 
Index of Authors 493 
Subject Index THE PATHOLOGICAL PHYSIOLOGY OF 
SURGICAL DISEASES 
CHAPTER I 
DIGESTIVE ORGANS 
Digestion begins in the mouth. With the assistance of teeth, tongue 
and cheeks, the food is comminuted, molded and thoroughly mixed with 
the first digestive secretion—saliva (i). This fluid is a product of the 
parotid, submaxillary and sublingual glands, and these organs are of 
particular interest from the standpoint of the study of glandular secretion 
for, on account of their accessibility and the ease with which their products 
can be collected, they have early provided classical material for the study 
of secretion in general. Foremost among the investigators in this subject 
are Ludwig (2) and Heidenhain (3) upon whose fundamental work numer- 
ous followers have built. The first observations of the detailed processes 
which occur in cells during activity were investigated microscopically 
in the salivary glands. 
The innervation of these structures is from two sources; sympathetic 
fibres from the carotid plexus and autonomic fibres from the glossopharyn- 
geal nerve. According to Kohnstamm (4), the submaxillary gland is con- 
trolled by a special center which lies between the nucleus of the facial 
nerve and the motor trigeminal (nucleus salivatorious). Fibres from the 
nucleus travel at first with the pars intermedia of the facialis and then 
as the chorda tympani of the lingual nerve. 
The fibres to the parotid arise in the petrosal ganglia of the glosso- 
pharyngeal as the tympanic, and continue as the superficial petrosal 
minor nerve to the otic ganglion of the trifacial. The parotid is supplied 
from this ganglion through the auriculotemporal nerve. Proof that 
all the secretory fibres to the parotid are supplied through this particular 
nerve, was first given by Claude Bernard. From the practical point 
of view, Leriche (5) and later Tronyl (6) deduced that the secretion in 
salivary fistulse could be abolished by section of the nerve, which fortu- 
nately is not difficult to find. The results were good. During the 
ORAL CAVITY, SALIVARY GLANDS, TONGUE AND ESOPHAGUS 
1 2 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
war, this operation was occasionally performed to control unbearable 
salivation (7). 
Glossopharyngeal saliva is serous and contains very few salivary 
corpuscles. It has the very interesting property of being about 
degrees warmer than the blood in the carotid artery, a proof that the 
formation of saliva is not merely a filtration but is coincident with con- 
siderable oxidation within the gland. These investigations were made 
chiefly on the submaxillary gland of dogs but the same principles apply 
to the parotid gland. Stimulation of the tympanic, that is, the superficial 
minor petrosal nerve, gives results similar to those obtained in the sub- 
maxillary glands by stimulation of the chorda. The processes in the three 
salivary glands may therefore be discussed jointly. 
Stimulation of the chorda produces marked dilatation of the vessels 
within the submaxillary gland and the saliva secreted is serous. Stimula- 
tion of the sympathetic fibres which accompany the blood vessels gives 
rise to a scanty amount of stringy saliva with considerable mucus. Stimu- 
lation of the sympathetic in the neck causes a marked constriction of 
the blood vessels. 
Under normal conditions, secretion is reflex, and occurs from the cortex, 
as shown in the flow of saliva initiated by seeing or smelling palatable 
food. Stimulation at the periphery, especially in the mouth and throat 
also brings about secretion. The salivation in stomatitis and after injuries 
to the oral mucosa is well known. But impulses originating in other parts 
of the body may also cause salivation. Thus, according to Gaultier (8), 
there is often marked salivary secretion in a very early stage of esophageal 
carcinoma, and similarly, according to the same author, the often trouble- 
some salivation during esophagoscopy is explained by the same reflex 
relation between the esophagus and the salivary glands. 
These nerve impulses regulate not only the quantity but also the 
quality of the saliva to an extraordinarily delicate degree. Pawlow (9) 
found the response to dry food greater than to moist food, and strongly 
stimulating substances such as acids, excited considerable salivary 
secretion. But it was not even necessary to bring these substances into 
actual contact with the oral mucosa. Secretion followed when an animal 
was offered food with which he was familiar by sight. Brunacci (10) 
has recorded the qualitative changes in his own saliva which followed the 
application of various stimuli. That which was secreted under mechanical 
stimulation differed the widest from that produced by sour substances, 
and between these extremes, all possible varieties were poured out. 
According to Popielski (11), the amount of saliva produced on stimulation 
by acids, is in direct proportion to the number of hydrogen ions present, 
irrespective of the kind of acid. It might be mentioned that ether is one DIGESTIVE ORGANS 
3 
of the substances which produces a marked flow of saliva through stimula- 
tion of the oral mucosa, and consequently there is considerable salivation 
in the early stages of anesthesia. 
This interesting adjustment of the quality and quantity secreted after 
different peripheral stimuli, has been further investigated by Jappeli (12), 
who found that differences in the physicochemical composition depend on 
stimulation of different areas in the central nervous system. Furthermore, 
he found that a flow of saliva could not only be stimulated from the brain 
and cerebellum, but also inhibited. It is quite possible, though not known, 
that the diminution observed in fever may be attributed to irritation of 
these inhibitory centers (13), though the diminution in deep anesthesia 
is probably not caused by such depression. In addition to being under 
nervous control, the quantity and concentration is also dependent on 
the water content of the blood (14). Thus there is dryness of the mouth 
after perspiration, and this in its turn leads to the sensation of thirst. 
Investigations of the chemical composition of normal saliva have been 
extensive and accurate, and will be dealt with later (15). In studying 
salivary secretion, particularly by means of chemical analyses, it is very 
important to remember that there are constant normal changes during the 
day in both the quantity and composition, especially of the enzymes (16). 
[A distinction should also be made between mixed saliva and the saliva 
from the individual glands.] 
What functional significance has this secretion? Beginning with 
the observation that lesions in the mouth usually heal promptly although 
they are by no means aseptic, and that in dogs primary healing of almost 
any kind of a wound takes place when the animal can lick the site, and 
finally that many plant seeds will not germinate if saliva has been added 
to the earth (17), the conclusion is almost forced that the saliva must have 
powerful antiseptic action. But in spite of considerable experimental 
work, first by Sanarelli, and recently by Clairmont (18), who also reviews 
the investigations of former authors, the question is not definitely settled. 
According to the latter, the saliva has no actual bactericidal power. 
Nevertheless, a number of bacteria, among them the common pyogenic 
staphylococci and streptococci find saliva an unfavorable medium for 
growth. The latter grow in long chains and this seems a sign of injury. 
On the other hand, certain bacteria, such as pneumococci grow, well so that 
Grawitz and Steffen (19) recommend its addition to culture media. The 
saliva with the strongest disinfecting power is secreted by the parotid 
gland, according to the experiments of Clairmont (18). The chemical 
substance usually held responsible for this action is potassium sulpho- 
cyanid. It is said to arise from nitrogenous metabolism, but the details 
cannot be elaborated here (20). Suffice it to say that a compound is then 4 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
supposed to be formed which has stronger bactericidal power than the 
simple substance itself. The objection has, of course, been raised that 
potassium sulphocyanid is inactive in the strength in which it is present 
in the saliva, but this does not seem to have been satisfactorily proved. 
The influence which substances may have on bacteria within the animal 
body can never be safely judged by their influence in the test tube, for 
substances entirely inactive in the latter may be strongly bactericidal in 
the animal body, or vice versa. 
The sulphocyanid content in smokers is greater than in non-smokers 
(15) and as Clairmont has shown, the addition of food to saliva com- 
pletely neutralizes its bactericidal effect. Particles of food are also good 
culture media. Mechanical cleansing of the mouth after every meal is 
therefore advisable. 
In addition to its effects on bacteria, saliva shows a destructive action- 
on certain toxins. Wehrmann (21) demonstrated, for instance, a loss of 
the destructive action of the venom of snakes, and Carriere (22) found the 
same with tetanus toxin. 
These, and other similar experiments have thus given a certain 
amount of explanatory evidence for the numerous clinical observations 
that wounds of the mouth heal unexpectedly well, but Gottlieb and Siches 
(23) showed that injuries to the mouths of dogs heal just as well if the 
salivary glands have been extirpated, or their ducts ligated. From this it 
seems to follow, that the quick healing of wounds in this part of the body 
does not depend on the presence of saliva and that its value in wound 
healing must not be overestimated. -For the present, the subject must 
rest here. 
The significance of saliva in digestion is given ratings which differ 
greatly. In general, the more accurate investigations of later years have 
shown that, in reality, it plays quite an important part, and that it was 
unjustly underrated for a long time. In the first place, by reason of its 
water content, it acts as a solvent for various food stuffs (15); with its help 
the bolus is formed, made slippery, and fit to be swallowed. [There are 
those who believe that this is its most important function.] It helps the 
sense of smell. It is easily reabsorbed in the stomach and Hammarsten 
believes that it carries dissolved substances with it. Its alkaline reaction 
can diminish the acidity of foods, [fermentative products or regurgitated 
stomach contents, and thus protect the teeth], and finally it contains an 
amylolytic enzyme which splits starch into sugar, and this may be con- 
sidered its most important function. [However, as Luciani remarks 
(24) the saliva of carnivora as that of infants is destitute of ptyalin as 
might be expected from teleological considerations, and this is the best 
proof that the principal function of saliva is mechanical, i.e., formation DIGESTIVE ORGANS 
5 
of the bolus. Attempts to show that the saliva of dogs, for example, 
developed amylolytic power when carbohydrate diet was given have been 
refuted.] The ptyalin may, however, be very active, as shown by Sal- 
kowski and others (25) and according to the well known findings of 
Grutzner, its action may continue in the stomach, since the food admixed 
with saliva is deposited in that organ in such a manner that the bolus last 
swallowed forms the central part of the mass. Hydrochloric acid, there- 
fore, which inhibits its action, does not reach the center for some time and 
thus carbohydrate digestion continues in this portion of the stomach 
contents, contrary to the former view that ptyalin was destroyed as soon 
as it reached the stomach (Claude Bernard). 
Still another property has been assigned to saliva, namely, that of 
stimulating the production of hydrochloric acid in the stomach. Strieker, 
and later Biernacki (26) found that the quantity of this acid secreted 
after feeding through a stomach tube was less than that produced follow- 
ing naturally chewed and swallowed food. In such experimental methods, 
however, psychic factors cannot be excluded and we know from the work 
of Pawlow, and others, that these factors have considerable influence, 
on gastric secretion (see later). [The alleged presence of a gastric hor- 
mone has also been refuted.] 
The first condition in the pathology of salivary secretion which merits 
a short discussion is increased flow, or salivation. Since the saliva is 
swallowed under normal conditions, and we are not conscious of the 
amount produced, there is great temptation to assume an increased 
production in conditions in which it flows from the mouth as, for example, 
in facial palsy; caution is necessary in these cases. True salivation is 
found in a number of diseases accompanied by intense pain (15) such 
as trifacial neuralgia, gastric crises, etc. It accompanies inflammatory 
conditions of the oral cavity and tonsils. It occurs in a whole series 
of gastric and intestinal diseases (esophageal carcinoma, pyloric steno- 
sis, intestinal parasitism, etc.). Certain poisons produce salivation 
—mercury, iodine, cocaine on the buccal mucosa, ether, and phenol. 
Finally, there is a class of substances which acts as true sialogogues such 
as muscarin, pilocarpin, nicotin, etc. Of these latter, it is known that 
pilocarpin, physostigmin and muscarin stimulate the autonomic nerve 
endings, while nicotin acts on their ganglion cells (27). Salivation also 
occurs in a number of organic and functional diseases of the nervous sys- 
tem. The increased flow of saliva during pregnancy (28) may belong in 
this category, but the explanation of this condition is in some doubt. So- 
called “ paralytic secretion,” however, belongs to this group. Destruction 
of the chorda tympani, or of Jacobson’s ganglion has, as an immediate 
result, complete inhibition of salivary secretion. After the lapse of about 6 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
twenty-four hours, the gland again secretes, but continuously (paralytic 
secretion, Claude Bernard), (36) and this ceases only after complete 
degeneration of the gland has occurred (30). It is not clear how this is 
brought about. Langley (31) believes that the central end of the chorda 
is in a state of increased irritability after section so that it influences the 
secretion reflexly from the centers. This paralytic salivation is of interest 
to surgeons because it is often observed in high degree in submaxillary 
(32) or parotid tumors (33). It may be so annoying that patients “desire 
operation on account of this symptom” (Kuttner (32)). Thus far, no 
explanation has been offered for this phenomenon but we may perhaps 
imagine a destruction of the secretory cranial nerves. [It has also been 
seen in the gland of the opposite side after hemisection of the cord 
(Heidenhain).] 
Successful attempts to stimulate salivary secretion by chewing paraffin, 
rubber, etc. are occasionally made for therapeutic reasons, as for instance 
to mitigate the thirst after operation. It is also believed that pathological 
transudates of all sorts such as ascites, and hydrothorax may be more 
quickly absorbed following an outpouring of saliva (34). 
The chemical and physical changes in the saliva during the course of 
general diseases have received much less investigation than the quantita- 
tive changes, i.e., salivation. There have been large numbers of single 
observations of the reaction made, however, in all sorts of febrile conditions 
and in diseases of the abdominal organs. It is often acid (15), (25). Altera- 
tions in its enzymic power and in its sulphocyanide content have also been 
demonstrated, the latter especially in involvement of the chorda in otitis 
media (35). An attempt has even been made to use the sulphocyanid 
content as a diagnostic sign in gastric carcinoma, but generally speaking, 
all these investigations, interesting as they are as single observations or 
biological facts, do not have any direct practical value at present. 
Diminution or actual absence of salivary secretion is found in cachectic 
individuals and in diabetes, cholera, dysentery, etc. presumably on 
account of the great loss of fluid. Massive loss of blood may also lead 
to diminished salivary secretion, and furthermore, it is an accompanying 
symptom in a number of febrile infectious diseases such as typhoid fever 
and pneumonia (13). 
Absence of salivary secretion on the corresponding side, is often 
observed in middle ear infections if the chorda tympani has become 
involved in suppuration, or has been disturbed by operation. A case 
has also been observed of destruction of the salivary nucleus, probably 
luetic, in which a complete loss of salivary secretion occurred (36). The 
cases of “ idiopathic asialia ” are especially peculiar, and by no means clear. 
This condition is occasionally observed in certain psychoses. Buxton DIGESTIVE ORGANS 
7 
(37) describes a case of absent salivary secretion following mumps, in 
which a cure was affected by treatment with continuous electric current. 
X-ray treatment of tuberculous lymph nodes of the neck often leads 
patients to complain of dryness of the mouth. This is probably due to 
injury of the substance of the salivary gland which is followed by a 
diminution of function. In patients, the results of considerable diminu- 
tion, or complete absence of salivary secretion are clear from what has 
been said regarding the physiological importance of saliva, and do not 
require detailed enumeration. Subjectively, the principal annoyance 
is extreme dryness of the mouth, compelling the patient in the instance 
mentioned by Buxton to moisten every particle of food with water, and 
making speech almost impossible. 
The results of complete loss of salivary secretion have also been studied 
experimentally (38). All authors are in complete accord in finding that 
after extirpation of the glands there is a decrease in the amount of gastric 
juice secreted and in addition, a marasmus which can not be explained 
merely by the absence of the external secretion of the salivary glands, but 
seems to require in addition, the assumption that an internal secretion 
is also lacking (39). In dogs, for instance, the lessened secretion of gastric 
juice after extirpation of the salivary glands did not return to normal, 
even when the animal was given food which had been well chewed and 
mixed with saliva by another dog. Improvement was obtained, how- 
ever, following the transplantation of a salivary gland into the abdominal 
cavity or after intravenous or intraperitoneal injection of the juice 
expressed from a normal salivary gland. [This is contradicted by work 
of Swanson in which he concludes there is no hormone in the salivary 
glands of dogs which stimulates secretion of gastric juice (40). The 
rise in acidity which he observed may be due to the absence of alkaline 
saliva, and the retardation of the maximum secretion rate to absence of 
the water of the saliva. There must also be a diminished pyschic secre- 
tion on account of the dryness of the mouth and impaired taste.] 
Clinical observations also point to an internal secretory function of the 
salivary glands (see Buxton’s case) and in a manner not yet clear, it seems 
that there is a certain correlation with the genital gland (see Biedl (41)). 
Such a relation is indicated by the “sympathetic” inflammations of the 
testes in parotitis, and vice versa, by the parotitis frequently observed 
after ovariotomy. The only remark that can be made in reference to the 
first mentioned condition, is, that the sympathetic affections of the testes 
in parotitis have been observed to be more frequent in some epidemics 
than in others. Every hypothesis for the reason, has failed to be sub- 
stantiated. It has been stated in the French literature that the pancreas 
may also be involved in mumps, but the necessary pathological anatomical 8 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
investigations are absent (42). [The fact that diabetes mellitus has 
been known to follow mumps has been cited to show such a relation, but 
more evidence is necessary for a final decision.] 
A disease of great practical importance for the surgeon is post-opera- 
tive suppurative parotitis. It usually appears quite suddenly with high 
fever, after all kinds of abdominal operations, and is attended with a high 
mortality (approximately 30 per cent., Wagner (43)). The opinions of 
authors concerning the route of this infection, i.e., ascending—up the 
larger ducts, or hematogenous, are still divided. This is plainly seen in the 
two newest German references to this subject, which appeared at about 
the same time, that of Heinecke (1) and that of Kuttner (32). The first, 
after an exhaustive critical review of the literature, comes to the conclu- 
sion that only in a few cases of parotitis in typhoid fever, has it been 
possible to demonstrate, a hematogenous source of infection by finding the 
specific organism in the pus from the gland; while Kuttner on the contrary 
remarks “that the view of the hematogenous origin of infections of the 
parotid has again gained considerable ground.” 
These diametrically opposed results carried out in simultaneous 
investigations on the very same subject, become comprehensible when 
the different viewpoints from which these two authors approached the 
problem is borne in mind. 
Heineke, and with him, many other authors (44), start from anatom- 
ical findings, and conclude that positive proof has been brought forth in 
all the cases in which an histological examination was made, that the 
first change in suppurative parotitis is the appearance of pus or bacteria 
in the ducts, and that from these structures the infection is carried second- 
arily to the other parts of the gland. Thus far, there are only two cases 
described in the literature in which an anatomical investigation led the 
authors to assign another route for the infection, viz., through the blood 
stream. In the one described by Sabrazes and Faguet (45), Stenson’s 
duct was found free of pus, while a lobule of the parotid was completely 
softened by suppuration. Unfortunately no information of the condition 
of the ducts in the affected part of the gland is given, so that this case has 
no real value. A second case observed by Robert, is found cited by 
Claisse and Dupre (44). The veins within the parotid as well as those in 
the neck were found full of pus. In this case also, no histological examina- 
tion was made. 
If we, therefore, accept anatomical findings as the basis, we must 
conclude that suppurative parotitis is always an ascending infection. But 
Rost (46) demonstrated that anatomical findings do not always show 
what is expected of them. Using dogs, he injected pure cultures of 
bacteria into the internal maxillary artery which supplies the parotid, and DIGESTIVE ORGANS 
9 
in the glands extirpated between the third and fourteenth day he found 
that only the ducts were filled with pus, and that no suppurative thrombo- 
sis or embolism had occurred. As injection of the vessel shows, the rapid 
production of pus in the ducts depends on the very rich blood supply of 
the salivary glands. 
There occurs therefore in the parotid, a suppurative inflammation of 
the ducts similar to a type found in the kidneys. Orth (47) showed that 
there is a special form of suppurative nephritis of hematogenous origin 
which he characterizes as a “simple metastatic suppuration,” in which the 
microorganisms penetrate the walls of the capillary loops of the glomeruli 
and are carried with the urine to the collecting tubules (nephritis papillaris 
mycotica). 
The decision of hematogenous or ascending infection in a given case of 
parotitis need therefore not be entirely influenced by the anatomical 
findings but may be settled by the clinical course alone. There is no 
difference in the anatomical picture between the ascending and the 
hematogenous routes of infection. 
We may now examine the arguments on which a clinical opinion may 
be based (48). The first point to consider is that foreign substances are 
easily excreted by the salivary glands. It must, however, be remarked 
that there are really only a few substances which are eliminated through 
this channel; among them are iodine, bromine, mercury, lead and certain 
alkaloids such as morphine and quinine (27). Furthermore, it has been 
pointed out that suppurative parotitis occurs in the majority of instances 
after operations for conditions that are not completely aseptic (1) and the 
clinical picture of sudden unexpected onset with the high mortality of 
about 30 per cent. (Wagner (43)) fits in perfectly with sepsisor pyemia. 
In addition, a large number of the cases which have come to autopsy 
showed pus foci in other parts of the body (49). It seems forced to explain 
the very high temperature at the onset of a post-operative parotitis, by 
the local condition alone. 
Formerly, the fact that the disease was found almost exclusively after 
ovariotomy was looked upon as an important proof of its hematogenous 
origin. The relation between the genital and salivary glands, which was 
mentioned by Hippocrates (48) and which, although little understood, 
finds expression in the orchitis following mumps (50) or the parotitis 
following contusions of the testicle (51) or in the vicarious swellings of 
the parotid gland during absent or scanty menstruation, etc. (52), was 
recognized, and the conclusion drawn that ovariotomy produced vaso- 
motor disturbances in the parotid gland in some manner or other, and re- 
duced its resisting power against infective organisms circulating in the 
blood. It is at once obvious that the latter part of this conclusion is not 10 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
at all necessary. Because even if ovariotomy should cause an injury to 
the parotid gland, it does not necessarily follow that infection of the paro- 
tid must occur by way of the blood stream, and cannot be ascending. 
After all, post-operative parotitis does not occur relatively so frequently 
after ovariotomy, because at the time these statistics were compiled, ovar- 
iotomy was the most frequent operation in which a laporotomy was per- 
formed. This is now changed, and statements of the relation of the 
antecedent procedure to parotitis at the present time include all kinds of 
abdominal operations. As already mentioned, it is seen principally 
after operations in fields not aseptic, i.e., suppurative appendicitis, 
cholecystitis, gastric operations, etc. (i). 
Furthermore, the fact that it is the parotid and only rarely the other 
salivary glands that are attacked, is hard to reconcile with the view that 
it is an ascending infection. It is not satisfactory to believe that Stenson’s 
duct occupies a particularly favorable position for the entrance of infection 
(Hanau 44) since foreign bodies are found much more frequently in the 
duct of Wharton, and the possibility advanced by Heineke that the 
mucin content of the saliva from the submaxillary and sublingual glands 
inhibits the development of pyogenic organisms has up until the present 
time received no experimental support. On the contrary, according to 
the newer investigations (see above), it is the parotid saliva which has the 
strongest bactericidal power. It is, therefore, not clear why the parotid 
only should become diseased through an ascending infection. The pre- 
dilection of certain tissues in hematogenous infections is more familiar, 
even if we cannot explain it. Finally, the fact that suppuration of the 
parotid often appears very late after an operation also argues against an 
ascending origin of the infection. It often occurs at a time when this 
origin cannot be further considered (see below Hallendahl (53)). Further- 
more, a suppurative parotitis is almost never observed as a result of 
stomatitis; indeed in the most common inflammation of the parotid, viz., 
mumps, an inflammation of the oral cavity is rarely seen, as emphasized 
by Schottmuller (54). 
Nevertheless, the salivary glands are subjected to a number of trau- 
mata after and during an operation, and these are quite capable of favoring 
an infection from within the oral cavity. The first influence is the loss of 
water, and its resulting diminution of salivary secretion. The patients 
usually fast before an operation, and they often lose much water by cathar- 
sis. After the operation they often receive nothing or very little by 
mouth, and are dependent on enteroclysis or infusions. Parotitis has 
also been observed in the course of certain treatments for ulcer, in which 
very small amounts of water are given and the salivary secretion is 
diminished (55). The operation itself leads to a diminished salivary secre- DIGESTIVE ORGANS 
11 
tion. Pawlow (56) has shown experimentally that laparotomy alone, or 
the pulling forward of a loop of bowel leads to a diminution or complete 
cessation of secretion, and that which is formed is viscid and turbid. 
Anesthesia also leads to a diminished secretion (57). A very marked 
increase is found during the early stages of chloroform anesthesia and 
it is still more marked with ether. During deep anesthesia, secretion 
ceases (58), partly on account of the exhaustion from the preceding 
hypersecretion, and partly also from inhibition of the secretory nerves. 
All of these factors interacting during the operation, diminish the quantity 
of saliva for several hours afterwards. Finally, it has been stated that too 
energetic or unskillful pressure over the parotid during the anesthesia may 
lead to injury of the gland (Wagner (43)). The infection that follows can 
naturally occur just as readily through the blood stream as through the 
ducts. [Opinions in the American and English literature are also fairly 
evenly divided. Most authors believe that parotitis following operation 
may be either hematogenous or ascending in origin. Accordingly, 
operations in septic fields, dehydration of the body, trauma during anes- 
thesia etc. are all recognized and procedures are recommended for 
prevention on these grounds.] 
In addition to suppurative parotitis, the disease picture known as 
pneumatocele should be mentioned. It occurs in glass blowers, and 
especially in those who blow principally with their cheeks. The entrance 
of air through Stenson’s duct is favored by the flabbiness of the 
cheeks, the latter of which in addition are often injured by repeated 
inflammations (59). 
Inflammatory changes are also at the basis of sialolithiasis, i.e., the 
formation of salivary calculi. These have been observed in the great 
majority of cases in the duct of Wharton, and only rarely in Stenson’s 
duct. To understand their mode of formation we must unquestionably 
call upon the newer physicochemical investigations regarding calculus 
forming processes in general. According to these, calculi must be con- 
sidered as “ mixed precipitations of colloids and crystalloids” (Schade (60)). 
All the fluids of the body in which calculi form, urine, bile, saliva, etc., 
are colloidal solutions. Precipitation occurs in such liquids, under the 
most diversified conditions, the details of which are unknown to us, but 
broadly, such colloids may be divided into those which are reversibly 
and those which are irreversibly coagulable. As an example of a reversible 
coagulation or precipitation in the human body, Schade mentions the 
uric acid infarcts in the new born, which as is well known, disappear later 
and leave no trace. Actual calculi, gall stones, urinary and salivary stones 
belong to the type of irreversible colloidal precipitates. Schade succeeded 
in imitating such calculus formation in a test tube by adding calcium THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
12 
phosphate, calcium carbonate or triple phosphates to blood plasma. In 
the absence of fibrin, for instance, when blood serum instead of plasma was 
used, the experimental calculus formation did not succeed. It follows 
that an inflammation of the glands or its ducts must be assumed as a 
primary cause of the formation of salivary calculi since fibrin is needed. 
Dal Fabbro (cited by Kroiss) and Kroiss (61) came to the same conclusion 
on other grounds. Inflammations of the kind that lead to the precipita- 
tion of colloids and crystalloids need not necessarily cause a lasting change 
in the gland. Otherwise it would be inexplicable why there is so seldom a 
recurrence when the first stone has been removed (i). Furthermore, not 
every inflammation of the salivary glands leads to the formation of calculi; 
otherwise parotid calculi would be much more frequent than submaxillary, 
and the reverse is the case. Either the inflammation must be of a special 
type, “a calculus forming catarrh” or other factors favoring calculus 
formation in addition to the inflammation must be present. All the 
theories which have been advanced to explain the formation of salivary 
calculi might be mentioned here, such as stenosis of the ducts, chronic 
irritation from pipe smoking (62), entrance of foreign bodies (63), bac- 
teria and so on (see also Kraus (64)), but on the whole, the actual factors 
operating in the salivary glands are known no better than those in the 
kidney. Foreign bodies especially leptothrix threads have been found at 
times, in the center of salivary calculi (65). In such cases, there is a 
general tendency to assume that these foreign bodies or bacteria are the 
direct cause of the calculus formation and that they form a nidus of 
crystallization. A special biological activity of certain bacteria is also 
mentioned as a possibility. Klebs actually calls such leptothrix threads, 
lime-algae, in analogy to those well known to geologists, which form whole 
mountains by precipitating carbonates from solutions of bicarbonates, 
and Galippe found hard concretions the scaffolding of which consisted of 
viable leptothrix threads, in normal saliva which he had kept tightly 
corked for four and a half years. These experiments are, of course, not 
conclusive in illuminating the etiology of these calculi, for a saliva saturated 
with bacteria is certainly not normal after four and a half years. Such a 
decomposition of saliva as occurs in this experiment cannot take place in 
the animal body when the saliva has a free means of outflow; also the fact 
that such concretions in colloidal solutions, preferably form around a 
foreign body as a center, here represented by fungus threads, proves very 
little of the origin of those calculi. This behavior is, however, easily 
explained on physicochemical grounds; precipitates in colloidal solutions 
“on account of the relatively great surface tension at the phase between 
foreign body and solution (here saliva) are accumulated at this border” 
(Schade (60), p. 79). DIGESTIVE ORGANS 
13 
The primary factor, therefore, is always precipitation in a colloidal 
solution, which in its turn is dependent on some form of inflammatory 
process in the gland. Such a foreign body, or bacterium, in the saliva, 
urine or similar fluid, can never be a crystallization center for reasons 
which cannot be further discussed here, but which are well known in 
crystallography. Such salivary calculi produce the so-called salivary 
colic and the “ tumor salivarium.” The latter is a painful swelling of the 
gland and ducts following the flow of saliva which always results during 
eating or even at the appearance of food (see above mentioned psychic 
salivation). Usually the saliva finds its way around the concretion, or it 
may force the stone out of the duct, and spontaneous cure will result. But 
the gland may become permanently enlarged by a stone remaining im- 
pacted for a considerable time; it then becomes indurated and microscopic- 
ally shows considerable connective tissue hyperplasia (66). 
An obstruction of long duration finally leads to complete degeneration 
of the gland. Occasionally, such a complete obstruction of the duct of 
Wharton is congenital, and there is found a cystic tumor in the region 
of the submaxillary gland which corresponds to the dilated ducts. It is 
interesting that this tumor has been observed immediately after birth 
which proves that salivary secretion occurs in intrauterine life (67). 
The results of ligation of the salivary ducts have often been studied 
experimentally with the view of discovering a method of healing salivary 
fistulae in man in a manner similar to that which has long been known 
to veterinarians (68). Such authors as Viborg, Pelschinsky (66), Rolando 
(69), Claisse and Dupre (44), Marzocchi and Bizzozero (69), Langemak 
(66), Kroiss (61) found histologically that ligation of the salivary duct 
produces, first, a dilatation of the ducts, then an hyperplasia of the 
connective tissue, perhaps as a result of venous hyperaemia, and finally, 
necrosis of the parenchyma. Experimentally, this degeneration of 
the gland takes place without particular inflammatory reaction, but in the 
few cases in which the duct was ligated in humans with salivary fistulae, 
severe inflammation resulted (Hirschfeld (70), von Bramann 3 cases) and 
this method had to be abandoned. In these cases the procedure must 
be done of course in pathological and infected tissue. 
TONGUE, ACTIVE DEGLUTITION, AND ESOPHAGUS 
The tongue has three functions; it is the organ of taste, it assists in 
the comminution and propulsion of food, and it is of great importance 
to speech. 
The nerve of taste is the glossopharyngeal which supplies the tongue 
with direct specific taste fibres, especially in the region most sensitive 
to impressions of taste, the base (circumvallate papillae), and indirectly 14 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
by way of the chorda tympani which travels in the same course as thp 
lingual nerve (71). In the last analysis, however, all taste fibres have 
their origin in the trifacial nerve, for this function is completely suspended 
after extirpation of the Gasserian ganglion (72). The tongue receives its 
motor impulses from the hypoglossal nerve, while its sensory fibres are 
supplied through the lingual nerve, and in a very small area, by the supe- 
rior laryngeal nerve. The tongue is the most sensitive part of the oral 
cavity, especially to thermal and mechanical stimulse; parts of the oral 
mucosa, such as the cheeks, perceive changes in temperature to a much 
less degree (73). 
The sense of taste, however, does not depend entirely on the presence 
of the tongue, but as shown in examinations of patients from whom the 
organ was completely extirpated on account of malignancy, other parts 
of the buccal cavity are also supplied with taste receptors. Thiery, 
and later Ehrmann (74), to whom we owe the most accurate investigations 
of tongueless men, found that, although their sense of taste was somewhat 
impaired so that they could not exactly be called “epicures,” they never- 
theless could taste to a certain extent in the soft palate, the palatine arches, 
and also perhaps in the posterior pharyngeal wall. Even at present, we 
do not know of all the points at which taste impressions may be received 
in the digestive apparatus, and there is, according to Thiery, hardly a 
place from the red margin of the lips to the stomach itself which has not 
been at one time or another, considered by physiologists to be involved in 
this function (75). The diminution following partial destruction of the 
glossopharyngeal and the lingual nerves, after extirpation of tumors, for 
example, is naturally more insignificant, and self explained by their 
anatomical distribution (case of Halban (76)). 
While the diminution of taste may be more or less unimportant, the 
loss of another function—speech—may be of much greater import. Even 
an insignificant wound, or a mild inflammatory process on the tongue, 
as well as the more serious lesions of the hypoglossal nerve (77), or the 
hemiatrophy of vertebral caries (78), may cause loss of the distinctness of 
speech. Speech disturbances are naturally greatest when the whole 
tongue is removed, or when both hypoglossal nerves are destroyed (77). 
Observation of the effects of removal of the tongue were made roughly, 
even in the earliest time of human history, when tearing and cutting out 
the tongue were favorite punishments. In our times this mode of punish- 
ment is supposedly still practiced in the interior of Persia. It is generally 
said that these individuals could make themselves understood fairly well, 
even shortly after the injury, but these statements do not have much 
scientific value (79). Thiery and Ehrmann have made accurate examina- 
tions of patients at various intervals after total extirpation of the tongue, DIGESTIVE ORGANS 
15 
to discover the type of sounds which could be produced (see also Schulten 
(80) They found that among the consonants, the lip sounds were nor- 
mal, but those which require the tongue are articulated very poorly 
even a considerable time after the operation. All nasal and friction 
sounds become very indistinct. An explosion-like “P” is produced 
instead of a “K” and a “T.” No distinction is made between “A” 
and “AE” or between “0” “OE” and “E.” The examples described 
by Schulten make it clear that these patients can be understood only 
by those who are accustomed to their speech, and to the alteration in 
their mode of articulating the consonants. 
A slight improvement is noticed if a small thickening of the mucosa 
develops on the floor of the mouth. This is occasionally produced in an 
effort to replace the lost organ (Ehrmann). Kettner’s observation on 
a boy four years old, who, in addition to other malformations (cleft palate, 
etc.), had almost complete absence of the tongue, shows that even with 
a small portion of the root of the tongue, speech is relatively intelligible 
(81) 
Probably in the olden times, a stump remained when the tongue 
was torn out, and with its help these miserable people made themselves 
fairly well understood. Experiences during the war, however, have shown 
that even a small injury of the tongue, such as an adhesion or the loss 
of the tip, leads to considerable disturbance of speech. 
That function of the tongue which is undoubtedly of the most impor- 
tance is its share in the act of deglutition. Swallowing is an extraordinar- 
ily complicated procedure, in which so many muscles take part, that it 
must be viewed as a whole, without undue emphasis on the part played 
by the tongue. Numerous investigators in all countries have busied 
themselves with this problem from ancient times to our own; a multitude 
of single facts and separate observations have been recorded, and still 
it cannot be said that the act of deglutition is understood in all its details. 
Indeed, it has not been sufficiently investigated to satisfy practical surgical 
needs. 
Many authors separate a bucco-pharyngeal phase and an esophago- 
pharyngeal phase of deglutition, although both blend inseparably into 
each other (82). If we follow a bolus of food on its way downward (83) 
we see, as the first preliminary act, a movement of the tongue, beginning 
with the tip, by which it presses firmly against the hard palate, pushing 
the food backward toward the pharynx. This action is by no means 
confined to the muscles of the tongue proper (vertical, longitudinal, 
transverse), but is shared by others which have their origin and insertion 
on the hyoid bone, chiefly by the mylohyoides and hyoglossus (84) and 
also by the geniohyodeus, genioglossus, and indirectly by the thyrohyoideus 16 
TLtE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
which contracts at least a fraction of a second later than the first named 
muscle. This partially explains the difficulties in swallowing after opera- 
tions for goiter, although other factors must be considered. This initial 
movement is important because it gives the bolus an impetus, which alone 
—at least as Kronecker and Meltzer assume—propels it to the cardiac 
opening. Schreiber’s investigations, however, have added an important 
point, viz., that the propulsion of food through the esophagus, is, as a rule, 
assisted by movements of the esophagus itself. Nevertheless, the part 
played by the tongue and the upper muscles of the neck must be valued 
quite highly. Meltzer’s (85) experiments, furthermore, have shown 
that experimental section of the nerve to the mylohyoid muscle is suffi- 
cient to produce considerable disturbance of deglutition, so that the 
animal must throw its head backward to permit food to enter the, pharynx. 
When the bolus has reached the border of the soft palate, the root 
of the tongue presses against the posterior pharyngeal wall while the soft 
palate raises itself, and touches the so-called Passavant cushion (formed 
from the posterior pharyngeal wall), and this closes the pharynx from 
above. Couvelaire (86) studied the movement of the soft palate in a 
patient whose nasopharyngeal spaces were exposed after the removal of 
a carcinoma of the inner canthus. Einthoven has also made similar 
observations on a living patient (cited by Eykmann (87)). 
When the bolus has reached the isthmus of the fauces, lifting of the 
larynx begins. This is of extreme practical importance. The hyoid bone 
places itself close under the* margin of the inferior maxilla, and chiefly 
by the contraction of the thyrohyoid muscle, the thyroid cartilage, and 
with it, the whole larynx, moves closer to the hyoid bone. It may be 
mentioned briefly that simultaneously with the larynx and the trachea, 
all those structures connected to them are lifted. This gives us an impor- 
tant point in the diagnosis of adherent tumors, tuberculous lymph nodes, 
etc. The lifting of the entire larynx upward, and probably somewhat 
forward, is a protection against choking, inasmuch as the subhyoid fat 
cushion presses the epiglottis strongly backward and thereby closes 
the larynx (87). At the same time, probably by a backward bending of 
the upper part of the larynx (from muscle traction and by the root of the 
tongue), the epiglottis forms a roof over the opening into the larynx. 
It is not definitely proved, however, that the glottis is covered completely. 
Observations on operated patients (Eykmann), and particularly the 
India ink experiments of Passavant (88) on man, seem to show that during 
swallowing, the epiglottis lies on the floor of the upper laryngeal cavity. 
The latter painted India ink on the rim of the epiglottis and found, after 
swallowing, imprints on the false vocal cords. The somewhat elementary 
opinion, formerly prevalent, that the epiglottis acts like a lid and is pushed DIGESTIVE ORGANS 
17 
into position by the bolus passing over it, must be abandoned on the 
basis of these later researches. To further ensure closure of the larynx, 
the glottis contracts simultaneously with the mylohoid muscles (at the 
beginning of swallowing), a fact which has been known since Czermak (89) 
and was recently demonstrated again by the animal experiments of Meltzer. 
At the same time, or immediately afterwards, the arytenoid cartilages 
move closer together and bend themselves so strongly downward and 
forward, that they almost touch the anterior wall of the thyroid cartilage. 
A further protection against the entrance of food into the larynx is 
provided by the interruption of breathing during swallowing (90). A 
number of observers assume that the centers of deglutition and of respira- 
tion are in close relation to each other, partly because of the fact that 
dyspnea induces swallowing movements (91) but the conditions are not 
as simple as this, since their observations, for example, water in the stomach 
of the drowned (see also Cahn (91)) can be explained in other ways. 
That all these extraordinarily complicated movements designed for the 
protection of the larynx could be observed when the bolus is in the isthmus 
of the fauces, may be accepted on the ground of numerous single observa- 
tions, and differences of opinion exist only as to whether'the bolus has 
already passed downward at the moment when the epiglottis touches the 
posterior pharyngeal wall. Most authors assume this on the basis of 
simple theoretical considerations, but Schmid and others believe that the 
bolus does not pass the opening of the larynx, but slips laterally into the 
esophagus through the piriform recess. The epiglottis would then adjust 
itself posteriorly before the bolus slips over it, an occurrence which seems 
more probable. This explanation appears plausible, especially from the 
appearance of the upper part of the pharynx from behind (see Spal- 
teholz’s Atlas, first edition, third volume, p. 502) and at the same time 
this would be a good explanation of why needles usually lodge in the 
piriform sinus. With this, the buccopharyngeal phase, the most impor- 
tant in the act in swallowing, is concluded. The bolus slides into the 
opening of the esophagus which has been closed during rest, but is now 
open (92). Before we discuss the next steps, we will consider the func- 
tional impairments which result from surgical interference, and from 
those diseases of the tongue of surgical interest. 
By excision, or paralysis of the tongue, the act of deglutition can be 
very seriously impaired. Such a patient usually throws his head backward 
to enable the food to reach the posterior pharynx (Thiery, Ehrmann). 
Another disturbing factor also comes into play—the food is less well 
chewed and mixed with saliva when the tongue is absent, and there is 
really considerable difficulty in eating larger pieces. When the muscular 
floor of the mouth can be preserved it offers a certain amount of compensa- 18 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
tion, and the cheeks learn to carry on much more extensive movements 
than in normal individuals. It is therefore advisable to preserve both as 
much as possible. When the bolus has reached the posterior pharyngeal 
wall, the patients attempt to bring it past the epiglottis by turning the 
head. This usually succeeds, although in the absence of the base of the 
tongue, the epiglottis cannot be closed normally. The other above 
mentioned mechanism for its closure is, however, still active, so that, 
even after removal of the whole pharyngeal part of the epiglottis, a dog 
can drink without choking, provided it can fake its time and is not 
excited (93), (87). Furthermore, Morgagni (94) describes a man at 
whose autopsy a complete absence of the epiglottis was discovered, 
and Rosenbaum (95) describes a case in which extirpation of the epi- 
glottis caused no disturbance whatever in swallowing. Therefore, it seems 
that in man also, the epiglottis may be completely or partially absent 
without impairment of deglutition (96). The opinion of Schiff that it 
interposes chiefly between the drops falling from the roof of the palate, 
the pharyngeal wall and the larynx, after the actual swallowing, has much 
in its favor. 
There is also considerable disturbance in the bucco-pharyngeal phase 
of swallowing after paralysis of the soft palate (diphtheritic), and in 
defects in this structure, or in the hard palate, when the closure of the 
buccal against the nasal cavity is incomplete. For example, in children, 
with cleft palate, food, especially if fluid, readily flows from the nose. 
Finally, there are paralyses of the pharyngeal musculature which also 
lead to interference with swallowing. These occur, for example, during 
the agony in typhoid fever, in apoplexy, etc., but they have hardly any 
surgical interest, and need not be discussed. The paralyses of the orbic- 
ularis oris muscle in lesions of the facial nerve are worth mentioning, 
because when the lips cannot close, fluids run out of the mouth. This 
is also true in the incomplete closure of the mouth in hare-lip, which as is 
well known, is often accompanied by defects of the palate (cleft palate). 
In this case, food flows from the mouth and nose, and suckling is interfered 
with. The same conditions result from wounds, especially war wounds. 
The most pronounced disturbances, even complete inability to swallow, 
are found in fractures or slight injuries (luxations) of the hyoid bone, 
especially of the great cornua, a fact first pointed out by Valsalva 
(Dysphagia Valsalvae (97)). The importance of this bone in swallowing 
is shown by the fact that after the injury such patients must be fed with 
a stomach tube for some time. The prognosis is very grave (about 50 
per cent, mortality), and not the least reason for this is the impairment of 
swallowing, and the danger of pneumonia from food entering the air 
passages. DIGESTIVE ORGANS 
19 
The results of section of the mylohyoid muscle or of its nerves, have 
already been mentioned. It is more serious if the other muscles belonging 
to this group are also cut, especially the genioglossus, and the geniohyoid. 
When the middle portion of the lower jaw is resected and the genioglossus 
is cut, the base of the tongue sinks backward, partly on account of its 
weight, and partly on account of “spasm” of the antagonists (hyloglossi, 
styloglossi, stylohyoid). It then covers the entrance to the larynx and 
serious danger of asphyxia occurs. Since the geniohyoid and mylohyoid 
will probably also be severed, the hyoid bone loses its support anteriorly, 
and in its turn increases the respiratory difficulty. These conditions have 
been studied experimentally by Szymanowsky (98). Similar observations 
were made in gunshot wounds of the face, and during the war, special 
bandages were constructed to prevent this backward sinking of the tongue 
(99) 
The act of swallowing has been divided into a bucco-pharyngeal and 
a pharyngo-esophageal phase. Naturally such a division, like any other 
in a quickly occurring process, is arbitrary, but it has advantages from 
the practical standpoint. Physiologically, it is more correct to consider 
the movement of the bolus by the tongue to the isthmus of the fauces 
as belonging to the act of mastication. These movements are under 
the control of the will. But the contraction of the constrictors of the 
pharynx, the lifting and roofing of the larynx, the movements 
of the esophagus, etc. are purely reflex, as emphasized by Magendie 
(100) and as such are exposed to numerous disturbances of importance 
surgically. 
Unfortunately, our knowledge of the innervation of the esophagus 
and the pharynx in man is very imperfect, although it has been increased 
by the more general use of local anesthesia. We must still, however, 
rely to a great extent on the facts found by experiment on animals. In 
the sensory part of the reflex arc are involved, the second branch of the 
trigeminal, the glossopharyngeal, the superior, and probably the inferior 
laryngeal nerves. In rabbits, swallowing movements result on touching 
the soft palate (second branch of the trigeminal) (101), while the glosso- 
pharyngeal contains the inhibitory fibres (Kronecker and Meltzer). 
The former also transmits swallowing reflexes in the monkey, while dogs 
and cats swallow when the posterior wall of the pharynx is touched 
(glossopharyngeal). In man, Wassilief could not discover a point on the 
tongue, palate or pharynx, which when touched, would always produce 
swallowing movements. Nevertheless he believes the swallowing reflex 
may be initiated from the sensory region of the pharynx (perhaps the base 
of the tongue). This is supported by the fact that after cocainizing this 
region, swallowing is difficult for about a quarter of an hour. We do not 20 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
know, however, the route by which this impulse is transmitted toward 
the center. Transmission anesthesia might be used successfully in this 
connection, but at present observations regarding inhibitions in swallowing 
after anesthesia of the second branch of the trigeminal have not been 
published, and just as little attention has been given to the glossopharyn- 
geal nerve in relation to these questions (102). Even some time after 
operation for tuberculous glands of the neck, it has been occasionally 
observed that the patients easily choke. In the case of goitres which 
reach far upward it is generally assumed that the superior laryngeal nerve 
is injured (103) but the cases have not been investigated very carefully 
thus far. 
The epiglottis, the third place from which impulses causing deglutition 
might be carried centripetally, is supplied on the sensory side by the supe- 
rior laryngeal nerve. Section in man is done chiefly in tuberculosis of 
the aryepiglottic fold to abolish the pain in swallowing (lit. see Zencker 
(104)). No ill effects have been observed after this operation, but such 
cases are really unsuitable for physiological investigations. The sensory 
tracts of the esophagus run in the recurrent nerve, but there are also 
communications with the spinal ganglia (105). According to Zimmer- 
mann’s investigations (73), the lower portion of the esophagus is insensible 
to touch and electrical stimuli, while in its upper part it reacts to them. 
It is insensitive to pressure and temperature differences, and also to some 
chemicals (alcohol). Other chemicals, such as menthol, are perceived 
by the sensation of cold, approximately'as far as the level of the larynx, 
but not further along the alimentary tract until it is placed immediately 
above the anus (106). The motor nerve of the pharynx and esophagus 
is the vagus, and it carries fibres which cause contraction of the muscula- 
ture, and others which determine muscle tonicity (107). 
In addition to this connection with the brain, the esophagus, similar 
to the whole intestinal tract, has a second center in sympathetic ganglion 
cell groups lying in its wall. The innervation is further complicated by 
the intermingling of the different nerves supplying the various muscle 
regions (108). 
The swallowing center lies in the medulla above the respiratory center, 
therefore the connection between swallowing and respiration. This 
briefly described complex reflex arc can be interrupted in any of its parts. 
We do not know, of course, which separate part of the arc is involved in 
the individual disturbances of swallowing, but this is not surprising 
considering our defective knowledge of these tracts in man, especially in 
the esophagus. Nevertheless some details are known to us. It has been 
mentioned that cocainization of the pharynx results in disturbances of 
deglutition, furthermore, in bulbar paralysis, through destruction of the DIGESTIVE ORGANS 
21 
center, difficulties in swallowing appear. Explanation and location of 
the deglutition disturbances (spasm) in tetanus and in rabies offer con- 
siderable difficulties (109). 
Before we select any of these disturbances for discussion, we must 
first investigate the normal part played by the esophagus during swallow- 
ing. Kronecker and Meltzer (84) by the clever expedient of introducing 
a small balloon into the esophagus to register the movements during 
swallowing, discovered that the food (chiefly semi-fluid and fluid sub- 
stances) was projected by contraction of the mylohyoid muscles like a 
shot to the cardia. This finding was questioned by Schreiber (82), who 
assigned a much greater importance to the movements of the esophagus 
in the transportation of the bolus and who, doubtless incorrectly, denied 
the squirting process completely. As proven by Cannon and Moser (no) 
by means of #-ray observation, fluids can certainly be squirted directly 
from the mouth to the cardia. Solid food is carried downward by the 
musculature, and as Schreiber demonstrated, with differing velocities in 
the cervical and thoracic regions. This may be correlated with the fact 
that the cervical part has cross striated, while the thoracic part has smooth 
musculature. A brief pause in the movement of the bolus occurs at the 
entrance to the esophagus, and at the cardia. 
Meltzer also ascribes a greater importance to the peristalsis of the 
esophagus in the transportation of the food (in). He found, further- 
more, in the dog, the esophagus of which contains only striated muscle, 
that the upper part is more irritable than the lower. This perhaps 
explained the differences in the velocity of propulsion in the several parts 
of the esophagus in this animal. In man, semi-fluids and fluids pass 
downward entirely from their own weight. When artificial nourishment 
is needed after operations in the pharyngeal region, it suffices, therefore, 
to pass a feeding tube through the mouth or nose to the beginning of the 
esophagus (112). Fluids can be poured into it at will without inciting 
the movements of swallowing. A fluid enters the stomach without 
meeting obstruction, since the cardia opens on account of the pressure 
on its walls. Those cases in which an artificial substitute has been made 
are of special surgical interest; Kaznelson (113) among others, describes 
such a case in which a rubber tube reached from the fistula in the neck 
to a fistula in the stomach. The bolus passed easily through this artificial 
passage, which leads Kaznelson to believe that the esophagus can be 
credited with only slight active participation in the transport of food. 
Schreiber investigated a case of Lexer, in which, using Roux’s method, a 
piece of small intestine was introduced under the skin of the chest to the 
thoracic aperture (82). The bolus moved downward very slowly, and was 
always mixed with air. In passing, it might be mentioned that Albert 22 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Wolff (114) observed movements of the axis during swallowing following 
a traumatic injury. 
Great importance has been attached to the so-called narrow places 
in the esophagus in reference to the location of erosions, the lodgement 
of foreign bodies, and the development of malignant tumors (lit. see 
Enderlen (115)). The statements of authors in this connection vary 
greatly. Thus, Sappey describes only one narrow place; Virchow (116) 
and others, three; Mehnert, thirteen, but the old teaching of Virchow 
still has the greatest following. His three narrow places are below the 
lower rim of the cricoid cartilage; about 2 cm. below the bifurcation of the 
trachea; and about 2 cm. above the hiatus esophagi. The accurate 
measurements of Telemann (117) have somewhat altered this teaching. 
According to him, if the esophagus is opened longitudinally and measured, 
no narrow places are found. Those described are to be considered as 
purely functional, occurring partly through unequal contraction of adjacent 
segments (cardia, hiatus esophagi), and partly through pressure from 
surrounding structures (bifurcation, cricoid cartilage). The physiolog- 
ical importance of these places, however, is not touched upon in Tele- 
mann’s work, as we shall see later. 
Of the various parts, the cardia deserves especial attention. Accord- 
ing to Openchowski (118) the centers for its closing are located in the 
posterior parts of the corpora quadrigemina, and in the anterior columns 
of the spinal cord. The fibres from the brain are transmitted chiefly 
through the vagus, and those from the spinal cord mostly through the 
splanchnics; both end in the plexus of Auerbach. The center for opening 
lies chiefly in the anterior inferior portion of the caudate nucleus; its 
fibres also traverse the vagus. Stimulation of the cortex in the region of 
the crucial sulcus also results in opening of the cardia. That the cardia is 
closed during rest can be verified at any time by the esophagoscope (112), 
(119). As the tube approaches, it opens, and the tube can be pushed into 
the stomach without encountering a strong resistance. Similarly, under 
normal conditions, the tonic closure of this muscle relaxes automatically 
when pressure in the lower part of the esophagus reaches a certain degree, 
whether this pressure is brought about by artificial pumping in of air, 
or the pouring in of fluids, or by the act of swallowing (v. Mikulicz). 
This sphincter mechanism is therefore regulated reflexly from the esopha- 
gus. Retzius describes the anatomy of this region as follows: there is no 
annular sphincter (120) but the longitudinal muscle fibres continue into 
the stomach and close the cardia, not by narrowing of the ring, but by 
longitudinal contraction (121). There is thus developed, a sort of valve. 
On the fundus of the stomach, to the left of the esophageal opening, is a 
fold which also acts as a valve, but its size varies within wide limits. DIGESTIVE ORGANS 
23 
Finally, fibres from the diaphragm also help in the closure by encircling 
the esophagus just above its junction with the stomach (122). 
Disturbances in the nervous innervation lead to the symptom complex 
known as cardiospasm. According to the newer investigations of Fleiner 
(123) conducted by the arrays and by stethoscope, the obstruction is not 
due to the cardiac orifice alone, but the musculature of the gastric sinus is 
also involved in forming too narrow a channel for the food to pass (see 
later). This causes the sounds, as heard through the stethoscope, to cover 
an area from 10 to 15 cm. wider than the region of the cardiac orifice. 
On the other hand, the operative results of Heller (124) (longitudinal 
incision of the muscles at the cardia about 3 cm. long), and those of Wen del 
(124) (longitudinal incision 7 cm. long through the whole cardia and 
transverse suture), show it must still be accepted that the circumscribed 
spasm of the cardiac orifice is the most important feature in cardiospasm. 
Congenital and acquired types are differentiated (125). The clinical 
symptoms of each are alike. The patients can swallow food; it does not 
enter the stomach, but remains in the lower part of the esophagus, or in 
the upper part of the stomach after which it is carried upwards by a strangu- 
lation which differs from vomiting by the absence of nausea, among other 
things. The other subjective symptoms, especially pain, differ widely. 
This may be very severe and some patients feel as though something had 
been torn in their chests (126). Probably everyone has experienced an 
uncomfortable sensation from contractions of the esophagus upon a 
closed cardia after eating or drinking hastily. 
The esophagus becomes widely dilated above, and it is usually assumed 
that this is purely passive from the stasis of food. In most cases, how- 
ever, it is more probably due to atony of part of the esophagus coincident 
with the cardiospasm. It was formerly considered as the primary factor 
(Stark (127), Rosenheim (119)) probably because at autopsy, the dilata- 
tion of the esophagus was found (Vormagen, Fleiner (126)) when naturally 
the spasm could no longer be demonstrated. Another fact which seems 
to support a nervous origin is that high grade dilatations such as are seen 
in cardiospasm are seldom met in organic obstructions from strictures or 
from stenosing carcinomata even when located near the cardia (151) 
(Gottstein (119), p. hi). Food can often be forced mechanically through 
the orifice if it is lying at the cardia (128). Kraus (129) found both vagi 
diseased in a case with marked dilatation. Similar cases are described by 
Paltauf and Heyrowsky (130) in which other symptoms due to the 
vagus had been observed clinically. Thus Kaufmann described a case 
in which the pulse rate sank to 40 beats a minute on those days when the 
cardiospasm was especially pronounced, and in which the vagus irritation 
was considerably relieved by atropin (131). 24 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Experimentally, Krehl (132) observed paralysis and dilatation after 
section of the vagus nerves in the neck. When the section is made below 
the hilus of the lungs, no effect is demonstrable either on the cardiac 
orifice or on the esophagus (133), (122). 
On the other hand, the investigations of Kronecker and Meltzer, Schiff, 
A. Bernard, Sinnhuber (134), and others have shown that after section of 
the vagi in the neck, the cardiac orifice goes into a state of contraction 
and remains hardened for days, on account of the independent action of 
the sympathetic ganglion cells lying in its walls. It is only later that it 
becomes paralyzed and dilates, as the studies of Krehl have shown. 
Cardiospasm with secondary dilatation of the esophagus is therefore to be 
considered as a vago-paralytic process (129), or as in the case of Kaufmann- 
Kienbock (131) as a result of vagus irritation. The particular part of 
the nervous system in which these changes have their primary site is 
unknown, but it probably differs in the various individual cases. The 
observations of Goltz (107) who saw a lasting spasm of the esophagus in 
the frog not only after section of both vagi, but also after destruction of 
the medulla oblongata, probably indicate that the affection may also be 
brought about by cerebral conditions. In many cases, it is probably not 
to be expected that gross changes in the nerves will be found, at least 
this thought is supported by the fact that prompt relief can often be 
obtained by a single energetic stretching of the musculature (Gottstein, 
Wilms, and others). In others there is an increased irritability of the 
vagus as a whole (vagotony), in which spasms of parts of the intestines 
are also present (135). In such a case, the cardiospasm must be classed 
as a constitutional disease. 
It should be mentioned in passing, that according to the summaries of 
Widmer, Tilmann, Reich (136) and others, unilateral section of the vagus 
in the neck in man, results, with the exception of permanent injury to the 
recurrent nerve, in nothing but a quickly subsiding acceleration of the 
pulse. Pulling or stretching, i.e., irritations of the vagus, are, however, 
extremely dangerous and have often caused death. This danger may be 
avoided by previous cocainization (137). 
In addition to this combination of flaccid paralysis of the esophagus 
with contraction of the cardia, localized paralyses of isolated parts above 
the cardia are also found. Complete paralyses occur in bulbar-palsy, 
multiple sclerosis, and similar affections of the central nervous system, 
usually, however, in the terminal stage. Gottstein (119) has described a 
post-diphtheritic paresis of the esophagus, i.e., paralysis following disease 
of the peripheral nerves. A weakening of the esophageal musculaturle 
and not a complete paralysis, is spoken of as “atony.” It occurs usualy, 
as a part of a general atony of the entire body and can be diagnosed with DIGESTIVE ORGANS 
25 
certainty only by x-ra,y examination (138). Small quantities of soft food 
are transported very poorly ; they are spread over the walls of the organ 
and remain there for some time. The cause of this atony is as little 
known as the underlying anatomical basis. 
In addition to the dysphagias from paralyses, there is also a spasmodic 
dysphagia in the upper parts of the esophagus (139). The anatomical data, 
briefly sketched above and the findings of Goltz, who observed reflex con- 
tractions of the esophagus in frogs, after irritation of the esophageal wall or of 
the sciatic nerve, are of value in understanding these conditions. Unfor- 
tunately no corresponding investigations seem to have been made in larger 
warm blooded animals. Our clinical experiences, however, especially 
with spasms in inflammations of the esophagus, and in the irritations of 
foreign bodies, etc. support the view that those spasms, particularly in 
the more central parts of the esophagus are reflex processes, incited by 
peripheral irritations of various kinds. The spasms in swallowing 
observed in the hysterical have thus far not been explained very 
adequately. 
[In a consideration of all these processes, i.e., swallowing movements 
of the esophagus, cardiospasm, etc. it must be borne in mind that the vagus 
nerve about which much of these mechanisms center, probably carries in 
man not only motor but also inhibitory fibres. There is great variation 
in the response in different species of animals as well as in the relative 
proportion of smooth to striated muscle. This makes the drawing of 
analogies precarious. Smooth muscle will contain Auerbach’s plexus 
and other local ganglia while in striated muscle they will be absent. The 
inhibitory control of the vagus seems to obtain in primitive types, and as 
Carlson and Luckhardt suggest, if this predominates in a species, cardio- 
spasm could be produced not by “vagotonia” but by vagus “hypotonia.”] 
Spasms at the entrance to the esophagus are of particular importance. 
Killian (92) described a special ring of muscle in that part of the constrictor 
pharyngis (M. fundiformis), which, like the cardia, is said to be closed 
during rest, while the remainder of the esophagus is an open, air filled 
tube (v. Mikulicz (112), Sauerbruch (140). Killian considers that spasms 
at this entrance may be the primary cause of so-called pulsion diverticula 
(141). They often offer great difficulties to the introduction of food. 
These diverticula, also called Zenker’s diverticula (142) are “sac-like 
outpouchings of the posterior or lateral esophageal walls at the junction 
of the pharynx and esophagus, caused, or further developed, by continuous 
pressure from within” (143). Explanation of their development has 
always been difficult. They have been considered as malformations, or 
as related to the branchial clefts, or as indicating an atavistic tendency 
(e.g., the mouth pocket in the pig), but all these theories have very little 26 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
corroborative material in embryological facts (143). For these reasons, 
the old Zenker-v. Ziemssen idea of a purely mechanical origin still has its 
place. “A circumscribed area of the wall of the esophagus loses its 
resistance because of a localized injury to its supporting muscle fibres, 
and gives way from pressure acting from within during swallowing” 
(Zencker, V. Ziemssen (142), p. 58). We actually know from the normal 
anatomy, that there is such a weak place in the posterior wall at the 
esophageo-pharyngeal junction, for Laimer (144) has described a three 
cornered space in which the longitudinal muscle fibres are lacking, and 
it is these latter which, on the whole, are considered the most important 
support for the pharynx and esophagus. 
That this weak place should be bulged by the pressure of a large bolus 
swallowed with particular force, especially when the entrance to the 
esophagus is spasmodically closed, seems rational (this assumption had been 
made by Monro in 1811 (144) and, as additional evidence this place has 
been found to have the least elasticity (143)). But this theory is not 
generally recognized, even though it does explain the causal relations 
fairly well. The lateral diverticulae, especially those situated at the 
entrance to the esophagus, are regarded by many as remnants of branchial 
clefts (145) although in the embryonal life of man, the branchial clefts 
never extend downward this far. Further investigations are necessary in 
this field, especially directed toward discovering whether the diverticulae 
have muscular layers, a point on which v. Bergmann lays special stress, 
and whether there is some lesion in the nerves. It is quite conceivable, 
though not shown thus far, that above the spastically contracted 
esophageal entrance, an atony of individual muscle bundles with 
eventual degeneration of the nerve elements, similar to that occurring in 
cardiospasm, is present. 
There are, however, true congenital diverticula. These are situated 
higher than the Zenker diverticulae, i.e., in the pharynx itself, and are 
derived from an internal incomplete fistula of the neck. 
There are also pulsion diverticuli in other parts of the esophagus, 
situated almost exclusively on the anterior wall, either directly above the 
cardia (epicardial), or above the left bronchus (epibronchial). Some of 
these structures must certainly have originated from traction, and their 
enlargement is due to pressure of the food trapped in them (traction- 
pulsion diverticuli) (Stark). Others may be considered congenital, 
arising during the division of the early common intestino-respiratory tube, 
by the pulling outward of bands of adhesions attached to the esophagus. 
Weak places may also be acquired through inflammatory ulceration, pres- 
sure ulcer, etc. (see later). These have, so far, not been described as a 
cause of pulsion diverticuli in the middle section of the esophagus, but DIGESTIVE ORGANS 
27 
it has been frequently asserted that these diverticuli are often exciting 
causes of spastic spasms of the musculature, another statement without 
definite proof (146). 
Most of those found at autopsy, often accidentally, are traction diver- 
ticuli of the middle and lower esophagus formed by the pull of adherent 
lymph nodes sclerosed by anthracosis and fibrous tissue. These may 
occur without symptoms. They often, however, break through into 
adjacent tissue and lead to very grave clinical conditions, such as medi- 
astinitis, esophageo-tracheal fistulse, etc. In addition to the disturbances 
in the motility of the esophagus, there are also sensory disturbances. 
As the investigations of Zimmermann show, the lower part of the esophagus 
is insensitive to touch and electrical stimuli, while the upper part feels 
them (73). It is sensitive throughout its whole length to pressure and 
temperature, to concentrated alcohol, but not to 1 per cent, hydrochloric 
acid. Anesthesia and hyperesthesia have been repeatedly observed during 
esophagoscopy in hysterical individuals (Gottstein (119)). But more 
accurate examinations of the sensory conditions, such as Rosenheim tried 
to make on his patients, have thus far lead to no results. We do not know 
if the sensitivities of the esophagus suffer in diseases of the central nervous 
system. 
Organic stenosis is less difficult to understand physiologically than 
nervous spasm and dilatation. These stenoses may be divided into 
those due to disease of the esophagus itself, i.e., stricture per se, and those 
caused by pressure from without. This latter condition is sometimes 
observed in strumous patients. The true strictures result chiefly from 
caustics. Their usual situation is at the “three narrow places” described 
above, viz., at the entrance to the esophagus, opposite the bifurcation of 
the trachea, or at the cardia. The latter are often quite extensive, and 
lead to later tubular constrictions which often reach far upward. This is 
explained by the act of normal deglutition described above, as demon- 
strated, particularly by Telemann by his comparison of the deglutition 
curve of Schreiber with Zenker’s corrosion curve (117). The irritation 
of the caustic produces a coincident cardiospasm by which the fluid is held 
for considerable time in the cardia (von Mikulicz (112)). Above the stric- 
ture, an hypertrophy of the musculature develops, with dilatation, the 
latter, however, of not very high grade. This combination of dilatation 
and hypertrophy reaches to the narrowest part of the stricture, as is 
easily understood, so that the change from dilatation to constriction is 
quite sudden. This is the reason that it is often very difficult to introduce 
a bougie from above, while it is easy to find the narrowest place from below. 
In the absence of dilatation, the stricture opens downward gradually like 
a funnel, in which case there is great danger of forcing a false passage 28 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
from above. As von Hacker (147) has shown, perforations at the level 
of the bifurcation occur always on the left side of the wall of the esophagus, 
because at that point it turns to the right. Conversely, a perforation 
above the cardia is usually situated on the right side of the wall, since it 
turns to the left as it passes through the diaphragm. 
Congenital stenosis or complete absence of part of the esophagus can- 
not be discussed here. They are easily explained on embryological 
grounds (148). 
That the esophagus, which is exposed to the most varied kinds of 
thermic, chemical, bacterial, and mechanical irritations is also, at times, 
the seat of inflammation, is not astonishing, but because of the excellent 
protection offered by the lining epithelium, these inflammations are rela- 
tively rare. Surgically, it is important that spasms which lead to dis- 
turbances of deglutition can be incited by catarrhal conditions, difficult 
to explain without esophagoscopy. It is also important to remember that 
during the course of scarlet fever (149), and other infectious diseases deep 
ulcerations may appear, and lead secondarily to strictures. The most 
serious of the diffuse inflammations is a phlegmon, which, except when it 
follows the presence of a foreign body, corresponds to phlegmonous 
gastritis. Its origin is as little understood as the origin of the latter 
condition. 
Circumscribed ulcers are also infrequent. The luetic, actinomycotic 
and the tuberculous types may be mentioned. The latter have recently 
been described. It is not known with any degree of certainty whether 
they are produced by the entrance of tubercle bacilli from the blood, or 
by local invasion (150). They often cause extensive loss of tissue, which, 
however, causes remarkably little discomfort. 
Pressure ulcers form a special group. These also appear by preference 
at the three physiological contractions, where as already stated, the walls 
have the least elasticity. Thus Kermauner (151) has described cases in 
which permanent sounds have caused extensive necrosis at the hiatus, 
bifurcation, and cardia. Such ulcers form during the agonal period, 
especially at the level of the cricoid cartilage, when the larynx sinks 
backward and presses against the spinal column. Pressure necroses 
appear also when tumors or tumor-like growths press on the organ from 
without. The most varied things, such as aneurisms, tuberculous glands, 
varices, etc. have been described. The most dangerous, in this respect, 
are the exostoses of the vertebral column (152). We know, therefore, of a 
great variety of external factors which cause ulceration, but we do not 
know why the necroses occur at these particular points, or why the 
esophagus, with its great elasticity, is attacked at all by pressure ulcers. 
Perhaps investigations of the blood vessel distribution may be helpful. DIGESTIVE ORGANS 
29 
The peptic ulcer is a much debated affection of the esophagus. Even 
in the comprehensive work on the diseases of this organ by Zenker and 
von Ziemssen, their occurrence is disputed. Recently, however, a series 
of about sixteen undoubted cases have been observed and described 
(compiled by Kappis (153)). A number of the patients had, in addition, 
ulcers in the stomach or in the duodenum, which indicates a correlation. 
Regarding the etiology, of which we know very little, it may be worth 
mentioning that islands of gastric mucous membrane were found in the 
esophageal lining in some cases, making it possible that the peptic 
ferment necessary for the formation of the ulcer, came directly from the 
esophagus itself, and not, as in most other cases, from regurgitated gastric 
contents. Vomiting alone cannot, of course, ever be a cause; other addi- 
tional influences of which we know very little in detail are needed (see 
gastric ulcer). Toxic injuries can be excluded, for there is found, as Rost 
has described (154), in the vomiting and injury of the esophagus from 
toxemia (peritonitis), a severe edema, but no ulceration. 
During impairment of the circulation, particularly during the agonal 
period, the digestive action of the vomitus or of the back flowing gastric 
contents through an open cardia, has been held responsible for the develop- 
ment of esophagomalacia, and the quite frequent rupture. 
The present view in this latter, much debated question, is that such a 
softening may actually take place, but only during the agonal period. 
Vomiting may then lead to rupture (Zenker, von Zeimssen (142), Cohn 
(155)), but a spontaneously appearing esophagomalacia such as was sup- 
posed to occasionally occur in healthy persons, has not been observed 
beyond question. Sudden rupture during vomiting must therefore be 
explained on other grounds. According to the compilation of Cohn, this 
condition occurs almost exclusively in middle aged men who are heavy 
drinkers. The rupture as found, is usually a longitudinal tear, and is 
typical of rupture from excessive pressure within. This can be easily 
imitated by closing a rubber tube at one end and attaching the open end to 
a water faucet; when the pressure is turned on, the tube will tear longitu- 
dinally at a given moment (156). In the esophagus, the question resolves 
itself to these points—does the rupture occur because the internal pressure 
becomes too high during the vomiting, or, as has been assumed, from 
kinking or contortion of the organ after pleurisy; or from the presence of a 
strong broncho-esophageal muscle; does a certain muscle segment go into 
spastic contraction, etc. or does it occur under normal pressure in an organ 
with abnormally weak walls? Thinning has often been described, and 
usually follows ulcerative, sclerotic, or arteriosclerotic processes. Brosch 
has measured the strength of the wall of a normal esophagus and found 
that there are considerable differences in the thickness of different seg- 30 
THE PATHOLOGICAL PHYSIOLOGY OE SURGICAL DISEASES 
ments. A thin strip is often found anteriorly in the region of the trachea. 
Furthermore, it is known that the strong musculature of the esophagus can 
slide under the mucosa to a considerable extent. For this reason, 
during esophagotomies, the incised area must be fixed at once with loops 
of thread to keep the edges separated, otherwise the musculature slips 
over the hole in the mucosa (147). It is quite conceivable that an area in 
the esophagus, otherwise normal, can momentarily be made thin through 
such a displacement of the muscularis. Roy (152) describes a case of 
rupture in which an exostosis of the thoracic vertebral column produced a 
demonstrable thinning of the wall. Both possibilities of sudden tearing, 
therefore, are quite conceivable, but it would seem in the case of a transverse 
tear, that the conception of a weak place in the wall is more logical 
(see Cohn’s list), while in a longitudinal tear, in which no microscopical 
changes in the torn place are demonstrable, the logical cause is a suddenly 
increased internal pressure (see Petren and V. Lichtenberg (157)). 
In closing this chapter, attention might be called to a peculiar anomaly 
in the course of the right subclavian artery which leads to a difficulty in 
deglutition, often extremely difficult of differential diagnosis. This 
artery may arise from the left side of the arch of the aorta, and may turn 
to the right between the esophagus and vertebral column, or between the 
esophagus and the trachea, and thereby cause disturbances to the trachea 
or esophagus, or both. Girard and Mouton (158) have recently reported 
two such cases of dysphagia and dyspnea lusoria. 
LITERATURE TO SALIVARY GLANDS AND ESOPHAGUS 
1. Heinecke: Deutsch. Chirurg., 1913, 33. Notnagel’s Handbuch, 16, part x. For 
lit. see Kraus. 
2. Ludwig: Wiener med. Wchschft., i860; 31st Naturforscherversam, 1856; Ztschr. 
f. rat. med., 1851. 
3. Heidenhain: Pfluger’s Archiv., 1872, V. 5, p. 309. 
4. Kohnstamm: Anat. Anzeigen, 1902, 21, 362. 
5. Leriche, R.: Zentblatt f. Chirurg., 1914, No. 41, 754. “Behandlung der perma- 
nenten Parotisfisteln durch die Entnervung der Speicheldruse.” 
6. Tronyl: Zentralbl. f. Chir., 1917, No. 48. 
7. Rost: Lehrbuch der Kriegschirurgie Borchard-Schmieden, 1920, 2 Ed. “Gesicht 
v. Mundhohle.” 
8. Gaultier, R.: “Le syndrome oesophago-salivaire de Roger daus le cancer de 
l’oesophage,” Arch. des. malad. l’appareil digestiv, 1909, Bk. 3, 590-606. 
9. Pawlow: Ergeb. der. Physiol., 1904, 3-1, pp. 177-184. 
10. Brunnacci: Arch, de Fisiol., 8. 
11. Popielski, L.: “Ueber die Gesetze der Speicheldrusentatigkeit,” Pfluger’s Archiv., 
1909, 127, 443. 
12. Jappeli, G.: “ Untersuchungen uber die Speichelabsonderung 2. Speichel- 
varietaten und Einfluss des Reizungsortes auf die physikochemischen Eigen- 
schaften des Unterkieferspeichels,” Ztschr. f. Biol., 1908, 51, 42 and 127. DIGESTIVE ORGANS 
31 
13. Jawein: Wiener med. Presse, 1892, 15. 
14. Jappeli: “Uber die physico-chemischen Bedingungen der Speichelabsonderung,” 
Ztschrf. f. Biol., 1906, 43, 398. 
15. Fleckseder: “Der gemischte speichel des Menschen, sein normales verhalten 
und seine Veranderungen in Krankheiten,” Ztschrft. f. Heilkunde, 1906-27 
(abstr. M. S. 231) (lit.). 
16. Hofbauer, L.: “Tagliche Scbwankungen der Eigenschaften des Speichels,” 
Pfluger’s Archiv., 1897, 65, 503. Chittenden, Richards, Am. J. Physiol., 
1898, 1, 462. 
17. Flo rain, L.: “Essse sur la salive Humaine et sur les proprietes physiologiques 
du sulfocyanate de potassium,” Gaz. med. de Paris, 1899, 7, 6, 3x7. 
18. Sanarelli, G.: Centralblatt f. Bact., 1891, 10, 817. Clairmont, P.: Wiener klin. 
Wchschrft., 1906, p. 1397. 
19. Grawitz, E. and Steffen, W.: “Die Bedeutung des Speichels und Auswurfs fur 
die Biologie einiger Bacterien,” Berlin Klin. Wchsrft., 1894, 31, 419. 
20. Edinger: Deutsche med. Wchscrft., 1895, 381. 
21. Wehrmann, C.: “Contribution a l’etude du venim des serpents,” Annales Past. 
Inst., 1898, 12, 510. 
22. Carriere: Annales Past. Inst., 1899, 435. Carriere, G.: “Due sort de la Toxine 
tetan. introdinte dans le tube digestif des animaux,” Comp. r. soc. Biol., 
1899, 51, 179. 
23. Gottlieb and Sicher: 85th Naturvorscherversammlung, Wien, 1913. 
24. Luciani; Trans, by Frances Welby. Human Physiol., MacMillan, 1913, V. 2, 
p. 158. 
25. Salkowski, E.: “Zur Kenntniss pathologischen Speichels,” Virchow’s Archiv., 
1887, 109, 358. 
26. Biernacki, E.: “Die Bedeutung der Mundverdauung and des Mundspeichels 
fur die Tatigkeit gesunden and Kranken Magens,” Ztschrf. f. Klin. Med., 
1892, 21, 97-H7- 
27. Mayer Gottlieb: Die Experimentelle Pharmacologie, 1910, p. 141. 
28. Schramm: Berliner klin. Wchscrft., 1886, Dec. 
29. Bernard, Claude: Journ. de 1’anat et de la Physiol., 1864, 507. 
30. Maximoro: Zentralb. f. Physiol., 1900, 249. “Die Veranderungen d. Speichel- 
drusen nach durchtrennung der chorda Tympani.” 
31. Langley: J. Physiol., V. 6, p. 71. 
32. Kuttner: Handbuch d. prakt. chir., V. 1, p. 743 and 718. 
33. Rost: Personal observation. 
34. Leube: Festschft. z. 50 j. Bestehend. Wurzburger phys. med. Ges., 1899. 
35. Alexander and Reko: Weiner klin. Wochschft., 1902, 1089. 
36. Zagari: “Policlinico,” 1907, Feb. Cited in Ztrblatt f. inn. Med., 1907, p. 473. 
37. Bunton, A. St.: “Complete suppression of saliva after mumps,” Lancet, 1883, 1, 
1087. 
38. Hemmeter, J. C.: “Die Wirkung der Total extirpation semtlicher Speicheldrusen 
auf die sekretorische des Magens beim Hunde,” Biochem. Ztschft., 1908,11, 238. 
Morano, G. P. and Baccarani, U.: Cited in Zentralbl. f. Chirur., 1902. “Sugli 
effetti dell’asportazione delle glandole parotidi e sotto-mascellari nei coniglio. 
Milano, F. Vallardi, 1901-12. 
39. Mohr.: Ztschft. f. Geb. and Gynak, 1913, 408. 
41. Biedl (Artur): “Die Innere Sekretion,” 3 Ed. Urban and Swarzenberg, 1916. 
“Ihre physiologischen Grundlagen und ihre Bedeutung fur die Pathologie.” 32 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
42. Auchi: Journ. de med. de Bordeaux, 1905, 44. Guerin: Journ. de med. de 
Bordeaux, No. 49, 1905, No. 44, 1908-38. 
43. Wagner: Wiener Klin. Wchschrft., 1904, p. 1414. 
44. Hanau, A.: “ Ueber die Entstehung der eiterigen Entzundung der Speicheldrusen,” 
Ziegler’s Beitrage, 1889, 4, 48, p. 7. Nicol: “Ueber genuine eitrige Parotitis,” 
Ziegler’s Beitrage, 1912, 54, p. 385. Muller: Inaug. Diss. Halle, 1883, p. 26. 
Claisse, P. and Dupre, E.: “Les infectious salivaires,” Arch. de. med. exp., 
1894, 6, 41 and 250. Dittrich, P.: “Uber einen Fall von eiteriger Parotitis und 
deren etwaigen Zusammenhang mit ausseren verletzungen,” (Prag.) Ztschrft. f. 
Heilkunde, 1891, 12, 269-280. Wendt, E. C.: “A contribution to pathological 
histology of acute parotitis,” N. Y. Med. Journ., 1880, 32, 248. Virchow: 
Alte Charite Annales., 1858-8, 3rd. half. 
45. Sabrazes, J. and Faguet, C.: “Infection puerperale staphylococcigul, pelva peri- 
tonitie, endocardite, ulcers-vegetante, parotidite suppuree d’origine embolique,” 
Gaz. des Hop., 1894, 67, 1039, 41. 
46. Rost, F.: “ Experimented Untersuchungen uber eitrige Parotitis,” Deutsch. 
Ztsch. f. Chir., 1914, 130, 305. 
47. Orth: Lehr. d. spez. path. Anat., 1889, 2, 64. Orth: Nachr. v. d. kgl. Ges. d. 
Wissensch, Gottingen, 1895, p. 19. 
48. Hellendahl: Med. klin., 1908, 452. Moricke: Ztschft. f. geb. u. Gynak., 1880, 5, 
348. Ruttermann: Inaug. Diss. Berlin., 1893. Bumm: “Uber parotitis nach 
Ovariotomie,” Munch. Med. Wchsft., 1887, 36, 173. 
49. Levy, R.: “Discussion on post. op. parotitis,” Berlin, klin. Wchscrft., 191-2,49-1, 
765- 
50. Herb, E.: “The combination of these diseases has also been shown experimentally 
by Herb,” Zentralblatt f. innere Med., 1900. 
51. Billroth. Cited in Wagner (43). 
52. Mohr: Versam. des deutsch. Ges. f. Gyn. Halle, 1913. Krapp: Phila. Med. 
Times, 1879. 
53. Hallendahl: Med. kliniks., 1908, 452. 
54. Schottmuller: “Parotitis epidemica,” Notnagel’s spez. Path. u. Therap., 1904, 3, 
P- 37- 
55. Gaultier: Archiv. des. malad. l’appar. digestiv., 1910. 
56. Parolon: Pfluger’s Archiv., 1878, 12, 272. 
57. Berth: “Uber parotitis nach gynak. operation,” Inaug. Diss. Greifswald, 1886. 
58. Buttermann: “Parotitis nach Ovariotomy,” Inaug. Diss. Berlin, 1893. 
59. Narath: Deutsch. Ztschr. f. Chirur., 19x2, 119, 201. 
60. Schade: Munch, med. Wchnsft., 1909, 142 and Med. klinik., 1911, 565. 
61. Kroiss: Bruns Beitrage, 1905, 47, 470. 
62. Haurrel: Wiener klin. Wchnsft., 1900, 163. 
63. Auerbach: Jahrbuch f. Kinderheilkunde, 1910, 22, 213. 
64. Krauss: Nothnagel’s Handbuch, 16, 1 part xst. half. 
65. Galippe: Compt. rend de seanc. de l’acad., 1893, No. 19. Klebs: Archiv. f. exp. 
Path., 1876, 5, 350 and 365. Alexandre: Rev. de Chir., 1906, 1, 732. 
66. Langemak: Virchow’s Archiv., 1904, 175, 299. 
67. Sultan: Deutsche Ztschrft. f. Chir., 1898, 48, 133. 
68. Viborg: Virchow’s Archiv., 1904, 175, 299. 
69. Marzocchi and Bizzozero: Centrlbl. f. Chirurg., 1903, 1295. Rolando: Zentral- 
blatt f. Chir., 1899, 985. 
70. Hirschfeld: Inaug. Dissert., Berlin, 1889-1890. DIGESTIVE ORGANS 
33 
71. See Corning: “Topographical Anatomy, 1911, 3rd edition. 
72. Bircher: Deutsch. Ztschft. f. Chir., V. 109. 
73. Zimmermann: Mitt. a. d. Grenzgebiet., 1909, 20, 454. 
74. Ehrmann: “Funktionsstorungen an Geschmacksin Sprache, und Schluck- 
bewegungen nach Totalextirpation der Zunge,” Bruns Beitrage, 1894, n, 595. 
Thiery: “Untersuchungen uber d. Geschmachsempfindungen usw. eines 
Zungenlosen,” Arch. f. klin. Chir., 1885, 32, 4x4. 
75. See also Giesoro and Hahn: “Ueber Geschmacksempfindungen im Kehlkoff,” 
Ztschr. f. Physiol, and Psychol, d. Sinnessogane, 1902, 27. 
76. Halban: “Zur Physiol, d. Zungennerven,” Wien. klin. Rundschau, 1896, No. 4. 
77. Deutsch. Chir., 34, No. 132. 
78. Ranzier: Montpellier med., 19x3, V. 36. 
79. Bronadel: Anftales d’Hygien, 1904, refer, to Zentralblt. f. Chir., 1904, p. 1167. 
80. Shulten: Deutsch. Ztschrft. f. Chir., 1893, 35, 417. 
81. See Zentralbl. f. Chir., 1907, p. 193. Also Weil in Maschkas; Handbuch d. 
Gerichtlichen Medizin, 1881, V. 1, p. 258, who observed a patient operated by 
Billroth for carcinoma of the tongue. He could articulate fluently even though 
but a small part of the tongue had been left remaining. 
82. Schreiber: “Ueber den Schluckmechanismus,” Arch. f. exp. Path. u. Pharm., 1901, 
46, 446; also Arch. f. exp. Path. u. Pharm., 1911, 67, 72; Grenzgebiet, W 24, 
P- 35- 
83. Scheier: “Zur Verwertung der Rontgenstrahlen f. d. Physiol, des Schluckactes,” 
Fortschrit auf. d. Gebiet d. Rontgenstrahlen, 1911-12, 18, 377. 
84. Kronecker and Meltzer: “Der Schluckmechanismus, seine Erregung und Hem- 
mung,” Arch. f. Anat. u. Physiol., 1882-1883, suppl., p. 328. 
85. Meltzer: Arch. f. Anat. u. Physiol., 1880, p. 296. 
86. Couvelaire: “Sur le rote du voile du palais pendant la deglutition, etc.,” Journ. 
de Physiol., 2, p. 280. 
87. Eykmann: “ Sitzungsbericht Akad Wissenschaft,” Wien. klin. part 3, 1891. 
88. Passavant: Virchow’s Arch., 104, p. 444. 
89. Czermak: Collected Writings, V. 6, p. 2. 
90. Marckwald: Ztschrft. f. Biol., N. F., 1889, V. 7. 
91. Schwartz, Cahn, Ducchesi: Zentralbl. f. Physiol., 1905, 19, 995. 
92. Killian: Munch. Med. Wchschrft., 1907 and 1908, No. 34. 
93. Magendie Longet: “Lecons sur la physiologie de la digestion, 1868, 13th lesson. 
94. Morgagni: “De sedibus et caus morborum,” 1761, Book 3, No. 13, Venedig. 
95. Rosenbaum: Arch. f. klin. Chir., 1894, 49, 773. 
96. Schmidt: “Die Krankheiten des oberen Luftwege,” 1894, p. 44. 
97. Albert: Lehrbuch d. Chirurgie, 1881, V. 1, p. 425. 
98. Szymanowsky: Cited by Konig in Lehrb. d. Chirurg. 2 ed., 1878, p. 304. 
99. Rost: Gesicht u. Mundverletzungen in Borchard-Schmieden Lehrbuch d. Kriegs- 
chirurgie, 2nd edition. 
100. Magendie, cited in Luciani: Human Physiol., V. 11, p. 143. 
101. Kahn: Arch. f. Anat. u. Physiol., 1903, p. 386. 
102. Hirschel: Munch, med. Wchschrft., 1912, 2. 
103. v. Eiselberg: In Handbuch d. prakt. Chir., 4th ed., 1913, V. 2, p. 386. 
104. Zencker: Munch, med. Wchschrft., 1919, p. 1167. 
105. Luscher: Ztschrft. f. Biol., 1897, V. 35. de Witt: Journ. of comp. Neurol., 1900. 
10, 382. 
106. Schwenkenbecher: Munch. Med. Wchschrft., 1908, No. 28. 34 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
107. Goltz: Pfluger’s Arch., 1872, V. 6, 616. 
108. Kahn: Arch. f. Anat. u. Physiol., igo6, p. 355. 
109. Rose: Deutsch. Chir., V. 8. 
no. Cannon and Moser: Am. J. Physiol., 1898, 1, 435. 
in. Meltzer: Zentralbl. f. Physiol., 1907, 21, 94 and 70. 
112. v. Mikulicz: Mitt, aus d. Grenzgebiet, 1903, 12, 509. 
113. Kaznelson: Pfluger’s Archiv., 1907, 118, 327. 
114. Wolff, A.: Berlin, klin. Wchschft., 1918, p. 422. 
115. v.Hacker: Handbuchd. Chirurg.,4thed., V. 2,p. 13. Lit. see Enderlen:Deutsch. 
Ztschrft. f. Chir., V. 61. 
116. Virchow: Virchow’s Arch., 1883, V. 2. 
117. Telemann: Dissert. Konigsberg, 1906. 
118. v. Openchowski: Arch. f. Anat. u. Physiol., 1889, p. 551. 
119. Gottstein: Mitt. aus. d. Grenzgebiet, 1899-1901, V. 6 and 8. Rosenheim: 
Deutsch. Med. Wchscrft., 1895, No. 45. 
120. Retzius: Cited by Fleiner Naturhist. med. Verein Heidelberg, 1919. 
121. Kelling: Arch. f. klin. Chir., V. 64, p. 402. 
122. Sauerbruch and Haecker: Deutsch. med. Wchschrft., 1906, No. 31. 
123. Fleiner: Munch, med. Wchschrft., 1919. 
124. Heller: Mitt. a.d. Grenzgebiet, V. 27. Wendel: Verh. d. Deutsch. Ges f. Chir.,' 
1910. 
125. Fleiner: Munch, med. Wchschrft., 1910; p. 982. 
126. Fleiner: Munch, med. Wchschrft., 1900. 
127. Stark: “Die diffuse Erweiterung der Speiserohre,” Deutsch. Praxis, 1903, 
Munchen. 
128. Obemdorffer: See Munch, med. Wchscft., 1911, p. 1988. Dietler: Ztschrft. f. 
Rontgenkunde, 1912, 14, No. 9. 
129. Kraus: Festschr. f. Leyden, 1902, V. 1. 
130. Heyrowsky: Wien. klin. Wchschrft., 1912. Paltauf: Wien. klin. Wchschrft., 
1908. 
131. Kaufmann: Wien. klin. Wchschrft., 1908 and 1909. 
132. Krehl: Arch. f. Anat. u. Physiol., 1892, suppl. p. 278. 
133. Stark: Munch, med. Wchschrft., 1904. 
134. Sinnhuber: Ztschrft. f. klin. Med., V. 50. Bernard, A.: Cited by Kraus. 
135. Neugebauer: Wien. klin. Wchschrft., 1914. Wilms: Deutsch. Ztschrft. f. Chir., 
V. 144. 
136. Reich: Brun’s Beitrage, V. 56. Widmer: Deutsch. Ztschrft. f. Chirurg.. V. 36. 
Tillmann: Deutsch. Ztschrft. f. Chir., V. 48. 
137. Heller and Weiss: Ztschrft. f. d. ges. exp. Med., V. 2. 
138. Holzknecht and Olbert: Ztschrft. f. klin. med., V. 71, p. 91. 
139. Hofmann, F.: “De Morbis oesophagi spasmodicis opera omnia,” Edit. Geneva, 
p. 130. Cited by Zenker and Ziemssen. 
140. Sauerbruch, Bruns Beitrage, V. 46, p. 423. 
141. Beck: Naturhist. med. Verein. Heidelberg, 1917. 
142. v. Ziemssen’s Handbuch, V. 7, 1st. appendix. 
143. Stark: “Die Divertikel der Speiserohre,” Leipzig, 1900, p. 45. 
144. Laimer, Monro: “The morbid anatomy of the human gullet, etc.,” Edinburgh, 
1911, p. 12. 
145. v. Bergmann: Munch, med. Wchschrft., 1890, p. 819 (Virchow’s discussion). 
146. Jacobs: Deutsch. med. Wchschrft., 1912, p. 997. DIGESTIVE ORGANS 
35 
147- v. Hacker: Handbuch d. prakt. Chirurg., 4th ed., V. 2, p. 513. 
148. Guiscz: Soc. des Chir., Paris, Nov. 18, 1910. 148. Kreuter: “Die angeborenen 
Verengerungen und Verschliessungen des Darmkanals, etc.” Leipzig, 1903. 
149. Frankel: Virchow’s Arch., 1902, 167, 92. 
150. Kummell: Munch, med. Wchschrft., 1906, p. 453. 
151. Kermauner: Wien. klin. Wchschrft., 1898, p. 974. 
152. Heinlein: Munch, med. Wchschrft., 1911, p. 436. 
152. Roy: Lancet, 1911, p. 1765. 
153. Kappis: Mitt. a. d. Grenzgebiet, 19x0, 21, 746. 
154. Rost: Deutsch. med. Wchschrft., 1912, No. 36. 
155. Cohn: Mitt. a. d. Grenzgebiet, 1908, 18, 295. 
156. Brosch: Virchow’s Arch., 1900, 162, 114. 
157. v. Lichtenberg: Naturh. med. Verein., Heidelberg, 1907; also Munch, med. 
Wchschrft., 1907. Petren: Brun’s Beitrage, 1909, 61, 265. (Lit. from Scandi- 
navia.) 
158. Girard: Chirurg. Kongres, 1913. Mouton: Brun’s Beitrage, 1919, V. 115. CHAPTER II 
STOMACH 
The advent and subsequent general use of the :r-rays and fluoroscopy 
have made possible a far more thorough and precise study of the form 
and movements of the stomach than the older methods of investigation 
used in experiments on animals which necessarily perverted the physiology. 
Pathologically, a whole series of new disease pictures have been discovered, 
and new symptoms added to known diseases. Many of these local 
diseases are not only curable, but their treatment often brings about 
considerable improvement of the general body health. 
From the surgical standpoint, greater emphasis must be laid on investi- 
gations of the motor function of the stomach, than on its secretory activi- 
ties, although both are very closely related. In examinations of the 
former with bismuth meals, the objections have often been raised that 
they are unphysiological, and give artificial results (Stiller). But experi- 
ments of Best and Cohnheim (i) have shown that the objections are 
groundless, except in the instance when bismuth is given with meat in 
dogs with fistulge. In this case, evacuation shows later than it really 
occurs, and is due, in all probability, to digestive liquefaction of the meat 
and a consequent quicker evacuation of the food than of the bismuth. 
This latter substance, itself, causes slight retention of food both in the 
stomach and the intestine, so that barium sulphate is to be preferred, 
since it is free from this objection. However this may be, it is necessary 
before proceeding further, to make certain that the form and movements 
of the stomach are not altered by bismuth but are shown in their true 
physiological relations. A number of procedures have been employed to 
demonstrate this very important point, and the instructive one of Grodel 
and Seyberth may be mentioned (2). They sewed silver beads to the 
greater and lesser curvatures of the stomachs of dogs, and took #-ray 
pictures with and without bismuth meals. In both cases the shape and 
movements of the stomach were identical. 
When x-r&y work was in its earliest stage, it was not very certain to 
anatomists that the stomach had a “fish hook ” shape (Rieder), or the 
shape of a cow’s horn (Holzknecht), as shown in the roentgenograms, but 
they soon satisfied themselves of the truth of the pictures. Among other 
methods, the organs of executed criminals were fixed very quickly after 
death by the intravenous injection of formalin, and then it was discovered 
36 STOMACH 
37 
that the shape of the stomach was the same as that shown by x-ray 
methods in the living (His, Simmonds, (3)). As a matter of fact, this 
procedure had been done some time earlier, and a few surgeons and anat- 
omists had a fairly clear knowledge of the shape of this organ, but only 
with the increasing use of the x-rays has this knowledge become general 
(4) According to the newest investigations, the cow’s horn shape of 
Holzknecht must be regarded as the physiological one. Even the siphon 
form is a sign of visceroptosis, although it is seen in so many individuals 
that, without further findings, it cannot be considered pathological, 
especially since the evacuation time in this type may be quite normal 
(5) Further important details of its shape may be summed up as follows: 
the empty stomach is a pouch with many folds, whose walls lie, ribbon 
like, in contact (6). The plaster model of His shows beautifully that the 
greater curvature is forward when the arcuate fibres contract, so that 
the anterior surface of the stomach faces superiorly. The pylorus then 
points backward, and is covered in part by the greater curvature (7). 
Functionally, three divisions of the stomach must be recognized, 
the cardiac portion, the pyloric antrum, and the pylorus itself. [It is 
perhaps even more convenient and certainly better for purposes of 
thought to further subdivide the stomach, as done by Cannon. Accord- 
ingly, the cardiac portion is subdivided by a line drawn horizontally 
through the cardia. Above the line is the fundus, below and to the 
incisura angularis is the body. The pyloric portion is also divided into 
the pyloric vestibule and the pyloric canal (8).] The cardiac end is the 
largest part, and represents, so to speak, a store room; while the antrum 
is the motor portion for the transport of its contents (9). There is, of 
course, no sharp anatomical boundary between these two divisions, but in 
man, as well as in dogs (10), a deep annular indentation can be observed, 
which is constant in position and is formed by a pulling in of the greater 
and lesser curvatures. This represents, so to speak, a functional sphincter 
(n). These contractures at various places of the stomach have excited 
considerable interest of late, chiefly from the investigations of Aschoff (9). 
Anatomically, the “narrow passes” as he calls them, are formed from 
contractions of the musculature and from folds in the mucous membrane 
(12). The more detailed architecture of the musculature and its relation 
to the shape are discussed by Forssel (13). 
Interesting details of the nature of gastric peristalsis have been given, 
especially by Schwartz (14). It seems that the form of a contraction wave 
depends on the thickness of the musculature. In a stomach with thick 
walls the contraction wave is short and deep; conversely, in a stomach 
with thin walls it is long and shallow. But according to the studies of A. 
Muller (15), the number of layers of a stomach varies; separate muscle 38 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
bundles may lie above or below each other, depending on the state of tonus 
of the wall at the particular time. In general, the muscle increases in 
strength towards the pylorus. The contraction waves therefore become 
deeper as they approach this part. Since the lumen decreases at the same 
time, the opposite walls of the antrum finally touch during a strong con- 
traction and there results a trapping of the food mass by the action of the 
so-called “sphincter antri.” Such trapping occurs in other parts of the 
stomach under pathological conditions (12). We assume from the mode 
of formation of this “sphincter” that it does not always appear at the 
identical anatomic place, but always approximately there, and that, as 
Kastle, Rieder, and Rosenthal emphasize (16), it constantly relaxes and 
reforms as peristaltic waves progress from the fundus along the greater 
and lesser curvatures. 
The fasting stomach is a lumenless, closed pouch, and when food enters, 
it expands, not so much by the weight of the food, as by the action of 
a nervous mechanism in the stomach itself. The recognition of this 
active unfolding is of great importance in understanding many physiolog- 
ical and pathological conditions. Why, for instance, does food which does 
not tempt the palate like some favorite dish, satisfy so quickly? Fleiner’s 
(12) (p. 113) explanation is that complete unfolding does not take place; he 
calls it quite apropos, “defense reflex,” and quotes a number of correlated 
examples occurring in various gastric diseases (17). The expansion 
of the stomach is also dependent on the consistency of the food, for in the 
case of solids, it remains in the highest part of the fundus for some minutes, 
and then, slowly and wedge-like, pushes downward, gradually overcoming 
the tonus of the musculature (18). Several minutes are necessary after 
the last bolus has been swallowed for the chyme to reach the most depend- 
ent part. Fluids, however, flow downward very quickly, like a rivulet, 
and only expand the stomach laterally when they have reached the lowest 
level. They are said to flow along a gutter on the lesser curvature when 
the stomach is filled with solid food (sulcus gastricus) and to quickly 
reach the pylorus without diluting the contents at all (19). The fact 
that the erosions are usually found along the lesser curvature in cases in 
which caustics are swallowed after a heavy meal, is supposedly dependent 
on this distribution. According to Kastle (20), however, this gutter 
cannot be demonstrated by the x-ray, and Schuller (21) questions its 
presence in man. 
Generally speaking, the movements of the fundus and antrum are dis- 
tinctly different. Those of the former are chiefly of the nature of tonic 
contractions; kneading and mixing does not take place here but the food 
simply accumulates in layers as it is swallowed and the masses which 
enter last, lodge in the center of the food bulk (22). Liquefaction STOMACH 
39 
proceeds at the surfaces and as the food is digested it is forced toward the 
pylorus by peristaltic waves which show roentgenologically, as shallow 
segmentations of the curvatures (23). Finally, the food is pressed into 
the actual motor segment, the antrum. Here, the movements are very 
powerful and consist of rythmic contractions and relaxations. As demon- 
strated in the studies of Ducchesi (24) there is an actual “systole and 
diastole.” They are therefore mixing and propulsive, and succeed 
each other with amazing regularity. Cannon (23) who introduced 
the a;-ray method in the study of digestion, states that in cats, they occur 
at the rate of six per minute, and can be observed in action with machine 
like regularity for over seven hours. In man, according to Holzknecht,. 
the contractions occur about every 22 seconds. Kastle (20), (11), however, 
with his co-workers, has made kinematographic studies of these move- 
ments and states that such a division of the stomach into antrum and 
fundus is not possible as far as the gastric movements are concerned. 
The stimuli which excite gastric motiity are first, mechanical; and 
second, chemical. The empty stomach is usually quiescent, but every 
hour and a half to two hours and a half, there is activity of the entire gas- 
trointestinal tract, lasting about 10 minutes, and directed towards moving 
the contents forward. This was first observed by Pawlow and Boldireff 
(25), who also found that the digestive glands secrete during this period. 
Very slight mechanical stimulation is sufficient to initiate movements (24) 
even touching with a bougie, but the temperature of the food seems to 
have little influence, particularly on the rate of evacuation (Egau (26)). 
Of chemical stimulants, hydrochloric acid and pepsin, both physiological 
products of gastric glands, are by far the most active. 
[But the increasing amounts of digestive products, probably after 
absorption, are also a potent stimulus. As Ducchesi points out, gastric 
movements are initiated by the entrance of food, further stimulus is 
provided by the secretions, particularly the acid, and the final one by 
the digestive products themselves.] 
It is interesting to observe that hydrochloric acid seems to act an- 
tagonistically in the fundus and antrum; it increases the peristalsis of the 
former and diminishes that of the latter, and in high concentration, may 
not only completely inhibit the movements of the antrum, but actually 
incite anti-peristaltic waves (Ducchesi (24)). 
[In other words, the excitability of the neuromuscular apparatus 
varies not only quantitatively but also qualitatively in the several parts 
and is almost antagonistic in the region of the antrum as compared to other 
parts of the stomach (Ducchesi).] 
The third functionally distinct part is the pylorus. It is open in 
the fasting stomach and .v-ray studies have shown that when food first 40 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
enters, it can be pushed through into the duodenum by pressure 
applied to the abdominal walls (5). The movements of the pylorus, which 
in opening and closing are directed toward the bowel, are regulated min- 
utely by reflexes arising in the mucosa of the stomach and duodenum 
(27), (19). If, for example, in a dog with a duodenal fistula, the ileum is 
empty, the antrum during each contraction projects a stream of chyme, 
at first well digested, later imperfectly so, through the fistula (28). But 
if the material escaping is now injected into the duodenum, distal to the 
opening, the pylorus closes, and remains contracted until the acidity of 
the injected material is neutralized by the alkaline intestinal secretions 
(Tobler). Thus the pylorus closes when acid is brought into contact with 
the duodenal mucosa, and the same phenomenon occurs with fat. It also 
closes when solutions of a strength other than isotonic are introduced into 
the stomach (29); when the temperature of ingested substances differs 
considerably from that of the stomach (30), and when painful stimuli of 
all sorts are present (9). 
[The acid control of the pylorus has undoubtedly been overempha- 
sized. Cannon, who elaborated this theory, early recognized its inade- 
quacy in the explanation of many of the facts observed in the emptying 
of the stomach, notably in the emptying of fluids. Recent experimental 
work on man and animals, using various methods, have correlated the 
opening and closure of the pylorus with the movements of the stomach 
itself. Thus under normal conditions the human pylorus opens regularly 
at the end or height of each tonus contraction. To use the expression of 
Cole, during the systole of each gastric cycle the pylorus opens and allows 
a small stream to be forced through. During diastole the pylorus may be 
closed, and Cole believes, this prevents the chyme from dropping back into 
the stomach as the intragastric pressure diminishes. Furthermore, since 
it is the so-called “duodenal cap” which is filled when the stomach con- 
tents leave the pylorus, particular interest, especially from roentgeno- 
graphic studies, is attached to this portion of the duodenum. Numerous 
considerations lead to the conclusion that it should be classed with the 
stomach and not the intestines. It seems that further work is necessary to 
determine the factors which influence the emptying of this cap. Prob- 
ably the state of fullness of the small intestine is a very important factor, 
but the reaction, or the fluidity of the contents of the cap may also play 
their parts. These questions are of extreme importance in a consideration 
of duodenal ulcers, the great majority of which occur in the first portion 
of that organ. Luckhardt, Phillip and Carlson (31), for example, found 
in their experiments that the intragastric contents as they issued from a 
duodenal fistula were acid to phenolphthalein, although they rarely 
showed free acid to other indicators (32)]. STOMACH 
41 
The secretory function of the stomach is of somewhat less interest to 
the surgeon than the motor, and even though the former has been much 
more extensively studied, it is not the better understood division of gastric 
physiology (33). The gastric juice is supplied chiefly by the fundus, where 
the long tubular glands are crowded closely together and consist, as we 
know from Heidenhain’s time, of the chief and the parietal cells. The 
former are said to secrete pepsin, the latter, hydrochloric acid, but this has, 
as yet, not been proved beyond doubt. The gastric juice furthermore 
contains a lipase (34), a lab ferment, many inorganic salts, a nucleoprotein, 
whose import is not clear, and mucus. 
The function of these glands has been studied successfully only 
since Pawlow (35) devised methods in his classic experiments, for con- 
structing miniature stomachs and for utilizing stomach and duodenal 
fistulae (Tobler (27), Cohnheim (9), and others). We know now that the 
secretion of gastric juice is essentially a reflex process and may be initiated 
not only from the mouth by chewing and swallowing, but even the desire 
to eat, leads to secretion. It can probably also be regulated from the 
duodenum, for Cohnheim and Marchand (36) found that the introduc- 
tion of hydrochloric acid into that organ was followed by a diminution of 
hydrochloric acid production in the stomach. Conversely, soaps in the 
duodenum arising from fats, lead to an increased secretion of acid. This 
latter fact has a certain significance, as we shall see later, in the secretion 
of gastric juice after cholecystectomy. Thirdly, the activities of the 
glands of the fundus are stimulated from the antrum, it is said, by means of 
a hormone (37) which is formed when digestive products are absorbed 
from the mucosa of that part of the stomach. That this is probable may 
be concluded from the observation, among others, that after atropin is 
given, the nervously controlled gastric secretion is inhibited, but abundant 
secretion can be elicited from stimuli arising from the antrum (38). 
Nor should the importance of the intragastric ganglia to secretion be 
underestimated, for the stomach will continue to secrete, even when all 
the extrinsic nerves have been severed (39). In this case it is possible that 
certain chemical substances, after absorption, are carried to the intrinsic 
nervous mechanism and thus activate the glands without the cooperation 
of the extrinsic nerves (see Babkin (33)). 
The gastric glands secrete a juice which is often qualitatively and 
quantitatively quite different under the influence of these different 
stimuli. This extraordinary sensitiveness can be seen from Pawlow’s 
investigations, in which the juice secreted varied considerably with the 
type of food ingested. Thus with bread, meat, milk, etc. an entirely differ- 
ent composition was found. Warming the food has a decided effect, so 
that temperature is also a further factor. Since much of our knowledge 42 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
of these processes has been gained from animals, great importance is 
attached to the studies on man, which show that the animal results in 
general can be applied directly to human physiology (40). 
The gastric juice, like other digestive fluids, when first secreted con- 
tains its enzymes in a form inactive for digestion. The name given to 
these pre-enzymes is zymogen, and there are usually special substances 
which are best adapted to activate them. In the case of pepsin, it is the 
hydrochloric acid. This enzyme is the principal one of the gastric juice 
and therefore in the stomach it is the protein of the food which is attacked, 
since the activity of pepsin is applied to these substances. Cleavage is 
carried to albumoses or proteoses (41). 
Carbohydrates are not attacked, but on the contrary, the ptyalin of the 
saliva is destroyed. Since, however, the food masses are deposited in the 
center of the stomach and do not at first come in contact with gastric 
juice (22), carbohydrate digestion may progress from admixed saliva for 
some time. An actual digestion of fat does not occur in the stomach, it is 
only liquefied there. Rennin has great physiological importance during 
the suckling period. It coagulates milk by precipitation of the casein and 
renders it more freely digestible. [The question of the identity of rennin 
and pepsin is often in controversy. There seem to be more facts in favor 
of their separate identities, but more investigation is needed to decide the 
matter conclusively. There are also assertions that fat may be digested 
in the stomach. These need corroboration.] 
The question of absorption from the stomach, particularly of proteins, 
has been generally answered in the affirmative, mainly from Tobler’s 
(27) investigations. Recently, however, a paper has appeared by Tsche- 
kunow (41) which is worthy of exceptional notice. According to his 
work, no absorption whatever of proteins takes place in the stomach, and 
Tobler’s findings must be considered due to experimental errors. Tsche- 
kunow’s work was done so carefully, that we must conclude not only that 
absorption does not take place but is actually improbable. 
The ability of the stomach to absorb water is a particularly important 
question for surgeons. Under ordinary conditions, the amount absorbed 
is negligible. The process begins first in the ileum, therefore, in pyloric 
stenosis, the patients often become desiccated. [Other substances such as 
glucose and alcohol are absorbed with a fair degree of facility, and prob- 
ably also hydrolyzed protein. These absorbed products go to make gastrin, 
the hormone which stimulates secretion after the psychic flow ceases.] 
The normal physiology of the gastro-intestinal tract of the suckling 
infant may be found,discussed by Uffenheimer (42). 
These complicated motor and chemical activities of the stomach are 
regulated by a marvelously delicate nervous mechanism. The funda- STOMACH 
43 
mentals of the innervation of the entire gastrointestinal tract are similar, 
so that the general principles may be first discussed, and then the differ- 
ences in various parts elaborated. Our knowledge of the innervation 
was gained chiefly through the work of Langley (43) and his school. 
Additional work was contributed by Openchowsky (44), Magnus (45), 
Pawlow (46), Bayliss and Starling (47), Elliot and Smith (48), Popielski 
(49), Goltz (50), v. Frankel Hochwart and Frohlich (51), Courtade and 
Guyon (52) and many others. 
In the first place all organs containing smooth muscle fibres, possess 
ganglia lying in the muscle substance. These are known as the plexus of 
Auerbach and by means of this nervous apparatus, the intestine is able to 
execute rhythmic movements and propel any contents forward even when 
removed from the animal body. 
The second nervous apparatus in the intestinal wall is the plexus of 
Meissner which controls the movements of the muscularis mucosae (Exner 
{53)). This thin band of muscle protects the mucosa from injury by pulling 
it away from sharp or jagged objects, or rather by a lowering of tone, it 
allows the mucosa to belly away. 
Two groups of nerves, which in general, have opposing actions enter 
Auerbach’s plexus. The first are sympathetic fibres, and the second are 
fibres from the cranio-sacral system, i.e., from the brain and spinal cord. 
Broadly, the antagonism of these.two groups is such that when stimulation 
of the one produces contraction of the muscle, stimulation of the other 
produces relaxation, although in a given case, it cannot be predicted 
which of these two effects will be produced. It must always be remem- 
bered that a stimulus flowing through a nerve does not go directly to the 
muscle, but to Auerbach’s plexus, in which it may be further elaborated. 
And then again, the separate segments vary in the degree of influence 
exerted on them by central innervation. The ileum is the most independ- 
ent, while the stomach is very considerably under the control of the extrinsic 
nerves, even though it does, like the ileum, carry on rhythmic movements 
outside the body. V. Openchowski (44) assumes in the case of this organ 
that the independent activity occurs by reason of sp cial groups of gang- 
lion cells located under the serosa and demonstrated by him with the gold 
chloride method. These cell groups are said further to correspond 
broadly to Remak’s cells in the heart. 
The impulses from extrinsic sources, transmitted to the stomach through 
the vagus and sympathetic may be divided into motor, sensory and secre- 
tory, and the motor function, especially of the vagus, has been investigated 
very extensively (54). 
Summing up, this nerve carries both stimulating and inhibitory fibres 
to the stomach, so that stimulation of the peripheral stump causes first 44 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
inhibition (55), then increase of gastric motility, while bilateral section 
in the neck causes slowing of the movements (Cannon (56)). Those of the 
antrum in particular, are made more active by vagus stimulation (Braun- 
Honckgeest (57)). 
A communication exists between the right and left vagi on the anterior 
surface of the esophagus (Ducceshi (58)), so that on section of one in the 
neck, no motor disturbance of the stomach is demonstrable. On the 
other hand, since communications do not exist in the stomach itself that 
half of the stomach whose vagus has been cut is not affected by stimulation 
of the other nerve. On section of both vagi the gastric movements be- 
come slower and more superficial (Cannon (56)). We may assume there are 
separate tracts, corresponding to the different functional divisions of the 
stomach. In like manner, there are separate centers in the brain to which 
these tracts belong, although they must be in close communication (see 
Openchowski (44)). 
The splanchnic nerves, as antagonists, carry chiefly inhibitory fibres 
to the stomach and stimulation of the sympathetic at the upper level of 
the dorsal spinal cord leads to inhibition of peristalsis (see Openchowski 
(44)). Section leads to no demonstrable change in gastric movements, so 
that even when all four are cut, the difference in the evacuation time of 
carbohydrates and proteins persists (Cannon (56)). The cross relation of 
the vagus and the sympathetic, which will be discussed under “Vomit- 
ing,” is shown in the experiments of Klee (59). The results following 
nerve separations will be discussed later. 
The center of inhibition of both large and small intestines is the coeliac 
plexus (Popielski (49)). Its destruction leads to pronounced increase in 
motor activity as a clinical case (tumor metastasis) and the investigations 
of Exner and Jaeger (60) show. Ileus may even be suggested by the 
intense spasms of the ileum and colon. 
How far this increased intestinal motility can be brought into relation 
with the vaso-motor functions of the sympathetic, i.e., with constrictions 
and dilatations of the vessels, is unknown at the present time. The 
motor activities of the stomach, on the other hand, are not influenced to 
any noteworthy degree by either section of the sympathetics (Cannon (56)) 
or by extirpation of the coeliac ganglion (Aldehoff and v. Mering (28)). 
Secretion of gastric juice also takes place in a stomach devoid of nerves 
(Popielski (38)). 
[At this point, the theory of intestinal movements as propounded by 
Alvarez may be introduced. According to most text-books, food material 
is said to move aborally because of the myenteric reflex or Bayliss and 
Starling’s “law of the intestines” which declares that stimulation at any 
point produces contraction above and relaxation below. This is inade- STOMACH 
45 
quate to explain many of the normal phenomena and is of less help in 
pathological conditions. It had been observed by a number of writers 
that the small bowel varies in its muscular strength and tone, and in its 
rhythm and irritability in different segments. In a series of papers, 
Alvarez and his co-workers have brought out the fact that there is a 
gradient in these properties from the stomach and including that organ, 
downward. Strength, tone, rhythm and irritability, all diminish as the 
terminal ileum is approached. When food is introduced into the stomach, 
its tone, using the word in a loose sense, rises and the contents are moved 
into a less active and less sensitive region. The tone of this portion then 
increases, and the contents are again moved forward and so on. Reverse 
peristalsis would occur if, for any reason, a lower segment should become 
hyperactive or if the tone of a higher segment should become less. Since 
ordinarily the higher segments are the more sensitive and active this 
would hardly occur except for short stretches or in disease. Furthermore, 
the intestines in spite of their length, act very much as a unit, so that each 
segment knows so to speak, what the other is doing, probably by way 
of short nerve paths through Auerbach’s plexus and through the mesentery 
and ganglia. One part of the tract responds almost instantly to changes 
in another. Reference to this subject will be made again. In discussing 
the emptying of the duodenal cap (p. 40), it was said that the state of 
fullness of the intestines was an important factor. Applying the theory 
of gradient, the tone below may be increased on account of the presence 
of food to a point where it is equal to that in the duodenal cap. The 
gradient of forces then becomes a horizontal line and no progress is made 
no matter how great the other activity throughout the tube (61).] 
Of the pathological changes in gastric motility, only that of vomiting 
will be mentioned here. With Openchowski (44) we may picture great 
restlessness in the viscera followed by spastic closure of the pylorus. 
Meanwhile saliva mixed with air accumulates and distends the lower end 
of the esophagus. A forced inspiration is made with the glottis closed, 
so that more air is sucked in. The cardiac orifice relaxes, and with it the 
cardiac end of the stomach, while strong contractions occur in the entire 
pyloric end. The organ assumes a pear shape and partly by its own move- 
ments and partly by the compression of the abdominal muscles, the 
contents are ejected upward. 
In the final analysis vomiting is a result of stimuli reaching the center 
in the medulla, but they may be either direct or indirect. Certain chem- 
ical substances act directly (apomorphin, also morphin); other stimuli may 
arise in almost any part of the body, but particularly from the pharynx 
and throat, from the gastric mucosa, or the peritoneum. [The duodenal 
mucosa is a particularly favorable place from which to elicit vomiting 46 
the pathological physiology of surgical diseases 
(31).] We will return to a discussion of the peritoneum in this, 
connection later. 
Two paths for the innervation of vomiting are described by Openchowski,, 
depending on the type of emetic used; the one through the vagi, the other 
by way of the splanchnics, the branches of the sympathetic to the spinal 
cord, and from there to the quadrigemini. Klee (59) could show in 
decerebrated cats that stimulation of the vagus consistently produced 
vomiting, and the sequence of events in this case was first, closure of the 
pylorus, then diminution of peristalsis, contraction of the pre-pyloric part 
of the stomach, and finally opening of the cardiac orifice. The closure of the 
pylorus is a very important part of the act and since it is dependent 
on the splanchnics, vomiting was prevented when Klee sectioned these 
nerves. 
On the basis of the considerations mentioned above, a number of 
remedies have been proposed for the vomiting during and after anesthesia 
(v. Brun (62)). Washing of the stomach with sodium bicarbonate has 
been used (Lenewitsch, Gunby); giving vinegar by which the chlorin 
derived from chloroform may be combined; finally, compression of the 
vagus and phrenic nerves lateral to the jugular vein (Joos) are all pro- 
cedures, among many others which have been recommended. Individual 
differences and sensitiveness play such an important role in this type of 
vomiting, however, that any results from treatment must be judged with 
the greatest caution. [A particularly pernicious vomiting after anesthesia 
occurs in individuals whose renal function is impaired. We have often 
observed it following prostatectomy. The administration of sodium 
bicarbonate as suggested above, has certain experimental and clinical 
justification. In these renal cases, there are a number of factors operating 
in a vicious circle. There is not only retention of metabolic products, but 
a perversion of metabolism which gives rise to the well known ketone bodies 
and probably other as yet unidentified partial oxidation products. This 
determines a tendency to acidosis, which in its turn leads to the formation 
of additional acids, and so on. Fluids freely given, are of great benefit, 
but the question of whether the addition of an alkali assists is difficult of 
solution. This subject will be discussed in more detail in the following 
pages.] 
The sensory tracts of the stomach lie both in the vagi and splanchnics. 
In the former, the communication between the two nerves on the anterior 
surface of the esophagus is doubtless as important in sensory phenomena 
as in motor. The sympathetic fibres enter first the coeliac ganglion; from 
here they travel via the major splanchnic, through the rami communi- 
cantes to the posterior roots of the spinal cord (7th to 9th according to 
Head, see Foster and Kuttner (63)). Thus when sensory stimuli reach the STOMACH 
47 
yagus centers from the gastric mucosa, they give rise reflexly to motor 
and secretory responses which are then transmitted to the stomach. This 
entire arc is of course below the centers of consciousness; at least, in opera- 
tions under local anesthesia, patients feel nothing when the gastric mucosa 
is cut and sewed. We will speak of the sensory phenomena in more detail 
in discussing the sensitivity of the abdominal cavity as a whole. 
The question of the origin of the pain in gastric ulcers has been much 
discussed. Lennander (64) is of the opinion that its perception comes 
through the parietal peritoneum and it may even arise from the absorp- 
tion of an abnormal lymph, e.g., one with a high hydrochloric acid content. 
Muller (65), Talma (66), and others believe that the hydrochloric acid, 
per se, excites the pain. But that this opinion is not correct, has been 
shown by J. H. Schmidt (67) and others who poured hydrochloric acid 
into the empty stomach of patients with gastric fistulae and no pain 
was elicited. 
On the other hand, all sorts of psychic emotions like joy and pain, 
produce both increase and decrease of the activities of the stomach. 
Cannon’s observations with the x-ray on the slowing of antrum movements 
when his cats were teased, Pawlow’s obtaining the same results by sensory 
stimuli from the periphery, give us fundamental facts in the application 
of diets for our patients. 
[Psychic states play such an important role in all the functions of the 
stomach that great care is necessary in the interpretation of any studies 
of its secretory and motor activities. Not only does tasting or chewing 
food produce an abundant flow of gastric juice, but even the sight or 
smell of it stimulates secretion of what has been called the “appetite 
juice.” But a distinction must be made between appetite and hunger. 
The former is highly complex involving the highest centers whereas the 
latter has a much simpler basis. Particularly through the work of Carlson 
and his associates, it has been shown that hunger is related to contractions 
of the stomach. His studies have been made on lower animals, on a man 
with a gastric fistula made because of esophageal stenosis, and on normal 
men. By the use of balloons in the stomach connected to suitable mano- 
meters and recording devices and by the use of two balloons, one inside 
the other and separated by a layer of bismuth paste, so that x-ray obser- 
vations could be made, he has described two main forms of contraction 
in the empty stomach. The first is a “tonus rhythm,” caused by tonic 
contractions of the fundus, and the second is of the nature of powerful 
rhythmic contractions which are superimposed on the tonus rhythm. 
These may increase in amplitude and frequency until a tetanus results 
which after persisting for a short time subsides and is succeeded by a period 
of rest after which the same cycle is repeated. It is during the periods of 48 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
contraction that the sensation of hunger is experienced, and the sensation 
varies directly with their strength until, during tetanus, veritable pangs 
may be felt. 
The origin of these contractions has been carefully studied and it 
seems that so far as they are dependent on tonus and motor stimuli 
through the vagi, the impulses do not originate in the cerebral hemispheres. 
Complete section of the splanchnics leads to increase of tonus and augmen- 
tation of the contractions, while section of the vagi in the chest gives rise to 
hypotonus and disturbance in the rate and regularity of the rhythm. 
Much data indicates that the neuro-muscular apparatus of the empty 
stomach is somewhat unique in its freedom from control by afferent 
impulses and central processes. The contractions are not only present 
during sleep when practically all other similar mechanisms exhibit lowered 
tone, but may even be augmented. Since it is the contractions which 
are reflected into the consciousness as hunger, the actual sensations may be 
deadened or abolished by concentration on other subjects, as for example, 
doing a sum, or reading. But the contractions continue whether they 
are perceived or not. The idea has been expressed that the ordinary 
routine of eating three meals a day is largely a habit which can be changed 
at will. A man may accustom himself to two meals a day and experience 
no hunger. Careful research has shown that while such individuals may 
not experience hunger, there occur nevertheless, gastric contractions 
as soon as the stomach is empty or practically empty, and the sensation 
is not perceived because of strict attention to other matters. 
These questions are of intense practical as well as theoretical interest. 
Many a case of hunger contraction has probably been called hyperperistal- 
sis. To return to the question of the pain in gastric ulcers, it is not an 
unusual history whiph says that the patient places a glass of milk and some 
crackers or other food beside his bed so that he may allay the pain which 
often wakes him at night. In fact, it has been remarked, facetiously 
perhaps, but there is truth in it, that with such a history, the diagnosis 
can be made over the telephone. We know hunger contractions occur 
during sleep and it is most interesting that a study by Carlson (68) 
should show contractions during the pain in one of his subjects. This 
line of investigation may prove of occasional diagnostic importance in 
diseases of the upper abdomen, although if the ulcer pains result from 
contractions, either from hunger or digestion, similar pains may be pro- 
duced also by other pathological conditions which excite hypermotility 
or normal motility with hyperexcitable nerves, a thought which agrees 
perfectly with clinical experience. 
It is not surprising if the pain is due to contractions, that the acidity 
does not parallel the intensity of the pain. Movements of the stomach STOMACH 
49 
are independent, to a certain degree, of the reaction of the contents, but 
the pylorus is more sensitive, and hyperacidity may augment its contrac- 
tions as well as those of the duodenum. In this case especially, the 
administration of alkali would temporarily ease the pains. That many 
ulcers should be accompanied by very little or no pain is also clear. There 
are variables in the forms of gastric, duodenal and pyloric contractions, 
inflammation and edema, proximity to nerve endings, viz., the vagi, and 
the inherent nervous stability of the individual. It also follows directly 
that the cessation of pain is no criterion of healing of the ulcer (69).] 
The vagus also carries secretory fibres to the stomach, for as Pawlow 
found, electrical stimulation causes an outpouring of gastric juice. Sec- 
tion leads to abolition of the reflex flow, i.e., of the appetite juice during 
feeding (46). But the statements regarding the influence of innervation 
on the secretion of gastric juice are by no means beyond criticism (see 
Babkin (33), Rheinboldt (70)). It is said that high section of both vagi 
brings about an increased production of hydrochloric acid, which leads 
to spastic contraction of the pylorus and subsequent gastrectasia (Katsch- 
kowsky, Fritsch (71)). The formation of pepsin is also diminished and 
fermentation of the stagnating food is likely to occur. 
Aldehoff and v. Mering found diminution of acidity at first after section 
of both vagi below the diaphragm, but this effect disappeared in about 
fourteen days. Nothing is known of the influence of the sympathetic on 
this process. 
The extrinsic nerve supply of the stomach has recently become of 
quite especial interest to the surgeon, because modern operations on the 
thorax, especially on the esophagus, often come in conflict with the vagi, 
and secondly, section of these nerves has been advised in the gastric crises 
of tabes. At times good results have followed this operation (Forstner 
and Exner). 
Gastric crises are a complex of sensory, motor and secretory stimuli in 
the region of the stomach. Forstner and Kuttner assume that the sensory 
phenomena are primary, and reflexly these excite motor and secretory 
changes whereby vomiting and gastric secretion occur. Reasoning in this 
manner, Forster and Kuttner (63) severed the sympathetic fibres, which 
as stated, lie in the seventh to ninth dorsal segments, and they as well as 
other operators, obtained good results in a large number of cases. Not 
all were benefited, however; vomiting, especially, was often entirely unin- 
fluenced, so that Exner (72) was led to sever the second tract which controls 
vomiting—that running in the vagus—by cutting that nerve at the 
cardia. His results were also good. From the pathological physiological 
standpoint, it must be admitted that both methods are based on good 
logic. Disease of the vagus nuclei in tabes has often been described and 50 
THO PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Exner could actually demonstrate inflammatory changes in the peripheral 
vagus in a number of his operative cases. 
On the other hand, vomiting may also be incited through the sympa- 
thetics, and that operative method which not only removes one symp- 
tom, but like Forster’s, improves all of them more or less, deserves the 
preference. Most surgeons therefore destroy the sensory part of the reflex 
arc, and thus all of the symptoms, especially the pain are improved. If 
vomiting is not terminated by this, the advisability of section of the vagus 
must be considered. The effects on the stomach of this latter operation 
are less in subdiaphragmatic vagotomy than after higher section. Alde- 
hoff and v. Mering sectioned the vagi, then cut transversely across the 
esophagus just above the cardia and reunited it. They found no changes 
in the motility or secretion of the stomach and especially no secondary 
dilatation following this operation except during a short time in which 
a delay in the evacuation and a reduction in hydrochloric acid secretion 
were observed. After section in the neck, below the point where the 
fibres to the heart separate, there are slowing of the movements, increased 
hydrochloric acid production, pylorospasm, and gastrectasis (Cannon, 
Katschkowsky, Fritsch). 
With good care, animals remain alive after high vagus resection, 
but their digestive tracts are extremely sensitive (Krehl (73)). The differ- 
ence in the behavior of the stomach after this operation and subdiaphrag- 
matic vagotomy, seems to lie in the fact that sympathetic fibres are also 
cut in the latter procedure and according to Cannon (56) gastric move- 
ments are practically undisturbed when both vagi and splanchnics are cut. 
Whether similar conditions hold true for secretory processes, is as yet, 
unknown, although it seems not improbable. Complete section of all 
sympathetic and vagus fibres is done when a so-called circular resection 
is performed. We shall return to the subject of gastric movements after 
resection in discussing operative methods. 
Gastric movements are altered when the pylorus is closed too tightly. 
The ability of the remaining part of the stomach to move remains normal, 
but it must labor against an abnormal resistance. The first type for 
consideration is that occurring in infants, which according to numerous 
investigators, is probably a spastic contraction of an hypertrophied 
pyloric muscle (74). Such cases of pylorospasm are also occasionally met 
in adults, although the contractures are not so severe and lasting. Wilms 
(75), especially, has called attention to this condition, and has advocated 
£-ray therapy. Manasse (76) has described cases of pylorospasm, in 
which varices and similar conditions existed in the stomach wall. These 
pylorospasms should probably be considered secondary. They occur 
quite frequently with ulcers, and much clinical evidence has shown that STOMACH 
51 
the ulcer need not be at the pylorus, but may be distant. In fact, other 
conditions in the stomach, as well as in the intestines, with or without 
mechanical obstruction to the pylorus, may lead to six hour retention 
with secondary pylorospasm as its cause. Holzknecht and Luger (17) 
have described secondary spasms in other regions of the stomach. 
[From what has been said of gastric movements, regarding the theory 
of gradients, and from other considerations, it is clear why pylorospasm 
should result from diseases of other viscera, e.g., the gall bladder.] 
There are, furthermore, symptom complexes, in which, with a normally 
functioning pylorus, there is defective evacuation of food which must be 
attributed to a paralysis of the body of the stomach. Even in a stomach 
previously healthy, a sudden motor insufficiency from the action of cer- 
tain injurious factors may occur. Immense quantities of gastric juice, 
bowel contents, and consumed fluid, collect, to be vomited periodically. 
Since water is not absorbed by the stomach, desiccation of the patient 
takes place and finally death ensues. 
In acute dilatation, a condition of the utmost interest to surgeons, it is 
necessary to sharply differentiate between two forms of the disease, that 
due to a mechanical obstruction, the so-called arteriomesenteric ileus and 
the true paralytic form. Either may undoubtedly exist alone, but they 
often exist in combination; the former may be the cause of the latter, and 
thus the symptoms may be much confused. In the first place (Braun, 
Tuffiers, Payers (77)) there is an individual predisposition to this dilatation 
but its exact nature is not clear since the histories of the patients, as 
reported in the literature, give data concerning the gastric motility as it 
was affected during the attack, and not as it was before. The most 
probable explanation is that there existed a chronic insufficiency 
and an acute attack was superimposed, but there are a number of 
injurious substances which may produce sudden dilatation of the 
normal stomach. 
Anesthesia should be mentioned first and accurate investigations on 
anesthetized humans have been carried out by A. Payer. In anesthetized 
animals the stomach may be enormously distended without rupture 
while in conscious animals this is not possible. Authors agree that 
anesthetics paralyze the stomach but their further opinions are conflicting. 
Kelling (78) believes the paralysis is confined to the “ evacuation 
reflex” and assumes there is a special valve mechanism in the cardia, 
whose opening is prevented by the anesthetic. Braun and Seidel (79) 
believe from observing the stomach ‘Tying motionless under the abdominal 
walls” that there is a paralysis of the gastric center, and that the valve 
observed by Kelling is a secondary result of the distention. Payer’s 
criticism of Kelling’s valve theory is quite just. Such patients vomit 52 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
really enormous quantities and this fact contradicts any mechanical 
■closure at the cardia. 
According to Kuru (80) the primary factor in acute post-operative 
gastric dilatation is an insufficiency of the adrenals. 
If we assume, then, that in this condition there is a motor paralysis 
of the stomach as a whole, the question arises, on which part of the nervous 
apparatus does the anesthetic produce its effect? That vagotomy leads to 
gastric dilatation and delayed evacuation has already been mentioned. 
Apparently the vagus can have no relation, however, to post-anesthetic 
gastric dilatation, because after section of the nerves as in Mangold’s 
experiments (81) the same disturbances of innervation were observed. 
At least this occurred in birds. In Braun and Seidel’s experiments, the 
splanchnics, sympathetics, and spinal cord were all sectioned and still the 
same phenomena were noted. Therefore, Payer’s view that Auerbach’s 
or Openchowsky’s plexus is damaged is much more acceptable. Accord- 
ing to him, it would otherwise be inexplicable “why motor insufficiency of 
the stomach lasts so much longer than the other effects of the anesthetic.” 
But it must be remembered that such gastric dilatation may occur 
without general anesthesia and may be found after operations under local 
anesthesia, or even without operation; for example, after applying a con- 
stricting bandage, such as a plaster corset (Kelling); during or after a 
debilitating disease such as typhoid fever; or in chronic suppurations 
(Kuru (80)); after catheterization of the bladder (Braun (77)); or of the 
ureters (Leguen (77)); after a fall (Tuffir (77)); after excessive eating (Korte 
(82)); and so on. While the blame in certain operations, e.g., cholecystec- 
tomy, is laid on a local peritonitis or perhaps the gauze tamponade, in 
other cases the reflex factors must be considered, which are possibly 
similar to those producing the dilatation of the bladder so often seen after 
all sorts of operative procedures (Bier (83)). 
A case of Haberer (84) was very characteristic in this respect, he 
observed a gastric dilatation presumably of reflex origin following the 
packing of gauze against the parietal peritoneum. The same influence is 
also shown in the investigations of Cannon and Murphy (85) who by 
merely manipulating the stomach and intestines, could demonstrate 
considerable delay in the evacuation of the stomach. In short, a large 
number of surgical procedures have been reported after which gastric 
dilatation occurred, and every experienced surgeon has seen cases in which 
this condition interfered with the operative success. 
Gastric dilatation may kink and obstruct the third part of the duo- 
denum by strapping down the root of the mesentery and its superior 
mesenteric artery. But this condition which is called arteriomesenteric 
ileus may take place without gastric dilatation (see Haberer (84)). STOMACH 
53 
A large number of factors may cause displacement of the root of the 
mesentery, among them, lordosis, enteroptosis, abdominal drainage, 
post-operative displacement of abdominal contents, adhesions of loops of 
ileum in Douglas’ cul de sac, from localized peritonitis (author’s autopsy 
observation), emaciation, and so on. It is very often impossible to 
differentiate in a given case. The experiments performed by P. A. 
Albrecht (86) and repeated by P. Muller (87) serve rather to demonstrate 
the effect of the pull on the mesentery exerted by the ileum hanging down 
in the pelvis, than to clear up the etiology of arteriomesenteric ileus. 
They allowed the mesentery in a cadaver to hang with the pull directed 
toward the pelvis, and found the duodenum so completely kinked that, 
water would pass into the jejunum only under very high pressure. 
In addition to this acute type, there is also a chronic variety in which 
food remains in the stomach for an abnormal length of time and leads 
thereby to considerable nutritional disturbances (Mathieu and Roux (88)). 
In this condition also, the pylorus is patulous at first, but it is often 
combined with ptosis of the stomach (gastroptosis of Glenard (89)). 
There is a recent disposition to regard this chronic motor insufficiency of 
the stomach as a local symptom of a constitutional disease, an “asthenia” 
in Stiller’s sense (99) (see Bauer (90)). Histological changes in the smooth 
muscle consisting of cloudy swelling and fatty degeneration have been 
described as an anatomical basis (Kussmaul (91)) but these are perhaps a 
result rather than a cause of the insufficiency, which finally depends on 
disturbance of innervation. Just what and where this disturbance is, 
whether it is along the vagus tract, or what seems more reasonable by 
analogy with acute dilatation, in Auerbach’s plexus, is still entirely 
unknown. 
In the first stage, it is the fundus which is particularly affected. As 
stated above, in the normal stomach, the longitudinally folded pouch is 
filled with fluid through almost its whole length before it begins to expand 
laterally; in atonic stomachs the walls are relaxed and lateral expansion 
takes place as soon as fluid enters, nor do they close tightly around the 
contents. Clinically, this is manifested by splashing noises when the 
stomach region is percussed. But emptying of the stomach contents may 
be nearly normal in this type, because, as was stated, the fundus only is 
affected, and not the pyloric portion which is the actual motor part. 
Retention occurs later, however, and if gastroptosis is present at the same 
time, it is assumed that the abnormal relations of the pyloric portion to 
the duodenum add another difficulty to evacuation. This is quite pos- 
sible, and becomes even more probable if a small ulcer is found at the 
pylorus, as often happens in such cases. This type of ulcer is probably 
secondary to the nutritional disturbances in the sharply kinked portion 54 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
(see Krempelhuber (92)). But another cause of incomplete evacuation is 
an increasing motor insufficiency. The stomach is then like a flabby bag 
which shows only weak defective movements under the rr-ray. In such 
advanced cases, as Rovsing (93) has repeatedly emphasized, gastro- 
enterostomy does not help, for the stomach lacks sufficient motor power 
to empty itself even through this opening. 
[This opinion is now shared by practically all surgeons.] 
The author can only support this much disputed opinion. He himself 
has lost a number of cases of gastroenterostomy done for marked retention, 
and at autopsy no other cause of the defective evacuation of the stomach 
could be found. The ultimate cause of the symptom complex is unknown. 
Reichmann (94) believed that a pathological hypersecretion of gastric 
juice was primary and overstretched the stomach. But Hayem’s (95) 
anatomical investigations have shown that in almost every case of Reich- 
mann’s disease there is mechanical obstruction, either an ulcer or its 
scar. The hypersecretion should, therefore, be considered secondary, 
the result of a gastritis caused by stasis. 
Before considering the changes in the motor and secretory functions 
of the stomach after various operative procedures, it is necessary to know 
something of the histology of normal repair in gastric and intestinal 
wounds (96). Small defects in the mucosa heal quickly and without any 
noteworthy disturbance. The lesion is narrowed by muscular contraction, 
and epithelium grows from the edges and covers it completely. The same 
principles apply to healing of the larger ulcers (Matthes (97)). The cover- 
ing is derived partly from glands, and partly from the surface epithelium 
of the adjacent mucosa. Regeneration of glands occurs last, as a rule. 
Wounds of the musculature are reunited only by connective tissue. The 
healing of the serosa is the most important from the practical standpoint 
(Graser (98)) because fibrin is exuded over this coat at the slightest 
provocation and adherence to adjacent tissue takes place, but the endothe- 
lial cells are not necessarily destroyed by this exudation. If two serous 
surfaces are brought in contact and sutured, as is done so often in gastro- 
intestinal operations, the fibrinous adhesions are organized; in a few days 
spindle cells and new blood vessels appear, and a firm union results. .These 
fundamentals of repair are found after all gastro-intestinal operations. 
In most cases of gastroenterostomy (Marchand (96)), the mucosa of the 
bowel at the border toward the stomach is probably destroyed, even 
though the mucous surfaces are sutured most carefully. The repair of 
this area proceeds by granulation (Wilkie (99)) and the opening may narrow 
by cicatricial contraction (100). 
The very nature of the conditions necessitates that gastric and intest- 
inal sutures are early subjected to strain. The question arises, “How STOMACH 
55 
much can they stand, without giving way?” Chlumsky (ioi) has tested 
on successive days following operation and under normal and pathological 
conditions, the strain to which various suture methods and buttons might 
be subjected without tearing. As controls, he used intact bowel and found 
that the healthy ileum of the dog supported a weight of 400 to 500 mm. 
Hg., while the ileum of man supports only about 200 mm. The greatest 
strength is shown by the submucosa, the weakest part in man is at the 
mesenteric attachment. In peritonitis, the bowel ruptures under much 
less weight. A double layer of sutures, just applied, will support a 
pressure of 150 and 200 mm. Hg. The Murphy button gives practically 
the same results. During the first four days, the firmness of the suture 
line becomes constantly less (as low as 20 mm. Hg.), then increases until 
about the eighth or tenth day, when it reaches a strength equal to that 
of the intact organ. Thus the greatest danger of rupture is from the 
third to fifth day. 
If the figures for internal tension of the walls of the stomach during 
digestion, which, according to v. Kelling are from 8 to 10 cm. of water, are 
compared with these, it is seen that even under the most unfavorable 
conditions (third to fifth days) moderate amounts of fluids strain the line 
of suture only to one-third of its possible resistance. Kelling calculates 
even more favorably, and believes that with liquid diet the pressure rises 
only to about one-seventh of the danger point. At the same time, he 
cautions against solid food until the union of stomach and bowel is of 
connective tissue, since muscular contraction may increase the pressure 
considerably, and lead to rupture. Vomiting increases the internal pres- 
sure, but even in this case he believes that it will amount to only about one- 
fourth of the critical pressure. 
The most frequent operative procedure on the stomach at the present 
time is gastroenterostomy, and in considering the changes in motor and 
secretory function following operations, this will be dealt with first (102). 
When the pylorus is present, but obstructed, the time factors of gastric 
emptying are very little changed and the belief that food leaves the stom- 
ach very quickly after gastroenterostomy is incorrect, as many careful 
studies have shown (103). When the stomach is empty, its walls are in 
contact and the gastroenterostomy opening is closed. Unfolding occurs 
only on the entrance of food, and filling proceeds normally. Its move- 
ments are in no way interfered with during respiration by the attached 
loop of bowel. When the last bolus of a meal was swallowed, that is, at 
the same time as in a normal stomach, Schuller could observe under the 
fluoroscope that some of the chyme separated and passed into the intestine. 
The contents do not leave in a continuous stream, but in single jets exactly 
as through the pylorus. When the gastroenterostomy opening is in the 56 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
antrum this similarity is more manifest because as Schuller could demon- 
strate in animals, the contents flow out in tune to the rhythm of the antrum 
movements. When it is in the fundus, the weight of the food is a more 
important factor and the stomach empties itself in irregular squirts (104). 
Herre (105) could also show a certain irregularity in the evacuation of the 
chyme. Since there is no ring shaped muscle at the operative gastro- 
enteric anastomosis (106) it must be assumed with Kocher (107), and 
Schuller, that the periodic opening and closing is due to peristalsis of the 
loop of jejunum. Indeed, this was observed by Kocher during a laparot- 
omy in a patient in whom a gastroenterostomy had been done previously. 
But perhaps a share in this emptying is assumed by the folds of the mucosa 
described above and by the contractions of the musculature in the so- 
called “narrow pass.” At all events, the time of emptying of the stomach 
after gastroenterostomy is approximately normal; at least, it is not 
accelerated. 
The clinical observations on this question are not in entire agreement, 
probably because they were made* on pathological stomachs. We must 
therefore return to animal experiments, and especially to those done with 
the pylorus obstructed (Schoemaker (108)). If a gastroenterostomy is 
done either at the fundus or at the antrum, without coincident closure of 
the pylorus, the largest part of the chyme passes through the normal way 
and only occasional bits through the new opening (Kelling, Borszeky (109), 
Cannon and Blake (no), Legget and Maury (111), for opposite, see Kuttner 
(112). Schoemaker performed his experiments with the pylorus closed, 
amd after gastroenterostomy or gastro-duodenostomy found by injecting 
acid into the intestine that the first squirt of chyme was evacuated into 
the bowel in about the same time as in the normal. He could obtain after 
either operation, a closure of the opening, which, however, was of shorter 
duration than the normal pyloric reflex. The evacuation of the stomach 
was especially quick after gastro-duodenostomy. Schoemaker points 
out, correctly enough, that these results obtained in animals cannot be 
applied in all respects to man. Nevertheless numerous clinical observa- 
tions (Schuller (103), Barsony, and others (113)) some of which were under- 
taken to determine the usefulness of different methods of closure of the 
pylorus, have shown that gastric contents escape through a gastro- 
enterostomy, provided it is large enough, in about the same time as in 
the normal stomach. Therefore the motor activity is little altered by 
this operation, but as we shall see, the change in the chemistry is quite 
considerable (114). 
In the first place, there is a continual backflow of alkaline intestinal 
juice (115). Through this, and by alterations in the outflow conditions, 
gastric digestion is markedly influenced and proceeds quite differently. In STOMACH 
57 
general, there is less hydrochloric acid in the stomach (Krause (116)). 
This has been correlated'with the idea that after gastroenterostomy, 
there is less stasis of food in the stomach. But, in most cases, the reason 
must be that the acid is neutralized by backflow of alkaline juices (Katzen- 
stein (117), Schuller). In addition to this, so to speak, test tube neutraliza- 
tion, experiments with Pawlow’s miniature stomach (Katzenstein) have 
shown that the presence of small quantities of intestinal juice results in 
a reflex inhibition of hydrochloric acid production. According to Kausch 
and Kaplan (118), this backflow of intestinal fluid ceases during subse- 
quent years. This does not seem to be the rule, however, for Schuller 
could not find increased hydrochloric acid in his patients when he re-ex- 
amined them some time after operation. As soon as the alkaline intestinal 
juice enters the stomach, pepsin digestion is interrupted, for this enzyme 
digests only in the presence of acid, and a trace of alkalinity destroys its 
ferment activity. But the digestion of protein in the stomach is not 
completely lost because trypsin in the backflowing pancreatic juice takes 
over this function (119). Trypsin is much less sensitive to changes in 
reaction than pepsin, and its digestive power for protein is only checked 
and not completely destroyed (Katzenstein). The other two pancreatic 
enzymes, diastatic and lipolytic, are also resistant to acid and thus, after 
gastroenterostomy, digestive processes take place in the stomach which 
ordinarily occur only in the bowel. Carbohydrates are broken down by 
the diastase, fats by lipase and bile. The rennin from the stomach is 
replaced by a similar enzyme from the pancreas. Altogether, the absent 
gastric digestion is compensated so well, that no changes are demonstrable 
in the total metabolism of either nitrogen, carbohydrates or fats (Hein- 
sheimer (120)). This latter may, however j depend partly on the fact 
brought out by Dagaew’s investigations (121), viz., that the passage of 
food through the small intestine is considerably slowed. Thus, the food 
is probably comminuted and absorbed in an approximately normal 
manner, before it enters the colon. 
But since after gastroenterostomy and pyloric closure, the food does 
not pass over the papilla of Vater, how are the pancreas and the gall 
bladder stimulated? The principal stimulus to pancreatic secretion 
is the secretin, which is formed from prosecretin by hydrochloric acid, 
is absorbed from the intestinal wall and carried to the pancreas 
by way of the blood stream (Bayliss and Starling (122)). Since 
prosecretin is present in the jejunum also, the flow of pancreatic juice 
after gastroenterostomy is easily understood. But normally, there 
are a number of other substances, chiefly soaps and oils, which act 
as direct stimuli to the pancreas, probably through nervous paths (see 
Cohnheim and Klee (123)). 58 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
According to the investigations of Bickel (124), who extirpated the 
duodenum in a dog and sutured the papilla of Vater to the abdominal 
walls as a fistula, these reflexes may also arise in the jejunal mucosa. This 
holds good for both pancreatic juice and bile. For the digestion of any 
sort of food, it is principally the bile which has been in the gall bladder 
and the bile ducts, and not newly formed bile which is important (125). 
Schoemaker obtained the same results (108); he observed, after closure 
of the pylorus and gastroenterostomy in dogs with fistulae, the regular 
action of these reflexes. 
Katzenstein (117) (p. 138) assumes from his investigations, that im- 
pulses from the stomach may also give rise to pancreatic secretion and 
bile flow. His experiments are, however, open to doubt, since the pylorus 
was not cut through and a flow of stomach contents into the duodenum 
can never be excluded after simple gastroenterostomy. 
But there is still another possibility regarding the secretory mechanism 
of bile and pancreatic juice. Kelling (126) observed a considerable 
backflow of food into the duodenum after resection of the stomach with 
duodenal fistula. In such cases, the food flows over the papilla of Vater 
and may thus directly stimulate the glands. 
Casagli’s (127) histological investigations have shown that when the 
duodenum is eliminated even partially from the digestive processes there 
results a sclerosis of the submucosa and of Brunner’s glands, as well as a 
thinning of the musculature. 
Regurgitation of bile and pancreatic secretion into the stomach has 
been observed when patients vomit for a long time after operation, as 
in the condition which occurs particularly in so-called vicious circle, 
of which we will speak later. It was believed on account of this, that the 
vomiting itself and the rapid downfall in such patients was a result purely 
of the entrance of bile and pancreatic secretion into the stomach. This 
idea was pursued in many experiments, and even though our conception 
of the cause of vomiting in vicious circle has undergone change, these 
studies not only have historic interest, but they give us a key to under- 
standing many-lesser disturbances after gastroenterostomy. 
Chlumsky (128) cut through the intestine of dogs just below the 
duodeno-jejunal plica, and sutured both openings to different places 
of the stomach, thereby leading duodenal fluid into the organ through one 
opening and allowing its emptying through another. It is true the dogs 
did not vomit, but they died after a few days, and showed no satisfactory 
cause of death. They displayed great thirst and at autopsy, the intestines 
were filled with dark brown fluid feces. The introduction of bile by 
anastomosis of gall bladder and stomach was followed by recovery of the 
animals (129), but death occurred again in a manner similar to that de- STOMACH 
59 
scribed above, when the bile was eliminated by a cholecyst-enterostomy 
and only pancreatic fluid was allowed to enter the stomach. Different 
results were obtained by Steudel (130) who varied this experimental 
method by sectioning the bowel at the same place, and then closing the 
duodenum, so that its contents had to pass periodically through the 
pylorus. Chlumsky explains these latter results by assuming that a 
periodic discharge of bile and pancreatic juice is less harmful to the 
dogs than a continuous one. But the conclusions which Chlumsky 
draws from his own wrork are certainly too far reaching. The fact that a 
dog dies after an operation on its stomach proves very little, because dogs 
generally do not stand laparotomies very well (Pawlow, Cohnheim (9)), 
particularly when the operation or even the manipulations include the 
pylorus. Often enough, dogs die with exactly the same symptoms and 
autopsy findings as Chlumsky describes, after entirely different operative 
procedures on the gastrointestinal tract, e.g., simple gastroenterostomy 
(author’s own observation). Furthermore, Kelling (131) succeeded in 
keeping a dog alive and perfectly healthy for a long time after an exactly 
similar operative technic. While it is true that more critical analyses are 
needed here, perhaps with the help of fistulae, it nevertheless cannot be 
denied after these experiments, that backflow .of bile and pancreatic juice 
may under certain conditions cause trouble. According to Stuber (132) 
a backflow of trypsin in animals leads to the formation of gastric ulcers, 
which do not appear to differ from those found in man in whom these 
have not as yet been described. The possibility must, however, be kept 
in mind. Furthermore, apart from changes in gastric digestion, a mixture 
of hydrochloric acid, bile and proteins, leads to the formation of bile 
acid salts, which are very difficult for enzymes to attack (21). 
On the whole, regurgitation produces no trouble in man, but now and 
then, individuals appear who for a longer or shorter time after gastro- 
enterostomy have eructations of bile, nausea, and other symptoms which 
must be attributed to this condition (133). Why trouble should occur 
in some individuals and not in others with the same pathological conditions 
cannot be answered with certainty. Psychic, or if you like, neurasthenic 
processes may play some role. 
As stated, this backflow is observed principally in connection with the 
so-called vicious circle, or as it is probably better called by Peterson (4), 
gastric ileus. This very undesirable complication of gastroenterostomy 
occurred even at the cradle of this very beneficial operative procedure. 
Indeed Wolfler (134) in his first communication on gastroenterostomy 
reported such a case. Physiologically, quite a number of different condi- 
tions are included under this name (135). In the first place, a backflow 
of duodenal contents may occur through an open pylorus, secondly, duodenal 60 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
contents in larger quantity may flow into the stomach from the proximal 
loop. In the third place, stomach contents may enter the proximal loop, 
instead of the distal, flow backwards through the duodenum and pylorus 
into the stomach, then into the proximal loop again and so on (vicious 
circle). With a closed pylorus, combinations of two and three would 
occur. Fourth, a backflow of intestinal contents from the distal loop has 
been observed as a cause of vicious circle. 
The reasons for gastric ileus after gastroenterostomy are found in tech- 
nical errors, which have gradually become so well known, thanks to the 
studies and experiments of numerous authors, that this complication is 
a rarity at the present time. Since it occurs much more frequently after 
anterior gastroenterostomy on account of the torsion and compression 
of the jejunal loop, the posterior operation is preferred. Furthermore, 
a long loop favors antiperistalsis, therefore it is made as short as is consis- 
tent with reaching comfortably from the duodeno-jejunal plica to the 
place of anastomosis (136). The loop cannot therefore be of the same 
length in each case, but must be longer with a deeply situated, dilated 
stomach, than with one of normal size (4). Even this consideration 
does not always hold, for the stomach may change its size after operation 
and spur formation, larger than ordinarily occurs, will result. Such a spur 
acts like the dam in a mill race and vicious circle is often the result. 
Finally, with the pylorus wide open, and a failure of the sutures in 
the mucosa the gastroenterostomy may shrink and a vicious circle arise 
from this cause (128). All these difficulties in evacuation are found more 
frequently in relaxed than in normal stomachs. 
This is not the place to discuss the methods which have been devised, 
to obviate vicious circle (see Tavel (135), Peterson (4), and others). Their 
principles explain themselves from what has been said above. Summing 
up our present knowledge, the so-called vicious circle is a true, high situated 
ileus resulting from a more or less complete mechanical closure of the bowel. 
The enormous dilatation of the duodenum which has been described in 
this condition can be explained by the same considerations (137). We will 
discuss the general pathological physiological consequences of ileus, the 
causes of death, etc. in a separate chapter. 
The diarrhea which is occasionally observed after gastroenterostomy 
has been explained (138) in certain cases by the sudden entrance into the 
bowel of decomposed material which had stagnated in the stomach before 
the operation, e.g., in carcinoma (139). [This must occur very seldom 
because in well appointed clinics a gastric lavage before operation is routine. 
This, however, may fail to remove some contents.] Where such a condition 
cannot be found, an explanation is more difficult. In these cases, an 
assumption is made based on investigations of Matthes (97) who found STOMACH 
61 
that the injection of gastric juice into the ileum causes severe enteritis 
and that hydrochloric acid when injected into the jejunum produces 
diarrhea (131). This idea has not received general recognition, chiefly 
because hypoacidity is found much mpre frequently after gastroenteros- 
tomy on account of the backflow of alkaline intestinal juices. Conversely, 
Schuller calls attention to the diarrhea which occurs with ordinary anacid- 
ity and believes there is an analogy in gastroenterostomy. This question 
has, however, not yet been answered. 
[Diarrhea so severe that it ended fatally has been seen after gastro- 
enterostomy (140). With the idea of gradient in mind (Alvarez (61)), the 
process can be attributed in some cases of gastroenterostomy to a rapid 
outpouring of food which enormously raises the tonus and irritability of 
the upper intestine, perhaps by the very distention, and leads to a hurried 
passage of the contents.] 
The communications reported by roentgenologists regarding the pro- 
gressive movement of the contents through the ileum and colon after 
gastroenterostomy are contradictory. A number of authors report a 
slight slowing of the passage through the ileum (Schuller (103)). Others 
state that the shadow of bismuth appears at the left flexure in five hours 
(141). Doubtless the subjects investigated (human patients), showed too 
many individual differences, so that slowing or acceleration of peristalsis 
must be correlated with factors other than gastroenterostomy. 
Another very disagreeable complication of gastroenterostomy is the 
development of ulcers at the site of the anastomosis to the jejunum. The 
similarity of all ulcers in the region of the stomach and intestines, and the 
numerous investigations to determine how this condition arises will be 
discussed in the paragraph on gastric ulcers, but certain peculiarities of 
jejunal ulcers may be pointed out. 
According to our present viewpoint, these, like all other peptic ulcers, 
are formed by the digestion of an intestinal wall previously devitalized by 
injury. According to Van Roojen (142) in 41, out of 56 cases, they were 
located at the gastroenterostomy opening, in two cases, at the place of 
Braun’s anastomosis; while the remainder were scattered in different 
parts of the bowel. On the whole, they are rare. 
[In the experience at the Lankenau Hospital they were found in about 
2 per cent, of cases of gastroenterostomy.] 
Gasset believes they occur more frequently after anterior gastro- 
enterostomy (143), but according to von Haberer (144), they are more 
frequent after the posterior operation with short loop. They are especi- 
ally dangerous because they perforate readily, usually into the free ab- 
dominal cavity since fixed parenchymatous organs to which they might 
adhere and which are in the neighborhood of ordinary gastric ulcers, are 62 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
distant. Isolated cases of jejunal ulcer have also been observed without 
previous gastroenterostomy (von Roojen). In one of the cases an ex- 
tensive burn of the skin was the cause of death. From the very beginning 
there was a difference of opinion ,as to wrhether they resulted from the 
entrance of gastric juice into the bowel, since the bowel is not normally 
adjusted to acid gastric juice, or whether other factors also came into 
play. Katzenstein (145) and Kathe (146) isolated loops of intestine in 
the stomach of dogs but retained their connection with the mesentery 
and thus disturbed the nutrition as little as possible. They found that 
intestinal mucosa has no resistance to the digestive power of the gastric 
juice, and is completely dissolved in a short time, but gastric mucosa 
implanted into the stomach shows a much greater resistance. Katzen- 
stein concludes from his experiments that the latter contains an anti- 
enzyme which is absent in the mucosa of the intestine. More recent 
investigations (147), however, indicate that these results may have another 
explanation. The digestion of the loops of intestine as found by Katzen- 
stein is due entirely to nutritional disturbances resulting from an inade- 
quate circulation. 
The doctrine that specific protection against autodigestion is possessed 
only by the gastric mucosa cannot be accepted in the form elaborated by 
Katzenstein. Among other ways this was shown by the investigations 
of Titze (148) who sutured omentum as a protection into an injured gastric 
wall. He observed no digestion at all and this method has gained con- 
siderable favor in operations for perforating gastric ulcers. 
Nevertheless, it is doubtless correct that the jejunal mucosa is very 
sensitive to hydrochloric acid for when Matthes (149) injected hydrochloric 
acid and pepsin into dogs through a fistula into the intestine, he observed 
that the acid first killed the cells and then the digestive action of the pepsin 
began. He could obtain extensive destruction of bowel mucosa in this 
way. Matthes is therefore still of the opinion that the jejunum can be 
so injured by an hyperacid gastric juice as to cause the development of an 
ulcer. The importance of hyperacidity in the formation of jejunal ulcers 
is further illustrated by statistics. Von Roojen found hyperacidity 
present 21 times in his cases; it was normal or below normal 12 times; 
and Patrion (150) reports 13 cases of hyperacidity in 18 jejunal ulcers. 
Consequently jejunal ulcer is rare after gastroenterostomy for carcinoma 
because hypoacidity is usually present in such cases. Ordinarily the 
gastric juice, which comes in contact with the bowel wall, is not strongly 
acid, because, as stated above, in the majority of cases, it is neutralized 
by the backflow of bile and pancreatic juice. 
Doubtless, this is a considerable protection for the jejunum, and it 
helps explain why jejunal ulcer is more common when those operative STOMACH 
63 
methods are used which either prevent or diminish this regurgitation. 
After Braun’s anastomasis (151), Neuhaus (106) could demonstrate that 
no bowel secretions can re-enter the stomach, and this is also true of 
Roux’s “Y” anastamosis (statistics of Von Roojen: compare this with 
Von Haberer (144)). Exalto performed gastroenterostomies in seven 
dogs and fed them mixed food and hydrochloric acid daily for some time 
without finding jejunal ulcers, while, of seven other dogs operated by the 
“Y” method and fed similarly, five died of perforating jejunal ulcers. 
Bickel’s investigations (124) yielded the same results. He extirpated the 
duodenum in a dog and deflected bile and pancreatic secretions to the 
exterior. This animal also died of perforating jejunal ulcer. The back- 
flow of bile and pancreatic secretions into the stomach evidently can neu- 
tralize even a high grade hyperacidity, and thus make it harmless to the 
jejunum; for to mention another experiment (Borszeky (109)) performed 
gastroenterostomies on 12 dogs and gave them two tablespoonsful of 
strong hydrochloric acid daily for three months. He then found a fatal 
perforating jejunal ulcer at the gastroenterostomy site in only one dog. 
Although we have seen that the principal reason for the formation of 
jejunal ulcers is the action of hydrochloric acid on the jejunal mucosa, 
the fact must not be overlooked that jejunal ulcers may occur, though 
rarely, even in diminished or absent acidity (Mikulicz, Kocher, Heiden- 
hain and many others (107)). In these cases another factor must be con- 
sidered, namely, that the vitality and resistance of the jejunal wall has 
been injured by some substance other than hydrochloric acid. Naturally, 
such injuries occur frequently to the jejunal epithelium during the opera- 
tion and especially at the place of the gastroenterostomy opening where 
the mucosa may be injured by the pull of the sutures or the pressure of a 
Murphy button. In discussing the histology of the repair of wounds of 
the stomach, it was pointed out that the mucosa of the intestine frequently 
breaks down at that place, so that healing proceeds by granulation. Such 
unprotected wound surfaces offer an especially good point of attack for the 
digestive action of the gastric juice, and statistics actually show that ulcers 
are most frequent at the opening. According to Haberer’s (144) experi- 
ence, however, they are, as a rule, not situated along the line of suture, 
but are usually distal to it. 
The importance of mechanical injury to jejunal mucosa as a cause of 
ulceration, is very well brought out in a communication by William Mayo 
(152). He observed only three jejunal ulcers among a large number of 
gastroenterostomies—one was caused by a Murphy button inserted three 
and a half years before, and still in situ; the second had formed on the floor 
of a suppurating hematoma in the transverse meso-colon; and in the third, 
an infected silk suture was found. In reference to the last observation, 64 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
the danger of silk as a suture material for the mucosa is especially 
emphasized in the English (Wilkie (99)) and French literature. In a recent 
publication, von Haberer (144) also expressed the opinion that silk 
thread, by daily friction, produced an ulcer a short distance from the 
line of sutures, and after observing this case, he infers that the jejunal 
mucosa may be so irritated by the mechanical action of food that ulcers 
result. 
The motor activity of the stomach is influenced to a much greater 
degree by pyloric resection than by simple gastroenterostomy. Three 
years before it was first done in man (Pean (1879)), Gussenbauer and 
Winiwarter had shown that the dog could withstand removal of this part 
of the stomach. These experiments, as well as those done as early as 
1810 by Merrem, pathfinding though they are, give us only a general 
idea of the effects on gastric function. Only in recent years have accurate 
investigations of the activities of the resected stomach been made with the 
help of the x-rays and fistulae (von Mering, Schuller, Dagaew, Kaplan 
and others (153)). Von Mering found no change in the evacuation time 
when he resected the pylorus and sutured the duodenum to the stump of 
the stomach. His statements, however, are only very general. The 
motor function was examined more carefully by Dagaew and later by 
Kaplan on the same dogs in the London Institute of St. Petersburg. 
These authors found a slowing of gastric evacuation which remained 
unchanged for years. This is very varied and is less after operation by the 
first method of Billroth than after the second. The contraction of the 
attached small intestine maintains periodicity of gastric evacuation and 
also slows it by the resistance of its pendulum movements (Dagaew). 
If other factors were inoperative, the resected stomach would empty 
rather more quickly than the normal, for the reflexes arising in the bowel 
and ordinarily acting on the pylorus, now act on the fundus. Anatomic- 
ally, there is of course no sphincter developed, but von Mering found that 
by introducing a finger, the gastric opening into the bowel closed under 
stimulation just as perfectly as when the pylorus was preserved. 
Investigations (Gocke (154) and others) have shown that conditions are 
more favorable in man than in animals probably on account of his upright 
position, and quite normal evacuation of the stomach may be present 
even with Billroth’s second method. According to Gocke, the evacuation 
time depends on the position of the remainder of the stomach. The 
steeper this is, that is, the shorter the remaining part of the greater curva- 
ture, the quicker the stomach empties itself. This explains the contra- 
dictory results obtained in animals and in man, as recorded by Schuller 
(155). In some of his patients, all of whom were operated by Billroth’s 
second method, the evacuation took two and one half to four hours, i.e.} STOMACH 
65 
it was approximately normal. In others, it was considerably accelerated. 
In one case, three years after operation, the stomach was quite empty in 
five minutes. In patients who were examined more than once, it was 
found that the evacuation time varied on different days; for instance, the 
individual whose stomach emptied in five minutes, returned two months 
later and at that time retained the chyme for one hour after eating. 
According to Schuller, the cause of this irregularity is chiefly mechanical, 
and is influenced by gravity since the actual gastric motor, the antrum 
pylori, has been removed. Compressions and kinkings, as well as shrink- 
ing of the attached bowel may result. Generally speaking, the same 
considerations regarding backflow of bile and pancreatic juice that were 
discussed under gastroenterostomy, hold good for resection. 
When the fundus was resected in animals, Kaplan (118) could demon- 
strate an accelerated gastric evacuation which was practically independent 
of the size of the resected portion. 
The results, following transverse resection, have been investigated very 
carefully from all standpoints both in animals and in man by Kirschner 
and Mangold (54), Gocke (154), von Redwitz (156), and others. Kirsch- 
ner and Mangold could show that such an incomplete section of the 
sympathetic and vagus fibres as occurs in this resection has no noteworthy 
effect on the antrum movements and reflexes; there is an outspoken 
autonomy here. According to von Redwitz, if a large part of the fundus 
is removed, the mixing of food is interfered with, but the emptying of the 
liquefied gastric contents into the duodenum is less affected. Further- 
more, transverse resection has also no appreciable influence on the quality 
of the gastric juice but the food, especially proteins, tends to remain longer 
in the stomach since the diminution of secretion to digest the food is 
proportionate to the amount of stomach removed. The numerous #-ray 
studies after transverse resection in man, have not yielded entirely similar 
results (157). Kummell could observe a deep spastic contraction at the 
site of the resection. Faulhaber and von Redwitz found only a shallow 
contraction in this area, caused perhaps by the sutures. According to 
Gocke, the peristaltic wave does not pass across the area of resection. 
But it is especially the findings regarding gastric evacuation which vary. 
In some cases rapid evacuation was observed; in others, it was normal. 
The experiments of Kaplan, mentioned above, seemed to support the 
statement that accelerated gastric evacuation results if much of the 
fundus is resected. Von Redwitz does not share this conclusion, but 
believes with Gocke that the rapidity depends on the shape of the remain- 
ing part (see above). On the other hand, Perthes believes that rapid 
gastric evacuation can only be explained by assuming that the pylorus 
remains open. This, however, is not the case according to the animal 66 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
experiments of von Redwitz. The relation found by Perthes between the 
rapid evacuation of the stomach and the appearance of hunger sensations, 
is very interesting. Sense of hunger was absent when a six hour residue 
remained in the stomach. Other investigators, like Gocke, could not 
demonstrate any parallelism between gastric evacuation and hunger 
sensation and the findings seemed to point to the conclusion that hunger 
sensation is not dependent on the presence of the stomach. According 
to Thoma (L. R. Muller) (158) these sensations are brought about by a 
deficit of nutritive substances in the blood, the presence of which normally 
quiets the hunger center in the mid-brain. 
[See page 147 and Carlson’s article in “ Harvey Lectures ” 1915-1916.] 
Total resection is now being performed more frequently since a large 
number of surgeons have abandoned simple gastroenterostomy for 
the treatment of peptic ulcer distant from the pylorus. The number of 
published cases, about forty, is probably not the real figure (159). The 
first of such investigations was made by Czerny in dogs (Kaiser (160)). 
One of these animals which lived five years after the operation, was later 
examined by Ludwig, i.e., Ogata. This animal has gained a certain fame 
in literature, which, however, is not quite justified, since at the autopsy 
it was found that a piece of stomach had been left at the cardia and had 
expanded into a small bag. In the dog reported by Monari (161), a 
strip of stomach remained, although distinctly smaller than that in 
Czerny’s dog, and at least no new gastric pouch formed from it. The 
same is true of the dog of Matthes-Grohe (159), but Dagaew (121) suc- 
ceeded in doing an anatomically proved total gastric resection uniting the 
esophagus to the duodenum. DeFillippi (162) could not demonstrate 
any changes in metabolism in Monari’s dog which was similarly operated. 
At autopsy, it was shown that both the lower part of the esophagus and 
the duodenum were distended like a pouch. The enlargement of the 
cardiac end of the esophagus results probably from the section of vagus 
fibres. Enlargement also occurs in man as described by Cohn (163) in a 
case operated by Unger (164). Accurate analyses of the processes of 
digestion have been made in a few of those cases in which good results 
followed the operation (159) and these have shown that neither the sensa- 
tion of hunger nor of satiation (Cohn) is felt although a peculiar pressure 
sensation in the abdomen warns them when the upper portion of the 
bowel and the esophagus are filled, that they must stop eating. The food 
remains for a very short time in this bag-like dilatation of the esophagus 
and then is transported through the intestines very slowly, taking 24 
hours to reach the cecum; but the statements regarding hunger sensations 
in total or subtotal gastric resection vary quite considerably. A man 
operated years ago in this clinic shows only one discomfort, and that a 67 
STOMACH 
continuous sense of hunger and an enormous quite untimely appetite (see 
also transverse resection). 
The slow passage through the intestines should probably be considered 
as due chiefly to vagus resection. At least, it cannot be deduced from 
Ogata’s experiments (165), that the presence per se of food which had not 
been in the stomach, slowed its passage through the small intestines. 
His work was done on dogs which he fed through fistulae in the small 
intestine, and thus excluded gastric digestion. Unger’s patient was very 
constipated after the operation. This also may possibly be considered 
due to the cutting of vagus fibres (Cohn). In a case of Schlatter (166) 
(the first successful gastrectomy (1897)) although no constipation resulted, 
huckleberries, given as a test substance, did not appear in the stools until 
72 hours after ingestion. 
Now what functions must be assumed by the small intestines after 
total gastric resection? We have seen above that the chief function of 
the stomach is to act as a mechanical reservoir in which food is liquefied, 
that is, brought to a consistency most useful to the bowel. At the same 
time, it regulates the supply and admits only small quantities at a 
time. The slight dilatation of the esophagus cannot receive consideration 
as a substitute. We must, therefore, give finely comminuted food in 
small amounts to facilitate the work of the bowel. We have seen, in 
discussing gastroenterostomy, that the digestive processes of a chemical 
nature can be carried out perfectly by the pancreatic juice and the bile. 
Pepsin is replaced by trypsin and in a similar manner the other less impor- 
tant enzymes, including the milk curdling ferment, are present in pan- 
creatic and intestinal juices (167). Consequently there is nothing to fear 
in regard to the chemical splitting of food and, really, the only anomaly 
demonstrable is the absence of bile acids in the feces, which must be due to 
the lack of hydrochloric acid. This conclusion was reached after numer- 
ous examinations of urine and feces made when food was given through a 
duodenal fistula (Ogata (165)) when the entire stomach was resected as in 
the dog of Monari (de Fillipi) and in the human gastrectomy of Schlatter 
(168). In the latter case, no microscopical abnormality was found in the 
feces, nor were decomposition products such as scatol or indol, detected 
in the urine or in abnormal amounts in the feces in spite of the absence 
of the disinfecting power of the stomach (see also Ssolwjeff (169)). It 
follows when complete compensation does not occur in a patient (Cohn),, 
but disturbances in the evacuation and the condition of the feces are 
present, that these must necessarily be charged to secondary factors, 
(severe anemia, cachexia, etc.). 
In examining the histories of patients who have had a total gastric 
resection, it is often found that the patients vomit. This of course in 68 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
the absence of the stomach attracts attention and two types must be 
differentiated, one similar to that occurring in cardiospasm in which stag- 
nating masses in the lower end of the esophagus are emptied without 
nausea (Cohn), and second, an actual vomiting of the food which has been 
in the small intestine (Schlatter). 
Even when, as stated, the small intestine satisfactorily takes over the 
functions of the stomach, evidences of this abnormal activity are left 
behind principally in the form of atrophy of the intestinal mucosa 
(Dagaew). It is interesting that such a change may occur in the 
duodenum even after simple gastroenterostomy (Casagli (127)). The 
small intestine, therefore, seems more sensitive to all these operative 
procedures than examinations of the metabolism would indicate. 
When the resection is not quite complete, a dilatation of the stump 
may occur in the course of time. The duodenum also dilates, and a 
gastric pouch finally results, which, in Schuchardt’s case (170) almost 
approached the original stomach in size. 
Gastric, duodenal and jejunal ulcers (see above) are, according to our 
present viewpoint, not specific diseases. For their formation, two inter- 
acting factors must be considered. The first is injury to gastric and intes- 
tinal cells which must always occur before the second factor, namely, the 
digestive action of gastric juice, can operate. 
Without previous injury the stomach wall is not digested. A very large 
number of hypotheses have been proposed and investigated to explain the 
protective power of the mucosa against self digestion. In the first place, 
mucus, probably through its mucin content, acts as a protection by cover- 
ing the epithelium (Roux and Riva (171); Claude Bernard); (Klug (172)); 
on the other hand, Danilewsky assumes the presence of a so-called anti- 
pepsin (173). Kaufmann demonstrated a consistent lack of mucus in 
gastric ulcer (174), but it can be shown experimentally that this substance 
does not give absolute protection. Payr, for instance, produced typical 
ulcers by causing thrombosis of gastric vessels even when the distribution 
of mucus over the epithelium was not changed in the least. 
Pavy’s old theory that the blood circulating in the gastric vessels 
becomes richer in alkali because the gland epithelium deprives it of the 
chlorine to manufacture hydrochloric acid enjoyed general recognition 
for some time, but no proof has ever been offered for its truth. On the 
contrary, Edinger (175) has shown that the acid reaction is present not 
only on the surface of the mucosa, but also in the deeper layers. This 
rather elementary theory can therefore be discarded and search for the 
immunity to digestion of the uninjured stomach wall must be directed to 
properties possessed by the cells themselves. The question is simply this: 
Is resistance to digestion a general property of all living uninjured cells STOMACH 
69 
as Hunter believed (176) or is it a specific property of gastric epithelium? 
Hunter’s teaching seemed disproved by the famous experiment of Claude 
Bernard (177) in which he placed the thigh of a living frog through a 
fistula into the stomach and found that it was promptly digested. Pavy 
observed the same result with a rabbit’s ear. These experiments, however, 
do not demonstrate the fact for which they were designed; for in both 
cases it was not the living, but a previously devitalized protoplasm which 
was digested. This is shown especially in the well planned experiments of 
Matthes (178), who demonstrated that by these methods, the hydrochloric 
acid of the gastric juice, acting as protoplasmic poison, kills the cells before 
they are digested. In Claude Bernard’s and Pavy’s investigations this 
injurious action of the acid was probably further favored by the circulatory 
disturbances incident to the ligation of the frog’s thigh or the rabbit’s ear. 
“In the presence of living uninjured tissue, digestive enzymes are inac- 
tive” (Matthes). 
The question has now been concentrated to this: Why does hydro- 
chloric acid produce no injury to the gastric mucosa? Matthes’ investi- 
gations give at least a partial answer to this. He found that a natural 
gastric juice with a high acidity digested proteins more quickly and 
thoroughly than an artificial one of even lower acidity, but acted less 
injuriously on living tissue. Doubtless this depends on a partial neutrali- 
zation of the hydrochloric acid by albumoses and peptones and also, 
perhaps, on protection by the mucus so that natural gastric juice seems 
less injurious than its content of the acid would indicate. This restric- 
tion of the action of the acid in the stomach cannot, however, be the only 
reason why the mucosa is normally uninfluenced, for then it would be 
difficult to understand why gastric juice which has had no influence on 
mucosa, digests the skin over which it flows from an open gastric fistula. 
This experience, so familiar to all surgeons, therefore obliges us to assume 
some sort of a specific protective property inherent in gastric epithelium. 
This must be accepted, simply as a fact, without any clear explanation. 
Other studies of Matthes have shown that the other tissues of the 
body vary in their susceptibility to the action of hydrochloric acid and it 
seems that the stomach wall itself is not absolutely protected. He states 
that in dogs, ulcers produced by trauma heal more slowly if about 50 c.c, 
of 0.56 per cent, solution of hydrochloric acid is given by mouth on 
an empty stomach. Naturally, these investigations did not remain 
unchallenged (Neumann (179)). The objection was made that such a small 
quantity of hydrochloric acid hardly increased the per cent, of acid in 
the stomach contents. But this objection may not be valid, for as stated 
above, artificially introduced hydrochloric acid is more irritating than 
the natural, because the latter is partly bound. * 70 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Kehrer (180) performed the following experiments with dogs on the 
same problem. After cutting the biliary and pancreatic ducts, he diverted 
these secretions into lower bowel segments. The chyme remained acid 
for a longer period in the duodenum, the pylorus remained closed and the 
fluid in the stomach became strongly acid. As a matter of fact in a few 
cases he did obtain ulceration of the gastric mucosa. But this does not 
necessarily mean that high acidity should be considered particularly 
important, for, according to the newest statistics, hyperchlorhydria is a 
frequent, but by no means constant accompaniment of gastric ulcer. In 
many cases it is brought about by pyloric stenosis (see above) and as Vir- 
chow (181) emphasized long ago, such a hyperchlorhydria, without local 
injury, would give rise to only a gastromalacia and never to a circumscribed 
ulcer. 
Matthes’ experiments practically prove that the stomach does not 
digest itself because of a special resistance to hydrochloric acid, but its 
immunity to pepsin must also be taken into account, since large experi- 
mental lesions of the mucosa quickly cicatrize and never lead to typical 
ulcers. This idea was again brought into prominence when so-called 
antipepsin was first demonstrated in the gastric juice and blood. All we 
know of this antienzyme is that the activity of pepsin is frequently checked 
and that quite different substances may be involved. From certain 
properties which it exhibits it may be assumed that it does not belong to 
the actual antibodies. Such pepsin inhibitory substances occur in the 
mosjt diverse, and in the lowest forms of life, as for instance, in bacterial 
extracts (Krasnogorski (182)); so that there is nothing specific about its 
presence in gastric juice or in intestinal parasites as it was once believed. 
Some surgeons, however, are still of the opinion that gastric ulcers must be 
attributed to an absence of antipepsin in the stomach wall (183). Katzen- 
stein was one of these and to prove this view, he transplanted sections of 
intestine, spleen, omentum, etc. into the stomach and found, without 
exception, that they were digested; implanted stomach wall, however, was 
not affected. Furthermore, he could produce chronic perforating gastric 
ulcers in animals by destroying the antipepsin. The same objections as 
those mentioned in connection with Claude Bernard’s experiments hold 
good for this first group; it was not a question of digesting living intact 
tissue, but tissue with its nutrition disturbed. 
Other authors (184) had already obtained contradictory results from 
similar experiments before Katzenstein’s work, andLicini (185) and Hotz 
(186) who repeated them with similar technic, but with especial care of the 
nutrition of the implanted part, found no digestion of either the spleen or 
intestine. On the other hand, Best (186) has recently obtained opposite 
results again. Obviously in experimental methods of such a nature, STOMACH 
71 
negative results have more weight than positive, because disturbances of 
nutrition can never be excluded with certainty. In his second group of 
experiments, Katzenstein injected dilute hydrochloric acid into the gastric 
wall or the blood stream to weaken the antipepsin, which supposedly acts 
only in alkaline media, but results by this method may be also explained on 
different grounds. The injection itself injures the tissues and this injury 
may be increased by reflex vessel cramp (see later) after the acid is 
introduced into the blood stream. 
Thus the theory that the protection of the stomach against auto- 
digestion resides in an antipepsin, and that a diminution of this substance 
in the stomach wall is followed by gastric ulcer, is yet to be proved. 
Stuber (132) recently expressed another opinion; that it was not the 
gastric juice which attacked the stomach, but trypsin, and that the pan- 
creatic juice entered the stomach through a “ neurogenically insufficient 
pylorus.” He attempted to prove the correctness of this theory by 
experiments on animals. In five dogs, he obtained multiple gastric 
ulcers, some of them calloused, by partial resection of the pyloric muscle 
and the administration of sodium bicarbonate. These experiments 
should be repeated and their merit determined since they are of great 
importance, especially in the treatment of gastric ulcer. 
The primary factor in the formation of gastric ulcer is injury to gastric 
or intestinal mucosa. There is doubtless a certain analogy to leg ulcers. 
Wounds on other parts of the body surface tend to heal without difficulty, 
but wounds on the lower leg from the ankle to the middle, are often very 
stubborn. Similarly, according to the experiments of Ribbert (187) 
artificially produced ulcers in the stomach, provided they are of sufficient 
size, show no tendency to heal, even in healthy animals. Nutritional 
disturbances following insufficient blood supply, are factors of the highest 
importance for consideration (Virchow (181)). Many unsuccessful 
attempts have been made to injure the nutrition of the stomach wall by 
ligation of vessels, sufficiently to produce a typical ulcer (187). Disse 
(188) may be consulted regarding the blood vessel supply of the gastric 
mucosa. According to Braun (Alberts (189)), four-fifths and more of the 
gastric vessels may be ligated without danger of gangrene, but Fibich 
(190) obtained progressive ulcers of the mucosa by the ligation of arteries 
and the excision of a portion of the mucous membrane with cauterization 
of the base. Generally speaking, however, the anastomosis of the gastric 
vessels is sufficiently free to provide adequate blood supply so that even 
artificially produced defects of the mucosa with simultaneous ligation of 
the arteries, heal easily. Clairmont (187) in attempting to repeat Fibich’s 
experiments could not confirm his results. Since these experiments failed, 
the logical procedure was to interfere with the gastric circulation through 72 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
capillary thrombosis, especially since Panum had shown (191) that the 
introduction of wax pellets, etc. into the femoral artery against the blood 
stream was followed by ulceration in the stomach and intestines. Cohn- 
heim (192) injected chrome alum into the gastric artery and found “large 
ulcers with steep margins and perfectly clean bases in all the animals which 
died or were killed within one or two days.” Payr (193) by the injection 
of dermatol, India ink, and particularly formalin, obtained typical ulcers, 
but they were also progressive so that they were very similar to those 
found in man. Ulcers produced by ordinary embolism healed very quickly, 
and this latter fact is essentially different from human gastric ulcers. 
But since Payr always obtained progressive ulcers by the injection of 
formalin, it seems to show that if the vascular injury is extensive enough, 
ulcers will form. Hauser (194) had already assumed this on the basis of 
his pathological anatomical studies. V. Redwitz (195) also after extensive 
histological examinations stated that thrombosis is very frequent in the 
region of an ulcer. Of course the question immediately arises, are these 
thromboses primary or secondary? Does pathological anatomy give any 
good reason for believing that thrombosis or embolism precedes gastric 
ulcer, as they do when the nutrition of the gastric wall is shut off experi- 
mentally? As a matter of fact, a number of such cases have been reported 
in the literature. Thus v. Recklinghausen (196), and later Merkel (197) 
have described cases of ulcer following embolism, and at least one case of 
hemorrhagic infarction of the stomach wall has been reported by Hauser 
(194). Such embolic showers are usually the result of an endocarditis, or 
of an extensive venous thrombosis, as in v. Recklinghausen’s case. They 
seldom offer opportunity for surgical interference on account of the grave 
general condition of the patients. 
Those ulcers observed following resection of the omentum belong 
perhaps to the same group, but they deserve considerable clinical atten- 
tion (198). The keen controversy which was waged some years ago, as to 
whether the emboli following resection of the omentum occurred only in 
the presence of infection has now been settled. Infection is not necessary, 
but in its presence, thrombosis and ulceration are probably much more 
frequent (see also Sprengel (199)). It is useful to differentiate those cases of 
hematemesis which occur post-operatively and in which the operation 
played the chief role, from those occurring in non-operated cases in which 
the offender is in all probability an infection, particularly of the peritoneum. 
This has not been done in the literature, and it has added another confusing 
factor in this very difficult field. After ligation of the omentum, throm- 
boses have been found, not only in the vessels of the stomach but also in 
those of the liver and they have been accompanied by focal necroses. 
This seems to show that a retrograde process occurs in the region of the STOMACH 
73 
portal vein. The underlying conditions have been studied very carefully 
by Payr (193) who produced thrombosis by freezing the peripheral parts 
of the omentum, and then followed its progress by the injection of foreign 
bodies. Experiment thus showed him that “emboli in the course of the 
veins could move toward the stomach and produce all the changes which 
had long been attributed to them.” 
This retrograde embolism is favored in the first place by the relatively 
Straight course of the veins, and further by the fact that according to the 
investigations of Hochstetter (200) no valves remain in the veins of 
individuals over 20 years of age. By a like reasoning, the presence of 
valves in children is said to prevent post-operative gastric ulcers. The 
researches of Payr have been checked by the investigations of Yatsushiro 
(201) who concluded that Payr obtained retrograde embolism simply 
because he used too high pressure in his injections. Finally, it is believed 
by some, especially by internists, that it is not a question of embolism 
in post-operative ulcers, but reflex vessel spasm (see later). It is a fact 
that embolism and thrombosis are not found frequently enough at autopsy 
to account for the very often severe hematemesis (“vomito negri”). 
Nitsche (202) has reported a case of hematemesis following appendici- 
tis, which showed microscopic necroses and hemorrhages in the mucosa 
three hours after death. These he attributes, in the absence of thrombi, 
to an excretion of toxic substances by the gastric glands, just as alkaloids, 
for example, are excreted. This excretion “injures” the glands, and 
would be of course a special form of septic injury, not embolic, but toxic. 
In other cases, a so-called “parenchymatous” bleeding is dealt with 
(Reichard (203)), of which we know only that it occurs in certain family 
groups. Ulcers are not present nor do they occur in “ bleeders,” though 
trauma may initiate them. 
Among the pathological anatomical observations which are said to 
show circulatory and therefore nutritional disturbances in the gastric 
mucosa, the erosions following passive congestion, following certain brain 
affections, and vomiting (Orth (204)) may be mentioned. Finally, we may 
also consider those in individuals with a more or less extensive arterio- 
sclerosis and degeneration in the vessels (Kaufmann (205)) and those follow- 
ing traumatic changes in the blood supply. It must require quite an 
extensive destruction of blood supply either through laceration of the 
vessels or reflexly by vessel cramp to produce an ulcer after trauma, 
because we know from numerous experiments that in the absence of 
extensive injury to vessels artificial defects in the mucosa show a pro- 
nounced tendency to heal. In connection with observations in Leube’s 
clinic, Ritter (206) studied the effect of blows delivered through the abdom- 
inal walls on the stomachs of dogs. He found that there resulted mainly 74 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
“a complete separation of mucosa from submucosa, with hemorrhage into 
the latter” and slight bleeding into the other layers of the stomach. He 
did not obtain a true ulcer. Chronic traumatism, the importance of which 
is very variable in the formation of an ulcer, may be caused by tight 
lacing, but it is very difficult to determine the significance of this factor 
in relation to gastric ulcer. Displacement of the position of the stomach, 
as in diaphragmatic hernia (207) may also lead to ulcer by disturbances 
of nutrition. Furthermore, injuries of every possible kind may affect 
the inner surface of the stomach and produce a defect in the mucosa. 
Decker (208) by repeated introduction under the mucosa of fluid warmed 
to 50 degrees, obtained hemorrhages and deep loss of tissue. It is a well 
known fact that cooks suffer comparatively frequently from gastric ulcer 
perhaps because they often taste very hot food, and ulcers are also quite 
frequent in mirror workers, metal workers, porcelain workers and others 
who swallow sharp particles. Doubtless, in the last mentioned cases, 
the factor of chief importance is vessel spasm rather than injury to mucosa. 
Strohmeyer (209) thinks he has found a chronic trauma in the pressure 
caused by the advancing ingesta. He arrived at this conclusion from the 
well known form of the ulcer, i.e., sloping sides like a funnel, which 
corresponds to the progressive movements of the stomach contents. He 
states that the accepted reason for the oblique form of ulcers, namely, 
the oblique course of the vessels, is not constant, but varies with the 
degree of filling of the stomach. 
An injury with subsequent ulcer can furthermore result from bacterial 
occlusion of the vessels (Neumann (179)). It has already been mentioned 
that many authors have accepted the theory of an infectious origin for 
those following resections of the omentum. Nauwerk (210) and recently 
Fritz Mayer (211) have given definite proof that bacterial embolism causes 
a large number of so-called erosions which, since Virchow, have been 
correctly regarded as forerunners of ulcers. From the literature and from 
cases of his own, W. Busse (198) concludes that hemorrhagic erosions, 
particularly those occurring post-operatively result from emboli, whether 
the latter are infected or not. Actually, many experimentors (212) 
could obtain ulceration of the gastric mucosa by the intravenous or sub- 
cutaneous injection of all sorts and varieties of bacteria. Singer (213) 
found gastric ulcers in 71 per cent, of rats kept under unhygienic conditions 
and fed with bread contaminated with their own feces, and Turk (214) 
found chronic progressive ulcers in dogs which had been fed large amounts 
of colon bacilli and housed in unfavorable surroundings. 
For the development of duodenal ulcer, Moynihan holds a previous 
appendicitis responsible, accepting, therefore, the theory of an infectious 
origin. This conception is not ratified by most German surgeons (215). STOMACH 
75 
[There is considerable circumstantial evidence in favor of ulcer follow- 
ing appendicitis in not a few cases. In the surgical clinic of our own 
hospital, we have had a number of notable examples in which a second 
laparotomy six months or later after operation for acute appendicitis 
has revealed ulcer. It is not certain that the ulcer developed subsequent 
to the appendicitis but careful questioning failed to reveal previous symp- 
toms suggestive of the condition. A long series of experiments on dogs 
and rabbits led to no conclusive results but other work with india ink 
(unpublished) showed that lymphatic drainage from the region of the 
appendix may carry material to the region of the duodenum and pylorus. 
At any rate, the idea that infection plays an important role in the origin 
of ulcer cannot be denied and the appendix need not be the source even 
if it is the commonest site of infection in the abdomen. The tonsils or 
other foci may be implicated. Rosenow’s work, while it can be criticized, 
is at least very suggestive.] 
Naturally, in the cases recorded in pathological anatomical literature 
as infectious, it cannot be positively determined whether the infection is 
primary or secondary, since ulcers provide such a suitable pabulum to the 
bacteria with which they are constantly surrounded. 
A case of Breus (216) is especially interesting in this connection. He 
reports an ulcer resulting from erosion by potash, which became second- 
arily infected by the tubercle bacillus. In addition to this case, other 
tuberculous ulcers have been described by various authors (217). Very 
little is proved by finding such ubiquitous organisms such as staphylococci, 
streptococci, colon bacilli, mycelia, etc. at the base of an ulcer (see cases 
of Sjubimowa (218), Rosenow (219), and others) while the presence of 
specific organisms and also of perhaps specific histological changes such 
as in anthrax, typhoid, syphilis and especially tuberculosis have a greater 
value but are by no means convincing. Tuberculous infection is relatively 
the most frequent of those named, and the portals of entry of this organism 
are better known (220). Infection may occur from the serosa or through 
the mucosa or by way of the lymph or blood vessels (221). 
It seems probable that in all cases in which infection is the cause of the 
ulcer, the primary factor must be a defective circulation whether it occurs 
mechanically by bacterial obstruction or reflexly through spastic contrac- 
tion of the nutrient vessels. 
The theory which seems to hold the center of interest at the present 
time, although in rejuvenated form, refers to the influence of the nervous 
system on the formation of ulcer. This was investigated experimentally 
as early as 1828 by Cammerer (222) who attempted to produce destruction 
of the stomach wall by resection of the vagus and administration of acetic 
acid. Talma (223) also speaks of the importance of this nerve. He says 76 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
that irritation leads to a contraction of the musculature “which, if pro- 
longed may cause the formation of round ulcers.” The experiments of 
v. Ijzeren (224) are very interesting in this connection. He sectioned the 
vagus below the diaphragm and among 20 rabbits he found 10 with ulcers, 
the oldest of which was 28 to 29 days. In addition to regenerative processes 
there were also “degenerative changes which prevented healing.” 
Lichtenbelt (225) and Antonini (226) found similar ulcers after vagus 
resection, but other authors had negative results in this respect (227). 
Clinically, Singer (228) observed a case in which the vagus nerve was 
surrounded by tuberculous lymph nodes and the symptoms of the patient 
were like those of duodenal ulcer. 
Furthermore, attempts were made to produce gastric ulcers by irrita- 
tion or destruction of the coeliac ganglion or the sympathetic nerve. 
Foremost among those to obtain positive results was Della Vedova who 
found 41 per cent, of ulcers after destruction of the coeliac ganglion, and 
60 per cent, after destruction of the splanchnic nerve. Kobogashi (229) 
and Kawamura (230) also observed multiple erosion in the gastric mucosa, 
not only after pricking or extirpation of the coeliac ganglion but also after 
section of the spinal cord, or ligation of the vagus nerve. Schiff (231), 
Ebstein (232) and others saw such ulcers after section of the optic thalami, 
cerebral peduncles, medulla oblongata, and spinal cord. In short, there 
is a large amount of experimental data in the literature which shows that 
gastric ulcers may be caused by disturbances in the equilibrium of the 
vegetative nervous system. There is much confusion, however. In many 
experiments on dogs, Gundelfinger (233) could never produce defects in 
the stomach or duodenum by procedures on the vagus, but always obtained 
them by extirpation of the coeliac ganglion. Nagamori (234) could produce 
them in rabbits by stimulation of the coeliac plexus. 
Just as it happens so often in the history of medicine, these findings 
have been given widely differing interpretations. Klebs (235) esteems the 
nervous system very highly as the causative factor in ulcers. He was 
of the opinion that the injury to stomach wall, which is the primary cause 
of the formation of ulcer, is brought about by vessel spasm, an opinion 
which Cohnheim (236) and after him many others, have disputed, because 
they believe such a spasm would not be of sufficient duration. The idea 
has been recently revived by Beneke (237), is now steadily gaining ground, 
and today we find it very widely recognized. Internists especially are 
its supporters, but there are also many among pathological anatomists 
(238). Thus Rossle (239) actually speaks of ulcers as “ secondary diseases,” 
because pathologically anatomically he has usually found with them other 
preceding changes, especially an old appendicitis, which are said to have 
brought about the reflex vessel spasm. According to Hart, this applies STOMACH 
77 
principally to the ulcers in older persons where coincident arteriosclerosis 
exists, and in whom, a priori, some sort of pathological process is to be 
assumed on account of the age. According to Lichter.belt, there are 
contractions of the muscularis mucosa which can be seen quite plainly 
with the .v-rays (von Bergmann (238)) and which are usually accompanied 
by cramp-like pains in the abdomen. This pathological contraction is 
said to result from increased irritability of the vagus. The investigations 
of Westphal (238) also support this conception. He obtained ulceration 
of the gastric mucosa by generous doses of pilocarpin and other substances 
which irritate the vagus. Furthermore, the experience of internists 
may be cited (Januschke (238)) who by giving atropine, have caused 
the prompt disappearance of painful colic. Rosier (240) tells of a number of 
interesting cases of ulcer in lead poisoning. In these, roentgenological 
contractures of the ring muscle in the form of hour-glass stomach could 
be demonstrated long before an ulcer appeared, and he concluded that 
ischaemia from vessel cramp was the immediate cause of the ulcer in these 
cases. 
Since experimental attempts to produce anemia of the mucous 
membrane by vessel cramp give somewhat irregular results, and especially 
since in animals it is seldom possible to produce chronic ulcers, as we see 
them in man, there must doubtless be assumed that a certain constitu- 
tional weakness operates in individuals affected by the disease (241). 
It had always been observed that weakly persons, especially chlorotic 
girls, are subject to gastric ulcer, and, therefore, particular physical condi- 
tions have been considered of much importance. In experimental 
animals, as has already been mentioned, such physical weakness has 
been established by caging them in dark, damp places with no oppor- 
tunity for moving about (Turk and others), or artificial anemia has been 
produced by bleeding (Quincke and Dettweiler (242)). Following such 
procedures, ulcers caused by thermic or chemical means healed more 
slowly. Silbermann (243) and Futterer (244) increased this artificial 
anemia by pyrogallol, and Litthauer (187) by pyrodin, all with positive 
results. The gastric lesions healed slowly or not at all. But this also 
is true of other wounds. They do not heal as well in anemic as in normal 
individuals. A gastric wound does not become a chronic ulcer just 
because of anemia. Experiments to produce vessel spasm and thus 
provoke ulcer formation were made by Licini with adrenalin (245) but the 
ulcers thus produced healed very quickly. 
If it can be shown that there is not only an indefinite “constitutional 
weakness” in those individuals with ulcers, but an actual predisposition 
of the vessels in the neighborhood of the stomach to cramp, a factor of 
importance will have been discovered. This presupposes an increased 78 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
irritability of the vegetative nervous system, a condition which in the last 
few years has been considerably illuminated, especially through the work 
of Eppinger and Hess (246). Great credit is due these authors for 
bringing into experimental reach the knowledge of constitutional weak- 
ness in the regions supplied by the vagus and sympathetics. They have 
introduced a “dynamic function test” and have shown that certain 
individuals respond strongly to atropin and pilocarpin while relatively 
insensitive to substances stimulating the sympathetic such as adrenalin. 
The reverse occurs in other individuals. 
Supported by these experiments, von Bergmann (247) has sought and 
found a similar constitutional weakness in the vegetative nervous system 
of his patients with ulcer. On the basis of later observation, the some- 
what too diagrammatic classification of vagotomy and sympatheticotomy 
has been abandoned (248). In most instances, the disturbances occur in 
both spheres (see Martius (241)) and even if a special nerve is notdiseasedr 
it does not exclude the possibility of a weakness in the vegetative system. 
According to Baur (90) it is a “degenerated soil” on which ulcers form, but 
it must remain an open question whether there is a lymphatic constitu- 
tional anomaly, or an asthenia, in the sense of Stiller (90) or some other 
form of degeneration. The regional distribution of gastric ulcer (for 
instance they are seldom observed in Brazil) also points to such factors 
(racial peculiarity) as well as to the influence of living conditions and 
nutritional circumstances (249). These findings, described above, fur- 
thermore, give us an explanation of why the old stomach remedy, bel- 
ladonna, gives us good results, and why morphin, which increases spasm 
and gastric secretion, fails so often in gastric pain. 
The spasms chiefly affect the pylorus, although the ulcers are distant 
from that region, or even when they are in the duodenum. Hunger 
pain, in duodenal ulcer, does not usually arise on an entirely empty 
stomach, rather the organ is filled with hyperacid fluid when the pylorus 
is spastically closed during a hunger pain. If the patient eats, the pylorus 
opens and the gastric fluid flows out. Probably this hunger pain is only 
a result of pylorospasm (see Haberer (215)). 
The results of Bolton (250) may perhaps be explained as following 
reflex anemia. He obtained a so-called gastro-toxic serum by the intra- 
peritoneal injection of stomach cells of heterologous species and then 
injected this serum into the stomach wall of an experimental animal. 
Deep ulcers resulted but thrombosis did not occur, as his accompanying 
pictures show. The description of the animal’s condition after the injec- 
tion, greatly resembles that seen in anaphylaxis. 
Gundermann (251) thinks the ulcers produced by him, after ligation 
of branches of the portal vein were due to liver injuries, that is, also of STOMACH 
79 
toxic origin and he does not believe they were due to thrombosis. The 
injection of liver extract into the ear vein of a rabbit was followed by 
subserous and submucous hemorrhages into the gastrointestinal tract 
and in some instances by collapse. Perhaps, as in uremic erosions, it is 
permissible to assume a reflex ischemia as the course of the ulcers. [All 
experiments of this nature are open to the objection of what might be 
called non-specificity. It cannot be too strongly urged that whenever 
extracts or fluids or other foreign substances are introduced into the body, 
two possibilities must be considered. When any result is obtained, ask 
first, is it general, and does it occur with any such substance; ask second, 
is it specific for the substance in question.] 
Krempelhuber (92) believes that anemia of the mucosa can be brought 
about purely mechanically by the gastroptosis which is present in some 
88 per cent, of cases of ulcer. 
The question now arises what operations can be done for gastric ulcer 
and how do they affect the disease? Resection of the ulcer bearing area 
is the easiest to understand. The changes affecting the mechanism and 
chemistry, following pyloric resection, have been previously discussed. 
But it cannot be denied that new ulcers may arise in other parts of the 
stomach after resection (252). 
The way in which a gastroenterostomy promotes healing is not easy to 
explain from a physiological standpoint, but that it does is a fact which 
must be accepted as proved by innumerable clinical observations. This 
is particularly demonstrable, as Kausch remarks (253) when a calloused 
ulcer is first treated by gastroenterostomy and then, after four to six 
weeks, on account of a suspicion of carcinoma, the radical operation is 
performed. The ulcer is then often found completely or almost healed. 
This is especially true of ulcers located at the pylorus and in these the end 
results, according to the study of von Redwitz, are just about as satis- 
factory as after resection. Other authors (254) believe that ulcers distant 
from the pylorus can also, in a large majority of cases, be made to heal by 
gastroenterostomy alone. This view is not universally accepted, although 
reports of healing after gastroenterostomy of the most severe type of 
ulcer, distant from the pylorus are plentiful (255). This alone interests 
us here, since we do not wish to discuss operative methods. In animals, 
von Izerem (224) found that after section of the vagus, he did not obtain 
an ulcer, as usual, when he performed a gastroenterostomy at the same 
time. Since, however, other authors have not consistently observed 
ulcers, following section of the vagus, care must be observed in the inter- 
pretation of this experimental result. Fibich (190) has further studied 
the healing of gastric ulcers after gastroenterostomy. He produced 
them by ligation of gastric vessels with excision and cauterization of the 80 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
mucous membrane, and they showed no tendency to heal without gastro- 
enterostomy. After this procedure, however, they healed in about 
three days like ordinary stomach wounds. All these experiments have 
aroused animated opposition especially since Korte, Clairmont and others, 
as above recorded, could never produce progressive ulcers under exactly 
similar experimental circumstances. For this reason, the results of 
Fibich are probably coincidences, which allow of no conclusive deduc- 
tions. Clairmont (187) following Fibich, repeated the experiments and 
came to the conclusion that up until that time (1908, before Payr’s work 
it had not been possible to produce a true gastric ulcer in animals), the 
healing of defects of the mucosa which occurred in about three weeks in 
the cardia and in six to seven weeks at the pylorus was not hastened, when 
a gastroenterostomy was performed at the same time. 
In spite of all this, how are we to explain the undoubted healing action 
of gastroenterostomy? Two factors may be taken into consideration; 
first, changes in the motor function and second, changes in the chemistry. 
We have seen that in comparison with the normal stomach the changes in 
the motor function are only of relatively minor importance. We must 
not forget, however, that in a large number of the cases operated for ulcer, 
the pylorus is not completely patulous because of mechanical obstruction 
either by an ulcer, or by a pylorospasm produced reflexly by an ulcer in 
another part of the stomach. In both cases, the gastroenterostomy 
opening operates purely mechanically; it undertakes the emptying of the 
stomach until the ulcer heals, and the obstruction to the pyloric opening is 
removed. It has also been observed in ulcers distant from the pylorus 
that pylorospasm disappears after operation (256). Undoubtedly, this 
better evacuation of the stomach cannot alone explain the rapid healing 
because the same injurious factor, digestive action of the gastric juice, 
is still active after operation. The second factor under consideration is 
the change in the chemistry (117, 257). Hydrochloric acid is neutralized 
by the backflow of alkaline intestinal contents and this inhibits its necros- 
ing effect on the cells of the stomach wall. Since the intestinal fluid can- 
not reach all parts of the stomach, but acts only in the neighborhood 
of the pylorus, it is easily comprehensible why ulcers in the cardia or on 
the lesser curvature heal with so much more difficulty than those at the 
pylorus, and Clairmont (258) has actually pointed out that results of 
gastroenterostomy in ulcers distant from the pylorus, are much poorer 
than those in ulcers at the pylorus. For this reason, a large number of 
surgeons treat the former principally by resection. 
When a gastrostomy is performed on account of stenosis of the esoph- 
agus, all the gastric stimuli from chewing, tasting, etc. disappear. The 
manner of response of the gastric glands to the sight of food, to chewing STOMACH 
81 
and to tasting, has been established by many experiments and was briefly 
mentioned before. The process when these are removed has also been 
studied (259). [In patients with gastrostomy openings, the flow pro- 
duced by the sight of food can, of course, be preserved although Carlson’s 
observations indicate that the amount is less than would be expected 
from Pawlow’s experiments on dogs. It will probably vary considerably in 
different individuals. It can also be tasted and chewed by these individ- 
uals.] Placing the food immediately in the stomach, however, also leads 
to secretion and digestion will thus proceed, although there is said to be a 
diminution of both hydrochloric acid and pepsin (Babkin The 
rv-ray studies of Cohn (260) give data regarding the motor activities under 
these conditions. He found that the usual contrast meal was quickly 
evacuated, but the addition of oil to the food slowed the emptying rate. 
The motor function of the stomach is therefore greatly dependent on the 
sort of food supplied. He could not observe peristalsis of the stomach but 
systematic studies sufficient to give useful information for the feeding of 
such patients are lacking. 
It might be mentioned in passing that feeding per rectum produces no 
gastric secretion whatever. 
LITERATURE TO STOMACH 
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Munch. Med. Wchscft., 1911, 58, p. 2732-2734. 
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3. Simmonds, Morris: “Ueber die Form u. Lage des Magens unter normalen u. 
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4. Petersen, Walther: “Anatomische und chirurgische Beitrage zur Gastroenter- 
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Verdauung and Ernahrung, Urban and Schwarzenberg, Berlin, 1908, p. 15. 82 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
See also Aschoff, Ludwig: (pamphlet), Ueber d. Engpass d. Magens Fischer, 
Jena, 1918 (Isthmus ventriculi ein Beitrag zum funkionell-Anatomischen Aufbau 
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f. exp. Pathol., 1886, 20, p. 291. 
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Roentgenogramme (Bio-Roentgenography) der inneren Organ des Menschen,” 
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Wochschift., 1919, No. 22, 579, No. 23, 623, No. 40, 1135, No. 41, 1169. 
13. Forssel, Gosta: “Ueber die Beziehungen der Rontgen bilder des menschlichen 
Magens zu seinem anatomischen Bau,” Grafe, Hamburg, 1913. 
14. Schwarz, G.: “Versuch eines Systems der physiologischen und pathologischen 
Magen peristaltik,” Fortschritte auf d. Gebiete d. Rontgenstrahlen, 1911, 17, 
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15. Muller, Albert: “Wie andern die von glatter Muskulaturumschlossenen Hohl- 
organe ihre Grosse?” Arch. f. Physiol., 1907, 116, 252. 
16. Kastle, Rieder and Rosenthal: Ztschrft f. Rontgenkunde, 1910-1911, 12. 
17. Holzknecht, G. and Luger, A.: “Zur Pathologie und Diagnostik des Gastro- 
spasmus,” Mitt, aus d. Grenzgebieten, 1913, 26, 669. 
18. Brauning, H.: “Die Entfaltung des Magens,” “Untersuchungen mit Roent- 
genstrahlen,” Munch. Med. Wochschift, 1909, 56, 277. 
19. Cohnheim, Otto: “Beobachtumgen ueber Magenverdauung,” Munch. Med. 
Woch., 1907, 52, 2581. 
20. Kastle: Fortschritte auf dem Gebiete d. Rontgenstrahlen, 1919, 26. 
21. Schuller: “Klinische und experimentelle Untersuchungen ueber die Function 
des Magens nach Gastroenterostomie und Pylorus resection,” Mitt. aus. d. 
Grenzgebieten, 1911, 22, 764. 
22. Grutzner, P.: “Ein Beitrag zur Mechanismus der Magenverdauung,” Pflugers 
Arch., 1905, 106, 463. Ellenberger: “Zum Mechanismus der Magenverdau- 
ung,” Pfluger’s Arch., 1906, 114, 93. 
23. Canon, W. B.: (1) “Movements of stomach studied by Rontgen Rays,” (2) “Pas- 
sage of food-stuffs from the stomach,” Am. Joum. Physiol., (1) 1898, 1, 
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24. Ducchesis, Virgilio: See Luciani, Human Physiology, trans. by F. Welby, Mac- 
millan, 1913, p. 192, etc. Vol. II. 
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im Magen,” Munch. Med. Woch., 63, 1916, 2, 37-40. 
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28. V. Mering and Aldehoff: 12 Kongress f. innere Med., 1893,471- Moritz: “Studien 
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30. Muller, Johannes: Ztschrft. f. diat. Therapie 8, Hft. 2. 
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83 
A. B., Phillips, H. T., and Carlson, A. J.: “The control of the pylorus,” Am. J. 
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32. Editorial: J. A. M. A., 1921, 76, 729. 
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34. Abderhalden, Emil: Physiol. Chemie, 1909, 661. Berlin, Urban. 
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36. Cohnheim and Marchand: Ztschr. f. Physiol. Chemie., 1909, 63, 41. 
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38. Popielski: Zentralbl. f. Physiol., 1902, 16, 121. 
39. Schiff and Contejean: Contrib. a. l’etude de la physiol, de l’estomac, These de 
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40. Bogen, H.: “ Experimentelle Untersuchungen ueber psychiche u. assoziative 
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42. Uffenheimer, A.: “Physiologie des Magen-Darmkanales beim Saugling und 
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43. Langley, J. N.: “Das sympathische u. verwandte nervose Systeme d. Wirbel- 
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47. Bayliss, W. M. and Starling, E. H.: “The movements and the innervation of the 
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THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
48. Elliot, T. R. and Smith, E. B.: “On the innervation of the ileocolic sphincter.” 
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49. Popielski, L.: “ Zur Physiologie des Plexus coeliacus (experimentelle Untersuch- 
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50. Goltz, F., Goltz and Ewald: (1) “Uber die Functionen des Lendenmarks des 
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51. Frankl-Hochwart, L. and Frohlich, A.: “Uber Tonus und Innervation der Sphink- 
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52. Courtade, D. and Guyon, J. F.: “Pneumogastrique,” Journ. de Physiol., 1899, 
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53. Exner, Alfred: “Wie Schutzt sich der Verdauungstract vor Verletzungen durch 
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54. Muller, L. R.: “Beitrage zur Anatomie, Histologie und Physiologie des nervus 
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55. May, W. P.: (1) “The movements and innervation of the stomach,” Brit. Med. 
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56. Cannon: Zentralbl. f. Physiol., 1906, 20, 613. Cannon, W. B.: “Motor activities 
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57. Dr. Van Braum-Honckgeest: “Untersuchungeo ueber Peristaltik des Magens und 
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58. Cited by Magnus: (2) “V. Ducchesi,” “Sulle funzioni Motricidello stomacho,” 
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60. Exner, A. and Jaeger: “Zur Kenntniss der Funktion des Ganglion Coeliacum,” 
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61. Alvarez: “The motor functions of the intestine from a new point of view,” 
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62. V. Brun, (K. O.), Max: Die Allgemein Narkose, Stuttgart, Enke, 1913. (In— 
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64. Lennander, K. G.: “Uber Hofrot Nothnagels zweite Hypothese der Darmkolik- 
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65. Muller, A.: “Der Einfluss der Salzsaure auf die Pepsinverdauung,” Mitt. aus. 
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66. Talma, S.: “Zur Behandlung von Magen,” Ztschft. f. klin. Med., 1884, 8, 407. 
67. Schmidt, J. E.: “Ein Beitrag zur Frage der Magensensibilitat,” Mitt, aus d. 
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68. Carlson: “The origin of the epigastric pains in gastric duodenal ulcer,” Am. J 
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85 
6g. For discussion and lit. see Carlson, A. J.: “On the nervous control of the hunger 
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70. Rheinboldt, M.: Int. Beitr. z. Pathol, u. Therapie d. Ernahrungsstorungen, 1910, 
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71. Fritsch, K.: “Das Ulcus ventriculi perforans als Etiologie der Pancreas necrosa,” 
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72. Exner, A., Schwarzmann: “Ein neues Operations verfahren tabetischer crises 
gastriques,” Mitt. aus. d. Grenzgebieten, 1914, 28, 31. Deutsche Zeitschr. f. 
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576-590 
73. Krehl, Ludolf: “Uber die Folgen der Vagusdurchschneidung,” Archiv. f. Anat. u. 
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74. Ibrahim: “Die Pylorusstenose der Sauglinge,” Die Erkennung u. interne Behand- 
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75. Wilms: “Die Rammstedtsche Operation beim hypertrophischen Pylorospasmus 
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76. Manasse: Berliner klin. Wochschft., 1917, 255. 
77. Brauns, Tuffiers, Payers, A.: “Die postnarkotische Magenlaehmung,” Mitt. aus. 
d. Grenzgebieten, 1910, 22, 446. 
78. Kelling, Georg.: “Ueber den Mechanismus der acuten Magendilatation,” Archiv. 
f. klin. Chirurgie, 1901, 64, 393. 
79. Braun, W. and Seidel, H.: “ Klinisch-experimentelle Untersuchungen zur Frage 
der akuten Magenerweiterung,” Mitt. d. Grenzgeb., 1907, 17, 533. 
80. Kuru, H.: “Ueber die akute Magenerweiterung (Mit. Bemerkuugen von B. 
Naunyn),” Mitt. aus. d. Grenzgebieten, 1911, 23, 169-190. 
81. Mangold, E.: “Die Lahmung des Magens durch die Inhalationsnarkose,” Munch- 
ener med. Wochenschrft., 1911, 58, 1861, 1863. 
82. Korte: Discussion by Korte in “Freie Vereinigung der Chirurgen Berlin,” Zen- 
tralbl. f. Chir., 1909, 36, 160. 
83. Bier: discussion by Bier in “Freie Vereinigung der Chirurgen Berlin,” Zentralbl 
f. Chir., 1909, 36, 160. 
84. Haberer, H.: “Der arterio-mesenteriale Duodenalverschluss,” Ergebn. d. 
Chirurg., 1913, 5, 475. 
85. Cannons, W. B., Murphy, F. T.: “The movements of the stomach and intestines 
in some surgical conditions,” Ann. Surg., Phila., 1906, 43, 512-536. 
86. Albrecht, P. A.: “Ueber arterio-mesenterialen Darmverschluss an der Duodeno- 
Jejunalgrenze und seine ursachliche Beziehung zur Magenerweiterung,” Virch. 
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87. Muller, P.: “Ueber acute post-operative Magendilatation hervorgerufen durch 
arteriomesenteriale Duodenal compression,” Deutsche Ztschift. f. Chir., 1900, 
56, 500. 
88. Mathieu, A. and Roux, I. C.: “Die klinischen Erscheinungsformen der motor- 
ischen Insufiizienz des Magens,” Ergebn. d. inneren. Med., 1910, 5, 252-279. 
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89. Glenard, Frantz: Les ptoses viscerales, Paris, Alcan, 1899. 86 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
90. Stillers: “Die asthenische Konstitutionskrankheit Springers Verlag,” 1917. 
Bauer, Julius: Konst. Disp. zu inn. Krankheiten, J. Springers Verlag., 1917, 
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91. Kussmaul: V. Volkmanns Sammlung. kl. Vortrage, 1880, 181. 
92. Krempelhuber, M.: “Zur Pathogenese des runden Magengeschwurs,” Deutsche 
med. Wochenschrift, 1919, 40, 1099. 
93. Rovsing, Niels, Thorkied: Translated from Danish by Georg Saxinger “Unter- 
leibschirargie,” Verl. v. F. C. W. Vogel, Leipzig, 1912, p. 194 ff. 
94. Reichmann, M.: “Ein Fall von krankhaft gesteigereter Absonderung des Magen- 
saftes,” Berliner klin. Wochenschrft., 1882, 40, 606. 
95. See No. 88. 
96. Marchand: “Prozess d. Wundheilung,” Deutsche Chirurg., i9or, 16, 300. 
97. Matthes, M.: “Untersuchungen uber die Pathogenese des Ulcus rotundum ven- 
triculi und uber den Einflusz von Verdauungsenzym auf lebendes und todtes 
Gewebe,” Zieglers Beitr., 1893, 13, 308. 
98. Graser, E.: “Untersuchungen ueber die feineren Vorgange bei Verwachsung peri- 
tonealer Blatter,” Deutsche Ztschift. f. Chir., 1888, 27, 533. Graser: Arch. f. 
klin. Chir., 1898, 50. 
99. Wilkie, D. P. D.: “ Gastro-jejunal and jejunal ulceration following gastroenteros- 
tomy,” Edinb. med. journ., 1910, n. s. v., 316, 327, 3 pi. 
100. Sonnenburg, case of Schroeter, F.: * ‘Ueber Gastroenterostomie,” Deutsche Ztschrft. 
f. Chir., 1894, 38, 305. 
101. Chlumsky, U.: “ Experimentelle Untersuchungen uber die Verschiedenen Meth- 
oden der Darmereinegung,” Bruns Beitrage, 1900, 25, 539. 
102. Perrier and Hartmann Monprofit: Chirurgie de l’estomac, Paris, 1900, Le Gostro- 
enterostomie, Paris, 1903. 
103. Kelling, Georg.: “Studien zur Chirurgie des Magens,” I Archiv. f. Klin. Chirurgie, 
1900, 62, 1. Hesse: “Roentgenologischer Beitrag zur Physiologie und 
Pathologie des Magen-Darm. Traktus,” Verhandlungen d. deutsch. Kong. f. 
innere Med. Wiesb., 1912, 29, 311-314. Zeitschrft. f. Rontgenkunde, 1912, 
14. Schuller: “Klinische und experimentelle Untersuchungen ueber die 
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104. Seringer: Chir. Kongresszentralbl., 1914, 5, 591. 
105. Herre: Zeitschr. f. Rontgenkunde, 1912, 14. 
xo6. Neuhaus, v. Volkmanns Sammlung klin. Vortrage, No. 486. 
107. Kocher: Chirurgenkongress, 1902. 
108. Schoemaker, T.: “Ueber die motorische Funktion des Magens,” Mitt. a.d. 
Grenzgebieten 1910, v. 21, 30, p. 719-728. 
109. Borszeky: “Die chirurgische Behandlung des peptischen Magen und Duodenal- 
geschwure und seiner Komplikationen und die damit erreichten end Resultati,” 
Brun’s Beitrage z. klin. Chir., 1908, 57, 172. 
no. Cannon, W. B. and Blake, J. B.: “Gastroenterostomy and pyloroplasty; an 
experimental study by means of the Rontgen rays,” Ann. of Surgery (Phila.), 
1905, 41, 686-711. 
in. Leggett, N. B. and Maury, J. W. D.: “Studies upon the function of the pylorus 
and stoma after gastroenterostomy has been performed,” Ann. of Surgery, 1907, 
46, 549- 
112. Kuttner, Herman: “Beitrage zur Chirurgie des Magens auf Grand von 1100 in 
Jahren behandelten Fallen (Aus der Chirargischen Klinik in Breslau)” Arch, 
f. klin. Chir., 105, 797. STOMACH 
87 
113- Barsony, Theodor.: “Aus der Chirurgischen Klinik zu Budapest,” Bruns Beitr. 
z. klin. Chir., 1913, 88, p. 473. 
114. Wettstein, A.: “Zur Chirurgie des Magens und des Duodenums,” Sammel- 
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115. Hartman, H. and Soupault, M.: “Les resultats eloignes de la gastro-enteros- 
tomie,” Revue de Chirurgie, 1899, 14, p. 137. Schlesinger, E.: “Ueber 
Gastro-Pyloro-Duodenoptose als Ursache des Einfliesens von Darmsaft, Galle 
und Pancreassaft in den Magen,” Zeitschrift. f. klin. Med., 1912, 75, p. 314. 
Kausch, W.: “ueber funkionelle Ergebnisse nach Operation am Magen bei 
gutartigen Erkrankung,” Mitt. a.d. Grenzgebieten, 1898, 4, 347. 
116. Krause, Fedor: “Erfahrungen in der Magenchirurgie,” Berliner kl. Wochenschrft, 
1903, No. 47, p. 1070. 
117. Katzenstein: “Ueber Aenderung magen Chemismus nach der Gastroenteros- 
tomie und den Einfluss dieser Operation auf Ulcus u. Carcinoma,” Deutsche 
Med. Wochenschr., 1907, 33-95. 
118. Kausch and Kaplan: Zeitschrift. f. physiol. Chemie, 1913, 87, p. 338. 
119. Abderhalten, Emil: Lehrbuch d. physiol. Chemie, 2 Aufl., 1906, p. 282, Berlin, 
Urban. 
120. Heinsheimer, F.: “ Stoffwechseluntersuchungen bei zwei Fallen von Gastro- 
enterostomie,” Mitt. a.d. Grenzgebieten, 1896, 1, 348. 
121. Dagaew, W. F.: “Aenderungen in den Verdauungsprozessen nach Gastroduo- 
denostomie und Gastrojejunostomie und nach total Magen extirpation,” 
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122. Bayliss, W. M., Starling, E. H.: (1) “Mechanism of pancreatic secretion,” 
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1902, 28, p. 325; 1903, 29, p. 174. 
123. c.f. Cohnheim, O. and Klee, P.: Zur Physiologie des Pancreas Ztschr. f. physiol. 
Chem. Strassb. 1912, 78, 464-484, Zur Physiol, d. Pancreas, Heidelberg. Akad. 
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klin. Wochenschrift, 1909, 46, 1201. 
125. Rost, F.: “Die functionelle Bedeutung der Gallenblase. Experimentelle und 
anatomische Untersuchungen nach Cholecystectomie,” Mitt. a.d. Grenzge- 
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126. Kelling: “Ein in physiologischer werther Fall von Magen resection nebst 
Bemerkungen zur Gastroenterostomie,” Deutsche Zeitschr. f. Chir., 1901, 60. 
S. 155- 
127. Casagli, F.: “ Modificazioni della parete del duodeno in sequito alia gastro- 
enterostomia, studio sperimentale,” Fireuze L. Niccolai, 1913, p. 173, 3 pi. 
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128. Chlumsky, V.: (1) “Ueber die Gastroenterostomie,” (2) “Uber die Gastroen- 
terostomie,” Bruns Beitrage, 1898, 20. 2312, 487. 1900, 27, 311, lit. 
129. Dastre quoted by Tavel, E.: “Reflux dans la gastro enterostomie,” cited by 
Tavel, Revue de chir., 1901, 2, 690. 
130. Dr. Steudel: “Die in den letzten Jahren an der Czernyschen Klinik ausgefuhrten 
Magenoperationen und die Endresultate der fruheren Operationen,” Bruns 
Beitr. z. klin. Chirurgie, 1899, 23, S. 387. 
131. Kelling, Georg.: “Studien zur Chirurgie des Magens,” 5 Arch. f. klin. Chirurgie, 
1900, 62, 307. 
132. Stuber: “Experimentelle Begrundung der Aetiologie des Ulcus ventriculi,” 
Deutsche med. Wohnschr. Leipzig and Berl., 1914, 40, 987; ibid. 1036, 88 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
“ Experimentelles Ulcus ventriculi Zugleich eine neue Theorie seiner Genese,” 
Zeitschr. f. exp. Path. u. Therapie, 1914, 16 and Munchner med. Wochenschr., 
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133. Mathiew and Roger: Inneres Kongresszentralbl. 8, 571. 
134. Wolfler, A.: “Gastro-Enterostomie,” Zentralbl. f. Chirurgie, 1881, No. 45, page 
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135. Tavel, E.: “Reflux dans la gastro-enterostomie” (see No. 129), Revue de Chir- 
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136. Bruns, P. et al. Editors: Walter G Kausch im HandbucH d. prakt. Chirurgie, 
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137. Rockwitz, C.: “Die Gastroenterostomie an der Strassburger Chirurgischen 
Klinik,” Deutsche Zeitschr. f. Chirurgie, 1889, 25, 502. Doyen: No. 128. 
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138. Anschutz, W.: “Ueber die Darmstorungen nach Magen operationen,” Mitt. a.d. 
Grenzgebieten, 1905, 15, 305. 
139. Boas, I.: “Ueber gastrogene Diarrhea by Pylorusstenosen,” Berlin Klin. Wochen- 
schr., 1912, 49, 337-339. 
140. Hertz, Arthur, F.: “Cause and treatment of certain unfavorable after effects of 
gastroenterostomy,” Ann. Surgery, 1913, 58, 466. 
141. Mathiew, A. and Tavignac, R.: “Etude sur les troubles intestinaux consecutifo 
a la gastroenterostomie,” Arch, des malad. de l’appar. dig. et de la nutr., 1913, 
S4i- 
142. Van Roojen, P. H.: “Ueber das Ulcus pepticum jejuni nach Gastroenterostomie,” 
Arch. f. Kl. Chir. Berl., 1909, 91, 381-448; Archiv. f. Klin. Chirurgie, 1910, 91, 
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143. Gosset, A.: “L’ulce’re peptique du jejunum appres gastroenterostomie,” Revue 
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144. v. Haberer, H. “ Ulcus duodeni und postoperations peptisches Jejunalgeschwur,” 
Arch. f. klin. Chir. Berl., 1918, 109, 413-566; Arch. f. Klin. Chir. v. 101 and 
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145. Katzenstein: “Der Schutz des Magens gegen die Selbstverdauung nebst einem 
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146. Kathe, H.: “Zur Frage der Verdauung lebenden Gewebes,” Berlin, klin. Wochen- 
schr., N: 1908, 48, 2135-2137, 1911 or 12. 
147. Hotz, G.: “Versuche uber die Selbstverdauung des Darmes in Magen,” Mitt. 
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148. Tietze, Alen.: “ Experimented Untersuchungun uber Netzplastik,” Bruns Bei- 
trage, 1900, 25, 411. 
149. Matthes, M.: (See No. 97) Zieglers Beitrage, v. 13. 
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d. Grenzgebieten, 1911, 23,15. 
151. Braun, Heinrich: “Uber Gastro-Enterostomie und gleich, zeitig ausgefuhrte 
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152. Mayo, Wm. J.: “ Gastrojejunal ulcers (pseudojejunal ulcers),” Sur., Gyn. and 
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153. Dagaew, W. F.: “Aenderungen in den Verdauungoprozessen nach Gastroduo- 
denostomie und Gastrojejunostomie und nach totaler Magenexstirpation,” 
Mitt. a.d. Grenzgebieten, 1913, 26, 176. Kaplan, S.: “Digestive processes 
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89 
S. Petersburg, 1913, F. Vaisberg and P. Gershunim, 169, P. 6 tab. 8, 
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f. innere Med., 1897, 433. Schuller, L.: “Klinische und experimentelle 
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Pylorus resection,” Mitt. a. d. Grenzgebieten, 19x1, 22, 742. 
154. Gocke, C.: “Beitrage zur Morphologie des Magens nach Resektionen,” Bruns 
Beitrage, 1916, 99, 294. 
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THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
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Roentgenstrahlen,i9i4-i9i5, 22, 377-384, 4 pi. CHAPTER III 
PANCREAS 
The pancreas has a double function. Its external secretion, 
takes a prominent part in digestion is poured through the duct of Wirsung 
into the duodenum (i); its internal secretion is given directly to the 
blood and has a most important effect on the general metabolism. Our 
knowledge of the external secretion is linked especially with the names 
of Heidenhain (2) and Pawlow (3) while recognition of the internal 
secretion is indebted to v. Mering and Minkowski (4) (1889), who observed 
glycosuria with subsequent cachexia, after total extirpation of the pan- 
creas, that is, they reproduced a typical diabetes mellitus. 
The external secretion of the pancreatic juice may be studied in dogs 
by two methods, viz., by suturing the opening of the excretory duct 
with its attached piece of duodenum to the skin, or better, by producing 
a duodenal fistula and providing a passageway for the bile after previous 
ligation of the common duct by suturing the gall bladder to the intestines 
(5) Stimulation to external secretion occurs principally, as far as we 
now know, when food passes through the duodenum, first, reflexly, 
through nervous influences, and second, by way of the blood from the 
action of absorbed secretin. The vagus and the splanchnics supply 
the pancreatic tissue, its blood vessels, and the autonomic centers, that 
is, the ganglion cells in the gland substance itself. Because of this very 
complicated innervation and because blood pressure changes play a very 
important part, the investigations of the effect of stimulation of these 
nerves on the external secretion, have lead to quite divergent results 
(6) In particularly careful experiments, Pawlow was finally able to 
consistently obtain a plentiful secretion of pancreatic juice by stimulation 
of the vagus; a scanty secretion followed stimulation of the sympathetic 
(see also Oppenheim, “Die Fermente,” Volume I, fourth edition, p. 468). 
The most active stimulus to external secretion, however, is not carried 
to the pancreas through nervous paths, but by the blood after the absorp- 
tion of a substance known as secretin elaborated by intestinal mucosa. 
The importance of this secretin was discovered by Bayliss and Starling 
(7) who demonstrated that there is first a prosecretin in the bowel mucosa, 
i.e., a pre-stage of secretin, and that this is changed to secretin under the 
influence of the hydrochloric acid from the stomach. Then, according to 
Bayliss and Starling, the secretin thus formed is quickly absorbed by the 
95 96 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
bowel and carried by the blood to the pancreas. The existence of a 
prosecretin has, however, recently been disputed (8) and the idea is 
expressed that the acid acts only as a solvent for secretin, and destroys erep- 
sin, which inhibits secretin. Popielski (9) furthermore, thinks that secretin 
acts only through the nervous system; but this view has been disproved 
by Fleig’s (10) experiments, which furnished positive proofs that secretin 
exercises its function by way of the blood stream. At the same time 
Fleig is willing to admit a nervous regulation. Secretion begins in about 
five minutes after hydrochloric acid enters the bowel. 
[Doubts of the specificity of secretin and also of gastrin have been 
expressed from time to time. Recently, these have crystallized in work 
by Luckhardt which he reported in 1921. In very carefully performed 
experiments he has shown that secretin or gastrin may stimulate the 
pancreas or the gastric glands or both, and further that very efficient 
secretagogues may be prepared from other organs than duodenal or gastric 
mucosa.] 
For studies of the histological changes occurring during activity and 
rest of the gland cells, the work of Heidenhain (2), Kuhne and Lea (12), 
and recently Bremer (13) may be consulted. 
As an example of the nervous influence, Cohnheim (14) states that the 
mere offering of food causes a flow. Thus there is a psychological factor 
just as in the stomach. The character of foods passing through the duo- 
denum also influences secretion for water as well as albumoses and oil 
lead to a scanty amount, while soap which is formed from oil stimulates 
the flow of larger amounts (5). Furthermore, the quantity secreted dur- 
ing a meal is dependent on the amount of gastric juice (15). It is larger 
after proteins than after carbohydrates and in the case of the latter sub- 
stance, differs according to their kind and mode of preparation. But 
Wohlgemuth (16) disputes this, and states that the quantity is greater 
after carbohydrate feeding. Heineke (17) on the basis of these state- 
ments, advises that patients with pancreatic fistulae be given such food as 
is ordered for diabetics. 
Observations of the secretion of pancreatic juice in operated patients 
with fistulae have been recorded by Schumm (18) and Glassmer (19). 
The important point has been brought out that there are no differences 
in the quality and quantity of pancreatic secretion in man and the dog. 
The most important physiological substances in the pancreatic juice 
are the digestive enzymes. Trypsin, the knowledge of which we owe 
principally to Kuhne (20) is proteolytic, and breaks down proteins not 
only to pepton, but carries the cleavage as far as amino acids. In the 
gland, it is present in a pre-stage, usually called zymogen, and according 
to Pawlow (21) it is activated by the enterokinase present in the intestinal PANCREAS 
97 
lumen. It acts particularly well in a strongly alkaline medium, such as 
that found in the normal pancreatic juice. Activation from trypsinogen 
to trypsin can be accomplished not only by the succus entericus but also 
by certain bacteria (22); calcium salts (Delezenne (23)), pressed liver sub- 
stance (Wohlgemuth (24)), and a number of colloids (Larguier des Banals 
(25)). By using special experimental methods, e.g., the injection of pilo- 
carpin, Camus and Gley (26) showed that the trypsin may be activated 
within the pancreas itself and thus there is a possibility that under certain 
circumstances, an active pancreatic juice may be secreted. Eberle 
(27) was the first to recognize that the lipase splits, not only neutral fats, 
but also lower esters into glycerin and fatty acids. The quantity present 
in the pancreas varies quite considerably and is said to occur in particu- 
larly large amounts in fasting animals (28). Steapsin when secreted is 
not a preenzyme but is active, although its activity may be increased 
considerably by the addition of bile acid salts (29). 
The diastatic action of the pancreatic juice, i.e., the splitting of starches 
to sugar, was first observed by Bonchardat and Sandras (30). It is 
found in varying degree in the pancreatic juice of all animals (31). Many 
experiments and clinical observations indicate that the amylolytic enzyme 
of the blood has a definite relation to the pancreatic amylase, because 
most of that in the blood has been secreted by the pancreas directly into 
that fluid. Thus it follows that after extirpation of the pancreas there is 
a diminution of this enzyme in the blood and an increase after ligation of 
the duct of Wirsung and the resultant stasis of the external secretion. 
Coincident with its increase in the blood, there occurs an increase in the 
urine and Wohlgemuth (33) on the basis of this finding, recommends its 
quantitative determination in the urine as a diagnostic help in obstruction 
of the duct of Wirsung. 
Of the other enzymes of the pancreatic juice, the nuclease might be 
mentioned (34). This enzyme is of diagnostic importance since the nu- 
clein test proposed by Schmidt (35) has, as a basis, its presence or absence; 
but it must be remembered that a nuclease is present in the intestinal 
mucosa also. The glutinase and casease which according to the newer 
investigations are probably identical with trypsin (see Oppenheimer, l.c., 
pp. 442 and 445) the hemolysin (36) and the necrotising, blood pressure 
reducing substances which have as yet not been fully investigated, 
may be passed over. 
According to the statements of Walther (37) (Pawlow), the quantity 
of the enzymes in the pancreatic juice varies considerably with the food. 
These statements of Pawlow and his school have, however, been sharply 
questioned, particularly by Popielski (6). Since the investigations of 
Walther were made before the zymogens (the pre-enzymes) were known, 98 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
his published figures cannot make any claim to absolute correctness, so 
that this point needs further investigation (38). 
Total extirpation of the pancreas is followed by a diabetes, and the 
glycosuria is not a result of a nerve lesion, nor of absence of the external 
secretion, but it depends on a failure of some substance which is supplied 
by the gland directly to the blood stream. The diabetes following extir- 
pation was discovered in 1889 by v. Mering and Minkowski (4) and at 
about the same time by de Dominici (39). 
Considerable controversy arose immediately, as to whether this 
diabetes followed because the external secretory function of the pancreas 
was abolished, or the internal, or both. The crucial experiment was sup- 
plied by Minkowski (40) who transplanted the uncinate process of the 
pancreas of a dog under the skin of the abdominal wall, leaving a pedicle 
of vessels for its immediate nutrition. The pedicle was later severed, and 
the entire remainder of the pancreas removed. Diabetes did not develop, 
nor did glycosuria appear until the transplant had been removed. Death 
then resulted from a severe diabetes. 
The appearance of sugar in the urine is a result of-hyperglycemia, but, 
according to the work of de Meyer (41) there may also be an increased 
permeability of the kidneys to this substance. It is not positively known 
at just what place in the complex metabolism of carbohydrates the 
failure of the internal secretory function of the pancreas makes itself felt. 
There are, however, many single facts, most of which are confirmed by 
experiments, and the most important theories of pancreatic diabetes may 
be mentioned in short outline (42). 
De Dominici’s assumption (39) that diabetes resulted from the absence 
of the external secretion after extirpation of the pancreas, and Pfluger’s 
that it is dependent on nervous regulation originating in the pancreas, 
have both been disproved by the experiments of Minkowski (40) men- 
tioned above and those of Hedon (43) among others. It must be accepted 
at present, that there is a pancreatic hormone, which, according to Biedl, 
reaches the blood stream by way of the thoracic duct, for, according to 
his figures, when the fluid from the thoracic duct escapes through a 
fistula, a lasting glycosuria results in from 66 to 88 per cent, of the cases. 
That it occurs when this vessel is ligated during operations in its vicinity 
or when it is done intentionally, e.g., in fat embolism (Wilms (44)), should 
also be borne in mind. Whether some enters the blood stream directly 
without passing through the thoracic duct is still an undecided question. 
How the pancreatic hormone acts in carbohydrate metabolism is the next 
question for consideration. The present day theories may be divided into 
two large groups. It is believed, first, that the pancreas in some way 
takes a prominent part in the destruction of sugar and second, that it has PANCREAS 
99 
a regulatory influence in the synthesis of this substance. Further details 
may be found discussed by Biedl (42, p. 361). At present it may be con- 
cluded from the numerous experiments, many of them extraordinarily 
accurate, that not only sugar formation but sugar consumption in the 
tissues is altered after extirpation of the pancreas, and that the hyper- 
glycemia is a result of this combined disturbance in carbohydrate metab- 
olism along with involvement of other internal secretory glands. 
There is also a diminution of antitrypsin in the serum after extirpation 
of the pancreas and Stawraky (45) believes this is responsible for the 
predisposition of diabetics to suppuration. 
The debated question of whether internal secretion comes from the 
islands of Langerhans is not completely settled, but, from the anatomical 
point of view, many investigations (46) have shown that there are definite 
histological changes in those structures in the largest majority of diabetics. 
These may be of the nature of hydropic or hyalin degeneration, or of an 
inflammatory process with resultant atrophy, etc.; and their constancy 
makes it necessary to assume that at least a par,t of the internal secretion 
of the pancreas is provided by these structures. If the gland acini also 
take part in the internal secretion is an open question, to which many 
very carefully planned experiments have been directed (47). These 
have consisted chiefly of histological examinations after ligation of the 
duct or after the injection of substances to stimulate or inhibit secretion. 
The relation of the acini to the cells of the islands were then studied (42/ 
p. 370). This was first done by Laguerre and his school but the details 
cannot be given. It must be admitted that the question has not been 
completely answered, although the theory has gained in probability. 
The same uncertainty surrounds the question of whether the islands take 
part in the external secretion (see Lombroso (48)). 
Up to the present, the only internal secretory function of the pancreas 
which has claimed our attention has been that concerned in carbohydrate 
metabolism. But there is another field in which it exerts a profound 
influence, for the investigations of a number of workers have shown that 
fat absorption in the bowel is almost entirely suspended after total extirpa- 
tion of the gland. But the splitting of fat is carried out approximately 
normally by the bacteria in the intestinal canal (49). 
After extirpation, the absence of the internal secretion so dominates 
the clinical picture, that we cannot obtain a real perspective of the results 
brought about by absence of the external secretion. Experimental liga- 
tion of the ducts has been done many times (50) but the results were not 
always of value, because, especially in the dog, there are often many 
accessory channels, and ligation of the duct of Wirsung and even another 
wider duct may not be sufficient to exclude all pancreatic fluid from the 100 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
bowel. In order to be certain, it is necessary to cut all strands found 
between the gland and the intestine with the exception of the vessels. 
Studies of the metabolism after complete elimination of the external 
secretion (as made particularly by Rosenberg and more recently by 
Holmberg) have shown that there is an early disturbance, in the 
utilization of protein, so that only about two-thirds of the nitrogen 
is absorbed. When later high grade destruction of the gland develops, 
the absorption of fat and carbohydrates also shows deviations from the 
normal. 
Changes in the splitting of proteins and of nucleic acid are not demon- 
strable. It is not easy to determine whether, as Rosenberg assumes, 
ligation of the pancreatic ducts leads to an absorption of larger quantities 
of the enzymes and subsequent excretion into the bowel “like iron,” or 
whether the absorption of proteins and fats is influenced chiefly by the 
internal secretory function (Lombroso). The former possibility helps 
explain the comparatively minor disturbances in the splitting and absorp- 
tion of the food material after the operation, but both possibilities may 
readily occur. At any rate, the opinion of Lombroso has gained consider- 
able ground, especially since the investigations of Fleckseder. The latter 
showed that fat digestion remains normal when the pancreas is implanted 
in the belly wall, by which procedure, of course, its external secretion is 
completely excluded. 
These questions of the internal secretion, and its relation to the external 
secretion, are particularly important to the surgeon in injuries of the 
pancreas (51). Frequently it is a case of a transverse tear which has 
been sutured, but thus far, the manner in which the pancreas functions 
and its fate anatomically, after such suture, are entirely unknown. The 
same is true of pancreatic cysts and their treatment. 
The anatomical changes which occur after ligation of the duct of 
Wirsung are first, a wide dilatation of the ducts, which are finally filled 
“with a clear, yellow alkaline fluid containing no enzymes” ((50) p. 403), 
and second a destruction of the gland cells, with gradual infiltration of 
connective tissue often dense enough to give the organ the consistency of 
cartilage. There are many collections of round cells and punctate hemor- 
rhages in this fibrous tissue. As Kuhne and Lea (52) and recently Ricker, 
Natus (53) and Knape (54) have shown, the pancreas in living rabbits 
may easily be observed microscopically. Natus studied these changes 
after ligation of the ducts by this method. 
According to the studies of Laguesse (55), W. Schulze (56), Ssoboleff 
(57) and others (on rabbits) the islands of Langerhans remain intact for a 
long time after ligation of the ducts, and this corresponds to the clinical 
observation that diabetes is usually absent in cases of pancreatic calculi PANCREAS 
101 
(see Lombroso (50)). In addition, the pancreas of young dogs has quite 
extensive powers of regeneration which extend also to the islands of 
Langerhans (58). Such observations have not been made on older 
animals. 
The histological changes following long standing stasis of secretion are 
quite similar to the usual picture of chronic pancreatitis in man, as Hess 
(59) among others has pointed out. Barth calls attention particularly 
to the fact that in chronic pancreatitis just as in experimental ligation of 
ducts, the islands of Langerhans are spared at first. The studies of 
Natus (53) on the pancreas of living rabbits are of particular help in 
understanding the beginning stages of this disease. By no means, how- 
ever, does chronic pancreatitis always depend simply on this stasis of the 
secretion; an infection carried by either the blood or lymph channels 
may play a far more important part. Unfortunately, we are not always 
in a position to determine, even at autopsy, the cause and the course of 
events in such cases. It might even have been the remains of a former 
acute pancreatic necrosis. To obtain a basis for the comprehension of 
the clinical picture, however, it is necessary to fall back on the conditions 
as found after ligation of the ducts. The failure of the external secretion 
in chronic pancreatitis may be occasionally demonstrated, according to 
Ad. Schmidt (61) by finding undigested muscle fibres and a fatty coating 
over the stools. Such findings are not constant; in fact, the diagnosis 
is very difficult and often cannot be made with certainty in spite of the 
many methods which have been proposed. This is perfectly clear when 
it is remembered that experimental incomplete ligation of the ducts (as 
performed by Rosenberg and others), leads to a sclerosis of a large part 
of the organ, but not to a recognizable alteration in metabolism. 
According to Barth (60) the severe pains to which patients with 
chronic pancreatitis are subject, and which often lead to a mistaken 
diagnosis of gall stone colic are due to an involvement of the neighboring 
solar plexus or its branches (62). 
From the therapeutic standpoint, it is usually assumed that chronic 
pancreatitis is caused by stasis of secretion and since it is also assumed that 
stasis of bile increases pancreatic stasis, free drainage of bile is established 
through a fistula of the gall bladder. 
[That form of pancreatitis which is more or less localized in the head of 
the organ and is very frequently associated with cholelithiasis or at least 
with cholecystitis, has given rise to considerable controversy in regard to 
its etiology. That it is very important cannot be denied; the records of 
the follow up department in the Lankenau Hospital indicate that those 
patients who have this condition associated with their cholecystitis do not 
as a rule recover health or well being after operation as promptly nor as 102 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
certainly as those with cholecystitis alone. Suffice it to say that they 
complain of pain in the upper abdomen and continued digestive disturb- 
ances. The theory of the lymphogenous origin has been championed in 
this country by Deaver. In his clinical experience he has followed the 
train of events in this wise; cholecystitis, lymphadenitis at the junction of 
cystic and common ducts, lymphangitis and lymphadenitis along the 
common duct and finally pancreatic lymphangitis leading to sclerosis of the 
head of the organ. The close relationship of this par t and the common duct 
is adequately explained on embryological grounds, and the lymphatics 
have been injected from the gall bladder. It is well knowm that infection 
of the gall bladder is very frequently present in its walls. On the other 
hand Archibald on the basis of experiments argues that the route of 
infection is via the common duct. A rise in pressure will force bile into 
the pancreatic duct and produce lesions in the gland. The sphincter of 
Oddi which closes the opening of the common duct is able to withstand 
quite considerable pressure, up to 600 mm. of water in dogs. Mechanical 
irritation, application of acid and other means are sufficient to throw this 
muscle into spasm, whence regurgitation of bile into the pancreatic ducts 
can ensue. It must be remembered, however, that the anatomical makeup 
of the common and pancreatic ducts varies, and until a very careful 
necropsy study of the arrangement of the ducts is made in cases of chronic 
pancreatitis the last word will not be spoken. Even one case of sclerosis 
of the head of the pancreas in which it is proved that bile could not have 
entered the pancreas via the common duct will be decisive. The opposite 
does not hold, of course. Even if it is shown that bile could have entered 
in this way, it does not follow that it necessarily did. Finally, if the lymph 
route is at fault, removal of the source of infection is indicated; if high pres- 
sure in the duct system is the cause, minimizing this is the proper 
procedure (63).] 
Very great surgical interest is attached to the so-called acute pancreatitis, 
or better, pancreatic necrosis, first described by Balser (64). The charac- 
teristic anatomical picture of this disease develops quickly and positively; 
and leads, without surgical interference, to a rapidly fatal outcome. It 
consists first of a destruction of the gland accompanied by extensive 
hemorrhage within its substance, and second, of necrosis of the surrounding 
fatty tissue because of leakage of the pancreatic steapsin. These innumer- 
able lentil-size areas of necrosis in the mesenteries and great omentum with 
their punctate, marble-white appearance, are so extraordinary that they 
have been the starting point of all the experimental work in this disease. 
It was doubtful if these fat necroses were related in any way to the pan- 
creas until R. Langerhans (65) succeeded in reproducing them in the 
subcutaneous fatty tissue of rabbits by the injection of pancreatic juice. PANCREAS 
103 
He then demonstrated that they depended on the splitting of fat and the 
formation of a calcium salt of the liberated fatty acids. 
Now that the fat necrosis is sufficiently explained by the action of the 
steapsin, the next question is, how is the steapsin liberated f om the gland, 
in other words, how is the destruction of the pancreas brought about? 
Two opinions are in conflict on his subject, and there is much experimental 
evidence in favor of both (66). The one, momentarily the favorite of the 
majority of writers, declares that the destruction of the pancreas is brought 
about in the same way that the fat necrosis is produced, viz., by the activi- 
ties of the pancreatic enzymes, particularly the trypsin. Chiari (67), there- 
fore, speaks of an “intravital self-digestion.” The same objection, 
however, is present as that in gastric ulcer. How does it happen that the 
pancreas suddenly becomes vulnerable to the action of its own enzymes? 
The views are divided on this point. Polya (68) and Kirchheim (69) 
believe that the toxic action is caused by the trypsin. Ricker, Natus, and 
Knape after observing the living pancreas in rabbits, reach the conclusion 
that the trypsin has nothing to do at first with the destruction of the gland. 
They showed experimentally how readily the pancreas reacts with stasis 
and hemorrhage to all sorts of irritations, and believe that in the explana- 
tion of the severe hemorrhage in pancreatic necrosis, the trypsin plays at 
most a secondary role. More important than this enzyme trypsin, accord- 
ing to the investigations of Knape, are the salts in the pancreatic juice. 
Knape believes that as soon as pancreatic juice has the opportunity of 
entering the surrounding tissues from the ducts, its salts exert such an 
intense irritative effect on the vasomotor nerves that severe hemorrhage 
into the pancreas occurs. The immediate stumbling block in this idea 
is the natural question, how can the pancreatic juice escape into the 
surrounding tissues in the first place? It might in high grade stasis, but 
in pancreatic hemorrhage, this condition is usually not found, at least as 
far as the pathological material goes. It is possible, of course, that a 
stasis of secretion can occur from a cause not readily demonstrable at 
autopsy such as a spastic closure of the sphincter of Oddi, as Archibald (70) 
concludes from various experiments. Once more, Knape states that some 
sort of a nervous stimulus arising in any part of the body may initiate 
spasm in the pancreatic vessels and be followed first by a small localized 
area of necrosis and second by the escape of the strongly irritant pancreatic 
juice after which destruction of the gland proceeds. He observed some- 
thing similar in rabbits. The primary factor would, therefore, be reflex 
vessel spasm, just as in gastric ulcer. He points to innumerable cases in 
the literature in which such pancreatic necrosis is said to have arisen 
reflexly from hanging, choking, lifting heavy weights, severe hemorrhages, 
etc. He himself had observed a man who while swimming, was seized 104 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
with an acute pancreatitis with anatomically extensive destruction of the 
organ. The man was drowned, and this shows how extraordinarily 
rapid the hemorrhage may be. Actually the assumption of a reflex process 
may not be far wrong. 
Indeed, even before the work of Ricker and his pupils, other writers 
had expressed the opinion that the destruction resulted from a change in 
blood supply. This was of course a very logical idea and corresponded 
very well with the views on the formation of gastric ulcers. Appropriate 
experiments were performed by Hildebrand (71), Payr and Martina 
(crushing of the pancreas) (72), and many others (for lit. see Guleke). 
Those of Bunge and Guleke (73) yielded the best results. They frequently 
produced anatomical changes very much resembling human fat and 
pancreatic necrosis by the production of venous thrombosis or by the 
injection of paraffin, oil, etc. into the arteries. The clinical case of 
Schultze (74) in which an aneurism of the pancreatico-duodenal artery 
was found as the basis of a pancreatic necrosis illustrates the value of 
these experiments. 
Then a second group of writers expresses the opinion that the most 
important factor in the destruction of the pancreas is the trypsin, which of 
course must first be activated. We have already seen that the entero- 
kinase is the normal activator of this substance. But dying cells, such as 
leucocytes, bacteria, etc. may also perform this service. To bring about 
such activation within the gland itself, Korte (75) injected a small amount 
of intestinal contents directly into the parenchyma, and Hlava (76) and 
Carnot (76) used pure cultures of bacteria for the same purpose. The 
changes obtained in this way, however, showed no similarity to human 
pancreatic necrosis. They usually found circumscribed abscesses, 
hemorrhages, scars, and sparsely scattered fat necrosis from which the 
only conclusion that could be drawn was that the pancreas was relatively 
immune to infection. The human type was much more closely imitated 
by the injection of intestinal contents, bacteria, bile, blood, sodium 
chloride, fats, soap, oils, fatty acids, etc., into the excretory ducts. It 
must always be emphasized however, as Knape and Ricker especially 
have done, that these experiments bring both activation of pancreatic 
juice and tissue injury into play, and the latter may very well act by way 
of reflex constriction of vessels. This idea is shown especially well in 
Rosenbach’s experiments in which he sutured the pancreas into the 
intestine and found that digestion of the gland occurred only if there was 
an injury produced at the same time. It may therefore be concluded 
with certainty that even the activated trypsin is unable to digest the 
living pancreatic tissue. But the fact remains that the injection of these 
various substances into the pancreatic ducts, has actually yielded changes PANCREAS 
105 
which are entirely comparable to the anatomical and clinical 
pictures of human pancreatic necrosis. They are, therefore, the most 
important of those mentioned. Seidel’s experiments have shown that 
duodenal contents may enter the duct of Wirsung, and with the help of 
steapsin and activated trypsin, produce typical pancreatic and fat necrosis 
in spite of the sphincter of Oddi. These results were obtained by ligating 
the duodenum after a previous resection of the pylorus apd posterior 
gastroenterostomy. A clinical case which illustrates the possibility of 
the entrance of intestinal contents is reported by Simmonds (77). Around 
worm was found in the pancreatic duct in acute pancreatic necrosis. 
It is well to remember that the anatomical make up of Oddi’s muscle 
is varied and its tonus also varies considerably in different individuals 
(dogs) (78). 
[In addition, the entrance of the pancreatic duct into the common 
duct varies in a very important manner not only in species but in the 
different individuals of the same species (man and animals) (79).] 
To sum up; on the basis of the experiments mentioned, we may con- 
clude that fat necrosis occurs when the pancreas is injured and activated 
pancreatic juice is set free, perhaps the latter is not eveti necessary. 
Experimentally, these preliminaries can be completed by a disturbance 
in the blood supply as well as by the introduction of intestinal contents 
into the ducts. At present, it is not possible to determine the mode in 
man and we are able to judge just as little of the possibly far reaching 
importance of the observation of Fischlers (80) who found that Eck- 
fistula dogs are particularly susceptible to pancreatic necrosis. 
Now that the anatomical changes in pancreatic necrosis have been 
partially explained, there still remains the problem of how the severe and 
fatal clinical course is produced. According to Maragliano (81) there 
exist the following possibilities. 
I. It may be an infection or an irritation of the peritoneum. 
II. An intoxication from soaps. 
III. An intoxication from enzymes. 
IV. An intoxication from substances, not identified, but formed in 
the disintegrating pancreas. 
Bergmann and Guleke (82), who have worked extensively on this prob- 
lem, were formerly of the opinion that death in pancreatic necrosis is due 
to trypsin poisoning, but recently they have reached the belief that the 
intoxication is not due to trypsin alone, but to a varied number of sub- 
stances arising in the autolyzed pancreas. Doberauer (83) holds the same 
opinion. V. Bergmann and Guleke believe further they could obtain an 
immunization of their experimental animals against the fatal effect of 
autolyzed pancreatic substance by previous injections of trypsin. 106 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
LITERATURE TO PANCREAS 
1. See Heiberg: Die Krankheiten d. Pankreas, Wissbaden, 1914 (Lit.). Lit. s. Bab- 
kin, Die aeussere Secretion d. Verdauungsdrusen, Springers, 1914. 
2. Heidenhain: Hermann’s Handbuch, 1883, 5, 1. 
3. Pawlow: Arbeit d. Verdauungsdrusen, 1898. 
4. v. Mering: Zentralbl. f. Klin. Med., 1889, p. 393; Arch. f. exp. Path. u. Phar- 
makol., 1890, 26. 
j. Cohnheim u. Klee: Zur Physiologie. d. Pancreas, Sitzungsbericht d. Heidelberger 
Akad. d. Wissensch., 1912, 3. 
6. Popielski: Pflugers Archiv., 1901, 86, p. 215. Pawlow: Nagels Handbuch d. 
Physiol., 1906, 2, p. 737. 
7. Starling and Bayliss: Zentralbl. f. Physiol., 1901-1902,15, 23 and Journ. of Physiol., 
1902, 28, p. 325. 
8. Salou: J. de Physiol. Pathol, gen, 1912, 14, p. 509. Gley: also Oppenheim, p. 471, 
J. de Physiol. Pathol, gen, 1912, 14, p. 241-530. 
9. Popielski: Pflugers Archiv., 1907, 120, 451. 
10. Fleig: Zentralbl. f. Physiol., 1902, 16, p. 24 and Arch, gen de Med., 1903, 80, 1473. 
11. Luckhardt, A. B., Henn, S. C. and Palmer, W. L.: “On the specificity of gastrin 
and pancreatic secretin,” Am. J. Phys., 1922, 59, 457. 
12. Kuhne undLea: Unter aus d. physiol. Inst. Heidelberg, 1878, p. 448. 
13. Bremer, F.: “Contribution a l’etud liistophysiologique de la secretion exteme du 
pancreas chez la chien (note preliminaire),” Ann. et bull, de la Soc. roy. des 
scienceo med. et natur. de Bruxelles, 1913, 71, 82. 
14. Cohnheim: Munchener med. Wochenschrift, 1907, p. 2581. 
15. Schlagintweit, E. u. Stepp, W.: “Studien uber die Pankreassekretion by Sekre- 
tionsstorungen des Magens nach experimenten am Dauerfistelhund,” Deutsches 
Arch. f. Klin. Med., 1913, v. 112 und Munch, med. Wochenschr., 1913, 60, 
1865-1867. 
16. Wohlgemuth: “Untersuchungen ueber das Pankreas des Menschen,” Berliner 
klin. Wochenschrift, 1907, 44, 47-51. 
17. Heineke, H.: “Zur Behandlung der Pankreasfisteln,” Zentralbl. f. Chir., 1907, 
34, 265-667. 
18. Schumm: Ztschft. f. phys. Chemie, 1902, 36, p. 292. 
19. Glassmer: “Ueber menschliches Pancreassekret,” Ztschrft. f. physiol. Chemie, 
1903, 40, p. 465. 
20. Kuhne: Virchows, Arch., 1867, 39, p. 130. 
21. Pawlow: Nagel’s Handbuch, 2, p. 731. 
22. Hekma, E.: “Ueber die Umwandlung des Trypsin-Zymogens in Trypsin,” Arch. 
f. (Anat.) u. Physiol., 1904, p. 343-365. Delezenne: Compt. rend, de la Soc., 
Biol. 54, p. 1989. Breton, M.: “Sur la role kinasique des microbes normaux 
de l’intestin, particulierement chez l’enfant,” Compt. rend, de la Soc. Biol., 
56, p. 35- 
23. Delezenne, C.: “Nouoelle observations sur la specificite des sels de calcium dans 
la formation de la trypsine,” Compt. rend, de la Soc. de Biol., 63, p. 274. 
24. Wohlgemuth: Biochem. Ztschrft., 2, p. 264. 
25. Larguier des Banals: “Activation du sue pancreatique pur sous l’influence com- 
binee des colloides et des electrolytes,” Compt. rend, de l’Acad., 141, p. 144. 
26. L. Camus und E. Gley: “Rechershes sur la secretion pancreatique; variations de 
l’activite proteolitique du sue pancreatique,” Journ. physiol, path., 1907, 
v. 6, p. 987. PANCREAS 
107 
27. Eberle: Physiol, d. Verdauung, Wurzburg, 1854. 
28. Grutzner: Pflugers Arch., 1876, 12, 285. 
29. Magnus, R.: “Die Wirkung synthetischer Gallensauren auf die pankreatische 
Fettspaltung,” Ztschrft. f. physiol. Chemie, 1906, 48, p. 376. 
30. Bonchardal und Sandras: Compt. rend. Soc. Biol., 20, 1845, I43> P- 1085. 
31. Langsdorff: Arch. f. (Anat. u.) Physiol., 1879, p. 1. Lepine und Barral: C. r. de 
l’Acad. des Sciences, 1891, 113, p. 729. K. Moeckel und Rost, F.: “Ueber den 
Ursprung und die Bedeutung des amylolytischen Blutferments,” Ztschrft. f. 
physiol. Chemie, 1910, 67, p. 459. Schlesinger, W.: “Zur Kenntniss des dia- 
statischen Fermentes im Blute,” Verh. d. 25 Kongr. f. inn. Med., 1908, p. 501. 
Wohlgemuth, I.: “Ueber die Sekretion von Pankreasfisteln und ihre Besin- 
flussung durch antidiabetische Diat; Bemerkungen zu den Arbeit von F. Kempf.” 
Deutsche Med. Wochenschrft, 1908, p. 765, und Bioch. Ztschft., 1909, 21, p. 
381.’ A. Clerk und Loeper: “Influence de la ligature du canal pancreatique 
sur le pouvoir amylolytique du sang,” Compt. rend. soc. Biol., 1909, 66, p. 871. 
32. Rosenberg: Inaug.-Diss. Tubingen, 1890. 
33. Wohlgemuth, I.: “Beitrag zur funktionellen Diagnostik des Pankreas,” Berliner 
klin. Wochenschrift, 19x0, part 3. 
34. Sachs: Ztschft. f. physiol. Chemie, 1906, 46, p. 336. 
35. Schmidt, A.: “Funktionelle Pankreasacheir,” Deutsches Arch. f. Klin. Med., 
1906, 87, 451-478. 
36. Wohlgemuth: Bioch. Ztschrft., 4, p. 271. Friedemann, U.: “Ueber ein komplexes 
Hemolysin der Bauchpeicheldruse,” Deutsche med. Wochenschrift., 1907, 
No. 15, 585-588. 
37. Walther: Arch, des Sciences biol. de St. Petersburg, 1899, 7, parts 1 and 2. 
38. Cohnheim: “Die Physiologie der Verdauung und Ernahrung 23 Vorlesungen fur 
Studierende und Aerzte-Berlin u. Wien, 1908, Urban Schwarzenberg, 492, p. 80. 
Die Physiologie der Verdauung usw., 1908, p. 81. 
39. De Dominici: Munchener Med. Wochenschrift., 1891. 
40. Minkowski: Arch. f. exp. Pathol, u. Pharmakol., 31, 1893. 
41. De Meyer: Arch. int. de Physiol. 9,1910, p. iox. Cited by Biedl. Innere Sekretion, 
Bk. 2, p. 351. 
42. Anofuhrl: Lit. cf. Biedl. Innere Sekretion, 1913, 2, 351. Biedl. Arthur: 
The internal secretory organs, their physiology and path., London, 1912, Bale, 
Sons and Danielson, 594 p. 8°. 
43. Hedon: Arch, de med. exp., 1892, p. 617. 
44. Wilms: Chirurgen kongress, 1910. 
45. Stawraky, W.: “Zur Frage nach der fermentativen, Tatigkeit des Blutes und der 
Gewebe bei Pankreasextirpation. 1. Ueber das Antititrypsin,” Ztschrft. f. 
physiol. Chemie, 1914, 89, 381-407. 
46. Heiberg, K. A.: “Die Entstehungsweise der Inselveranderungen und ihr Verhalten 
bei Diabetes mellitus,” Zeigler’s Beitrage z. path. Anat,, 1911,51, p. 178. Weich- 
selbaum, A.: “Ueber die Veranderungen des Pankreas bei Diabetes mellitus,” 
Wiener Klin. Wochenschrift., 1911, 24, p. 153-159. Lubarsch: “Pathologie des 
Diabetes,” Jahresk. f. serzth. Fortbildung, 1911, 1, 57-67. 
47. See Heiberg, Ergebn. d. Anat. von Merkel-Bonnet, 1909, 79 und Gelle, ibid., 1912, 
2, 20, according to Weichselbaum (Wien. Klin. Wochenschrft. 2, p. 155) regenera- 
tion of destroyed islands takes place only from ducts. 
48. Lombroso, U.: “Die Gewebselemente welche die innere Funktion des Pankreas 
besorgen,” Ergebn. d. Physiol., 1910, 9, 1-89. 108 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
49- Escherich: Die Darmbakterien des Sauglings, p. 158. 
50. Holmberg: Dissert. St. Petersburg, 1913, Ref. Chir. Kongressbl., Vol. 4, p. 831. 
Lombroso, U.: “Zur Frage ueber die innere Funktion des Pankreas mit beson- 
derer Rucksicht auf den Fettstoffwechsel,” Arch. f. exp. Pathol., 1907, 56, p. 
357 u. Ergebn. d. Physiol., 9, page 1. Rosenberg: Pflugers Arch., 1898, 70, p. 
371. Fleckseder, R.: “Ueber die Rolle des Pankreas bei der Resorption der 
Nahrungsstoffe aus dem Darme,” Arch. f. exp. Pathol, u. Pharm., 1908, 59, 
407-419. 
51. Garre, C.: “Totaler Querriss des Pankreas durch Naht.geheilt,” Beitrage z. klin. 
Chir., 1905, 46, 233-340. Homeyer: Munchener med. Wochenschrift, 1907. 
Heineke, H.: “Ueber Pankreasrupturen,” Arch. f. Klin. Chir., 84, 1112-1134. 
52. Kuhne undLea: Untersuch. a. d. physiol. Instit. Heidelberg, 1882, 2. 
53. Natus, M.: “Beitrage zur Lehre von der Stase nach Versuchen aus Pankreas des 
lebenden Kaninchens.” “Versuch einer Theorie der chronischen Entzundung 
auf. Grund von Beobachtungen am Pankreas des lebenden Kaninchens und von 
histologischen Untersuchungen nach Unterbindung des Ausfuhrungs ganges,” 
Virchows Arch., 1910, 199-202, 417-471. 
54. Knape, W.: “Deutsche Zeitschrft. f. Chir., 121 und Virchows Arch. 206. 
55. Laquesse, E.: “Ilots de Langerhans et secretion interne,” Compt. rend, de la Soc. 
de Biol., 59, p. 368. 
56. Schulze: Arch. f. Anatomie and Entwikelungsgeschichte, 1900, 56. 
57. Isoboleff: Virchows Arch., 168. 
58. Mora, Henri: “Pancreatectomies chez les jejunes chiens, leur influence sur le 
developpement et sur la glycolyse. These de Paris, 1913, Vigot Freres. 
59. Hess, O.: “Pankreas necrose und Chronische Pankreatitis,” Mitth. a. d. Grenzge- 
bieten, 1909, 19, p. 661. 
60. Barth: “Ueber indurative Pankreatitis,” Arch. f. Klin. Chir., 1904, 74, 2. 
61. Ad. Schmidt: Lit. to chronic pancreatitis: Fr. Muller. Deutsches Arch. f. Klin. 
Med., 1887, 12, Ad. Schmidt, Grenzgebiete, 1914, 26 und Arch. f. Klin. Med. 87, 
1906, Guleke, Ergebn. f. Chir. v. 14, Gross, Deutsches Arch. f. Klin. Med. v. 
108, 1912, p. 106, Riedel, Berliner, Kl. Wochenschrift, 1896, No. 1 a. 2, Barth. 
Arch. f. Kl. Chir. v. 74, Hess, Mitt. ausd. Grenzgebieten, 1909, v. 19, Ehrmann, 
Zeitschrft. f. klin. Medizin v. 69, Truhart, Pancreaspathologie Wiesbaden, 1902. 
62. Schmieden, V.: “Ueber die Zirrhose des Pankreas,” Munchener Wochen- 
schrift, 1906, 53, 2289-2292. 
63. Archibald, E.: Surg. Gyn. and Obst., 1919, 28, 529. Deaver, J. B. and Sweet, 
J. E., J. A. M. A., 1921, 77,196. 
64. Balser: Virchows Arch., 1882, 90. 
65. R. Langerhans: Festschrift, assistenten f. Virchow, 1891. 
66. Natus, M.: “Beitrage zur ihre von der Stase nach Versuchen am Pankreas des 
lebenden Kaninchens,” Virchows Arch., 1910, 199-202. Ricker, G.: “Zuratz 
ueber die Folgen der Unterbindung des Ausfuhrungsganges der Bauchspeichel- 
druse, etc.,” Bruns Beitrage 87, p. 729. Knape: “Die Pankreashemorrhagie,” 
Virchows Archiv., 106 und Deutsche Zeitschrift. f. Chir., 1913, 121. 
67. Chiari: Verhandlungen der Deutsch. path. Gesellschaft., 1901, 5. 
68. Polya, E.: “Ueber die Pathogenese der akuten Pankreaserkrankungen,” Mitt. 
a. d. Grenzgebieten, 1912, 24, p. 49. 
69. Kirchheim: Arch. f. exp. Pathol, u. Pharmak., 1913, 74. 
70. Archibald, Edward: (1) “Ideas concerning the causation of some cases of pancreati- 
tis,” Canad. J. M. and S., Toronto, 1913, 33. (2) “Experimental Production of PANCREAS 
109 
Pancreatitis in Animals as a result of the resistance of the common duct sphinc- 
ter,” Surgery, Gynecology and Obstetrics, June, 1919, No. 6, 529-545, 1 pi. 
17 Internat. med. Congress, London, 1913. 
71. Hildebrand: Zentralbl. f. Chir., 1895 and Arch. f. Klin. Chir., 57. 
72. A Payr und Martina, E.: “ Experimented Untersuchungen uber die Aetiologie der 
Fettgewebsnecrosen und der Leberveraenderungen bei Schadigung des Pankreas- 
gewebes,” Deutsche Zeitschrft. f. Chir., 1906, 83, 189-193. 
73. Guleke, N.: “Ueber die experimentelle Pankreasnekrose und die Todesursache 
acuten Pankeasnekerose und die Todesursache bei acuten Pankreaserkrank- 
ungen.” “Die neueren Ergebnisse in der Lehre der akuten und chronischen 
Erkrankungen des Pancreas, mit besonderer Berucksichtigung der entzundlichen 
Veranderungen,” Ergebn. d. Chr., 1912, 4, p. 408 and Arch. f. klin. Chir., 1906, 
78, 1908, 85. Bunge: Arch. f. klin. Chir., 1903, 71, p. 726. 
74. Schultze, W.: “Ueber zwei Aneurysmen von Baucheingeweidearterien; zugleich 
ein Beitrag zur Aetiologie der Pankreas blutungen,” Zieglers Beitrage, 1905, 38. 
75. Korte: Berliner Klinik., 1896, December. 
76. *Hlava: cited by Polya, Mitt, aus d. Grenzgebieten, 24, p. 49. Carnot: These de 
Paris, 1898. 
77. Simmonds: Deutsche med. Wochenschrift, 1915. 
78. Rost, F.: “Die funktionelle Bedeutung der Gallenblase; experimentelle und anat- 
omische Untersuchungen nach Cholecystectomie,” Mitt. a. d. Grenzgebieten, 
1913, 26, p. 759. 
79. For literature and discussion of the surgery see Sweet, J. E.: Internat. Clinics, 
1915, 4, 293. 
80. Fischler, F.: Deutsches Arch. f. Klin. Med., 100 und Grenzgebiete, 1913, 26, 4, 
p. 103. 
81. Maragliano, D.: “Le causauella morte per necrosi pancreatica,” Policlinica, 1912, 
19. 
82. Guleke, N.: “Ueber subcutane Pankreas verletzungen,” Munchener med. Woch- 
enschrift, 1910, p. 1673; med. Wochenschrift, 57, 75-79. v. Bergmann: “Die 
Todesursache bei akuten Pankreaserkrankungen,” Zeitschft. f. exp. Pathol, u. 
Therapie, 1906, 3, 401-424. 
83. Doberauer: “Ueber die sogenannte acute Pancreatitis und die Ursachen des 
schweren oft todlichen Verlauf derselben,” Bruns Beitrage, 48, u. Chirurgenkon- 
gress, 1906, 456-515. CHAPTER IV 
LIVER AND GALL BLADDER 
The liver, the physiological importance of which is indicated by its 
size, is interposed between the intestines and the greater circulation 
and serves to elaborate the energy values which enter the body as food (i). 
The liver has been compared to a sorting room, or a bank—well-selected 
comparisons since they imply that a division and purposeful reconstruc- 
tion of the many food substances which enter by way of the portal system, 
take place here. But to these remarks might be added that warm blooded 
animals can tolerate extensive elimination of liver activity; as, for example, 
after establishing an Eck fistula (anastomosis between inferior vena cava 
and portal vein, ligation of portal vein (see later)). 
The first and the most important place of metabolism must therefore 
be sought in the liver. Cessation of function, or what amounts to the 
same thing, its experimental elimination, can lead to a flooding of the 
circulation with substances which, although formed in the body from 
foodstuffs, are deleterious, and if not thrown off, poisonous. The liver 
regulates these metabolic processes by means of numerous enzymes, some 
contained in its own cells, and others received by way of the circulation, 
as for instance, from the pancreas. The different stages of metabolism 
within the liver are not carried on one by one, but they overlap in ways 
unknown in detail, making it still more difficult to grasp the complicated 
functions of this organ. Thus far, there is no evidence that these various 
functions take place in different sections of the liver as some French 
authors (see Hess-Serege (2)) claim, but it is remarkable that certain 
diseases seem to prefer special parts. 
Tropical liver abscesses are found almost exclusively in the right lobe, 
while cirrhosis usually begins in the left lobe (3). Glenard and Serege’s 
opinion, that the functions of the two lobes are independent of each other, 
to a certain degree, cannot be accepted at present. Nevertheless, there is 
a possibility, especially from facts in its pathological anatomy, that 
certain portions possess their own definite functions. If this were true, it 
would be of great importance to the surgeon, but such an assumption has 
no supporting evidence at present. 
We know from the experiments of Gluck (4) and Ponfick (5) that 
rabbits easily tolerate the removal of two-thirds of the liver. The livers 
of the operated animals have a very active regenerative power so that after 
110 LIVER AND GALL BLADDER 
111 
a short time the remaining portion is doubled in size (6), possibly because 
the original amount of blood with the original vascular tonus flows through 
a much smaller amount of liver tissue. This hyperemia governs growth, 
and the cells cease to grow as soon as equilibrium is established between the 
inflow of blood and the growth of tissue. It is desirable to investigate this 
interesting theory experimentally. This regenerative power is found in 
man also, as for instance, in echinococcus cysts and other affections 
which destroy liver tissue mechanically. 
These regenerated cells seem to function, although no investigations 
of changes in metabolism after partial resection have been published. 
The investigations of Gluck and Ponfik were confined to anatomical 
facts. 
In Ponfik’s experiments the other organs of the animals showed a 
comparatively slight injury. There was chiefly congestion in the abdomi- 
nal organs, leading to considerable enlargement of the spleen. 
We may now briefly review the various functions of the liver. 
First, it has special importance in carbohydrate metabolism. We owe 
to Claude Bernard (7), among many other things, the demonstration 
that the liver stores carbohydrates in the form of glycogen, which it then 
changes into sugar and supplies to the body according to requirement. 
We cannot discuss in detail how this occurs, or by what enzymes it is 
accomplished (1). There is a rather lively controversy, supplemented 
by many carefully planned experiments concerning whether the body 
elaborates glycogen from substances other than carbohydrates, i.e., 
from fats and proteins (8). This question, which is of special interest 
in the treatment of diabetes, has been generally answered to the effect 
that the liver does form glycogen from proteins, and perhaps from fat 
also. For this reason, it is now generally conceded that not merely 
carbohydrates but also proteins must be reduced in diabetics. For the 
surgeon, carbohydrate metabolism in the liver is of special interest, 
because its disturbances, which are comparatively easily demonstrated, 
are at present the most important diagnostic sign of liver lesions. The 
reduced tolerance to galactose is probably the most frequent. In simple 
obstructive jaundice, it is not present, but it is found in every icterus 
resulting from injured liver cells (9). 
The importance of the liver in relation to the anabolism and catabolism 
of proteins is also not trivial. Proteins, broken down in the intestines 
to amino acids, are practically all carried into the body by the blood cir- 
culation, not by the lymph channels, which means they encounter the 
liver by way of the portal vein. Since these split products have not yet 
been demonstrated in,the blood of the portal vein, it is assumed that the 
amino acids are synthesized in the bowel into complete protein molecules 112 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
and pass as such to the liver (io). The findings of Abderhalden and 
London (n), who replaced the food proteins given to Eck-fistula dogs 
by completely split proteins and yet had nitrogen equilibrium, support 
this view. How far the liver participated in this phase of the protein 
metabolism is by no means clear. Fischler on the basis of his experi- 
ments, believes the liver plays a prominent role in this process. 
[That the blood contains amino acids and that they increase markedly 
during digestion has been clearly shown. The normal concentration of 
about o.i per cent, may be nearly doubled in the portal blood of dogs 
after a heavy protein meal; furthermore, there is a greater fall in the 
amounts of amino acids during their passage through the liver (difference 
between portal and hepatic vein blood) than during passage through the 
entire remainder of the body (difference between arterial and vena cava 
blood) (12).] 
To the surgeon, this question is very important, especially because the 
loss of a part of the liver function through Eck’s fistula may be serious 
(see later). The catabolic products formed from the protein molecule 
are dangerous and poisonous to the body; thus, for example, the ammo- 
nium salts formed by the splitting of proteins are converted into urea, 
and sent into the greater circulation in a non-toxic form (13). Blood 
from the portal vein is very rich in ammonium salts and if it is conducted 
directly into the vena cava, as in an Eck fistula, it may result in symptoms 
of ammonia intoxication, which, however, is not usually fatal (see later). 
The details of the formation of urea from protein are still obscure and 
they cannot be discussed here (14). 
The liver is also concerned in purin metabolism which, of course, is 
merely a subdivision of protein metabolism. Proteins are classified into 
simple and compound proteins. Nucleo-proteins belong to the latter 
group, and are split into nucleic acid and a protein moiety by enzymes 
elaborated in various organs. Nucleic acid is broken down by enzymes 
through the various purin bases to uric acid which is quickly split further. 
As is well known, the disease “gout” is a disturbance of purin metabolism 
and we differentiate “renal” gout from “true gout.” In the former, after 
increased formation of uric acid, the kidneys do not eliminate at a rate 
sufficient to prevent its accumulation in the blood and deposit in various 
tissues; in the latter, the disturbance results from a defective enzymic 
catabolism- of purin bodies. Since enzymes which are active in the catab- 
olism of nucleins (uricolytic ferments, etc.) have been found in the liver, 
although only in autolysis, and since it has been shown that the urine of 
Eck fistula dogs contains five times the normal quantity of uric acid, a 
number of writers believe the liver has considerable importance in gout, 
an opinion which is not generally accepted (1), (15). LIVER AND GALL BLADDER 
113 
Some of the -ingested fat also traverses the liver, but by far the larger 
quantity enters the circulation through the chyle channels. As Fischler 
(i) expresses it, the liver has transferred its function in fat absorption to 
the intestine, since the bile formed by the liver is necessary to change fat 
into a water soluble form. 
The fats reaching the liver may be stored there, but they may also 
undergo a vaguely understood alteration as shown by their participation 
in the formation of acetone bodies. Histologically, fatty acids have not 
been demonstrated in the liver (Fischler). Part of the fatty bodies, 
especially cholesterol is excreted in the bile, the other portion is added to 
the general metabolism after it undergoes a very complicated analysis and 
re-synthesis (16). 
The detoxifying property of the liver, mentioned above, is active not 
only in reference to proteins, but to all sorts of ingested substances, which 
by conjugation, splitting, or in some other way, are made harmless to the 
organism. This applies especially to alkaloids, which for this reason 
are quickly fatal if introduced subcutaneously, but are comparatively 
harmless if taken by mouth when they can enter the Hver by way of the 
portal vein. Schiff (17) found that a dose of nicotine which quickly killed 
a frog, deprived of its liver, did not even poison a normal one; in the same 
manner, a mammal may be quickly killed by injecting strychnine, mor- 
phine and other poisons into the greater circulation, while the same dose 
injected into a mesenteric vein is harmless (lit. see Wohlgemuth (14), p. 196). 
Of course, this detoxifying process is not without its effects on the 
liver, and often its service rendered to the organism as a whole brings 
about its own destruction. This is evidenced anatomically, by the fatty 
degeneration following poisoning by phosphorus, alcohol, phloridzin, and 
a number of infectious diseases; by the loss of glycogen and finally by 
central necrosis of the lobules. 
The contention of whether the fatty liver in phosphorus poisoning is a 
result of degeneration or infiltration, may be decided by the investigations 
of Lebedeff (18) in favor of the latter. He starved dogs until they had 
lost practically all of their fat and then fed them with linseed oil and meat, 
poisoning them at the same time with phosphorus. Their liver cells 
contained linseed oil, but no dog fat; consequently there could not have 
been a change of protein into fat, or as it -is usually designated “fatty 
degeneration” of the cells. 
Central necrosis has considerable surgical interest since it occurs in 
chloroform poisoning. Fischler’s experiments have shown that the process 
is by no means simple, but is related in a complicated way to pancreatic 
activity (19). Ordinarily, chloroform does not injure the livers of healthy 
animals, but if the liver is short circuited by an Eck fistula, it produces 114 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
the typical central necroses very speedily and the animals die in a peculiar 
comatose condition (20). In animals with Eck fistulae, similar changes 
may be produced by poisons other than chloroform but some animals 
which have had these fistulae for some time, are not more sensitive to 
chloroform than normals. Fischler believes, therefore, that chloroform 
is merely an activator in the production of these changes. A liver injured 
in some way seems to be hypersensitive to the trypsin derived from the 
pancreas, for if an animal has been previously immunized to this enzyme, 
it does not develop a central necrosis, notwithstanding the Eck fistula 
plus chloroform (Bergmann and Gulecke). The correctness of this view 
is vouched for clinically by the observed coexistence of central necrosis 
and pancreatic fat necrosis (Adamski’s case (21)), a combination which 
has also been seen experimentally. According to Fischler, death in 
central liver necrosis results from a flooding of the circulation with liver 
substance split by trypsin, and is therefore a death from split protein 
intoxication. Clinical reports of death after chloroform anesthesia 
similar to the deaths of liver necrosis or acute yellow atrophy, have been 
frequently described in the literature (22), but in these cases, the authors 
failed to take into consideration the possibility of a hypersensitiveness of 
the liver to chloroform. This peculiarity of patients with icterus is known 
to every surgeon and for this reason ether is the preferred anesthetic. 
[A decisive factor in chloroform necrosis of the liver is the diet. Ani- 
mals who have been starved are much more susceptible and are injured 
to a greater degree. Interesting facts have been brought out, not only in 
this connection but also in the repair of such injuries, by Whipple and his 
associates. It seems that when the liver is injured by chloroform, the 
necrosis involves the lobules beginning in the center and extending outward 
to approximately the same degree throughout the entire organ. If 
therefore a small section is removed at intervals after poisoning, the 
process of repair can be followed with great accuracy. The necrotic 
debris is removed by autolysis and absorption, and new liver tissue then 
grows in. The rate at which this repair proceeds has been studied, and 
it was found that complete regeneration can take place in from seven to 
ten days. During starvation, the rate is slower; a diet of bread and 
skimmed milk is the best for repair, skeletal muscle is less favorable and 
so on. The amount of carbohydrate present is the important factor. 
Fats have no influence. 
Two problems of more general interest also have received light from 
these investigations. 
“The protein sparing action” of carbohydrates is well recognized 
through the efforts of Lusk and others. That is: during fasting, less 
nitrogen (protein) is lost if the body is well stocked with the carbohydrate LIVER AND GALL BLADDER 
115 
glycogen; the addition of added amounts of carbohydrates to a diet 
insufficient in proteins will decrease or prevent the loss of nitrogen; and 
finally, carbohydrates added to a diet already containing nitrogen suffi- 
cient to maintain equilibrium will bring about storage of protein. The 
mechanism of this action is not understood but it is believed by some that 
it occurs “at the source,” i.e., carbohydrates spare proteins by inhibiting 
the intracellular enzymes which destroy the latter. Others believe that 
it occurs by way of chemical union between partial oxidation products of 
carbohydrates such as lactic acid, and the end products of protein catab- 
olism. An actual construction of new tissue takes place from a portion 
of the carbohydrate molecule. 
These experiments on liver regeneration seem to support the latter 
view. The addition of sugar to the diet of the poisoned animals led to a 
marked diminution in nitrogen excretion, i.e., the nitrogenous bodies 
which would have been excreted were captured and combined with the 
sugar to help form new liver tissue. 
The second more general proposition concerns growth. The rate 
of repair of the liver is so rapid that fully 800 grams of liver grow in seven 
to nine days. Were a tumor to grow at the rate of 100 to 150 grams per 
day (about the size of a normal spleen or kidney), the surgeon would no 
doubt be dumfounded. This great capacity of the liver to repair and grow 
should offer a remarkable opportunity to study problems of growth in 
general (23).] 
In addition to these various functions, the liver is concerned in blood 
coagulation. The cause of delayed coagulation is either lack of fibrinogen, 
or an excessive amount of anti thrombin in the blood. We know that in 
experimental destruction of the liver by chloroform (24), phosphorus or 
other injurious substances, not only is there a lack of fibrinogen in the 
blood, but also an increase of antithrombin in the liver, a substance which 
inhibits blood coagulation (25). The latter is found in other organs also, 
but whether these antithrombins of various organs are identical is not 
known at present. 
It is naturally quite clear that we can interfere but little with our 
surgical equipment in this complicated metabolism of the liver; in other 
words, the surgical therapy of diseases of the liver is far from promising. 
The surgeon’s interest is centered especially upon the conditions in which 
an acute cessation of metabolism swamps the organism with poisonous sub- 
stances which endanger the benefits of some operation, possibly performed 
on an entirely different part of the body. Unfortunately, our knowledge 
in this respect is still fragmentary, but the investigations of death from 
chloroform have at least shown us in which direction to turn our 
attention. 116 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Surgical therapy in diseases of the liver confines itself to its circulatory 
conditions and to those of the portions of intestines dependent upon them. 
We must therefore become acquainted with the experimental investiga- 
tions of the hepatic circulation (26). In man, and in those animals which 
differ from the dog in not having extensive anastomoses, the anatomy of 
which is described especially well in Rio Branco’s (27) work, ligation, or 
embolic occlusion of the hepatic artery is followed‘by necrosis of large 
amounts of liver tissue. The numerous experiments on this subject 
have been compiled by Narath II. Of later investigators, we 
need mention only Cohnheim and Litten, Janson, Ehrhardt, Haberer, 
Narath (28). 
The results obtained by older authors do not agree in every detail, 
the reason being that the ligature was not always applied at the same place 
and many overlooked possible abnormal collateral branches, which are 
found at times in man, and more often in the ordinary laboratory animals, 
especially the dog. Haberer (28) with due consideration of all these 
possible sources of error, conducted a series of investigations by ligating 
the hepatic artery at various places, and immediately after death, following 
this by injecting the vessels through the aorta. He found that if the 
artery is ligated before the branching of the gastro-duodenalis, the collat- 
erals are sufficiently numerous, and act promptly enough to prevent 
changes in the liver. If this collateral circulation is narrowed down by 
applying a ligature between the gastro-duodenal, and the pyloric arteries, 
then small necroses are observed, while ligation of the hepatic artery 
proper leads to total destruction in spite of the arterial blood still flowing 
through from arteries in the diaphragm, or from possible abnormal hepatic 
branches. 
V. Haberer’s, and later Nicoletti’s experiments (29) have also shown 
the effect of ligation of the two end branches of the hepatic artery. 
Necrosis involves the lobe indicated only when it is comparatively iso- 
lated, as is the case in rabbits. According to Nicolleti, the broad junction 
of the hepatic lobes with each other in man, makes it possible to ligate the 
final branches of the artery, but Narath (28) and Thole (30), believe the 
danger of necrosis is too great. As a whole, the results of experimental 
and anatomical investigations have been confirmed on man in both the 
cases in which the artery has been ligated by accident or intentionally 
(aneurysm) as well as in the rare pathological condition of embolism 
(Chiari) (3), (28). According to Narath II, there are about 20 cases in 
the literature in which the hepatic artery or separate branches have been 
ligated operatively. Humans can undoubtedly tolerate ligation of the 
common hepatic artery; but ligation before the gastric artery branches 
off, leads to small liver necroses. Ligation near its origin is possible with- LIVER AND GALL BLADDER 
117 
out extensive necrosis, only when there is a well developed collateral 
circulation such as usually develops after ligation of the main branches 
(31). Everything depends on the collaterals, but their extent can hardly 
be estimated beforehand (see Narath). If, however, arteriosclerosis 
involving the hepatic artery or extensive adhesions are present about the 
liver, the collateral circulation is usually sufficient, and ligation of the 
arterv near the cceliac axis would be feasible. Bourdenko (32) has 
utilized this fact in animal experiments by suturing the omentum to the 
liver thereby obtaining a collateral circulation, and then after some days, 
tying off the hepatica propria. The results were by no means conclusive, 
but he believed that the necroses were less extensive. Villandes 
attempted to avoid the danger by slowly constricting the lumen of the 
artery before final ligation. 
Still another method was devised by Narath II (28) who established 
an anastomosis between the renal artery and the portal vein by means 
of a suture and found that his animals lived and showed only minor 
changes in the liver. He obtained similar results by implanting the 
severed hepatic artery into the portal vein, which amounted to the same 
thing. These experiments are intensely interesting from every standpoint. 
First of all, they show that the liver cells are able to extract the arterial 
blood necessary for their nutrition from the portal circulation when this 
contains it. This was demonstrated especially well in one of the dogs in 
which an embolus obstructed the portal vein to one lobe, which consequently 
became necrotic, while the other lobes were undamaged. Furthermore, the 
portal vein and its surrounding connective tissue are not dependent for 
blood supply on the vasa-vasorum, for even in the absence of these vessels, 
they do not perish from necrosis. But it is not known whether the vessel 
wall receives its blood supply from the portal vein itself or from other 
sources. 
Narath II and Steckmacher (33) studied histological changes in 
the liver after ligation of the hepatic artery. Among the more important 
findings are periacinar connective tissue proliferation and cyst formation, 
both described by Janson (28) also. It must be emphasized that this 
formation of connective tissue following necrosis has nothing in common 
with true cirrhosis of the liver (see Lissauer (34)). 
The changes after sudden ligation of the main trunk of the portal vein 
cannot be studied in animals because death usually takes place after a few 
hours (35), but in dogs and cats single branches can be ligated without 
fatal results (36). Ehrhardt stated that in the cat, nutritional disturbances 
of the liver cells resulted from ligation of the branches of the portal vein 
supplying them. The normal fat content of the cells oscillated and the 
blood content of the liver lobules became minimal. In a number, cicatri- 118 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
cial shrinking was found after two to three months. After more extensive 
ligation, the livers showed changes quite similar to cirrhosis. Solowieff 
(37) had observed this before, after a gradual occlusion of the portal vein, 
and he was enabled to keep the animals alive for months. Steenhuis 
also found in his extensive experiments on rabbits that after ligation of 
separate branches of the portal vein the corresponding lobes were, always 
shrunken, while the others showed a compensatory hypertrophy. Liga- 
tion of such isolated branches is not fatal because the portal system is 
not a closed unit, but anastomoses with branches of the superior and in- 
ferior vena cavae, and is in close connection with the hepatic artery also 
(Josselin de Jong's work discusses these anatomical relations). Changes 
in the liver in the sense of cirrhosis have by no means been consistently 
observed after ligation of the portal vein (38) and certainly not after its 
partial elimination as was undertaken by Cohnheim and Litten and others 
(39). They occluded the large vessels by introducing globules of wax into 
the portal vein, but found no alterations in the liver. On the other hand, 
Zahn (40) who used mercury for emboli, observed so called “red infarcts” 
which means foci of atrophy of liver cells with capillary dilatation. Chiari 
{41) points out that the type of liver change under these conditions 
•depends on whether the involvement includes the interlobular branches 
•or is only in the larger trunks. In the latter case, the interlobular anasto- 
moses with the hepatic artery remain intact, and these inner “portal 
vein roots” supply a large amount of the blood otherwise excluded. 
The results of these experiments are in perfect harmony with the 
changes following portal vein thrombosis (42). Of course, here too the 
secondary anastomoses formed by the portal vein play an important part. 
The esophageal and gastric veins dilate as do those of the abdominal wall 
(caput medusae), and a quickly fatal hemorrhage may result from rupture 
of these esophageal varices. Furthermore actual cavernous dilatation 
of the veins of the hepatoduodenal ligament has been observed and total 
obstruction of the portal vein may finally be compensated, thus prolonging 
the life of the patient (43). 
If, therefore, ligation of a branch of the portal vein is permissible 
and compatible with life, nevertheless, “the ligation of the main trunk 
of the portal vein generally kills the patient,” as Langenbuch (44) 
expresses it. 
What is the cause of death in total occlusion of the portal vein in man or 
animals? Numerous investigative results are available, for ligation of this 
vein is a particularly suitable method for studying the physiology of the 
liver; although the animals do not live for more than a few hours. Death 
is generally supposed to result from exsanguination into the enteric vessels, 
but yet they cannot hold enough to cause death from hemorrhage as LIVER AND GALL BLADDER 
119 
Tappeiner (35) points out, and Ehrhardt (36) has shown that no such 
remarkable stasis really occurs. 
Tappeiner carefully investigated blood pressure, rapidity of outflow, 
pulse, etc. during exsanguination, and also after ligation of the portal vein, 
but was not able to explain why “ the blood is placed in such a condition 
that it cannot participate actively in the circulation” after portal obstruc- 
tion ((35) p. 64). 
According to investigations of Thole (6), a notable depression of blood 
pressure occurs after experimental ligation of the portal vein with intact 
vagus, and the animals die in collapse. If the vagi are cut, these symp- 
toms develop more slowly, so that an infarct of the intestines appears. 
To sum up: We may say that death after ligation of the portal vein 
results either from collapse, or from intestinal congestion (infarction). 
Thus far, the cause of this collapse is unknown. 
That elimination of liver function is not the cause of death is obvious, 
since death results so quickly, and since the numerous experiments with 
Eck’s fistulae (45) have shown that mere short circuiting of the liver is a 
procedure entirely compatible with the life of an animal or man (see case 
of Rosenstein (46)). We cannot discuss here the changes in metabolism 
which follow Eck fistulae. A question of possible future surgical impor- 
tance is still debated, viz., whether animals with Eck fistulae may be per- 
mitted a meat diet, and on what the severe collapse, occasionally observed 
after such a diet, depends. The surgeon is interested in the Eck fistula 
chiefly because it relieves the peripheral stasis incident to portal ob- 
struction. We shall return to this in discussing ascites and its therapy. 
Furthermore, after establishing an Eck fistula, the whole liver may be 
extirpated in animals, but they live only a few hours (38). 
Experimental obstruction of the hepatic veins has often been used to 
study retrograde embolism (47). Arnold observed a very instructive 
case of this condition and made it the starting point of experimental 
investigations which showed that obstruction of the hepatic veins results 
in the appearance of red spots in the liver corresponding to engorged 
capillaries. In a number of clinical cases of thrombosis there were found 
nodular hyperplastic foci, capsular thickenings, increase of connective 
tissue along the hepatic vein which was tortuous, and degeneration of the 
parenchyma (48). 
It is interesting to note the reaction of the liver to temporary pinching 
off of vessels, especially those in the hepatoduodenal ligament. Its 
corollary—how the lesion resulting from this cause or from obstruction 
or stasis can be counteracted—is also of interest. 
To check hemorrhage during resection of portions of the liver the most 
rational method is, of course, temporary compression of the hepatoduodenal 120 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
ligament, and this has been done repeatedly both experimentally and in 
man (49). Opinions as to the results differ. Some state that its com- 
pression for as long as one hour does not cause observable lesions, while 
others consider this method of temporary hemostasis impossible, because, 
as stated above, rapid collapse and death followed either this procedure 
or ligation of the portal vein (Langenbuch). Ransohoff (50) also points 
out that a fall in blood pressure is caused by merely inserting a finger into 
the foramen of Winslow, while Burdenko observed chromatolysis in the 
abdominal ganglia. 
With these contradictory statements, it is probable that the differ- 
ences lie not so much in erroneous observations, as in individual variations 
in the animals and in the nature of the experiments. Thoele emphasizes 
that in man, the portal vein can be occluded for only a short time and then 
only after the arterial supply has also been closed off. Perhaps the 
differences in results depend on the simultaneous obstruction of both 
artery and vein. 
The most important, and for the patient the most distressing, result 
of stasis in the portal circulation is ascites (51). Its development, as well 
as that of edema is often considered due to mechanical causes, assuming 
that the fluid passes out of blood vessels somewhat like a creek overflowing 
its banks when its natural outlet is dammed; i.e., it is purely a result of 
obstruction. The fact is, however, that ascites may be due to various 
causes, which according to Quinke, may be grouped as follows (52) : 
I. Increase of inflow. 
(a) Increased inflow of lymph. 
(b) Increased secretory activity of the endothelium. 
(c) Increased permeability of blood vessel walls from congestion 
or inflammation. (In the latter, probably the altered activity 
of the endothelium is an important factor.) 
II. Decreased outflow. 
(a) From obstruction to efferent lymphatics. 
(b) From decreased absorptive power of endothelium. 
(c) From decreased absorptive power of the blood vessels, e.g., 
in passive congestion. 
Naturally this classification has only didactic value. As Quincke 
himself remarks, in some cases several of these factors are present or follow 
each other. But the ascites due to congestion is still differentiated from 
an inflammatory exudate by the greater albumen content and the more 
numerous leucocytes of the latter. But quantitative determinations 
show that such a comparison is not always possible because middle LIVER AND GALL BLADDER 
121 
values are found so frequently. Furthermore, in many cases there is an 
uninterrupted course of events from transudate to exudate. Pure obstruc- 
tive ascites, in the old sense of the term, can hardly be said to exist (53). 
For the development of any ascites there is required a disturbance in the 
intermediary water and mineral metabolism of the cells, chiefly perhaps 
the endothelium, but a disturbance which must be classed under the 
group of “inflammations.” According to our present opinion, the over- 
flow of fluid is not a simple leaking of serum through a more permeable 
vessel wall, but is a result of a specific activity: a “secretion” of the 
endothelium. Theoretically, therefore, it is not justifiable to draw a 
sharp distinction between obstructive and inflammatory ascites, since the 
difference between the two is one, not of kind, but of degree. 
But for practical purposes, the differentiation is highly important. 
An exudate ordinarily indicates a bacterial process, whether it be due to 
primary bacterial action, to infection from careless puncture, or to infec- 
tion of a transudate which on account of its long duration has rendered 
the intestinal wall more permeable to bacteria (54). Even though we may 
be able to determine in a general way that an exudate is due to bacterial 
processes, the actual factor which causes the inflammation and disturbs 
cellular metabolism so that fluid is poured out, remains unknown. Only 
when this is recognized, will we be in a position to understand the reasons 
for the frequent failure of our therapeutic measures, which in the main, 
attempt to improve the circulation. The question of whether or not this 
disturbing factor resides simply in the congestion itself, can perhaps be 
answered by experimental obstruction to the portal circulation. 
The very careful investigations of Ito and Omi (55) who .obstructed the 
portal circulation gradually, have demonstrated that no ascites is devel- 
oped in animals in spite of marked congestion. The clinical findings in 
slowly developing portal thrombosis are of less deductive value on account 
of the varied etiology (56), (42). The frequently cited case of Langenbuch 
in which ascites developed after numerous small branches of the portal 
vein were ligated during resection of a lobe of the liver, is not clear 
cut because as the author himself states, it was complicated by erysipelas. 
In a number of instances on record, portal thrombosis was associated 
with ascites, in others, such was not the case (53). On the other hand, 
not a few cases of cirrhosis of the liver show ascites when no trace of stasis 
in the portal circulation can be discovered at autopsy. The splenic tumor 
in cirrhosis of the liver is not due to congestion, but is inflammatory. It 
follows that we must be very careful in interpreting the importance of 
congestion in ascites, especially that following cirrhosis of the liver, and 
we must not be too optimistic in expecting a cure of the ascites by opera- 
tive improvement of the abdominal circulatory conditions (38). 122 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
The most common operation for this purpose is that of Talma and 
Drumond (57). These two surgeons, from anatomical considerations, 
simultaneously and independently proposed that a free anastomosis be 
established from the portal vein to the inferior vena cava by fixing the 
omentum, spleen, liver and gall bladder to the anterior abdominal wall. 
We know that in cirrhosis of the liver the natural communications between 
the portal vein and inferior vena cava are often much distended, leading 
among other things to the dangerous varices of the esophagus, or to the 
classical caput medusae. Experimental investigations were made of the 
possibility of eliminating the liver after omental fixation, i.e., to determine 
whether sufficient anastomoses would develop. Tillmann (58) ligated the 
portal vein after one of these operations in a dog, without important damage. 
But this well known experiment failed to answer its original question 
because at autopsy, not only was the portal vein only partially obstructed, 
but there were numerous collaterals in this area. Furthermore, many 
workers who did not suture the omentum to the anterior belly wall suc- 
ceeded in gradually ligating the portal vein in dogs without fatalities (59). 
On the basis of their investigations, Ito and Omi assume that the last 
mentioned writers unintentionally produced a peritonitis, which led to 
broad anastomoses between the abdominal organs and which may explain 
why the dogs escaped the consequences of their operations. 
Moreover, their experiments show that omental fixation does not 
always suffice to prevent death, and only the formation of broad adhesions 
of the abdominal viscera to the anterior abdominal wall and to each other, 
insures the development of sufficient collaterals. For this reason they 
suggest treating the ascites of cirrhosis by producing such adhesions. 
Referring to what has been said above regarding the cause of ascites in 
cirrhosis, it appears somewhat doubtful whether this quite dangerous 
method would be better than simple omental fixation. The same may 
be said in regard to establishing an Eck fistula, a method which has been 
used but seldom in man. At any rate, Rosenstein’s patient who survived 
the operation for some time was not entirely relieved of the ascites by 
this procedure (60). Detailed statistics of the operative results in about 
300 cases of the Talma operation are furnished by Bunge (61). He showed 
that ascites disappeared in only 30 per cent. Later figures appear to be 
somewhat more encouraging (see Hopfner (51)). 
The unsuccessful results of the various operations show with almost 
the certainty of an experiment, that stasis is not the only cause of ascites, 
although it must be admitted that it is a real and essential factor in the 
appearance of a transudate in cirrhosis of the liver. The practically harm- 
less Talma operation therefore seems justifiable. In passing, it may be 
mentioned that Talma himself did not consider the ascites in cirrhosis the LIVER AND GALL BLADDER 
123 
result of congestion alone. Up to the present, attempts to establish more 
clear cut and definite indications for Talma’s operation on the basis of 
hepatic functional tests, have failed and will continue to fail, for the simple 
reason that neither the place nor the mode of action of stasis is known. 
In the few instances of sudden death following Talma’s operation, 
Kretz attributed the fatal outcome to a sudden flooding of the circulation 
with substances which otherwise would have been detoxified in the liver. 
These deaths must, therefore, be considered analogous to those observed 
occasionally in Eck-fistula dogs (see above). 
In contrast to these procedures which combat ascites by improving 
stasis, are those which confine themselves to symptomatic treatment and 
remove the fluid by early and frequent puncture (Ewald (62) a.o.), or by 
permanent drainage. To make the latter possible, the saphenous vein 
with its opening into the femoral vein intact, is turned upwards and 
introduced as a drain into the abdominal cavity (Rouotte’s operation (63)), 
or silk threads, or silver wire (64) carried from the abdominal cavity into 
the subcutaneous tissues have been used to induce the growth of new 
lymph vessels (for other methods see Enderlen, Hotz, and Magnus- 
Alsleben (42)). 
In the cure of ascites by puncture or drainage, that is, without new 
blood vessel anastomoses, a number of factors must be considered (52). 
By paracentesis, substances are removed which are injurious and irritating 
to the serosa and which hinder absorption. The mechanical absorptive 
conditions are improved, the endothelium of the serosa is again placed 
under physiological conditions, and changes favoring a cure are promoted. 
In fact, ascites has been permanently relieved in certain instances by this 
means, and the importance of this form of drainage must not be under- 
estimated. Physiologically, it is at least as logical as Talma’s operation, 
and it is quite possible that the latter influences ascites not only because it 
relieves the assumed venous congestion, but also because it opens new 
connections between the lymphatics of the abdomen and the subcutaneous 
tissue, or in other words, it establishes permanent drainage. But after 
all, we know very little of the activity of the lymph channels in the forma- 
tion or the removal of ascitic fluid, although we do know that irrespective 
of the therapeusis of its underlying cause, the removal of fluid is desir- 
able, because the increase of intraabdominal pressure leads to circulatory 
disturbances. This will be considered more carefully in the section on 
ileus. 
A most interesting function of the liver is its bile formation and 
secretion (65). As it appears in the intestine, bile is a product of liver 
cells and of the epithelium of the bile channels, especially the gall bladder. 
It is delivered from the liver as a thin watery fluid; its peculiar viscid 124 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
consistency is due to the mucin secreted by the epithelium of the bile 
channels (66). But the consistency of bile changes not only with its 
mucin content but with its content of water. The chief constituents are 
the bile acids, which are conjugation products of cholic acid and glycocol or 
taurin (glycocholic acid and taurocholic acid), and bile pigments. 
For the other chemical substances found in the bile, the reader is 
referred to Wohlgemuth (67). The numerous investigations of the 
source of bile acids and bile pigments have now quite definitely established 
the fact that the acids originate mainly, if not exclusively, in the liver 
itself. A question of great importance in the etiology of gall stones is th£ 
source of the cholesterin found in the gall bladder. Since the bile of that 
structure contains more cholesterin than liver bile, Naunyn (68) assumed 
that it was a product of the gall bladder epithelium, but Aschoff (69) 
believes that it comes chiefly from the liver. 
In addition to these normal constituents, the bile also eliminates 
substances which have been ingested as medicines. We cannot discuss 
the details here (38). This is the basis of all efforts to dissolve gall stones 
by medicines, or to disinfect the bile channels (70). 
The formation of bile, as Barbera (71) attempted to prove in numerous 
investigations, is a result of the metabolism of the liver cells. The color 
and the chemical composition depend to a certain extent on the blood 
supply. At least, Colasanti (cited by Wohlgemuth) observed a colorless 
bile, very poor in bile acids in a gall bladder fistula dog, whose portal vein 
had been ligated. In the literature, a certain prominence is given to cases 
in which a nearly colorless bile is secreted, i.e., acholic stools without 
icterus. They are usually associated with extensive changes in the liver, 
such as tuberculosis or very advanced fatty degeneration and infiltration 
(72). Thus far, total failure to secrete bile has not been observed with 
certainty (73). Leukourobilin formation, in which the usual hydro- 
bilirubin has been further reduced in the intestine, as well as fatty and 
milk stools, are often mistaken for acholia. Nor must the colorless bile 
found in degeneration of the liver cells be mistaken for the white bile 
found in hydrops of the gall bladder (see later). 
The quantity of bile secreted varies within wide limits, and observa- 
tions made on man or animals with gall bladder fistulae, can be utilized 
only with caution. It is true that both man and the dog tolerate the 
complete absence of bile from the intestines comparatively well. Mayo 
Robson (74), for instance, was enabled to observe and experiment for 15 
months on a patient with a complete gall bladder fistula. Nevertheless 
this continuous and total loss of bile can scarcely be considered a matter of 
indifference to the general metabolism. Recent observations, especially 
of severe osteoporosis with gall bladder fistulae have taught us better. LIVER AND GALL BLADDER 
125 
The statements of the quantity of bile flowing from biliary fistulae 
must not be taken too literally, because the amount excreted may in 
reality be larger, or it may be less. Brand (75) compiled tables of the 
quantity secreted by different individuals in 24 hours, according to differ- 
ent authors. He gives figures ranging from 16 c.c. to 1122 c.c. Mayo 
Robson observed from 860 to 1133 c.c. in his patient. 
The liver, of course, secretes constantly, but in varying amounts. 
The daily curve of secretion usually begins to rise during the early 
morning and reaches one or two maxima during midday and evening 
hours, followed by a fall during the night until the early morning. The 
curve may be explained by the taking of food which undoubtedly influ- 
ences bile formation. In the details, the statements of the various workers 
are very conflicting; but it may be gathered that water has no influence, 
while a protein diet increases bile secretion (76). In regard to fats and 
carbohydrates, opinions are hopelessly contradictory. While some 
observed considerable increase after fat feeding (77), others found a 
decrease (Mandelstamm, Thomas, Stadelmann); clear proof that the 
much used method of the gall bladder fistula is very unreliable. 
From the investigations of Stadelmann and his followers which 
were made with every conceivable precaution, it can be stated that 
the increase in bile secretion observed after protein diet is seen only 
when compared to that in the same animal during starvation, and that 
immediate increase of bile formation after feeding is not consistently 
observed. 
Of the chemicals credited with bile stimulating action, very few have 
survived critical tests. The bile acid salts are of special interest because, 
according to the consensus of opinion, they always induce an increased 
bile secretion and are probably important in the physiological process 
(78). These salts are absorbed in the upper intestine, reach the liver 
through the blood, and then are re-excreted into the intestine with the 
bile, a process often designated as “ the biliary circulation.” Furthermore 
biliary secretion, according to Asher (79) and his pupils, is stimulated by 
the direct action of albumoses and peptones on the liver cells, but the 
secretin of the small intestine has very little, if any, such powers (see under 
pancreas (80)). 
The quantity depends moreover on the amount of blood which flows 
through the liver. Consequently, ligation, especially of the hepatic 
artery, leads to a change in secretion. It follows that the tonus of the 
blood vessels of the liver will have a modifying effect. But inasmuch as 
the hepatic artery and the portal vein have a contrary innervation, i.e., 
arterial vaso-constrictors travel with the vagus, and dilatators with the 
splanchnics, while in the portal vein the reverse is the case, it must be 126 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
assumed that the vessel tonus is more or less balanced (67). Rost, however, 
observed in animals that psychical stimuli influence bile formation, but 
the effect is not as marked as in the stomach. This is no doubt due to 
the absence of true secretory nerves in the liver. 
Bile from the liver cells is not discharged uninterruptedly into the 
intestine under normal conditions. As may be observed at any time in 
dogs with duodenal fistula, all the digestive glands rest during starvation, 
and only a few drops of a grayish brown, alkaline intestinal juice are 
discharged. But this quiescence is interrupted about every hour, when 
the so-called “emptying action” of all glands occurs and they secrete for 
about 10 minutes, during which time the gall bladder also discharges 
several cubic centimeters of bile, in two or three single jets (81). Apart 
from this, food as it passes through the duodenum causes contraction of the 
gall bladder, and opening of the sphincter of the papilla of Vater (82). 
Since Pawlow’s investigations, it is known that albumoses especially, 
i.e., protein derivatives, lead to this flow of bile. Hydrochloric acid may 
also be effective, but pure fat does not stimulate the flow, nor does pure 
sodium oleate (Rost). When fat has been split, however, either by the 
action of other digestive secretions, or by long standing (rancid), an 
abundant flow results; although it is not known what particular sub- 
stances formed in this chemical process are the stimulants (83). For 
practical work in nutrition, it is important to know that fat given by the 
mouth is split up sufficiently to stimulate a profuse flow. 
We are dealing with an extraordinarily delicate reflex mechanism 
when we experiment with the nerves which regulate the movements of 
the gall bladder, bile ducts and the musculature of the papilla of Vater. 
Doyon (84) supported by his experiments, stated that the splanchnics 
are the motor nerves of the bile passages, and, furthermore, that stimula- 
tion of the central stump of the vagus is followed by dilatation of the 
sphincter of the papilla of Vater and synchronous contraction of the gall 
bladder. Bainbridge and Dale (85), also Courtade and Guyon (86) in 
a later work, came to somewhat different conclusions for they found that 
stimulation of the splanchnics caused relaxation of the gall bladder, 
while stimulation of the vagus caused its contraction, with simultaneous 
opening of the papilla of Vater. It is not as yet known what part is played 
by the nerve plexuses in the gall bladder, and by the ganglia distributed 
throughout the bile channels. Their anatomical structure can be found 
described by Dogiel (87), who also made pressure calculations on the gall 
bladder. Reach (88) devised a method of studying the living bile passages 
and noted the influence of poisons on their motor conditions. 
The functional importance of bile in digestion has been frequently 
underestimated (89). In the first place, it is certain that the bile helps LIVER AND GALL BLADDER 
127 
in fat absorption, and in its absence, only from one-seventh to one-half 
of the normal quantity is taken up (90), and yet the well known observa- 
tion of Claude Bernard (91) showed that bile without pancreatic juice 
does not permit fat absorption. He found in rabbits, in which the 
entrance of the choledochus is higher than that of the pancreatic duct, 
that no fat is demonstrable in the chylus ducts between those two open- 
ings, but below the pancreatic duct the papillary lymph vessels are milky 
white and opaque. Dastres (92) experiment, on the other hand, proves 
that pancreatic juice alone does not emulsify fats, for after ligation of the 
common duct he produced a cholecysto-jejunal fistula and found the chyle 
ducts filled with fat only below the entrance of this fistula. It seems that 
the filling of chyle ducts with fat is brought about by a specific stimulation 
which bile and pancreatic secretion exert on the papilla of the intestines 
(93). That the fat splitting property of the pancreatic juice is intensified 
by the presence of bile acid salts in the bile, and that artificially prepared 
bile acid salts have the same property, is shown in the investigations of 
Rachford and Magnus (94). 
Exclusion of bile from the intestine leads to decomposition of the 
feces from this failure in fat absorption. For this reason, it was supposed 
that the bile was an antiseptic, but since the discovery that even in com- 
plete absence of bile, fecal decomposition does not take place on protein 
and carbohydrate diets, this idea was abandoned. This finding, however, 
has not been uniform among various workers (66). Bile is also active in 
protein digestion in checking the activity of pepsin. As Hammarsten (95) 
first demonstrated, and it can be easily verified in dogs with duodenal 
fistulse, bile forms a precipitate taking pepsin with it in the presence of an 
acid gastric content rich in proteins. On the other hand, it increases the 
protein digestive power of the pancreatic juice (96), so that it is not 
surprising that Rosenberg (77) found no change in the utilization of the 
nutritive substances when maximal quantities of proteins were given 
before and after establishing a complete gall bladder fistula. The amylo- 
lytic power of pancreatic juice is also supposedly increased, but the bile 
is said to contain a starch splitting enzyme (97). 
The salts of bile acids are used as cathartics because of their mild 
though effective action and in mentioning this influence of bile in 
stimulating peristalsis, we have completed, in rough outline, the 
picture of the physiological activities of this secretion (98). This 
review has shown that bile is a very essential factor in the digestive 
processes, and if Mayo Robson’s patient with her total gall bladder 
fistula remained in good health for 15 months, it only “proves that the 
animal organism in some manner always finds ways and means to replace 
lost functions” (99). 128 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Of all effects resulting from disturbances in the flow of bile, the most 
important and striking is icterus (ioo). Jaundice develops when bile can- 
not flow into the intestine because the ducts are obstructed. There is 
first a stasis in the bile channels, which results in rupture of the intracellu- 
lar bile capillaries, as demonstrated by Eppinger (ioi), and then, according 
to Fleischl’s'investigations (102) the bile passes either through the lymph 
channels of the liver into the thoracic duct and enters the blood by this 
route, or passes directly into the blood capillaries (103). In such cases 
of mechanical obstructions, as, for example, by calculus in the common 
duct, or from compression by a carcinoma, the stool is clay colored from 
the absence of bile pigments. Theoretically, the gall bladder should be 
distended, but in cases in which it is shrunken from previous inflammatory 
processes, at the time of occlusion, it cannot distend as it would in ordinary 
chronic calculus disease. On the other hand, with tumors in the pancre- 
atic region or at the papilla, the gall bladder is usually normal, and conse- 
quently, on occlusion of the bile duct, it distends considerably. This 
Courvoisier’s sign (104) is important in differential diagnosis. With such 
a complete occlusion of the common duct, no urobilin or urobilinogen is 
found in the bile, which is correlated with the “biliary circulation,” 
mentioned previously (38). 
[The question of how much of the duct system must be obstructed 
before clinical jaundice appears is interesting for several reasons. There is 
apparently no data available for the human subject, but McMaster and 
Rous have determined that the ducts from three-quarters of the liver 
substance in dogs and monkeys can be obstructed without pigment or 
cholate accumulation and that tissue icterus did not result when nineteen- 
twentieths of the liver substance was placed in stasis (105).] 
This mechanical form of icterus, easily understood physiologically, 
has always been distinguished from the so-called hemolytic or toxemic 
icterus, the distinction having been first made from the clinical observation 
that there are cases of icterus in which the feces remain bile stained. This 
condition, of course, does not follow simple stasis from obstruction of the 
larger bile channels. The common factor in the diseases leading to this 
form of jaundice is a destruction of erythrocytes which liberate hemoglo- 
bin. It was formerly thought that the liver was not concerned in this 
hemolytic icterus, especially because, in other places in the body, as for 
example, the subcutaneous connective tissues, extravasated blood is 
changed into hematoidin, which is chemically an isomer to the bilirubin 
of the bile (black and blue marks). But the error of this theory was shown 
by Minkowski and Naunyn (106) who poisoned geese and ducks with the 
strongly hemolytic arsine and did not obtain icterus if the liver had pre- 
viously been extirpated. Recently, McNee (107) repeated and amplified LIVER AND GALL BLADDER 
129 
these investigations, and on the strength of his histological findings, 
reached the conclusion that it is not the liver cells but the endothelium of 
the liver capillaries (Kupfer’s star cells) which is concerned to a large 
degree in the formation of icterus. Since similar endothelial cells are 
present in the spleen and bone marrow, and the iron free moiety of hemo- 
globin can be split off there, he considers it quite possible theoretically, 
that the endothelium of these organs also plays an essential part in this 
type of icterus. Observations along similar lines have been made by the 
determination of the bilirubin in the splenic blood in which it was found 
that this blood contained more than blood taken from the finger tip (108). 
But these investigations are all only beginnings and great care should 
be exercised in their interpretation (see Fischler’s (i) critique of the 
experiments). 
As a consequence of the increased blood destruction, the bile becomes 
much thickened and especially rich in pigments, so that the ducts cannot 
be emptied by the usual secretory pressure of the liver (ioo). The bile is 
thus dammed back, forced into the lymphatic system, and icterus results. 
This theory which thus classes hematogenous icterus with stasis, was 
supported by the demonstration that, as in stasis icterus, the bile channels 
rupture and thus directly cause icterus because bile capillaries are plugged 
with so-called bile thrombi (108). On the other hand, since this process 
is not clearly understood but is a consequence of blood changes, the differ- 
entiation of hematogenous and obstructive jaundice is perfectly valid, 
although the mechanism of the former is not as was formerly supposed, 
but approximates that of obstructive icterus. Finally, Kretz (109) points 
out that by the destruction of liver cells, communications are opened 
between bile capillaries and the smallest lymph vessels and this would 
probably lead to icterus. Whether alterations in the liver cells are respon- 
sible for certain still obscure forms (catarrhal, familial, neonatorum) by 
diverting the bile from its normal course, has not yet been established, 
although the indications seem to point in that direction (compare later in 
regard to hydrops of the biliary system). 
The blood changes which lead to hematogenous icterus are of a most 
varied nature, but as far as is known, they all have the one thing in 
common, viz., the escape of hemoglobin from the erythrocytes. This may 
be brought about by specific blood poisons such as arsine or toluen- 
diamin; by those which form methemoglobin, potassium chloride and 
pyrogallol; and by a large group of blood diseases classified under the 
name of pernicious anemia. These latter diseases are closely related to 
splenic pathology and will be discussed in that chapter (no). 
The cases of icterus associated with hematomata are especially interesting 
to the surgeon. Their mutual relationship is not clear, since the combina- 130 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
tion is more or less rare, and consequently has not been systematically 
studied. 
Toxic jaundice may also be referable to mechanical occlusion of the 
biliary capillaries by thrombi, and possibly to swelling of the liver cells. 
The results of icterus are first noticeable in the liver itself (lit. by 
Quincke (52), p. 57). In obstructive jaundice, i.e., stone in the common 
duct, there is distention of all the bile passages; in fact, cases have been 
observed in which approximately one liter of bile had accumulated in 
them. The liver cells continue to secrete for some time, but they are soon 
injured both by the mechanical pressure and by the chemical action of 
the bile. Glycogen accumulation, as well as the excretion of bile acids 
decreases, and later, the simplest morphological observation will show 
that a severe cell injury has occurred. In place of the destroyed 
parenchyma, connective tissue grows in, the bile ducts proliferate, and as 
Nasse showed in animals, the liver becomes shrunken and atrophic. 
These morphological changes have been frequently studied in animals 
and although the different species showed but slight variations in the final 
pathological findings, it was found that some animals tolerated the ligation 
of bile ducts better than others (hi). Icterus appears in three days 
after duct ligation, but if the thoracic duct also is tied off, the appearance 
of tissue icterus is delayed for weeks (112). Jaundice develops promptly, 
of course, if the bile is conducted directly from the gall bladder into the 
blood through a fistula into the vena cava, as was performed by Burger 
and Fischer (113). The changes in the liver are further complicated by 
adventitious infection, which is favored by the stagnation of bile. The 
importance of infection in the appearance of the histological changes 
described is doubtless great, because Frey and Harley (112) after ligating 
the common duct under aseptic conditions, did not find the foci of round 
cell, nor the cell necrosis, described by Cohnheim and Beloussow, but 
they did develop when peritonitis was superimposed (111). 
When bile enters the general circulation, the injury is not confined to 
the liver alone, but the entire organism feels its effects. The toxic process 
may be very complex and it seems to be due in large measure to cholic 
acid which irritates the central end of the vagus with resulting slowing of 
heart action, and later, paralysis of some of the medullary nuclei (114). 
But to what extent the cerebral phenomena—depression, delirium 
convulsions, etc.—depend on the same substance is not known. Hepatic 
insufficiency may be an underlying factor, or it may be the bile 
substances, especially pigments, to which suspicion has lately been turned 
(«s)» 
Morawitz and Bierich (116) investigated the delay in the coagu- 
lation time of the blood in jaundice, and found that the bile acid salts are LIVER AND GALL BLADDER 
131 
not at fault, because even in the most severe cases, the blood does not 
contain sufficient cholates to account for the delay. Furthermore, it is 
not proportional to the depth of the jaundice. Clinically, it is remarkable 
that not every jaundice leads to this decreased coagulability, and hence to 
those most disagreeable postoperative secondary hemorrhages. The 
impression is gained that catarrhal icterus is more prone to hemorrhage 
than the icterus following calculus in the common duct. 
A diminished fibrin content could not be demonstrated. Experiments 
were so devised that a properly chosen dose of hirudin was added to various 
samples of blood, to produce a great delay in the coagulation time of the 
sample from an icteric patient who bled freely, but not sufficient to cause 
change either in normal blood, or in blood from icteric patients who did 
not bleed freely. The deduction was made that the decreased coagulation 
of the blood is due to a delayed formation of the fibrin enzyme, probably 
on account of a deficiency of thrombokinase, but the reason is not clear. 
Kunika’s (117) opinion, that icterus is accompanied by absorption of 
substances liberated in the destruction of liver cells, is but an unproved 
hypothesis. 
The combination of anuria and jaundice is a peculiar one, their phy- 
siological relationship has not been determined (118). In eight out of 
thirteen dogs, there occurred a delayed elimination of indigo carmine and 
phlorizin sugar after ligation of the common duct, and renal injuries, 
similar perhaps to those in patients with anuria, were present. 
Gall stones are the most frequent cause of mechanical obstruction to the 
flow of bile. Modern knowledge of cholelithiasis begins with the work of 
V. Helmsbach (119) who drew an analogy between the calculi found in 
man, and pearl and shell formation in molluscs, by stating that an organic 
scaffolding was formed by some substance, perhaps from an inflammatory 
process, to which inorganic salts adhered, causing practically a petrifac- 
tion of the organic base structure. The actual form of the stone would be 
decided by its position and the pressures to which it was subjected. 
Naunyn (68) has elaborated this conception, and believes that gall stones 
form from the precipitation of substances which are normally contained 
in the bile, especially cholesterin, bilirubin and lime, and that the pre- 
cipitation of these bodies is primarily due to gall bladder infection, i.e., a 
calculus forming catarrh. 
The formation of calculi in the gall bladder, and in other parts of the 
body as well, presents a very interesting problem in colloid chemistry 
(Schade (120)). 
Calculi may develop in layers or strata. This presupposes colloidal 
precipitates such as fibrin, and other proteins which enter the bile in 
inflammatory processes. With these colloids, crystalloids are precipi- 132 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
tated. The architecture of the calculus is therefore stratified at 
first; later, through secondary rearrangement, especially due to crystalloids 
a radiating appearance develops. This type is usually represented in the 
common bilirubin lime calculi of the gall bladder, but urinary, salivary, 
pancreatic, and intestinal calculi are formed in a similar manner. All 
originate from an inflammatory process. 
Recently the pure cholesterin calculi have been contrasted with the 
inflammatory calculi, especially by Aschoff-Bacmeister (121), Schade and 
others, for Aschoff (122), approaching the subject histologically, found no 
inflammatory changes, either past or present, in a gall bladder which 
contained cholesterin calculi; but with calculi of the other type, such 
changes were always present. He concluded, therefore, that calculi could 
be formed simply by “slow precipitation” of cholesterin without bacterial 
cooperation, i.e., inflammation. Furthermore, on the basis of animal 
experiments, and observations with fresh gall bladders, he could not 
subscribe to Naunyn’s opinion that cholesterin is a product of the gall 
bladder epithelium, merely because these cells contain a larger amount than 
the liver cells (122). He believed that this may be due to absorption. Ac- 
cording to the same writer, stasis alone from mechanical factors such as 
lacing, pregnancy, etc. is sufficient to encourage the formation of choles- 
terin calculi. According to Hofbauer (123) the movements of the dia- 
phragm influence the emptying of the bile, and he thinks that the upright 
position of man, with its diminished diaphragmatic movement, is favor- 
able to gall stones. For this reason gall stones would be exceedingly rare 
in quadrupeds. 
Bacmeister actually obtained this cholesterin precipitation in the test 
tube, if bile was kept for about a month under sterile conditions. But 
there must first be some change in the bile before this takes place, and the 
process was markedly hastened if gall bladder epithelium was added. By 
combination of the positively charged protein ions with the negatively 
charged cholesterin particles, the precipitation occurs (124). The details 
of the colloid chemical conditions in this process are still matters of con- 
troversy. Schade (120) assumes that separation takes place when the 
solvent action of bile in cholesterin is altered, as is the case if the cholate 
disappears in stasis, and Exner and Heyrowsky (125) have demonstrated 
that this actually occurs in the autolysis of stagnant bile. They also 
found less cholate than normal in the bile from the fistula of a gall stone 
patient. 
On the other hand, in certain diseases such as arteriosclerosis (126), 
diabetes, during pregnancy (127), and in excessive protein intake, there is 
an increase of cholesterin in the blood and bile. But from a theoretical 
colloid chemical viewpoint, it is improbable that, unless it be very great, LIVER AND GALL BLADDER 
133 
this increase would lead to marked cholesterin precipitation. It is 
interesting that such single calculi are frequently found after pregnancy. 
Chalatoff (128) succeeded in obtaining precipitation experimentally in the 
gall bladder bile of rabbits by cholesterin feeding, and Verse (129) ob- 
tained a marked lipemia with cholesterin deposits in the cornea of rabbits 
after feeding them with cholesterin and oil. 
These demonstrations doubtless support the theoretical possibility 
that this type of calculus might form by autolysis in sterile stagnant bile, 
but the question still remains whether the results obtained in vitro 
apply to the conditions as they occur in man. 
According to Kretz (130) the older conception, that these calculi 
are the product of metamorphosis, still holds good, and on the basis of 
personal investigations, this theory is supported by Boysen (131); while 
Aschoff and Bacmeister defend the teaching of their aseptic origin (132), 
(130)* 
Kuru (133) believes he could always find fibrin in cholesterin calculi 
by means of Weigert’s stain, and Kretz regarded this discovery as very 
good evidence for their inflammatory origin. At the instigation of Aschoff, 
Aoyama (134) reinvestigated Kuru’s problem, and also found small 
amounts of protein scaffolding in the so-called crystallization centers of 
some true cholesterin calculi, while in others it was absent. In all pig- 
ment lime calculi, the protein scaffolding was very dense and easily 
demonstrable. Aschoff (132), however, pointed out that the value of 
Weigert’s stain in this problem is, to say the least, dubious. In agreement 
with other investigators, he accepts the theory of inflammatory origin for 
cholesterin pigment calculi. But he believes the pure cholesterin calculi 
may be formed under aseptic conditions and that the irritation from these 
stones may readily lead to a secondary inflammation of the gall bladder. 
There is no doubt of the practical value of this differentiation, irre- 
spective of the position assumed towards their origin. Clinically, it is 
not at all unusual to find gall stone colic with a cholesterin calculus 
occluding the cystic duct, unaccompanied by inflammation of the gall 
bladder or infection of its contents. Usually this is seen in the condition 
known as hydrops (see later) in which severe inflammation is seldom 
found, in spite of an enormously swollen gall bladder of dangerous appear- 
ance, so that we may safely await developments, and operate only if the 
attack is repeated. It cannot be reiterated too often that an operation 
is not undertaken on account of gall stones, but because of inflammation 
in the bile passages. Furthermore, the emphasis laid by Aschoff on the 
role which the cholesterin diathesis plays in gall stone formation, clears 
up many questions in gall stone pathology, as, for example, why they are 
much more frequent in women than in men. 134 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
According to the consensus of opinion, they form only in the gall 
bladder or in the large bile ducts, but after removal of the gall bladder, 
calculous deposits may occasionally arise in the common duct. Recently, 
Aufrecht (135) reported, on the basis of certain findings in the stools and 
in the bile ducts, that the first impulse to gall stone formation is actually 
given in the liver cells themselves. A practical, and much investigated 
question is whether gall stones can be dissolved within the gall bladder, 
v. Hansemann (136) introduced human gall stones into the gall bladder 
of dogs and was able to demonstrate dissolving effects similar to those 
observed on sectioning human gall stones. But Aoyama (Aschoff (132)) 
proved that the gall stones of man, although insoluble in human bile, 
dissolve in dog bile, which, according to McNee, is related to the fact 
that the bile of dogs, rabbits and cattle contains in comparison, very 
small quantities of cholesterin. The diet has a pronounced influence on 
the absorption of gall stones (137), in glycocol feeding, the calculus 
diminishes very slowly, but after cystin ingestion it disappears quickly. 
As already emphasized, the danger in gall stone disease consists not 
so much in the calculi themselves, as in the inflammation they induce in 
the ducts. In spite of the sphincter of Oddi, it is easy for intestinal bacteria 
to enter the bile ducts; that the muscle does not always close the opening 
completely, is illustrated by the fact that ascarides frequently find their 
way up to the liver. Bacteria which have once entered the bile passages 
are apt to remain alive and virulent for a long time, for bile is a good 
culture medium for all sorts of organisms. Indeed, Conradi (138) not 
only recommended its use for laboratory purposes, but even assumed that 
the bile more or less neutralizes the bactericidal action of serum, and 
permits unrestricted growth of the bacteria. Of course, it is not a suitable 
pabulum for all types of bacteria (139); pneumococci thrive poorly, but all 
sorts of intestinal bacteria grow very well, especially colon (140) and 
typhoid bacilli (141). In fact the organisms have been isolated and 
cultured from the gall bladder many years (decades) after recovery from 
typhoid fever (142). But organisms suspended in the bile, do not stir 
up an inflammation of the gall bladder, except when bile (143) or 
circulatory disturbances are superimposed (144). The degree of inflam- 
mation varies, but among many cases, especially of typhoid cholecystitis, 
are numbers which clinically give the impression of a very acute 
disease, but no marked alteration is found in the gall bladder wall, 
although the organ is fuller than normal, probably on account of swelling 
of the mucosa of the cystic duct. 
[For a discussion of the literature and valuable contributions on the 
mode of infection of the gall bladder, see Myeks, H. F., et al., Journ. 
Infect. Diseases, 1921, 28, p. 456.] LIVER AND GALL BLADDER 
135 
In addition to infection by way of the bile channels, anhematogenous 
infection of the liver may occur chiefly by way of the portal vein. For this 
reason liver abscesses are particularly common in tropical dysentery (145), 
and in suppurative appendicitis. 
[In the experience at the Lankenau Hospital, they are particularly 
prone to follow an appendicitis which involves the mesoappendix, espe- 
cially when the latter is gangrenous.] 
In such cases when rigor indicates the embolic transport of pus, 
ligation of the right colic, the vein which comes from the appendix, has 
been suggested (146). The subject of hepatic abscesses from retrograde 
extension has been discussed by Reiniger (147). 
The surgical procedure undertaken in gall stone disease consists either 
in removal of the gall bladder, or in opening it and establishing drainage 
by means of a fistula. The latter is only a temporary affair, but if drainage 
of bile to the outside is allowed to continue for a considerable period of 
time, severe illness, especially digestive disturbances result. (See above, 
functional importance of the bile.) Thus with a complete bile fistula, 
there is the interference with fat absorption. Pawlow (148) observed 
at autopsies of a number of animals with complete biliary, or intestinal 
fistulse, a marked softening and pliability of the bones, which had lead to 
fractures, especially of the ribs. Looser (149) afterwards examined the 
bones histologically, and proved that the changes were actually osteopo- 
rosis. Schmorl (described by Seidel (150)) observed the same condition 
with gall bladder fistulas in man. The osteoporosis in Schmorl’s case 
was differentiated from simple senile bone atrophy by the predominance 
of the absorptive processes. Thus far, however, it is not known whether 
this condition is present constantly with gall bladder fistulae, whether it 
is due to the absence of some important substance, or to some entirely 
different cause. 
Since cholecystectomy is an operation which removes an organ at one 
stroke, it is necessary to inquire into the function of this organ in the body 
economy. Some physiologists think that it serves only to produce mucus 
(Schroder von der Kolk); others say it regulates the flow of bile (Luciani); 
still others maintain that the viscid gall bladder bile mixes with the fluid 
liver bile and slows the current (151). While these writers lay more stress 
on the mechanical factors of bile flow, others see in the gall bladder a 
chemical-physiological function because of the increased usefulness of 
the thickened bile (152). Indeed, according to Hammarsten (153) the 
content of solids in gall bladder bile is eight times greater than that of 
liver bile. It is thus clear from the beginning that bile from the gall 
bladder must contain substances for digestion in greater concentration 
than liver bile. The experimental removal of the organ has given only 136 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
very general results, the workers being content to show that its removal 
was tolerated, which of course coincides with the fact that in man, small, 
shriveled, non-functioning gall bladders are frequently found and no 
clinically demonstrable conditions traceable to its loss can be established 
(154). Although Rosenberg (155) and Rost (154) could not find any 
change in the total metabolism of fat and protein after experimental 
cholecystectomy, Rost, corroborated in the essentials by Klee and Kluppel 
(156), found that there is an alteration of bile flow, in that bile is constantly 
being discharged by drops into the intestine. But in some of the chole- 
cystectomized animals a partial “continence” appears after a few weeks; 
bile is not discharged constantly, but it flows periodically, just as before 
operation, and the bile stored in the bile ducts enters the duodenum in 
jets. The interval between two periods of bile flow is short, especially 
in the first few months, but these pauses gradually lengthen, and finally 
a rhythmicity may be established which is almost as perfect as in th'e 
normal dog with gall bladder intact. This all depends on the functional 
capacity of the sphincter muscle, first described by Oddi (82), which 
closes the papilla. If it is strong and functions well, the bile is dammed 
back and collects in the large ducts, they then enlarge and form a sub- 
stitute reservoir. But when the sphincter is poorly developed, there is 
no dilatation of ducts but a more or less constant flow of bile, i.e.f there 
is a much poorer functional result. Rost could show on autopsy material 
that these same conditions result in man; he also observed that with 
a poorly functioning sphincter, the danger of an ascending infection 
increases, and no dilatation of the ducts takes place. We do not know 
why some of the previously normal animals become continent, while others 
do not. It should also be mentioned that not only do the bile ducts distend, 
but the gall bladder stump has a tendency to dilate into a new reservoir, 
especially when a portion of the cystic duct is left remaining (157). 
If continence is established in cholecystectomized animals, the flow 
of bile is as prompt as in normal animals, but of course the quantity 
expelled is considerably less, and what is probably more important, all 
the bile is discharged from the ducts at the first stimulus from the passage 
of the chyme in the duodenum, and none is left for the remainder of the 
food except as it is freshly secreted by the liver. Moreover, the bile in 
the ducts is only slightly concentrated and therefore must be poorer in 
active solids. Furthermore, Rost has shown that cholecystectomy influ- 
ences pancreatic secretion, and only about one-third of the normal amount 
of bile plus pancreatic secretion is discharged, to mix with a certain amount 
of food. This may possibly be due to exhaustion of the secretin, although 
why and in what manner secretion is influenced by the removal of the 
gall bladder, is unknown. This inadequacy of pancreatic and bile LIVER AND GALL BLADDER 
137 
secretion in its turn leads to a stasis of food in the duodenum, which 
reflexly diminishes the hydrochloric acid production in the stomach (158). 
This is probably the best explanation for the resulting hydrochloric acid 
deficiency which now causes numerous general disturbances such as 
vomiting, eructations, gastric pressure sensations, constipation, etc. (152). 
These symptoms are frequently attributed to adhesions, although in 
later laparotomies none can be found; but similar symptoms have been 
observed, when an aseptic calculus occluded the gall bladder (159). 
[The rate at which the gall bladder can concentrate bile has been 
determined in the ingenious experiments of Rous and McMaster. They 
found that a gall bladder emptied at the beginning of an experiment and 
left to fill from the liver concentrated 49.8 c.c. to 4.6 c.c. in about 22 hours. 
The gall bladder has, of course, often been considered a mere diverticulum 
in the duct system but it is apparent that its functions are more than that. 
It, of course, contains smooth muscle within its walls and it is assumed 
that it squirts its contents into the duodenum when the sphincter of Oddi 
relaxes. The contrary innervation, as Meltzer termed it, is said to be 
such that the relaxation of sphincter and contraction of gall bladder take 
place synchronously. But the experiments of Doyon and others following, 
have not demonstrated the existence of this mechanism. Indeed, attempts 
to record contractions of the intact gall bladder are beset with many 
difficulties and none have succeeded. The movements of respiration give 
records on tracings which obliterate any which the gall bladder may have 
made. By removing the organ and suspending it between levers in a 
bath of oxygenated Locke’s solution as done with intestinal segments, etc. 
a slow contraction and relaxation indicative of ordinary smooth muscle 
tonus is obtained, but no active contractions. When the papilla of Vater 
is observed through a duodenostomy with the incision in the abdominal 
wall closed as far as possible to restore intraabdominal pressure, it will be 
found that the bile runs out in a tiny stream as the sphincter relaxes 
and any spurts are absolutely synchronous with inspiration, i.e., when the 
diaphragm descends it presses the liver downward and squeezes out bile. 
In general it may be concluded that an expulsive power has never been 
demonstrated in the gall bladder any greater than the secretory pressure of 
the liver (250 mm. water). When the sphincter is closed, bile accumulates, 
and the pressure slowly rises; when the sphincter opens, the bile runs out 
because of the pressure under which it was confined, plus the pressure 
against the liver and gall bladder from surrounding structures. Ether 
was necessarily used in these experiments which were performed on dogs 
(r6o).] 
The results of cholecystenterostomy, by which operation the bile is led 
into the stomach, small intestine or colon, have been studied experiment- 138 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
ally by Viedemann (161), who paid particular attention to digestion as 
studied through fistulae. He found that allowing the bile to flow into the 
stomach did not influence gastric acidity, at least not on a milk diet 
(see also p. 58). Gastric motility is unchanged immediately after the 
operation but later shows perceptible slowing. Intestinal digestion is 
not impaired by bile drainage into the stomach, but appears to be altered 
when the bile is drained into the small intestine. 
In animals, a cholecystcolostomy exposes the bile passages to great 
danger of infection, but in spontaneous ruptures of the gall bladder into 
the colon, a subsequent cholangitis is not the rule. 
Experimental investigations of hepato-cholangio-enterostomy, i.e., anas- 
tomoses between branches of the hepatic duct and the gastro intestinal 
canal, were made by Enderlen and Zumstein (162). In normal animals 
the anatomical structure is not especially favorable for this operation, 
since the larger ducts are deeply situated under the surface of the liver. 
But in chronic obstruction the branches are reached more easily. 
Intestinal contents have no injurious effect on living liver tissue, which 
offers an interesting additional fact to the problem of autodigestion of 
living tissue, discussed above. 
When obstruction of the bile ducts by calculi or tumors is complete and of 
long duration, the bile stored in the ducts is often not greenish yellow, but 
is white. This applies particularly to occlusion of the cystic duct, in which 
case the gall bladder becomes distended with this clear white fluid (hydrops). 
But the rare cases of hydrops of the whole duct system from chronic 
occlusion of the common duct are of greater interest, and more important 
for the understanding of hydrops formation. Kausch (163) among 
others has described such a case in detail. It can be deduced that the 
quantity of bile depends on the secretion of the liver, on the secretion of the 
bile channels, and on the absorption of bile in the system. The amount 
of secretion from the bile passages can be very large, as Kausch shows in 
his case. 
There are two opposing theories in reference to the etiology of white 
bile (164). The one asserts that in stasis, the liver cells partially or com- 
pletely lose the power to form pigments (165). This only applies to 
occlusion of the common duct. But with this theory it seems inexplicable, 
as Kausch points out, that the patients are jaundiced and constantly 
excrete large quantities of bile pigments in the urine. The other theory 
states that the increase of pressure in the bile passages forces the bile 
secreted by the liver into the blood and lymph vessels (163), (166), and 
at the same time the mucosa of the bile passages hypersecretes (167). 
Hydrops of the gall bladder when calculi occlude the cystic duct, can be 
explained similarly. LIVER AND GALL BLADDER 
139 
[It seems that the gall bladder and ducts exert opposing influences on 
the bile; the gall bladder concentrates it, while the ducts dilute it with a 
thin colorless fluid which they can secrete against considerable pressure. 
In obstructed ducts either unconnected with the gall bladder or connected 
to one that is functionless, this fluid gradually replaces the bile and 
becomes the “white bile” of surgeons (168).] 
The subject of pain in attacks of cholelithiasis especially that radiating 
to the shoulder, will be discussed when dealing with the sensitivity of the 
abdominal cavity. 
In 1911, Clairmont and Haberer described a “bile peritonitis” (169), 
although the pathological anatomist could discover no perforation in 
the bile passages. These authors emphasized, in a later work (170), that 
there must have been a pathological condition of the walls of the gall bladder 
and bile channels to permit this abnormal permeability, but its nature 
was not explained. There was no microscopical investigation of this 
case, but the authors found a similar bile exudate in the abdomen in four 
dogs whose common bile ducts had been ligated for other reasons. Since 
attention was called to this condition, reports of similar cases 
were .rapidly forthcoming, and two years later, Sick and Frankel 
(171) were able to collect 18 cases in the literature and the number has 
since increased. The common feature in all is the biliary peritonitis, but 
opinions differ as to the etiology. Clairmont and Haberer in their second 
publication, group the pathological anatomical findings into those in 
which either an opening was found macroscopically in the bile passages 
or in wfiich leakage was proved microscopically, sometimes, however, 
only in the form of a subserous bile passage on the liver surface. But 
there still remained cases in which neither perforation nor inflammation 
could be found, and in which it was apparently a question of diffuse 
permeability (for instance, the case of Schievelbein-Ritter (172)). Since 
the perforations found were often exceedingly minute, and only visible 
microscopically, the majority of authors are inclined to assume that a 
perforation is a constant feature and may have been overlooked in the 
cases in which it was not found (173). A new light is shed on the question 
by Blad’s (174) investigations. He showed first in vitro, that the pig- 
ments in the colloidal bile cannot pass through a membrane. But when 
tryptic enzyme (Pancreon) is added and the colloids are destroyed, the 
pigment is “liberated” in some obscure way, and passes through the mem- 
brane. Furthermore, when a freshly removed gall bladder was used as a 
diffusion sac, the colloid would not pass through, while the crystalloids 
did very easily. He then elaborated these results in vivo by ligating the 
choledochus and injecting a tryptic enzyme into the gall bladder of dogs 
by way of the liver (duodenal juice plus bacteria). In another experi- 140 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
mental series, he injected the same ferment into the gall bladder through 
the papilla of Vater. An actual biliary peritonitis without perforation 
of the bile passages resulted. The gall bladder wall showed no inflamma- 
tion but was completely necrotic. Further observations must show 
whether this explanation holds good for all human cases. That reported 
by Risel (175) in which there was a sterile circumscribed gangrene of the 
gall bladder might be utilized in this connection, although the author 
himself believes it might have been a thrombotic process in the cystic 
artery. At any rate, necrosis of the gall bladder wall alone does not lead 
to an escape of bile, as is shown by a case of volvulus of the gall bladder, 
in which, in spite of total necrosis of the mucosa, submucosa and muscularis, 
no bile was found in the abdominal cavity (176). Many cases of suppura- 
tive cholecystitis illustrate the same point. 
The oldest discussion of the reaction of the peritoneum to bile is 
probably that of Bohn who attempted to discover why gall bladder injuries 
are usually fatal (177). He concluded from investigations on dogs, the 
gall bladders of which he removed with and without ligation of the cystic 
duct, that gall bladder injuries prove fatal, because bile escapes into the 
abdominal cavity (for other early experiments, see Rost, 81). Recent 
investigations are discussed by Erhard and Notzel (178). Furthermore, 
all cases of gall bladder perforations in man, and there are many in the 
literature, can be used in this study. Ehrhard and Notzel found that 
normal sterile bile does not call forth an inflammatory reaction in the 
peritoneum but the moment infectious organisms enter with the bile, a 
severe peritonitis begins. In fact Notzel showed that animals intraperi- 
toneally inoculated with bacteria of a certain virulence, remained living, 
but those treated similarly, but with addition of bile, all succumbed. 
These experimental findings correspond with clinical observations, and 
Hirschel (179) for example, reported eight cases of peritonitis originating 
from the gall bladder, all of them ending fatally. On the other hand, the 
prognosis is by no means so unfavorable in traumatic perforation of the 
gall bladder or in a ruptured hydrops. Such traumatic lesions, especially 
experimental ones, heal very promptly, a fact which was already observed 
by older authors. Enderlen and Justi (180) have studied the histology 
of healing in gall bladder wounds. 
In injuries to the liver, the escape of bile is of much less importance 
than hemorrhage. For this reason, the slowing of the pulse, reported by 
Finsterer (181) on the basis of clinical and experimental observations is not 
always found (see investigations by Rubaschow (182)). LIVER AND GALL BLADDER 
141 
LITERATURE TO LIVER AND GALL BLADDER 
1. Compilation and Lit. see Fischler: Physiologie u. Pathologie der Leber, Springers 
Verlag., 1916. 
2. Hess: v. Volkmanns Sammlung klin. Vortrage, N. F., 1900, No. 576. 
3. Kehr: Handbuch d. prakt. Chirurgie, 3, p. 611, 4 Edit. 
4. Gluck: Arch. f. Klin. Chir., 1883, 29, p. 129. 
5. Ponfick: Virchows Archiv., 1889, V. 118 and 119. 
6. Thoele: Neue deutsche Chirurgie, 1912, V. 4, p. 70. 
7. Claude Bernard: Compt. rend, de T Acad des Sciences, 1848, V. 27, p. 514 and 
L’oeuvre de Claude Bernard (Paris Bailliere et Fils). 
8. see Pfluger: Das Glykogen und seine Beziehungen zur Zuckerkrankheit, 1905 2 
Edit, and Abderhalden, Physiologische Chemie, 2, p. 409, espec. p. 430. 
9. Isaac, S.: “Die Funktionsprufung der Leber,” Berliner klin. Wochenschrift, 1913, 
p. 1167. 
9. Sachs: Ztschrft. f. klin. Med., V. 38, p. 87. 
9. Hohlweg: Deutsches Arch. f. klin. Med., 97. 
10. see Wohlgemuth in Oppenheimers Handbuch d. Biochemie, 3, p. 178. 
11. E. Alderhalden und London: “Weitere Versuche zur Frage nach der Verwertung 
von tief abgebautem Eiweiss im tierischen Organismus, ausgefuhrt an einem 
Hunde mit einer Eckschen Fistel,” Zeitschr. f. physiol. Chemie, 1907, 54, p. 112. 
12. see van Slyke, D. D.: “Chemistry of the proteins and their relation to disease,” 
Oxford Medicine, V. 1, p. 251. 
13. v. Schroder: Arch. f. exp. Path. u. Pharmak, 1882, 15, p. 364. 
14. see Abderhalden: Physiol. Chemie, 1909, p. 316 und Wohlgemuth in Oppenheimers 
Handbuch der Biochemie, 1907, 3, p. 183. 
15. Nencki und Pawlovv: Archiv. f. exp. Path. u. Pharmak., 1893, V. 32. 16. 
16. J. Frankel: Chemie der Lebensvorgange Dynamische Biochemie; Wiesbaden, 
1911, p. 383, J. F. Bergmann. 
16. K. Glassner und Singer: Med. Klinik., 1909, No. 51. 
16. M. Landau und Me Nee, J. W.: “Zur Physiologie des cholesterin Stoffwechsels,” 
Ziegler’s Beitr. zur prakt. Anat., 1914, V. 58, 667-699. 
16. Aschoff-Bacmeister: Die Cholelithiasis, Jena, 1909. 
17. Schiff: Arch, des sciences physique et naturelle, 1877, 58, p. 293. 
18. Lebedeff: Arch, fur (Anat. u.) Physiol., 1883, V. 31, p. 11. 
19. Fischler, F.: “Ueber das Wesen der zentralen Lappchennekrose in der Leber und 
uber die Rolle des Chloroforms bei dem sogenannten Narkosenspattod,” Mitt, 
a.d. Grenzgebieten, 1913, 26, p. 553 (further lit.). 
20. G. H. Whipple and Sperry, J. A.: “Chloroform poisoning; liver necrosis and 
repair,” John Hopkins Hosp. Bull., 1909, 20, p. 278-289. 
21. Adamski, Johann: “Lebernekrosen bei Pancreas fettgewebsnekrose,” Dissert. 
Munchen, 1912, C. Wolf and Sohn. 
22. Guleke: Arch. f. kl. Chir., V. 83, p. 602. 
23. Lusk Graham: “The Elements of the Science of Nutrition,” 1917, Ed. 3. 
23. Davis, N. C., Hall, C. C., Whipple, G. H.: “The rapid construction of liver cell 
protein on strict carbohydrate diets, etc.” Archiv. Int. Med., 1919, 23, 689 and 
711; 1921, 27, 679; 1921, 28, 21. 
24. Doyon: Oppenheimers Handbuch d. Biochemie, 1908, 2, 2. 
25. Morawitz: Ergeb. d. Inn. Med., 1913, 10. 
25. Nolf, P.: “Eine neue Theorie der Bloodgerinnung,” Ergebnisse der inneren Med., 
1913, 10; Ergebnisse der. inneren Med., 1912, 9, 275-341. 142 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
25- Doyon: “Rapports du foie avec la coagulation du sang,” Journ. de Physiol. 
Pathol, gen., 1912, 14, p. 229. 
26 for Lit: s. Kehr, neue deutsche Chir., 8, p. 150. 
27 Rio Branco: Essai sur 1’ anatomie et la medicine operatoire du trone coeliaque et 
ses branches, etc., Paris, Steinheil. 
28. Ehrhardt: Arch. f. klin. Chir., 1902, V. 62, p. 460. Janson: Zieglers Beitrage, 
1895, V. 17, p. 505. Haberer: Arch. f. klin. Chir., V. 78, p. 557. Narath: 
Brun’s Beitrage, V. 65. Narath, II: Deutsche Zeitschft. f. Chir., 1916, V. 135. 
Cohenheim and Litten: Virchows Arch., 1876, 67, 153. 
29. Nicolletti: Centralbl. f. d. Grenzgebiet, 1910, 13. 
30. Thole: Chirurgie d. Lebergeschwulst Neue deutsche Chirurgie, V. 7. 
31. Kehr: cit. see Kehr. Chirurgie d. Gallenwege, neue deutsche Chir., 8, p. 155; 
Munch, med. Wochenschrift., 1903. 
32. Bourdenko: cited by Kehr, 31. 
33. Narath II und S. Steckelmacher: “ Experimentelle Nekrose und Degeneration 
der Leber. Versuche mit vitaler Toluinblaufarbung,” Zieglers Beitrage, 1913, 
V- 57, 3I4-344- 
34. cf. Lissauer: Deutsche Zeitschrift. f. Chir., 1916, V. 35. 
35. Tappeiner: Arbeiten aus d. physiol. Anstalt. Leipzig, 1873, V. 7. 
35. Claude Bernard: Comptes rendus, 1850. 
36. De Josselin de Jong: “Ueber die Folgen der Thrombose im Gebiete des Pfort- 
adersystem,” Mitt. a.d. Grenzgebieten, 1912, V. 24 (Steenhuis, Dissert Gron- 
ingen, 1911). 
36. Erhard: Arch. f. klin. Chir., 1902, 68, p. 462. 
37. Solowieff: Virchows Arch., 1875, V. 62. 
38. Lit. Fischler: Lebercirrhose in Ergebn. d. inn. Med., 1909, V. 3 und Lissauer, 
Berlin, kl. Wochenschft., 1914 (collected ref.). 
39. Cohnheim und Litten: Cohnheim, ges. Abhandlungen. 
40. Zahn: Naturforscherversammlung, 1897, p. 9. 
41. Chiari: Zeitschft. f. Heilkunde, 1898, V. 19, p. 475. 
42. Josselin de Jong and Sax, R.: Zentralbl. f. Path., 13. 
42. Enderlen, Hotz, und Magnus-Alsleben: “Die Pathologie und Therapie des 
Pfortaderverschlusses. Experimentelle Untersuchungen uber die Ecksche 
Fistel,” Ztschft. f. d. ges. exp Medizin, 1914, V. 3. 
43. Verse: Zieglers Beitrage, V. 48. 
44. Langenbuch: Deutsche Chirurgie, 45, V. 2, p. 106. 
45. E. Magnus-Alsleben: Ueber die Ecksche Fistel, Verhandlung d. deutsch. Kong. f. 
innere Med., 1912, 29, 572-579; Lits. Fischler, Arch. f. exp. Path, and Pharmak 
61; Arch. f. klin. Med. 104 and in; Franke u. Rabe, Sitzungsberichte u. Abh. d. 
Naturforschenden Gesellsch. zu Rostock, 1912, Enderlen, Hotz u. Magnus 
Alsleben, Zeitschr. f. d. ges. Exp. Medizin, 1914, 3. 
46. Rosenstein: Arch. f. klin. Chir., 98. 
47. Heller: Arch. f. klin. Med., 1870, V. 7. 
47. Ribbert: Zentralbl f allg. Pathol., 1897. 
47. Arnold: Virchows Arch., V. 124, p. 385. 
48. Cases of Schuppel, Hainski, Lange, Thran, Umbreit, Eisenmenger: Lit. see Fischler 
( 1), p. 256. 
49. Cosentino: Cited by Thole, Leberverletzungen Neue deutsche Chir., 4, p. 101. 
Borgzecky: Brun’s Beitrage, V. 88, p. 466. Baron: Zentralbl. f. Chir., 1910. 
50. Ransohoff, J.: Ann. of. surg., 1908, 98, 247-257, 4 pi. LIVER AND GALL BLADDER 
143 
51. Hopfner, E.: Der Aszites u. seine chirurgische Behandlung, Ergebn. d. Chir., 1913, 
6, 410-480. 
52. Quincke: Therapeut. Monatshefte, July, 1914. 
53. see Klopfstock. Berliner kl. Wochenschrft., 1911, No. 3. 
54. Lubarsch: Naturforscherversammlung, 1912 Munster. 
55. Ito und Omi: Deutsche Zeitschrft f. Chirurgie, V. 62. 
56. Josselin de Jong: Mitt. a.d. Grenzgebieten, V. 24. 
57. Talma: Berliner klin. Wochenschr., 1900, 1898. Drumond: Brit. med. Journal, 
1896. 
58. Tillmann: Deutsche med. Wochenschr., 1899. 
59. Schiff: Neuere Schweizerische Ztschrft. f. Heilkunde, 1862, V. 1. Ore: Compt. 
rend, de l’Academie, 1856, V. 42. Golowieff: Virchows Arch., 1875, V. 62. 
60. Rosenstein, P.: “Ueber die Behandlung der Lebercirrhose durch Anlegung einer 
Eck’schen Fistel,” Arch. f. klin. Chir. Berlin, 1912, 98, 1082-1092. Chirurgen- 
kongress, 1912. 
6r. Bunge: “Die Talma—Drummondsche Operation; Ihre Judikation, Technik, und 
die bischer erzielten Resultate,” Wiener klin. Wochenschr., 1905, 18, 930. 
Klinisches Jahrbuch, 1905, 14. 
62. Ewald: Ueber Fruzeitige Punction von Aszites, Berlin, klin. Wochenschrift, 1888, 
16. 
63. Rouotte: Lyon med., 1907, 109, p. 40. 
64. Franke: Chirurgenkongress, i9rr. Handley, W. S.: “Abstract of the Hunterian 
lectures on the surgery of the lymphatic system,” Lancet, April, 1910. 
65. “Die functionelle Bedeutung der Gallenblase. Experimentelle und anatomische 
Untersuchuungen nach Cholecystectomie,” Rost, Mitt. a.d. Grenzgeb., 1913, 
v. 26, Lit. Babkin: Aeussere Sekretion der Verdauungsdrusen, Springers 
Verlag, 1914. 
66. Hammarsten, O.: “Zur Chemie der Galle,” Ergebnisse d. Physiologie, 1905, V. 4, 
p. 14. 
67. Wohlgemuth: Oppenheimers Handbuch d. Biochem, 1908, 3, 1 p. 202, Jena, 
1909, G. Fischer. 
68. Naunyn: Klinik. der Cholelithiasis, 1892. 
69. Aschoff: “We entstehen die reinen Cholesterinsteine?” Munchener med. Wochen- 
schr., 1913 (with compilation). 
70. Rabe: Festschrift, z. Feier des 25 jahr. Bestehung d. Eppendorfer Krankenhauses, 
1914. 
7r. Barbera: Arch. ital. de Biol., V. 26 and 31 und Bull, delle Sc. med. di Bologna 
Serie T. 7, 1896, 1898. 
72. Weintraud: In v. Noordens Handbuch d. Pathol, u. Stoffwechsels. Thorspecken: 
Mitt. a.d. Grenzgebieten, 1909, V. 19. Letienne und Hanot: Arch, generales 
de med., 1885, V. 1. 
73. Ostwald Adolph: Lehrbuch der chemischen Pathologie Veit and Co.,Leipzig, 1907. 
74. Majo Robson: Zentralbl. f. Physiol., 1890, V. 4, p. 634. 
75. Brand: Pflugers Arch., 1902, 90, p. 494. 
76. see Stadelmann, Der Ikterus, p. 81; Babera, Bull, della Sc. med. di Bologna, 1898. 
77. Rosenberg: Arch. f. Physiol., 1901, p. 528. 
78. Minkowski: Deutsche Klinik., V. 5, p. 681. Pfaff u. Balde: J. of exp. Med., 
V. 2, p. 49. Schiff: Pflugers arch., 1870, V. 3, p. 598. Tappeiner: Arbeiten 
a. d. physiol. Instit. Leipzig, V. 7. Stadelmann: Deutsche med. Wochenschrf t., 
1896, Zeitschft. f. Biol., 1897, 34, p. 1, Berliner Klin., Wochenschft., 1896, p. 
9-10. Doyon und Dufort: Arch, de Physiol., V. 9, p. 562. 144 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
79- Barbera: Zeitschft. f. Biol., 1897, V. 32. Bohm, P.: “Ueber die feineren Bau 
der Leberzellen bei verschiedenen Zustanden; zugleich ein Beitrag zur 
Physiologie der Leber, Zeitschft. f. Biol., 1908, V. 51, 409-434. Asher: 
Zeitschft. f. Biol., 1903, V. 45; Zentralbl. f. d. ges. Physiol, u. Pathol, d. Stoff- 
wechsels, 1911, No. 5. Pletnew: Bipch. Zeitschft., 1909, 21. Loeb, A.: 
“Ueber den Eiweissstoffwechsel des Hundes und uber die Abscheidung der 
Galle bei Futterung mit Eiweiss und Eiweissabbauproducten mit besonderer 
Berucksichtigung der zeitlichen Verhaltnisse,” Ztschrft. f. Biol., 1910, V. 55. 
Kusmine: Ztschft. f. Biol., V. 46. 
80. Rost, F.: “Die functionelle Bedeutung der Gallenblase. Experimentelle und, 
anatomische Untersuchungen nach Cholecystectomy,” Mitt. aus. d. Grenzgeb., 
1913, 26, p. 736. Henri und Portier: Compt. rend. Soc. de Biol., 1902, 54, p. 
620. 
81. Rost: Die functionelle Bedeutung d. Gallenblase. Mitt. a. d. Grenzgebieten, 
1913, 26, 5. Pawlow: Die Tatigkeit der Verdauungsdrusen, Wiesbaden, 1892. 
Cohnheim und Klee: Heidelberger Akad. d. Wissenschaften. Math, naturn. 
Klasse, 1912. 
82. Oddi: Arch. ital. de Biol., 1887, p. 317; also Helly, Arch. f. micr. Anat. V. 54, 
p. 614 und Hendriksen, Anat. Anz., 1900, V. 17, p. 197. 
83. P. Klee und O. Klupfel: “Experimenteller Beitrag zur Funktion der Gallenblase,” 
Mitt, aus d. Grenzgebieten, 1914, 27, p. 783. 
84. Doyon: Arch, de Phys., 1896, V. 5, p. 678 and V. 6, p. 19. 
85. Bainbridge and Dale: Journ. of Physiol., 1908, V. 33, p. 138. 
86. Courtade and Guyon: Compt. rend. Soc. de Biol., V. 60, p. 399. 
87. Dogiel: Arch. f. Anatomie, 1899, p. 130. Dogiel: Compt. rend. Soc. de Biol., 
1903, V. 55, p. 314. 
88. F. Reach: “Untersuchungen zur Physiologie und Pharmakologie der Gallenwege,” 
Zentralbl. f. Physiol., 19x2, V. 26. Wiener Klin. Wochenschrft., 19x4. 
Dastre: Arch. f. Physiol., 1889, V. 22, p. 800. 
89. Mayo Robson: Zentralbl. f. Phys., 1890, V. 4, p. 634. Copemann and Winston: 
Journ. of Physiol., 1889, V. 10, p. 213. 
90. Munk: Ueber die Resorption von Fetten und festen Fettsauren nach Ausschluss 
d. Galle v. Darmkanal. Virchows Arch., V. 122, p. 302. (Lit.) 
91. Claude Bernard: cited by Hammarsten, Physiol. Chemie, 1895, 3, Ed., p. 275. 
92. Dastre: Du role de la bile dans la digestion de matieres grasses, Compt. rend. 
Soc. de Biol., 1887, December. 
93. Lewin: Ueber den Einfluss d. Galle und des Pancreassaftes auf die Fettresorption 
im Dunndarm, Pflugers Arch., V. 63, p. 171. 
94. Magnus: Die Wirkung synthetischer Gallensaure auf die pancreatische Fett- 
spaltung, Zeitschr. f. phys. Chemie, V. 48, p. 376. 
95. Hammersten: Ueber den Einfluss der Galle auf die Magenverdauung, Pflugers 
Arch., 1870, V. 3, p. 53. 
96. Rashford and Southgate: Med. Rec., Dec., 1895. 
96. Delezenne: Compt. rend, de la Soc. de Biol., 1902, 54, p. 392. Bruns: Arch, de 
Science biol., 1899, 8, p. 97. 
97. Roger, H.: Gaz. d. hopitaux, 1910, p. 1516. Sidney, Martin, and Dawson, Wil- 
liam: Proc. of the Roy. Soc., 5, 1, 45, p. 292, V. 48, p. 358. 
98. Nepper: Ztschft. f. Biol., 1908, V. 51, p. 1. K. Glassner and G. Singer: “Gallen- 
sauren als Abfuhrmittel,” Wiener klin. Wochenschft., 1910, 23, 5. Schupbach: 
Presse med., 1913, V. 21, p. 137-139. LIVER AND GALL BLADDER 
145 
99- Abderhalden: Physiol. Chemie, Edit., 1904, 2, p. 690. 
100. Lit. see Stadelmann: Der Ikterus, Stuttgart, 1891, also Kretz in Handbuch d. 
allgem. Path. 22, 466; Quincke in Nothnagels Handbuch, 1899, 18. 
101. Eppinger: Zieglers Beitrage, V. 31, p. 230. 
102. Fleischl: Bericht uber d. Verh. d. kgl. sachs Ges. d. Wiss. zu Leipzig, 26 
103. Hurley: Arch. f. Anatomie u. Physiol., 1893, p. 291. 
104. Courvoisiers sign Kasuistisch—statistische Beitr. S. Pathol, u. Therapie d. Galle- 
wege, Leipzig, 1890. 
105. McMaster, P. D. and Rous, P.: “Biliary obstruction required to produce jaun- 
dice,” J. Exp. Med., 1921, 33, 731. 
106. Minkowski and Naunyn: Arch. f. exp. Pathol, u. Pharmakol, 1886, 21. 
107. McNee, I. W.: “Giebt es einen echten hematogenen Ikterus?” Mediz. Klinik, 
1913, p. 1125-1129. Lantz: Zentralbl. f. Chir., 1907, p. 617. 
108. Eppinger: Zieglers Beitrage, V. 33. von den Berg, A. A. H., Snapper, I.: “Unter- 
suchungen uber den Icterus,” Berlin, klin. Wochenschrift, 19x4, V. 24, p. 25 
and Vol. 51, 1109-1180. 
109. Kretz: Ergebn. d. allg. Pathol., No. 8. 
no. Stadelmann: Verhandt. d. med. Kongress, 1892, 11. Pick: Wiener klin. Woch- 
enschrft., 1874, 29, No. 26. Minkowski: Verhandt. d. med. Kongress, 1892, 
11. Liebermeister: Deutsche med. Wochenschrft., 1893, No. 16. 
in. Tischner: “Vergleichende Untersuchungen zur Pathologie der Leber,” Virchows 
Archiv., 1904, V. 175, 90-184. Tsunoda, I.: “Eine experimentelle Studie 
uber die Folgen der Stenose oder Obliteration des Ductus choledochus; zur 
Kenntniss der sog. biliaren cirrhose,” Virchows Archiv., 1908. Nasse: 
Arch. f. klin. Chir., V. 48, p. 886. Siegerbeek von Heukelom: Zieglers Beitrage 
z. pathol. Anatomie, 1896. Frerichs: Klinik. d. Leberkrankheiten. Beloussow: 
Arch. f. exper. Pathol, u. Pharmacol., 1881, V. 14. Bauer: Inaug. Diss. Ros- 
tock, 1882. 
112. Frey und Harley: Verh. d. 11. med. Kongr., 1892, p. 115 and Arch. f. (Anat. u ) 
Physiol., 1893, p. 291. 
113. Burger and Fischer: Ztschrft. f. d. ges. exper. Med., 1914, V. 3. 
114. Rywosch: Arbeiten d. Pharmakol. Instit. in Dorpat; Lit. in Stadelmann: Der 
Ikterus, p. 264. 
115. See Krehl: Pathol. Physiol., 1912, p. 372, F. C. W. Vogel. 
116. P. Morawitz and Bierich: “Ueber die Pathogenese des cholaemischen Blutungen,” 
Arch. f. exp. Path., 1907, V. 56, p. 115. 
117. Kunika: Deutsche Zeitschft. f. Chir., 118. 
118. Clairmont and Haberer: Mitt. a. d. Grenzgebieten, 1911, V. 22, p. 159. 
119. Meckel v. Helmsbach: Mikrogeologie herausgegeben von Billroth, 1856. 
120. H. Schade: “Ueber Konkrementbildungen beim Vorgang der tropfigen Ent- 
mischung von Emulsionskolloiden,” Munchener med. Wochenschrift, 1909, 
No. 1 and 2 and 1911, No. 14; Ztschft. f. exp. Pathol, u. Therapie, 1910, 8, u. 
Kolloid-chemische Beihefte, 1, p. 375. 
121. L. Aschoff-Bacmeister, A.: “Die Entstehung des Gallenstein-Leidens,” Die 
Cholelithiasis, Jena, 1909; Bacmeister: Ergebn. d. inn Med., 1913, 11, p. 1, 
1-31, 1 pi.; Lit. see Riese: Ergebn. d. Chir., 1913, 3. 
122. Aschoff, L.: “Zur Frage der Cholesterinbildung in der Gallenblase,” Munchener 
med. Wochenschft., 1906, 13, 1847; also Mitt. aus. d. Grenzgebieten, 1912, 24. 
123. L. Hofbauer: “Zur Pathogenese der Cholelithiasis,” Mitt. a. d. Grenzgebieten, 
1912, v. 24. 146 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
124- Lichtwitz, L.: “ Experimentelle Untersuchungen uber die Bildung von Nieder- 
schlagen in der Galle,” Deutsches Arch. f. klin. Med., 1907, V. 92, 100-108; 
Deutsche med. Wochenschft., 1910, p. 704. 
125. A. Exner u. Heyrowsky, H.: “Zur Pathogenese der Cholelithiasis,” Arch. f. klin. 
Chir. Berl., 1908, 86, 609-642; Chirurgenkongress, 1908, and Berliner klin. 
Wochenschrft., 1908. 
126. Larroche: cited by Bacmeister, Ergebn. d. inn. Med., n, p. 14. Chauffard: 
Inners. Kongressblatt, 9, p. 44. 
127. Naumann: Wiener kl. Wochenschrft., 1912. McNee, T. W.: “Zur Frage des 
Cholestearingehalts der Galle wahrend der Schwangerschaft. Mitt Bemerkung 
von L. Aschoff,” Deutsche Med. Wochenschrift, 1913, 39, 994-996. 
128. Chalatoff: Chir. Kongressblatt., 1914, 4, p. 561. 
129. Verse: Munchener Med. Wochenschrift, 1916. 
130. Kretz: Handbuch d. allgem. Pathologie, 2, p. 493. 
131. Boysen, I.: “The pathogenesis of gallstones (Swedish),” Inneres Kongress zentral- 
blatt, 1914, 11, p. 121. 
132. Aschoff, L.: “Wie entstehen die reinen Cholesterinsteine?” Munchener med. 
Wochenschr., 1912, p. 1753 u. 1913, No. 32. 
133. Kuru: Virchows Arch., 1912, V. 210, p. 433. 
134. Ooyama, T.: “Zur Frage der Cholelithiasis,” Zieglers Beitrage, 1913, V. 57. 
135. Aufrecht: Deutsches Arch. f. klin. Med., 1919, V. 128. 
136. v. Hansemann: Virchows Arch., V. 212, p. 319. 
137. Glaessner: Wiener klin. Wochenschrift, 1918, p. 549. 
138. Conradi, H.: “Ueber Zuchtung von Typhus bacillen aus dem Blut mittels der 
Gallenkultur,” Zentralbl. f. Bact., 1906. 
139. Frankel-Krause: Zeitschrift. f. Hygiene, 1899, V. 32, p. 106. 
140. Laubenheimer: Zeitschrft. f. Hygiene, V. 58, p. 64. 
141. Forster, I.: “Ueber die Beziehungen des Typhus und Paratyphus zu den Galle- 
wegen,” Munchener med. Wochenschrift., 1908, No. 1-6. 
142. Hendel: Arbeit, aus. d. Kais. Ges. Amt., 1908, V. 28. 
143. Ehret and Stolz: Mitt. a. d. Grenzgeb., V. 6, 7, 8, 10. 
144. Koch: Ztschft. f. Hygiene, V. 60. 
145. Gobel,C.: “UeberLeberabscesse,”Mitt. a. d. Grenzgebieten, 1906, V. 15,521-563. 
146. Wilms: “ Venenunterbindung bei eitriger Pfortaderthrombose nach Appendicitis,” 
Zentralbl. f. Chir., 1909, p. 1041-1043. 
147. Clara Reiniger: “Ueber die Entstehung von Leberabscessen auf rucktaufigen 
Wege,” Frankfurter Zeitschrift f. Pathol., 1913, V. 13, 103-113. 
148. Pawlow: Verhandt. d. Med. Gesellschft. in St. Petersburg, 1905. 
149. Looser, E. “Ueber Knochenveranderungen bei chronischen Fisteln der grossen 
Verdauungsdrusen,” Verh. d. Deutschen pathol. Ges., 1907. 
150. H. Seidel: “Permanente Gallenfistel und Osteoporose beim Menschen,” Munch- 
ener Med. Wochenschrift., 1910, p. 2034. 
151. Billard and Cavillie: Compt. rend. Soc. de Biol., 1900, p. 595, and 625 and 780. 
152. H. Hohlweg: “Ueber Stoerungen der Salzsaureabscheidung des Magens bei 
Erkrankungen und nach Extirpation der Gallenblase,” Deutsches Arch. f. klin. 
Med., 1912, 108, p. 255. 
153. Hammarsten: Nova acta Reg. Soc. scient. Upsala, 1894. 
154. See Zur Geschichte d. experimentellen Cholecystectomie. Rost, Mitt, aus d. 
Grenzgebieten, 1913, 26, p. 712. 
155. Rosenberg: Pflugers Archiv., 1893, 53, p. 388. LIVER AND GALL BLADDER 
147 
156. P. Klee and O. Kluppel: “Experimenteller Beitrag zur Funktion der Gallenblase,” 
Mitt. a. d. Grenzgebieten, 1914, 27, p. 785. 
157. Nasse: Arch. f. klin. Chir., 1884, 48, p. 885. Oddi: Bull, de sc. med. Bologna, 
1888. Florken: Deutsche Zeitschft. f. Chir., 113, p. 604. v. Stubenrauch: 
Arch. f. klin. Chir., 82, p. 667. De Voogt: Nederl. Tydschr. voor Geneeskunde, 
1898, 2, p. 236. Clairmont and Haberer: 33 Chirurgenkongress, 1904. 
158. Cohnheim and Marchand: Zeitschrft. f. physiol. Chemie, V. 63, p. 41. 
159. Riedel: “Der Gallenstein in Keimfreier Gallenblase,” Munchener Med. Wochen- 
schr., 1912, p. 8. 
160. Rous, P. McMaster, P. D.: “Concentrating activity of the gall bladder,” J. Exp. 
Med., 1921, 34, 47, see also Auster and Crohn, Proc. Soc. Exp. Biol, and Med., 
1921, 19, 117. 
161. Wiedemann: “Experimentelle Untersuchungen zur Lehre der Verdauung und 
Resorption verschiedener Nahrungsprodukte bei abnormalem Gallenzufluss in 
der Verdauungsapparat,” Bran's Beitrage, 1914, V. 89, p. 594. 
162. Enderlen and Funstein “Ein Beitrag zur Hepato-Cholangio-Enterstomie und zur 
Anatomie der Gallengange,” Mitt. a. d. Grenzgieben, 1904-1905, V. 14,104-119. 
163. W. Kausch: “Die Hydrops der Gesamten Gallensystems bei chronischem Chole- 
dochus verschluss und seine Bedeutung fur den Chirurgen,” Mitt. a. d. Grenz- 
gebieten, 1911, V. 23. 
164. Korte, W.: Beitr. z. Chir. d. Gallenwege u. d. Leber, 1908. Courvoisier: Kasuis- 
tische usw. Beitrage. z. Chirargie d. Gallenwege, 1890. 
165. Steiner: Wiener klin. Wochenschrft., 1914, No. 23. 
166. Quincke: Die Krankheiten der Leber in Nothnagels spec. Path. u. Ther.. 18. 
Bertog, J.: “Beitrag zur Frage der Entstehung der sogen. weissen Galle bei 
absolutem dauemden Choledochus verschluss,” Mitt. aus. d. Grenzgebieten, 
1913, V. 26. 
167. Berg: “Mitt. auS d. Grenzgebieten, 1912, V. 24. 
168. Rous, P. and McMaster, P. D.: “Physiol, causes for varied character of stasis 
bile,” J. Exp. Med., 1921, 34, 75. 
169. Clairmont u. Haberer: Grenzgebiete, 1911, V. 22, p. 154. 
170. Wiener klin. W7ochenschrift., 1913, p. 891. 
171. P. Sick and Frankel: Bruns Beitrage, z. klin. Chir., 1913, V. 85. 
172. Schiebelbein-Ritter: “Ueber galliche Peritonitis ohne Perforation der Gallen- 
wege,” Brans Beitrage, 1910, V. 71. 
173. C. Nauwerk and Leibke: “Giebt es eine gallige Peritonitis ohne Perforation der 
Gallenwege?” Berliner klin. Wochenschr., 1913, P. 624-627. 
174. Blad: Archiv. f. klin. Chir., 1917, 109, 101. 
175. Risel: Deutsche med. Wochenschrift., 1914, p. 1599. 
176. G. Kubig: “Ueber Volvulus der Gallenblase,” Munchener med. Wochenschrift., 
1912, 59,1998-2000. 
177. Bohn: De renunciatione valneram, Leipzig, 1755. 
178. W. Notzel: “Experimentelle Untersuchung zur Gallenblasen perforation peri- 
tonitis,” Arch. f. klin. Chir., 1910, V. 93. Ehrhard: Arch. f. klin. Chir., V. 64, 
and 74. 
179. G. Hirschel: “Die Behandlung der diffusen eitrigen Peritonitis mit 1% Kamp- 
feroel,” Brans Beitrage, u. Munchener med- Wochenschrift., 1910, V. 56. 
180. Enderlen u. Justi: Deutsche Zeitschrift. f. Chir., V. 61. 
181. Finsterer: Deutsche Zeitschrift., V. 121. 
182. S. Rubaschow: “Ueber Bradykardie bei Leberverletzungen (Erwiderang auf die 
Arbeit von H. Finsterer),” Deutsche Zeitschrft. f. Chir., 1913, V. 120, p. 515. CHAPTER V 
SPLEEN 
Splenectomy is doubtless the most frequent operation performed on 
the spleen (i). It was first done for injuries which without operative inter- 
ference, would usually have proved fatal from hemorrhage. Generally 
speaking, removal of the spleen is well borne, except in young animals 
(sucklings) which perhaps show some retardation of growth. But in this 
case the laparotomy itself, and not the extirpation of the spleen, may cause 
this disturbance (2). As an immediate consequence, vomiting of bloody 
gastric contents has been reported (3), to be explained perhaps by a 
retrograde thrombosis- into the gastric vessels such as occurs in resections 
of the omentum (v. Eiselberg, see later). Nevertheless, the loss of so 
large an organ is not without its results and study of the sequelae of splen- 
ectomy has materially increased our knowledge of its physiology. This 
better knowledge has led to more operative removals of the organ and has 
enabled us to cure or improve a number of diseases of the spleen, or rather, 
a number of general diseases in which the spleen occupies an important 
place, e.g., pernicious anemia, etc. Thus, splenic surgery has gained 
steadily in importance during recent years. 
Since the spleen has such an extraordinarily rich blood supply, it is 
natural that attention is directed to changes in the peripheral blood picture, 
but the data collected by various writers is not uniform concerning the 
effect of splenectomy on either the hemoglobin or the number of red 
blood corpuscles. This depends possibly, as Asher (4) and Vogel (5) 
have shown, on a relation between the iron content of the food and blood 
regeneration, inasmuch as the hemoglobin and the red blood cells remain 
steadily low on a diet poor in iron. In general, a diminution in the number 
of erythrocytes and in the percentage of hemoglobin, which is usually 
ascribed to the loss of blood from operation, is observed immediately after 
splenectomy (6). According to Vulpius (7), this diminution in erythro- 
cytes is never more than 20 per cent., and in one month it is again restored 
to practically the pre-operative count; Kuttner (8) actually records a 
count of 6,650,000 with 130 per cent, hemoglobin a year after splenectomy 
for gunshot injury; this probably can be related to the removal of its 
blood destroying activities. Peres (9) also describes a case in which 
there was a very rapid regeneration of hemoglobin. 
148 SPLEEN 
149 
But these are in the minority; the results in humans, as confirmed by 
many experiments on animals, may be summed up by saying that after 
splenectomy there is only a transient and minor diminution in hemoglobin 
and in the number of red blood corpuscles, which is completely compensated 
in a short time (lit. see Vulpus (7), p. 687). 
[An increased resistance of the red blood cells to hypotonic salt solu- 
tions, hemolytic sera, saponin, etc. has been found after splenectomy. 
Careful studies of this phenomenon have shown that this property 
resides in the red blood cell itself and is not due to an antihemolytic 
power of the serum or other similar factors. Its explanation is not 
clear but it is probably of importance in the decreased tendency to 
hemoglobinuria and jaundice seen after the administration of hemolytic 
agents (10).] 
Changes in the number and variety of white blood cells are found much 
more regularly than changes in the erythrocytes (Ehrlich (6)). Soon after 
operation, there appear a lymphocytosis and an eosinophilia which per- 
sist for many months, indeed for years (n), and which disappear very 
gradually. The absolute number of the leucocytes is also considerably 
increased. The reason is said to be a stimulus engendered by the removal 
of the spleen, which acts on the organs particularly concerned in the 
formation of lymphocytes and eosinophiles, i.e., on the bone marrow 
and lymph nodes. In monkeys, however, Kreuter (12) observed no 
influence on the peripheral blood picture; there was only a slight eosino- 
philia and no lymphocytosis at the end of the observation period. It 
seems, however, that physiologically, monkeys have a lymphocytosis. 
A similar change in the blood picture, i.e., lymphocytosis and eosino- 
philia, can be produced experimentally by the injection of substances 
which “act by increasing the tonus of the autonomic nerves,” while 
conversely, a polymorphonuclear leucocytosis and an a-eosinophilia, 
result from substances which increase the tone of the sympathetics and 
exert an intensive stimulation on the bone marrow (13). Substances 
which are able to influence the blood picture in one direction or another 
may be present in many organs even though the most of them have not 
yet been isolated in pure form. F. Schultze (14), pursuing this idea, was 
able to obtain a marked increase in the polymorphonuclears with diminu- 
tion of the mononuclears and eosinophiles by the injection of pressed 
spleen juice. He believes it may be concluded from these experiments 
that after destruction of the spleen, there is a preponderance of substances 
which act on the autonomic nerves; or as Bayer puts it in his iron metab- 
olism studies, a paralysing autonomic hormone is absent (15). Subse- 
quently, this internal secretory function is presumably taken over by the 
lymph nodes after which the blood picture returns to normal. Although 150 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
this theory is tempting on account of its simplicity, it must nevertheless be 
examined very carefully. It is, of course, not improbable that the normal 
blood picture is maintained by an equilibrium of the various internal 
secretions, but it must not be forgotten that our actual knowledge of the 
details in this field is still very meager. Very peculiar, and difficult 
to interpret, are the findings of Danilewsky and Selensky (16) who 
observed a marked increase in erythrocytes and hemoglobin after the 
injection of spleen and bone-marrow infusions even when the tissues had 
been previously boiled. On the strength of these results, attempts were 
made to improve severe anemias by administering “Lienin Pohl” and 
other preparations of spleen. 
With the exception of these deficiency symptoms after splenectomy, 
our knowledge of the role of the spleen in blood regeneration and destruc- 
tion is based especially on morphological studies. We know (17) that in 
embryonal life the splenic pulp shows erythropoetic masses but these never 
acquire the importance of those in the liver, but disappear before the 
embryonal period is concluded. The normal human spleen shows no such 
ery thropoetic masses, but they have often been observed under pathological 
conditions, such as severe anemias, even post-hemorrhagic; bone marrow 
carcinomata, and various infectious diseases such as small pox, diphtheria, 
malaria and syphilis. The erythropoetic foci are always found in the pulp 
and never in the purely lymphatic Malpighian follicles. The latter are 
concerned with the formation of lymphocytes in embryonal as well as in 
adult life. Myelocytes are also developed in the pulp of embryonal 
spleen, and this also points to a close relationship with the bone marrow. 
In adults, the pulp consists of cells whose function is still in doubt and 
while it normally gives rise to no myelocytes, it retains the ability to 
produce them under pathological conditions. Thus a myeloid transforma- 
tion of the splenic pulp is found in all sorts of infectious diseases; it can 
be produced experimentally, and finally it is often found in anemia and in 
tumors of the bone marrow. 
More important than its function to form blood corpuscles is its ability 
to destroy them. This function also resides in the pulp in which large 
endothelial cells, the macrophages, take up and dissolve those red blood 
cells destined to destruction. If an increased breaking down of erythro- 
cytes in the peripheral blood occurs from pathological causes, there arises a 
stimulus to the spleen; intense hyperemia of the organ develops, there 
results an hyperplasia of the cellular elements, and a splenic “tumor.” 
This is also seen experimentally, first in blood intoxications, and second in 
infectious diseases, particularly those in which marked destruction of 
erythrocytes occurs (18). The substances liberated, especially the hemo- 
globin, are carried to the liver and there elaborated into biliary pigments, SPLEEN 
151 
with the exception of iron which is stored in the spleen. As we have 
already seen, if the destruction of red blood cells is too rapid, and the pro- 
ducts are carried in too large a quantity to the liver, bile cylinders may be 
formed and lead to icterus. If the splenic function fails, the broken down 
red cells are taken up by the Kupfer’s cells of the liver, and thus they act, 
so to speak, as a substitute for the spleen (19). 
As stated above, the change in the blood picture after splenectomy, 
particularly the lymphocytosis and eosinophilia, must be considered as 
related to a stimulus which removal of the spleen produces not only on the 
lymph nodes and bone marrow, but also on a number of other organs 
which in their turn develop anatomical changes (20). Thus, as numerous 
writers have confirmed, there is swelling of the lymph nodes which renders 
about 20 per cent, of the superficial nodes enlarged to the touch (21). How 
often or how many of the deep lymph nodes are enlarged cannot of course 
be expressed in percentage, but according to autopsy records, the figure is 
quite high. In close histological relation to the lymph nodes are the so- 
called hemolymph nodes (22) which acquire a certain practical importance 
after splenectomy because they have often been confused with accessory 
spleens and have been described as such. These are structures which 
microscopically are identical with true lymph nodes, the only point of 
difference being that their sinuses contain blood. Because of this, they 
bear on superficial examination, a certain resemblance to splenic tissue 
and actually their function brings them in close relation to this organ since 
they contain erythrocytes and considerable amounts of the products of 
their destruction. Transitions into actual splenic tissue have, however, 
not been observed thus far. These hemolymph nodes also hypertrophy 
very markedly after splenectomy, and appear scattered in the mesentery as 
firm, dark red nodules, about the size of a finger nail, and grossly show 
great similarity to accessory spleens (23). All reports of the appearance of 
numerous accessory spleens after splenectomy must therefore be accepted 
with great caution. 
V. Stubenrauch (24), who terms these spleen-like bodies “splenoids,” 
thinks like Beneke, that they are from an implantation of torn and crushed 
spleen pulp. The experiments which he performed on the transplantation 
of splenic fragments showed, as a matter of fact, that these particles healed 
very well and were preserved for considerable time. Kreuter (25) also, 
on the basis of his experiments on monkeys, believes that the brownish 
nodules appearing in the peritoneum after splenectomy, are implants from 
liberated pulp. Cases similar to those of v. Stubenrauch have also been 
observed by others (26). Numerous (about 400) accessory spleens were 
discovered by Albrecht (27) in an individual who had not been 
splenectomized. 152 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
The oft cited statement of Giesker and Rosenmuller that accessory 
spleens are found at autopsy in 94 per cent, of southern Europeans and 
only once in every 400 northern Europeans and that this is related to the 
incidence of malaria in the former should be rigidly reinvestigated. In 
my experience, accessory spleens are found more often at autopsies in the 
north of Germany and other malaria free districts, than the published 
reports would indicate. 
After partial removal, the spleen is able to regenerate extensively. This 
occurs not only in lower animals such as frogs (Eberhard, cited by Vulpius) 
but also in mammals as shown in an experiment of Laudenbach (28) on 
dogs, and an observation on a human case by Kuttner (29). In the latter, 
four years after almost total splenectomy for traumatic rupture, a spleen 
the size of a peach was found. When the blood changes after splenectomv 
pass over very quickly, it has always been related to such regeneration or 
to the presence of accessory spleens. Whether this is correct or not, can 
naturally be determined but seldom. 
Of the other organs which are influenced by splenectomy, the bone 
marrow must be mentioned especially. As Mosler (20) first described, 
there are found hyperemia, active mitotic figures and increase in number 
of specific marrow cells with diminution in the amount of fat. The 
pressure of the increasing bone marrow leads to absorption of bone bridges 
which is evidenced clinically by gnawing pain in the long bones (Lohlein, 
cited by Vulpius), and also in a disturbance of ossification, although the 
latter is not always present. There are also occasional references to poor 
healing in fractures after splenectomy (Notzel cited by Meyer (1), (20), 
(3°)> (31))- 
An hyperplasia of the thymus has also been found, and Bayer (15) 
believes from his investigations on iron metabolism after splenectomy, that 
the thymus acts vicariously for the spleen (32). But v. Braunschweig (32) 
found no changes in the thymus under these conditions. Vulpius (7) 
describes swelling of the liver and many describe swelling of the thyroid (33) 
but it is very difficult to interpret these chapges physiologically at the 
present time; they are not found consistently so that they may only be 
chance results of the splenectomy. A certain satisfaction attends the use 
of the above mentioned theory of Schulze and Bayer that there is failure 
of a paralysing hormone acting on the autonomic system. Many of the 
changes described may be explained as a vagotonisation following this. It 
would also explain why all patients do not react to splenectomy with organic 
changes, but only those, if it may be so expressed, who have a particularly 
sensitive autonomic system. This applies especially to swelling of the 
thyroid. It is too elementary and meaningless to speak of the swelling 
of certain organs after splenectomy as “vicarious” manifestations. In SPLEEN 
153 
some cases the changes are probably only a result of the general operative 
shock. Thus a suddenly appearing Graves disease is occasionally seen 
after other severe operations, and, therefore, this condition is not character- 
istic of splenectomy and indeed it does not occur more often after this 
operation than after other laparotomies. 
The part which the spleen plays in iron metabolism is very important. 
Asher (34) found that the elimination of iron is considerably increased in 
splenectomized dogs. M. B. Schmidt (35) showed experimentally that 
the iron in the spleen is derived principally from destroyed erythrocytes 
and tissue cells, and that contained in the food is stored chiefly in the liver 
so that the spleen retains most of its contained iron even on an iron-free 
diet. A large part of this ultimately reaches the liver which thus “ assists ” 
the spleen. Whether other organs, e.g., the bone marrow, are also supplied 
with this stored iron to manufacture new red blood cells is not known with 
certainty. The results of Asher have been confirmed in humans by Bayer 
(36) who demonstrated an increased output of iron in several splenec- 
tomized patients. After splenectomy, the liver acts vicariously for the 
spleen, and assumes the storage of iron, but it is unable to hold it as tightly, 
and the hemoglobin of the blood diminishes, as Bayer found, after splenec- 
tomy during pregnancy. Lepehne (19) also demonstrated this increased 
output of iron by histological methods. [This disturbance in iron 
metabolism may, however, be a manifestation of increased blood destruction 
and not directly dependent on absence of the spleen.] 
We have thus far examined the functions of the spleen only from the 
standpoint of its importance in the blood picture. A further function is 
manifested in infectious diseases. It is able to ingest any bacteria which 
are circulating in the blood and destroy them in a manner similar to the 
destruction of functionless red blood corpuscles. This is one way in which 
the spleen helps in the struggle against infection. It may, however, set 
free bacterial antibodies from the remains of white blood corpuscles. 
Naturally, many experiments have been undertaken to discover if splen- 
ectomized animals are less resistant to infection, and a number of writers 
(Ludakewitsch, see the contrary, Piktin (37),Bardoch (37), anthrax) believe 
there is both increased susceptibility to infection and decreased resistance. 
But when one after the other of the inherent experimental errors in such 
investigations had been overcome, more and more writers reached the 
opinion, that a splenectomized animal, if it were otherwise in good condi- 
tion, shows no increased susceptibility. After splenectomy, as in every 
operative removal of an entire large organ, an animal is necessarily in a 
weakened condition and therefore any infection is more likely to be 
virulent. This lowered resistance however is not greater than after any 
other severe operation and is therefore not specific of splenectomy (Melni- 154 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
kow (38)). When the large number of factors concerned in an infection is 
considered, it is easily understood that a very large number of experiments, 
and marked differences in the results are necessary before conclusions 
which will withstand criticism can be drawn. Investigations of the 
bactericidal power of the blood serum, before and after splenectomy, are 
much more enlightening in this problem. Thus Montuori (38) found that 
the blood of splenectomized animals showed a diminished bactericidal 
power which lasted from 20 days to 4 months after the operation. Here 
also, it must be remarked, that loss of blood and operative shock alone 
can diminish the natural antibodies of the serum (normal agglutinins (39)). 
Perez (9), on the other hand, could, not demonstrate any change in the 
bactericidal and agglutinative power of the blood serum in a case in which 
he had removed a wandering spleen. Indeed there was even a slight 
increase in these powers. The practitioner is of course particularly 
interested in the resistance of splenectomized patients to infectious diseases 
and to sum up, it may be accepted that no positive influence was detected 
in any of the cases thus far described (Vulpius (7)). 
It is well known that the spleen is usually spared from metastases of 
tumors. This is spoken of as a sort of tumor immunity and it has been the 
subject of much study with mouse tumors. Oser and Pribrom (40) 
believe they could show that the sarcomata of rats grew more quickly 
after extirpation of the spleen, but nothing is known of anything similar in 
man (lit. see Schmincke (41)). 
What part the spleen plays in digestion is not definitely known. Gross 
(42) demonstrated a diminution in the pepsin of the gastric juice after 
splenectomy in a patient in whom it had been normal before the operation. 
Luciani (43) also states that the digestive power of the gastric juice is 
constantly diminished after extirpation of the spleen. This has been 
demonstrated in animals by Tarulli and Pascucci (44) and after the 
injection of extracts of spleen, this digestive power returned to normal. 
The old idea that spleenless individuals were possessed of large appetites 
was investigated by Richet (45) and he actually found, that for the same 
body weight, splenectomized dogs consumed more food in a day than 
normals. It would seem after these experiments and observations that 
the spleen does have some sort of influence on metabolism and the utiliza- 
tion of food. Further studies have led to the statement that splenecto- 
mized dogs have a reduced capacity for the assimilation of glucose, levulose 
and lactose, Quarta (1), but just how this occurs has not been demon- 
strated. It has been assumed that the spleen regulates the blood supply 
of the digestive organs and this conclusion has been drawn from several 
facts. As Schonfeld (46) has shown, first, the volume of the spleen is 
greatest during the time of digestion, second, contractile elements have been SPLEEN 
155 
demonstrated in the spleen, and finally Roy (47) detected rhythmic 
changes in splenic volume which occurred about every 60 seconds, and 
were independent of the fluctuations of blood pressure. The idea has 
been expressed in this way; the spleen acts as a “heart” for the portal 
system. But this regulation of blood supply can not alone explain the 
changes in digestive power, so an internal secretory power is suspected, 
but nothing definite in this direction has been discovered. Furthermore, 
the spleen has an influence on the motility of the intestines. As the 
animal experiments and the compilations of A. Meyer show (1) there 
often occurs a passing paralysis of the intestines with meteorism after 
splenectomy, but without other signs of peritonitis. Is this really more 
severe than after other operations? There are not sufficient records 
of prolonged constipation after splenectomy to answer this positively, 
even though it is said to have been observed. In opposition to these 
statements, Bayer (36) saw an increased activity of the intestines which he 
correlates with his theory of increased vagus tonus. Whether the splenic 
extract which Zulzer used therapeutically under the name of “Hormonal” 
owes its unquestioned ability to stimulate peristalsis to a hormone or 
only to a lowering of blood pressure on account of its content of “vaso- 
dilation” (Popielski, 48) has not been determined. At any rate it should 
not be concluded that the spleen is an especially important central organ 
for normal intestinal motility just because stimulation of peristalsis has 
been observed after the intravenous injection of “Hormonal.” At 
present, observations such as those of Soulie (1) in which a long lasting 
constipation was relieved by splitting the capsule of an enlarged spleen, 
must be evaluated very cautiously. 
Still more hazy is the importance of the spleen in psychic processes. 
Pohl (49) describes a case in which there was increased somnolence after 
splenectomy. Czerny (20) also observed nervous disturbances after 
the same operation. 
When one other fact is added, we will have completed the enumeration 
of the known symptoms and conditions which appear after splenectomy. 
In very young animals, there is an increase in the ash of their bodies which 
is chiefly from increased calcium and phosphorus, although there is 
relatively less of the latter (2). 
When the animals of Malassez and Pouchet (50) were bled a second 
time after splenectomy, the blood picture was apparently not altered, 
but others (51) believe that the usual symptoms are intensified by such a 
procedure although the latter do not give the details of their experimental 
results. 
A pathologically increased destruction of erythrocytes in the spleen is 
the crux of the situation in a number of diseases in which a severe anemia 156 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
occurs (52). These diseases among which are hemolytic jaundice, per- 
nicious anemia and Band's disease are often successfully treated by splen- 
ectomy. Their etiology and possibly that of a few others belonging to 
the same group is not known, nor are we entirely positive that different 
types of one and the same disease are not given separate names. We can 
only say with our present knowledge, that the spleen is fundamentally at 
fault, and with its removal, a large number of patients with these diseases 
may be cured or considerably improved. Eppinger draws an analogy 
between a number of loosely connected diseases formerly grouped under 
splenomegaly, and the hyperthyroidism in Basedow’s disease, justifying 
the comparison on the basis of therapeutic results. 
Jaundice is a symptom frequently present in all these diseases and as 
we have already seen, it is a result of bile cylinder obstruction in the capill- 
aries of the liver. The primary cause is a pathological hemolysis in the 
spleen. This can be imitated experimentally by administering tolu- 
endiamin to dogs. Banti (53) and Ivanovicz showed that it is more 
difficult to produce jaundice in splenectomized dogs with this substance 
than in normals, and the bile remains fluid in the former while it becomes 
viscid and dark from the extensive hemolysis in the latter. Therefore, 
we may conclude that the increased hemolysis is bound up with the presence 
of the spleen and it is only when the spleen participates in some manner 
that the toluendiamin becomes hemolytic. An approximate index of 
the degree of hemolysis can be obtained by estimations of the amount of 
urobilin in the stools. Eppinger and Charnass found a considerable 
increase in this substance in hemolytic icterus and in pernicious anemia. 
The conclusion is drawn quite correctly, that there is not insufficient 
formation of erythrocytes but an increased destruction of them in these 
diseases. 
The relation of pathological conditions in the spleen to diseases of the 
liver has been the object of much experimental investigation (54). Mal- 
lory, and later Breccia, demonstrated inflammatory and necrotic foci in 
the liver after such injuries to the spleen as crushing, heating, electrolysis 
etc. Foa injected tubercle bacilli under the capsule of the spleen and 
then found miliary tubercles in the liver which healed after removal of 
the spleen. Such foci in the liver were also obtained when the splenic 
vein had previously been ligated, although in this case, the anatomical 
picture was somewhat milder. Conversely, the injection of tubercle 
bacilli into the liver resulted in a severe infection of the spleen. 
It must be concluded from such experiments that the liver and spleen 
are in very close relation through their lymph and blood supplies, 
and that diseases affecting the one organ readily make themselves felt in 
the other. SPLEEN 
157 
In these diseases, the bone marrow is driven to supply sufficient red 
blood cells to compensate the enormous diminution. In hemolytic 
jaundice it succeeds very well; the blood picture remains fairly normal, 
but in true pernicious anemia all sorts of immature forms, nucleated 
corpuscles etc. are thrown into the peripheral blood. As an additional 
factor in this compensation for the loss of blood, the connective tissue 
proliferation in the spleen as it occurs in the classical Banti’s disease, 
should be regarded as an effort on the part of the organism at recovery 
(Eppinger). 
Even though the view that these hemolytic diseases may be regarded 
as an “ hypersplenism ” is in many ways open to criticism and has not been 
sufficiently substantiated in all its details, it has the big advantage of 
offering a starting point from which this difficult question can be viewed 
from common ground (55). Surgically at least, it is not necessary to 
deal with single types, usually named after their authors, but with a 
disease pathologically physiologically uniform and one which can be 
characterized briefly as increased hemolysis brought about by an alteration 
in the spleen. If the spleen is removed in these cases, the hemolysis 
ceases, and in the most favorable cases, especially those in which secondary 
changes have not progressed too far, the disease is completely cured. 
Approached from this standpoint, the etiology is of course entirely 
ignored. But it may be different in the various types, or, on the other 
hand, it may be but different degrees of one and the same process. The 
search for bacteria has been constant, particularly in Banti’s disease, 
and especially by Banti himself, who believes in an infectious origin, but 
up until now observations either by cultures or by inoculation have led 
to no positive results. In contradistinction to those writers who believe 
in a single bacterial or toxic cause, others believe that they result from a 
summation of injuries, especially previous infectious diseases, which have 
damaged the spleen. Perhaps in addition there is a congenital weakness 
of this organ (Banti’s disease of infantilism (56)). In connection with 
iron metabolism in Banti’s disease, Bayer (36) found considerable reten- 
tion of this substance in one individual and since there was also a lowered 
hemoglobin, he concludes, probably correctly, that the spleen of this 
patient could not supply its contained iron to the body as it was needed. 
The fact that an injection of adrenalin does not lead to an increase in 
white blood corpuscles in Banti’s disease as it does normally, is often cited 
as another indication that there is dysfunction of the spleen in this disease 
(57). Investigations of Blumenfeldt (58) have shown that this is not 
always true, for a leucocytosis did occur when he injected adrenalin into 
a splenectomized individual. This reaction is therefore not dependent 
on the spleen. 158 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
Injuries of the spleen and their results deserve short mention, since 
they have led to many experimental studies. In the mechanism of 
tearing wounds there are a number of factors which interact, but no one 
in particular should be especially emphasized. The soft consistency of 
the organ, Berger (59) states, makes it possible to compare it to a bladder 
filled with fluid and to apply Pascal’s laws according to which any pressure 
which is applied will spread equally in all directions. Investigations of 
Kon (60), however, have shown that the analogy is not fortunate because, 
while in any ordinary bladder, the pressure will spread equally, in the 
spleen, the capsule is less resistant to longitudinal than to transverse 
stretching. The reason for this is not known, but in all probability it 
explains why the great majority of tears of the spleen are transverse. 
A factor, leading to another limitation of Pascal’s law, is that the spleen 
is not freely movable but is more or less fixed in its position by fairly 
strong bands. A large number of the cases of rupture must therefore be 
regarded as tearing-off fractures, a view which has much justification in 
those cases resulting from indirect force such as the one of Waldeyer 
reported by Brogsitter (21). In direct trauma, the importance of the 
fixation bands of the spleen lies principally in their causing it to become 
bent on its convex surface while holding it fixed in position and therefore 
preventing it from turning aside (61). But in these bending tears, much 
depends also on which part of the spleen is lying on the structures beneath. 
This is usually the side endangered, as the experiments of Kon have shown, 
and the various positions of the spleen depend principally on the amount 
of contents in the stomach and intestines. 
If anhematogenous infection is engrafted on a splenic injury, it may lead 
to a sequestration of various portions, or even of the entire organ. In 
animals, Kuttner (62) could readily obtain such a splenic sequestrum by 
manual crushing of the organ followed by the injection of staphylococci 
into the ear vein. 
LITERATURE TO SPLEEN 
1. Lit. see coll. ref. by A. Meyer: Zentralblatt f. d. Grenzgebiete, 1914, Vol. 18, 
Hirshfeld, Deutsche Med. Wochenschrift, 1915, Schmincke, Munchener Med. 
Wochenshr., 1916. 
2. Droge: “ Einfluss der Milzextirpation auf die Chemische Konstitution des Tier- 
koerpers,” Pfluger’s Arch., 1913, 152, p. 437; Pfluger’s Arch., r9T4, 157, 486-500. 
3. Lieblein, V.: “ Ueber Magen—Darmblutungen nach Milzextirpation, zugleich ein 
Beitrag zur Kasuistik der isolierten Schussverletzungen der Milz,” Mitth. a. d. 
Grenzgebieten, r904, r7, 43r-446. 
4. L. Asher: “Die Funktion der Milz,” Deutsche med. Wochenschrift, 191T, 37, p. 
1252; Biochem. Zeitschft., 55, p. r3. 
5. Vogel, H.: Biochem. Ztschft., 18, p. 386. 
6. see Ehrlich: Die Anemia in Nothnagel’s Handb, 1898, 8 (Lit.). SPLEEN 
159 
7. Vulpius: Brun’s Beitrage, 1894, V. 11, p. 684. 
8. Kuttner: Chirurgenkongress, 1907, p. 25. 
9. Peres: 31 Jahresbericht f. chirurgie, 1907, 13. 
10. Pearce, R. M., Krumbhaar, E. B., Frazier, C. H.: “The Spleen and Anemia,” 
Lippincott Philadelphia, 1918. 
11. W. Notzel: Brun’s Beitrage, 1906, V. 48, 309-336. 
12. Kreuter: “ Experimented Untersuchungen ueber den Einfluss der Milzextirpation 
auf das periphere Blutbild,” Arch. f. klin. Chirurgie, 1914, Vol. 106, p. 191. 
13. G. Bertelle, W. Falta and O. Schweeger: “Ueber die Wechselwirkung der Drusen 
mit innerer Secretion.” 3. “Ueber Chemotaxis,” Zeitschrft. f. Klin. Med., 
1910, V. 71, p. 49. 
14. Schultze, F.: “Beitrag zur Splenectomy bei der traumatischen Milzruptur und 
zur Frage der dadurch bedingten Blutveraenderungen,” Bruns Beitrage, 1911, 
74, p. 482. 
15. R. Bayer: “Weitere Untersuchungen uber die Funktion der Milz, vornehmlich 
ihre Rolle im Eisenstoffwechsel mit besonderer Berucksichtigung des Morbus 
Banti,” Mitt. a. d. Grenzgebieten, 1913, 27, p. 311-340. 
16. Danilewsky and Selensky: Pflugers Archiv., 1895, 61, p. 264. 
17. see Naegeli: Blutkrankheiten, 1908, p. 72; Ehrlich, Die Anemia in Nothnagels 
Handb, 1898, 8, p. 56. 
18. Jawein: Virchows Archiv., 1900, V. 161, p. 461. 
19. G. Lepehne: “ Experimentelle Untersuchungen uber das Milzgewebe in der Leber. 
Ein Beitrag zum Hemoglobin-und Eisenstoffwechsel,” Deutsche med. Wochen- 
schft., 1914, p. 1361. 
20. Tizzoni: Arch. int. de Biol., 1882, 1, p. 34. Riegner: Berlin klin. Wochenschft., 
1893, P- i77- Mosler: Deutsche med. Wochenschft., 1884, Vol. 22, p. 338. 
Czerny: Wiener med. Wochenschft., 1879, p. 333. 
21. Brogsitter, C. M.: “ Splenectomie subkutane Milzruptur. Historisches, Kasuis- 
tisches und Kritisches,” Charite-Annalen, 1909, p. 558. 
22. Helly: Ergebn. d. Anat., 1902, V. 12, p. 207. Haberer: Arch. f. Anat. and Physiol., 
1901, p. 47. 
23. Momadi und Sisto: cited by A. Meyer (1). 
24. v. Stubenrauch: Chirurgenkongress, 1912, p. 214. 
25. Kreuter: Zentralbl. f. Chir., 1919, p. 554. 
26. Tizzoni: Arch. ital. de Biol., 1882, p. 36. R. Faltin: “Splenic formations in the 
peritoneum observed about 6}4 years after splenectomy caused by rupture of the 
spleen,” Deutsche Zeitschft. f. Chirurgie, 1911, no, p. 160. 
27. Albrecht: Zieglers Beitrage, z. pathol. Anat., 1896, 20, p. 513. 
28. Laudenbach: Virchows Arch., 1895, V. 141. 
29. Kuttner: cited by Stubenrauch, 24. 
30. Laudenbach: Arch, de Physiol., 1896, 28, p. 706. Emelianoff: Arch. d. sciences 
biol. de St. Petersbourg, 1893, V. 2, p. 135. 
31. Elliot: New York med. Journ., 1907. 
32. Klose, H. and Vogt, H.: “Klinik und Biologie der Thymusdruse mit besonderer 
Berucksichtigung ihrer Beziehungen zu Knochen-und Nervensystem,” Bruns, 
Beitrage, 1910, V. 69, 1-200. v. Braunschweig: Inaug-Diss. Dorpat, 1891. 
33. Winkler: Zentralbl. f. Chir., 1905, p. 257. Zesas: Arch. f. klin. Chir., 1885, V. 48 
and 31. Metzger: Zeitschft. f. Geb. and Gynekol, 1890, V. 19, p. 31. Crede: 
Arch. f. Klin. Chirurgie, V. 28, p. 401. Tiedemann: Ztschft. f. Phys., 1833, V. 5. 
34. Asher: Zentralbl. f. Physiol., V. 22. 160 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
35- Schmidt, M. B.: 15th Pathologentag., 1912, p. 91. 
36. Bayer, R.: “ Untersuchungen uber den Eisenstoffwechsel nach der Splenectomie ein 
Beitrag zur Lehre von den Funktionen der Milz,” Mitth. a. d. Grenzgebieten, 
V. 21, p. 338 and V. 27, p. 311. 
37. Piktin: Zentralbl. Bact., 15, p. 840. Ludakeevitsch: Annales de l’inst. Pasteur 
1891, Vol. 5. Bardach: Annales de L’inst. Past., 1891, V. 5, 1889, V. 3, p. 40. 
38. Melnikow: Montuori: Referred to in Centralbl. Bact., 1893, 13, 670. 
39. Rost: Inaug. Diss. Heidelberg, 1908. 
40. Oser und Pribram: Zeitschft. f. exp. Pathol., Therapie, V. 12. 
41. Schmincke: Lit. Munch, med. Wochenschrift, 1916. 
42. Gross, O.: “Ueber den Einfluss der Milz auf die Magenverdauung; Zugleich ein 
Beitrag zur Methodik der Pepsinuntersuchung,” Zeitschrft. f. exp. Pathol, and 
Therapie, 1910, V. 8, 169-180. 
43. Luciani: Lehrbuch der Physiol., V. 2, p. 152. 
44. Tarulli and Pascucci: Arch. ital. de Biol., 1901, V. 36, p. 188. 
45. Richet: Ref. Journ. de physiol., 1912, V. 14, p. 379. 
46. Schoenfeld: Inaug. Diss. Groningen, 1855. 
47. Roy: Journ. of Physiol., 1882, V. 3, p. 203. 
48. Popielski: “Die Theorie der Hormone und innere Sekretion,” Klinisch therap. 
Wochenschr., 1913, 20, p. 1134. 
49. Pohl: Deutsche Zeitschrift. f. Chirurgie, 104, p. 196. 
50. Malassez and Pouchet: Compt. rend. Soc. de Biol., 1878. 
51. Grunberg: Inaug. Diss. Dorpat., 1891, p. 58. Freiberg: Inaug. Diss. Dorpat., 
1892. Eliasberg: Inaug. Diss. Dorpat., 1893, p. 23. 
52. Eppinger, H. and Ranzi E.: “Ueber Splenectomie bei Bluterkrankungen,” Berl. 
Klin. Woch., 1893, u. Natusf. Vers., 1913, Eppinger u. Ranzi Mitt. a. d. Grenz- 
gebieten, 1914, V. 27, p. 796. 
53. Banti: Zieglers Beitr., 1898, V. 24. 
54. Lit. s. Ziegler, in Ergeb. d. Chir., 1914, V. 8, p. 683. 
55. Turk: “Die Blutkrankheiten und deren chirurgische Behandlung,” (Milzextirpa- 
tion) Deutsche Med. Wochenschrift., 19x4, V. 13, 14, Berl. Klin. Wochenschr., 
19x4, 51, 174. Muhsam, R.: “Die Blutkrankheiten und ihre chirurgische 
Behandlung,” (Milzextirpation) Deutsche Med. Wochenschrift., 1914, V. 13, 14. 
Mosse: Naturforscherversammlung, 1913 (surg. sect.). Decastello, H.: “Ueber 
den Einfluss der Milzextirpation auf die perniziose anaemia,” Deutsche med. 
Wochenschrift., 1914, V. 13, 14. 
56. Isaac: Schmidt’s Jahrb., 1912, 14, 315. 
57. FreyandLury: Zeitschft. f. d. ges. exp. Medizin., V. 2 and 3. 
58. Blumenfeldt: “Zur Frage der Funktionsprufung der Milz beim Menschen,” 
Herlin. klin. Wochenschrift., 1918. 
59. Berger: Arch. f. Klin. Chir., 1907, 83. 
60. Kon, J.: “Der Mechanismus und die pathologische Anatomie der subkutanen 
Verletzungen der Milz,” Vierteljahrsschrift. f. ger. Med., 1907, 34, 269-282. 
61. Leverenz, Schoenwerth: Cited by Michelsson, Ergebn. d. Chir., 1913, V. 6, p. 497. 
62. Kuttner, H: “Ueber sequestrierende Milzabscesse,” Beitrage z. klin. Chir. Tubing, 
1907. 54, 405-457. Chirurgenkongress, 1907, p. 23. CHAPTER VI 
THE PERITONEUM 
Because of their development from the common coelum, and because 
of their anatomical and physiological similarity in the sense of lining serous 
cavities, the peritoneum, pleura and pericardium have a large number of 
common physiological and pathological peculiarities. These will be 
discussed together in this chapter on the peritoneum. 
The serous coats are made up of a thin layer of connective tissue covered 
by a single layer of flat epithelium, or endothelium, as it is now called. 
Of all the attempts to differentiate this endothelium from epithelium and 
classify it with the connective tissues that of Kolozoff and v. Brunn (i) 
who detected cilia on the surface of the serosa, seems to supply the best 
proof of the epithelial character of these cells. 
[There is doubt that these projections were really cilia; possibly they 
were only artefacts such as tiny strands of fibrin. The term mesothelium 
has been suggested but in view of its long established usage, endothelium 
is probably to be preferred, especially so because of the doubt of the 
origin of the cells.] 
But their functional properties are also indicative of this origin. 
Uninjured serous surfaces do not adhere (v. Brunn); it is only when the 
vitality of the cells is reduced that fibrin is poured out and adhesions 
develop which finally, by organization, become dense and tight (2). 
According to the view of Marchand and Ziegler, fibrin appears as an exu- 
date of plasma from the surface vessels; but according to Neumann and 
Grawitz, its origin is a “fibrinoid degeneration of the uppermost layers 
and of the swollen cells of the surface” (cited by Heinz). The histological 
details in this question still give rise to differences of opinion (3). As in 
the skin, larger defects in the serosa are filled in, first by blood, and later 
by connective tissue; finally, endothelial cells grow in from the edges and 
cover the entire denuded area (4). / 
Peritoneal adhesions are not necessarily permanent, but may disappear. 
Ujeno (5) by using iodine solutions, produced abdominal adhesions in 
rabbits and after having assured himself of their presence by a second 
laparotomy, caused their disappearance by massage of the abdominal 
walls. The processes concerned in their removal consist of degeneration 
and absorption. New adhesions are prevented by the ingrowing covering 
161 162 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
of endothelial cells which are found as tube-like islands in the zone of adhe- 
sions (v. Brunn). What part enzymic processes play in the solution of 
such adhesions is not known with certainty. 
The histological processes in the course of the encapsulation of foreign 
bodies in the peritoneum have been studied by Monkeberg (6) who injected 
lycopodium into the abdominal cavity. The first change is degeneration 
of the endothelial cells and growth of surrounding connective tissue. The 
former cells then grow from the edges, and conditions return as close as 
possible to the normal. Thus the pathological anatomical course of the 
formation and disappearance of adhesions is fairly well understood. 
There are, however, a large number of physiological questions which 
require answers. For instance, it is not known whether the serosa of the 
abdominal, pleural and pericardial cavities, though embryologically 
similar, are equally subject to their formation. Lennander (7) believes 
that they are formed more readily in the peritoneum, while Burkhardt (8) 
thinks it is a case not of differing functions of the endothelium, but of 
mechanical changes. It is a fact that leucocytes may easily be obtained 
by light suction from the peritoneum but not from the pleura or peri- 
cardium. Since the preliminary step in the formation of adhesions is 
similar to the process of blood coagulation, the leucocytes are probably 
not unimportant as enzyme carriers. But the mere presence of blood in 
the peritoneum, does not favor the formation of adhesions for according 
to Schrunder (9), none developed even when the serosa was injured at 
the same time, but they did form very readily when microorganisms were 
added to the blood. 
Since adhesions are, to say the least, unwelcome, all sorts of substances 
and methods which Payr (10) has catalogued, have been tried (experiment- 
ally, and in man) to prevent their formation. In general, two methods 
have been employed. The first consists of spreading certain smeary 
substances over the visceral and parietal surfaces of the peritoneum, and 
the second, of stimulating the intestines to vigorous peristalsis immediately 
after operation in order to prevent the formation of adhesions at the very 
start (n). Of the substances recommended for introduction into the 
abdominal cavity to prevent adhesions, mention may be made of olive 
oil, camphorated oil, liquid paraffin, gum arabic, gelatine, egg white, etc.; 
further, gold beater’s skin, collodion, protective silk, etc., have been 
covered over the intestines (12). The results of all these experiments 
have been very meager. Some have believed that camphorated oil will 
inhibit them but others have recorded the opposite experience (13). It is 
of course necessary that an abdomen be reopened for adhesions in order 
that such cases may he evaluated. Of the other substances not one has 
stood the test of time. THE PERITONEUM 
163 
[It must, of course, be remembered that the formation of adhesions is 
part of the process of normal repair, so that the problem is really not the 
prevention, but the limiting of adhesions to a point just consistent with 
repair.] 
A particularly remarkable fact for surgeons to note is that blood remains 
fluid in the serous cavities, or to put it more cautiously, blood free in the 
peritoneal cavity is mostly encountered in a fluid or semifluid state. 
Many experiments have been performed to clear this question, but contra- 
dictory results were obtained. 
The works of older writers (Brucke (14), Lister) may be ignored, 
since they were performed on cold blooded animals and cannot be applied 
directly to humans. Trousseau and Leblanc (15), drew blood from the 
jugular vein of a horse and injected it into its pleural cavity through a 
funnel. The blood coagulated immediately, serum was pressed out just 
as in a test tube and was absorbed in the course of a few days. 
Extensive experiments were performed by Penzoldt (16), who allowed 
blood from one rabbit to pass through glass and rubber tubes into the 
pleural or peritoneal cavity of another rabbit. Examination for the coagu- 
lability of the blood was made either at autopsy or by puncture of the 
cavities. He found that there was always fluid blood present, even after 
nine days of hemothorax, but coagulation was also always found at the 
end of 24 hours. When blood was removed during the first two hours 
after its introduction, it was still fluid, but coagulation set in in vitro. 
On examination at later periods, coagulation did not occur until the fifth 
day, when it again set in but so slightly that Penzoldt concludes, prob- 
ably correctly, that it was not true blood coagulation, but coagulation of a 
pleural exudate. He could demonstrate inflammatory processes in the 
pleura in practically every case. 
When small amounts of blood were introduced into the abdominal 
cavity, no blood was found in three days, or perhaps only a few coagula. 
From this, Penzoldt concludes that the blood must have remained fluid 
for some time in the peritoneal cavity. Changes in the sense of a peri- 
tonitis were not demonstrable. This last point is of great interest for it is 
well known that hemorrhage into the abdomen, particularly in the upper 
abdomen (injuries to liver or spleen) gives rise to and in fact, to all 
the clinical symptoms of peritonitis (Trendelenburg). This will be dis- 
cussed later. It will also be shown that hemorrhage, in general, exerts 
a pronounced irritant effect on tissues, for blood out of its normal environ- 
ment is certainly not an indifferent substance. 
In work on the absorption of hemorrhage, Cordua (17) performed 
extensive experiments on the conditions occurring in intraperitoneal 
bleeding. He allowed the blood from the carotid artery of one dog to 164 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
flow through a tube into the abdominal cavity of another and by removing 
samples through fine glass cannulae, studied its changes. Of course, this 
method yielded only approximate figures of the amount of blood which had 
coagulated and the amount which remained fluid, but the results are use- 
ful as they stand. Certain technical errors are inherent in all these 
experiments. As soon as blood has left the body and is no longer in con- 
tact with living tissue but flows through glass tubing, it becomes very 
unstable and coagulation begins very quickly (18). Furthermore, strict 
asepsis was not observed in the experiments cited. In addition, a large 
amount was introduced quickly, while in the hemorrhages in man, at 
least in those amenable to treatment, the blood pours in much more 
slowly. Finally, an animal’s own blood and a foreign blood behave very 
differently, and this factor has not always been given sufficient 
consideration. 
Nelaton (19) avoided a number of these errors, by attempting to 
produce hemothorax from stab wounds of the lung, but in other cases, he 
also used the injection method. The findings are thus briefly summarized 
in his publication; blood is coagulated in 24 hours at the latest, and serum 
is then pressed out. Therefore his results correspond in general to those of 
Trousseau. Riedel (20), who observed a very rapid absorption after 
injecting blood into the pleural cavity, also found that the largest part 
remained fluid and only a small part coagulated. After injection into a 
joint, he states that one-third coagulates and two-thirds remains fluid. 
The fluid portion of the blood is absorbed, the coagulated portion is first 
organized and then removed in this somewhat complicated way. Jaffe 
(21) believes that blood in joints first coagulates and later becomes fluid 
again. Pagenstecher (22) who led blood directly from the carotid artery 
into the pleural cavity of the same animal, found almost all the blood 
fluid during the first two hours, and after six hours there remained a non- 
coagulable fluid resembling blood with floating coagula. 
Operative observations in hemorrhage into serous cavities, particularly 
the peritoneurri, show that there is always a mixture of clots and fluid blood 
present. The relative quantities of each can only be judged. In slow 
hemorrhage, e.g., secondary hemorrhage, there are more clots and less 
fluid; in rapid hemorrhage (rupture of liver or mesenteric hemorrhage) 
the findings are reversed. 
From this synopsis it is evident that the writers on this subject have 
divergent opinions. The French say, coagulation in toto takes place; the 
clot expresses serum which is absorbed. Riedel and others find a rapid 
absorption without coagulation. Penzoldt and Pagenstecher occupy a 
middle position. These differences in results must depend on the methods, 
and the reason for the differences will be found only when it becomes known THE PERITONEUM 
165 
why a certain part of the blood remains unclotted. In other words, 
chemico-physiological examinations are necessary to lead us further. 
This question brings up a more general one; why blood which coagulates 
so quickly outside the body remains fluid within the organism. Roughly, 
this subject has undergone the following vicissitudes. Brucke’s idea (23) 
is that there is some sort of a vital process of which we know nothing definite 
and the blood remains fluid only so long as the vessel wall is intact and 
living. Freund (24) believes that the absence of friction, that is, a pure 
physical process, is sufficient explanation. But the idea of slight friction 
is not entirely accepted and the “ vital process” opinion is not excluded. 
It is known that there are present in the blood, coagulation producing and 
inhibiting substances, or at least their precursors (25) and that, e.g., 
experimental injection of Witte’s peptone (26) or tissue extracts (27) check 
coagulation. The opinion is therefore held at present that such substances 
are also important in maintaining fluidity of the blood in the living vessels. 
Indeed, it is held that in the final analysis, the coagulation or fluidity of 
the blood when brought in contact with animal tissues depends on the 
balance of these coagulation producing and inhibiting factors (28). 
The view is often expressed that the same conditions which control the 
fluid state of blood in the vessels, also maintain its fluid character in the 
serous cavities. An antithrombotic property of the endothelium of the 
serosa has been spoken of but the thought has also occurred, that in addi- 
tion to this, the blood may have been defibrinated by the movements of 
the lungs and diaphragm (Riedel). Without doubt a recent hemorrhage 
(about twenty-four hours old) must be sharply differentiated from the 
sanguinous fluid obtained at a later puncture. Many workers have experi- 
mented with fresh hemorrhage into the pleural cavity, in the light of newer 
opinions on blood coagulation (29). Israel produced hemorrhage by open- 
ing the internal mammary artery and found it could “ not be antithrombotic 
substances, but only lack of fibrinogen which determined the absence of 
coagulation.” Clotting was readily brought about by the addition of 
fibrinogen and when increasing amounts of completed thrombin were 
added, the coagulum of this mixture was as firm as that of the controls. 
If inhibitory substances had been present, the coagulum would necessarily 
have been less firm. Furthermore, no inhibitory substances could be 
extracted from the endothelium. But while Zahn and Chandler believed 
certain changes occurred in the fibrinogen of the blood on contact with the 
pleural endothelium, Henschen, Herzfeld and Klinger regarded the process 
entirely as one of “defibrination.” The movements of the lungs, heart and 
abdominal organs whip out the fibrin just as it may be done with glass rods. 
The relative quantity of fluid and clotted blood, found at operation, 
either in the peritoneal, pleural or pericardial cavities, would therefore 166 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
depend entirely on the relative amount of movement which has been 
transmitted to the blood present. This opinion is supported by the finding 
of quantities of fibrin clots in such hemorrhages. In addition, it must not 
be forgotten that coagulation is further slowed by the very slight friction 
to which the blood is subjected in such serous cavities so that a less amount 
of agitation will lead to defibrination. That the movements of the intes- 
tines are not to be underestimated can be seen from the fact that air which 
has escaped from a partially covered perforation of the stomach is spread 
in small bubbles over the peritoneum. It would seem to indicate that a 
kind of “beating” of the air occurs. 
The erythrocytes, settle in the defibrinated fluid blood so that the 
fluid obtained by puncture of such old hemorrhages is poorer in hemo- 
globin and shows a diminution in the number of cells. These are gradually 
destroyed; numerous “shadow cells” appear and exudative processes are 
indicated by an increase in the number of leucocytes. These latter cells 
then predominate, so that paracentesis does not reveal a fluid hematoma, 
but an exudate (Ledderhose) which contains considerable mucoid material 
(30). Blood in a joint or serous cavity is therefore not an entirely innocu- 
ous substance and Bier has taken advantage of this fact to increase the 
formation of callous in pseudarthroses. But it does not of itself favor the 
formation of adhesions in the peritoneal cavity as the experiments of 
Schrunder (9) have shown. The pain in subcutaneous hemorrhage 
is considered by Pagenstecher as probably due to this tissue irritation. 
That the increased temperature, “absorption fever,” is also an effect 
need only be briefly mentioned. 
As already stated, hemorrhage into the abdominal cavity is a powerful 
irritant to the peritoneum and leads to peritoneal shock. The clin- 
ical picture in such intraperitoneal hemorrhage is apparently very 
serious. Actually, however, the danger from hemorrhage alone is often 
not very great (31). Even when patients appear exsanguinated after 
injuries to the liver or spleen, there may be found only a small amount of 
blood. Many gynecologists have recently become more conservative 
in their treatment of extra-uterine pregnancy. 
According to the calculations of Wegner (32) the total surface of the 
visceral and parietal peritoneum in a moderately developed female is 
17,182 sq. cm., while the total external body surface, according to the 
same author is 17,502 sq. cm. The surface of the peritoneum is therefore 
approximately as great as the total body surface and this explains the 
importance of the absorptive and exudative processes to the remainder of the 
body. Under the stimulus of this calculation, the absorptive and exuda- 
tive processes of the peritoneum have been studied from the surgical view- 
uoint, by ths most varied methods and under the most varied conditions. THE PERITONEUM 
167 
Wegner, himself, injected measured amounts of saline solution and serum 
into the abdomen of rabbits, and after killing them at intervals, measured 
the amount of fluid remaining. As these experiments show, the absorp- 
tive ability of the peritoneum is quite astounding. Its rapidity has been 
calculated by injecting small quantities of solutions of various substances 
which can be readily detected in the urine. Among them were potassium 
iodid (33), lactose (34), salicylates or potassium ferrocyanide (Schnitzler 
and Ewald) and dye stuffs such as methylene blue. Since the time 
between injection and appearance in the urine is dependent on both the 
rate of absorption from the peritoneum and the excretory rate and power of 
the kidneys, such methods yield only relative results. When, there- 
fore, excretion of iodin began in 15 to 20 minutes and lasted four to five 
hours, as in the experiments both of Schnitzler and Ewald and of Clair- 
mont and Haberer, absorption of this substance must have occurred much 
earlier. This conclusion may safely be made by analogy with other 
salts which are eliminated more rapidly by the kidneys as for example, 
salicyl, which can be detected in the urine more quickly (Schnitzler and 
Ewald). As Wegner showed, the injection of potassium cyanide is 
followed by almost instant death, as though the poison had been injected 
directly into the blood stream. Absorption, therefore, is very rapid, but 
pathological conditions may alter the speed and furthermore, absorption 
does not proceed at the same rate during longer periods of time (35). 
It is necessary now to study the paths by which soluble and insoluble 
substances leave the peritoneum. Dubar et Remy, Mafucci and Heusner 
(36) demonstrated that absorption takes place not only by way of the 
diaphragm, but also through the great omentum, the lateral ligament, 
Douglas’s cul de sac, the gastrohepatic omentum, etc. Both lymphatics 
and blood vessels take part. Danielsen (37) found by examinations of 
thoracic duct lymph and of blood, that colloids are taken up by the lymph 
channels and crystalloids by the blood stream. Bacteria belong to the 
group of colloids. Insoluble particles, such as oil and milk droplets, blood 
cells, india ink, etc. pass into the lymphatics of the diaphragm and then 
enter the thoracic duct. These paths were described by v. Recklinghausen 
(38) in 1863 and the rich supply of this muscle is shown in the anatomical 
investigation of Kuttner (39). The question of stomata in the vessels, 
i.e., clefts between the endothelial cells, whose presence was accepted by v. 
Recklinghausen, is also discussed by Kuttner, and they are proved to be 
absent (see also Muscatello (40)). The absorption of insoluble particles 
compared to that of fluids is relatively very slow. Oil and liquid paraffin 
can be found unabsorbed in the peritoneum even after 24 hours (41). 
In these studies and observations much depends, of course, on the position 
of the patient or the experimental animal, i.e., whether the diaphragm 168 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
was at the lowest level or not. For, as Muscatello showed, the region of 
the diaphragm is the only part of the peritoneum from which insoluble 
particles are absorbed. Thus absorption from the peritoneum may be 
very considerably diminished if the patient is so placed that the chest and 
upper abdomen occupy a high position and the pelvis the lowest (Fowler’s 
position). That solutions are also absorbed almost exclusively by the 
diaphragmatic peritoneum is shown by the experiments of Clairmont and 
Haberer in which they observed a very much delayed absorption of 
iodide solution after painting the under surface of the diaphragm with 
collodion. Substances tend to approach the diaphragm, as Muscatello 
and others have shown, not only on account of their weight, but also 
against the force of gravity. There is a current of fluid directed upwards, 
produced probably by the movements of the diaphragm and the intestines. 
The cause of this current is not entirely clear. At any rate, as v. 
Recklinghausen has already stated, up and down movements of the dia- 
phragm, even in a dead animal, cause a more rapid taking up by its 
lymphatics, of particles scattered over its surface. A portion of the 
corpuscular elements are also first phagocytosed by wandering cells, 
and may be absorbed by omentum or mesenteries and thus be transported 
in the lymph channels (Metschnikoff (42)). 
In contradistinction, fluids or true solutions enter the blood stream 
directly. Only a small quantity is carried away by the lymph. This can 
be demonstrated by pouring almost any dye solution into the abdomen 
and observing the lymph as it flows from a fistula of the thoracic duct. 
The urine is colored before the lymph (43) and even after the introduction 
of large quantities of saline solution into the abdominal cavity, no increase 
in the quantity of lymph from the thoracic duct can be observed (44). 
True solutions also are absorbed by the diaphragm. That this absorption 
of fluids is greatly dependent on the blood supply of the abdominal cavity 
is easily understood, since they enter the blood stream directly. A further 
demonstration of this point is afforded by the experiments of Klapp (45) 
who observed a greatly increased absorption after placing animals in a hot 
air chamber and producing an active hyperemia of the abdominal organs. 
Conversely, by producing venous stasis, Clairmont and Haberer 
demonstrated a diminished absorption. Cold applied to the abdomen 
diminishes absorption (37). Also, when the venous return is hindered by 
increased intra-abdominal pressure (e.g.; a large exudate) absorption is 
slowed. In such cases, the removal of a portion of the exudate relieves 
pressure on the veins; the return of blood is improved and the rate 
of absorption increases. 
How do pathological circumstances ajfect absorption, especially from the 
peritoneum; what are the conditions after operative injury, inflammatory THE PERITONEUM 
169 
processes, etc? (35). After simple laparotomy, absorption is slowed only a 
trifle, that is, the beginning of absorption is not delayed but it is found 
slowed if estimations are made over a longer length of time. If the intes- 
tines are pulled out of the abdominal cavity, the absorptive processes are 
much more disturbed, they begin very much later than normal but may 
be somewhat favored by moistening the intestines with warm saline solu- 
tion. Anesthesia per se has no appreciable effect but a diminution 
of peristalsis produces diminution of absorption (Schnitzler and Ewald, 
Clairmont and Haberer). Clairmont and Haberer stimulated peristalsis 
with physostigmin and believed absorption in the rabbit began earlier. 
Schnitzler and Ewald could not observe an increased absorption by other 
methods, e.g., tying off a low loop of bowel. Obviously the results 
obtained in experiments such as these depend much on the kind of animal 
used. The serosa of the rabbit is more sensitive than that of the dog. 
Much finer differences may, therefore, be obtained in the former animal. 
It is doubtful, however, if these particular experiments can be used as a 
basis for believing that the toxemia of peritonitis in man will actually be 
increased by the taking of food or cathartics (46). 
According to Clairmont and Haberer, an inflamed peritoneum absorbs 
more quickly in the first stages of peritonitis, and later the rate is slowed. 
This decrease of the absorption rate in the beginning is particularly 
evident if the inflammation is brought about by chemical irritants. In 
bacterial peritonitis the increase is not so clearly seen. In the later stages, 
Schnitzler and Ewald, and Clairmont and Haberer found a decrease in the 
rate by the potassium iodide method, but Glimm, using milk sugar, could 
not demonstrate it. Likewise Peiser, by injecting bacteria into the ab- 
dominal cavity, first observed considerable absorption and then later only 
a very slight amount. The divergence of results in these animal experi- 
ments is not very difficult to explain. The gross anatomical pictures 
of the peritonitides are not similar throughout, because in one instance a 
large amount of exudate is poured out and a small amount in another. 
Furthermore, the amount of fibrin varies in the same way. It seems only 
natural that absorption experiments carried out with bacterial infection 
should lead to differing results. 
A chronic inflammation of the peritoneum was produced by Schnitzler 
and Ewald by introducing mechanical irritants such as sand, glass, cellu- 
loid particles, etc. Wegner sought to produce the same result by re- 
peatedly injecting air. These experiments showed that the chronically 
inflamed peritoneum absorbed less than the normal membrane; a result 
which agrees, as Schnitzler and Ewald emphasize, with the clinical experi- 
ence, that sepsis occurs less readily from a peritoneum which is the seat 
of a chronic inflammation. It is well known, especially from experiments 170 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
of gynecologists, that the danger of a post-operative peritonitis may be 
diminished by previous injection of irritant substances such as camphor, 
oil, etc. (47). It may be mentioned that one or even many injections of 
air lead to no demonstrable anatomical change in the peritoneum. 
Apparently, transudation into the peritoneum is not interfered with 
by either dry or moist eventration, but the amount of fluid which escapes 
in acute inflammation is often very large. Increased transudation, ascites, 
has been discussed under cirrhosis of the liver. According to the state- 
ments of Wegner (48) the fluid which is poured into the abdominal cavity 
after the introduction of glycerin or hypertonic salt solution may equal 
the body weight in 12 to 23 hours. In the acute forms of peritonitis, 
however, the fluid does not accumulate as in the chronic forms, because 
in the former condition, the absorptive processes are not delayed, so that 
during a given time interval almost as much will be absorbed as has been 
poured out. Furthermore, the experiments of Wegner ((48) p. 85) show 
that, normally, the peritoneum is able to absorb in from to 30 hours 
an amount of fluid equal to the body weight of the experimental animal, 
which coincides with what has been said of the exudative powers of the 
peritoneum. The formation of an exudate depends on an injury to 
vessel walls (Cohnheim). For information concerning the anatomical 
conditions in the endothelial cells during exudation, Borst’s studies may be 
consulted (49). According to the investigation of Schrader (50) the 
injection of bacteria, dead or alive, or of bacterial filtrates leads to no 
increased transudation. 
The blood vessels of the peritoneum and of the abdominal organs are 
innervated by the splanchnics which send fibres not only to the arteries 
but also to the portal system (51). This vascular bed supplied by the 
splanchnics, is an extraordinarily large one, and, therefore, this nerve has 
been called the “regulator of the general blood pressure.” A dilatation 
of vessels in other parts of the body, e.g., skin surface is quickly compen- 
sated by a slight constriction of those in the splanchnic area. The pres- 
sure in the aorta therefore remains stable but it falls considerably when 
paralysis of the vaso-constrictor fibres of the splanchnics develops, e.g., 
in severe peritonitis. The individual is actually exsanguinated by bleeding 
into the vessels of his own abdomen. A good idea of the amount of blood 
which may be contained in these vessels can be obtained from an investi- 
gation of Mall (52). By stimulation of the splanchnic 3 to 27 per 
cent, of the blood in the portal system of a dog was driven into other 
vessels. This fall of blood pressure is one of the principal causes of death in 
peritonitis (see later). The details of the blood and lymph vessel supply 
of the peritoneum have been studied by Meisel (53). He found the visceral 
layers were far better supplied than the parietal, but both contained a very THE PERITONEUM 
171 
rich capillary network which ramified in the loose sub-endothelial tissue. 
Before speaking of the sensory nerves of the abdominal organs, it may be 
useful to discuss briefly the vegetative nervous system in general (54). 
It has been found, chiefly through pharmacological investigations, 
that it is advantageous to divide the nervous system supplying the organs 
which function involuntarily, into the sympathetic portion and the cranial, 
i.e.y sacral autonomic portion (55). This is a physiological, rathe than 
an anatomical division, since anatomically, the entire vegetative nervous 
system shows similarities insofar as the fibres which lead outwards from 
the various parts of the brain, do not pass directly to their respective 
organs, but first enter groups of nerve cells, the so-called ganglia. Here, 
in all probability, they are completely freed from any influence of the 
will and then pass as independent nerve structures into the tissues they 
innervate. The activities of the ganglia are paralyzed by injections of 
nicotin (Langley) and the functions of the pre-ganglionic fibres may then 
be separated from those post-ganglionic. 
When both the sympathetic and the cranial-sacral autonomic systems 
supply any organ, and most organs in the abdomen are so provided, their 
functions are to be regarded as antagonistic. If, for example, stimulation 
of the sympathetic leads to inhibition of the movements of the intestines, 
stimulation of the sacral autonomic or the abdominal vagus will lead to 
an increase of peristalsis. 
At this place we must refresh our knowledge of the anatomy of the 
sympathetic nervous system. In spite of its special functional importance, 
the sympathetic is anatomically to be considered “ only a part of the total 
peripheral nervous system which has become independent” (56). The 
visceral branches, which spring from each spinal ganglion cell, or more 
accurately, from the anterior root, represent a direct nerve supply to the 
viscera in lower animals (Petromyces). In higher animals this simple 
structure is complicated by the union of single rami viscerales (border 
strand of the sympathetic); by the addition of non-medullated fibres arriv- 
ing from the periphery; and by.the presence of ganglion cells along their 
course, which, in their development, represent displaced spinal ganglia, 
that is, the primitive centrifugal ramus visceralis and a few centripetal 
non-medullated fibres, is called in anatomy, the ramus communicantes. 
The largest, and from its function the most important of the ganglia in 
the abdomen is the solar ganglion, or, as it is also called, the coeliac plexus. 
Its most important branches are the major and minor splanchnic nerves. 
It is not known with certainty whether the vagus merely traverses the 
plexus or if it is connected with the nerve cells. Since sensory, motor and 
vaso-motor fibres all enter the ganglion, its function is very complex and 
the clinical symptoms following its destruction or compression may there- 172 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
fore be very varied. Strehl (57) has collected the investigations on this 
subject which have been carried out up to the time of his article (1905). 
The experiments of Popielski (58) and Exner and Jager (59) have already 
been discussed. According to these, stimulation of the intestines after 
extirpation of the ganglion is said to be answered by a contraction lasting 
for a decidedly longer time. If the animals remained alive, they became 
emaciated and passed very foul smelling excrement. In agreement with 
these experimental results, Exner and Jager found strong spasms of the 
small intestines in a case of probable destruction of the solar ganglion. 
At autopsy there are found (Strehl) hemorrhages and ulcers in the mucosa 
of the stomach, duodenum and upper small intestines, dilatation of the 
vessels and hyperemia of all the abdominal organs, with enlargement of 
the liver, periodic occlusion of the common bile duct, transient glycosuria, 
albuminuria, acetonuria, and emaciation with general body weakness. 
Accordingly, therefore, the vaso-motor and motor centers for the intestines 
are probably located in the coeliac ganglion. 
Strehl himself, however, did not observe changes in the mucosa 
of the intestinal tract following experimental extirpation of the plexus. 
The large glands seem to be little influenced by this operation but there 
have been no careful experiments done on this problem with fistula dogs. 
The only constant findings in the many experiments of a large number of 
workers, seem to be the accelerated emptying of the small intestines and 
the dilatation of the vessels supplying them. 
The sensitivity of the abdominal organs has been much investigated 
from the surgical standpoint during the last few years, especially since 
the introduction and ever increasing use of local anesthesia (59). In 
speaking of this problem, a distinction must be made between mechanical 
stimuli and those impulses inherent in the organs themselves. The 
sensitivity to mechanical stimuli, such as cutting, crushing, sewing, etc. 
has been much studied, especially since the work of Lennander (77). 
Lennander and Wilms (61) were first of the opinion that only the parietal 
peritoneum was sensitive to pain, because they observed that patients 
experienced no discomfort when the intestine was sutured as in a resection, 
but manipulation of the parietal peritoneum was immediately painful 
as was also ligation of the mesentery. This observation was soon con- 
firmed by Propping, Ritter (62) and many others, so that this point may 
be accepted as established. The part played by the nerves running 
along the blood vessels of the mesenteries is still evaluated differently 
by different workers. Lennander and Wilms held the view that these 
nerves in the mesentery, i.e., in the visceral peritoneum, are less concerned 
in abdominal pain than the nerves in the parietal peritoneum and they 
therefore believe that abdominal pains of all kinds are produced by a THE PERITONEUM 
173 
rubbing of the parietal peritoneal coats (Lennander) or by a “pulling” 
of the same membrane (Wilms). An actual inherent sensitivity of the 
intestines is denied by these writers solely on the basis of the results of 
their experimental investigations with mechanical stimuli. But the 
view of Nothnagel (63) must be more nearly correct; namely, that 
it is not entirely justifiable to compare the sensations which are 
obtained by mechanical stimulation of the bowel with those experi- 
enced when the organs are diseased. Newer work, such as that of Ritter, 
Propping, Kappis and others, also lays more stress on the pain nerves 
which traverse the mesenteries along with the vessels. A. W. Meyer 
(64) showed in animals that these sensory fibres reach from the mesenteric 
attachment approximately half way around the bowel, and the part of 
the intestine opposite this attachment could be gently distended with air 
or otherwise mechanically stimulated without eliciting pain. Naturally, 
such experiments can be of only border line value. It is not very probable, 
on the face of it, that these sensory branches end along a sharp line. 
It is better to assume that they become more sparse, so that there is a 
gradual diminution of sensation from the parietal peritoneum outwards to 
the intestine. The insensitiveness of the part of the bowel opposite 
the mesenteric attachment would then be only relative. This idea 
gains strength from the fact that the zones of sensation in the intestines 
vary widely in different species of animals. The intestine of man, for 
example, is distinctly less sensitive than that of the cat, which in its 
turn, is less sensitive than that of the dog (65). The presence of such 
individual differences is probably the reason a few writers (Ritter) have 
occasionally elicited pain in man by mechanical stimulation of the 
intestines. 
Kast and Meltzer (66), as well as Ritter, found in their animals that 
the intestine is sensitive to pain. They believe that the opposing results 
of other writers are due to their methods, particularly to injury from the 
laparotomy. In surgical practice it can nevertheless be accepted that 
mechanical stimulation in general elicits pain only from the parietal 
peritoneum and from the mesentery, and that the pain from the latter 
is less in degree than that from the former. On this question there is a 
satisfying unanimity of opinion which is daily confirmed at operation. 
But it is an entirely different question how non mechanical sensations, 
especially the pain in peritonitis, ileus, etc. are to be explained. As 
pointed out, a number of writers, like Wilms and Lennander, believe that 
all sensations in the organs of the abdominal cavity are initiated by pulling 
or pressure on the parietal peritoneum. When, as Wilms could show, a 
loop of small intestine is blown up with air, there is sufficient tension on the 
mesentery to produce a round hole when it is incised parallel to the THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
174 
intestine. This makes it plausible that the pain of ileus is a pul- 
ling pain. 
But not every pain in the abdomen can be explained in this way; there 
are many such sensations in the gastrointestinal tract, which cannot be 
considered due to a pulling of the organs. Lead colic, tabetic crises, pain 
of ulcer, and many others might be mentioned (67). In investigations of 
this subject, we are always confronted by the assumption that even if 
the abdominal organs are insensitive to cutting or puncturing or burning, 
they must be able to react with pain in certain kinds of diseases. The 
inherent sensitivity is attributed to the intestinal canal itself and not alone 
to the mesentery or the peritoneum. In addition, Nothnagel (63) states 
that “anemia is a stimulus sufficient to irritate the sensory nerves of the 
intestines; nerves which are otherwise insensitive to external stimuli, ” but 
at present this is not definitely proved, and is opposed by Lennander who 
could elicit no pain by producing anemia of the intestines with the Far- 
adic current. On the other hand, the clinical observation that in arterio- 
sclerosis of the mesenteric vessels, there is often severe abdominal pain 
(68), may be considered an argument in favor of the correctness of Noth- 
nagel’s views. 
The pain in ulcerative processes, particularly gastric ulcers, is said by 
Kappis to be due to the direct irritative effect of the gastric juice on the 
nerves in the lesser omentum running toward its attachment to the intes- 
tines. This opinion is supported by Kappis, among other ways, by the 
injection of turpentine in the stomach wall. At first there is no pain but 
when the fluid has spread out and comes in contact with the roots of the 
greater or lesser omentum, the animal gives evidence of distress. 
The tendency, therefore, of the later writers who have worked on this 
problem is to consider the sympathetic nerves which travel along the 
vessels particularly responsible for the inherent sensitivity of the viscera. 
As a matter of fact, this view is the natural one. Formerly, it was side- 
stepped only because it was taught in normal physiology that stimulation 
of the normal sympathetic did not elicit pain. The many experiments 
on this point have been critically reviewed in an admirable work by Buch 
(59). But now the investigations of Valentine, Brachet and others have 
actually shown that most severe pain is felt when the sympathetic or its 
ganglion is the site of an inflammatory change, as, for example, from 
exposure to the air for a time. It has therefore been argued that the 
experiments on mechanical stimulation of the intestines have not really 
shown what was intended, because no attention was paid to the damage 
done to the nerve by the laparotomy (66). As a result of this demonstra- 
tion that an inflamed sympathetic is painful, we may at least admit the 
possibility that pain sensations in the abdominal viscera can be carried by THE PERITONEUM 
175 
the sympathetic. In the final analysis, the whole question hinges on the 
fact that we are ignorant of the kind of stimulus to which the sympathetic 
responds with pain. May it not be possible that lead, when it produces 
its typical colic, not only stimulates the motor nerves of the intestines and 
causes spasm, but also irritates the sensory nerves in such a manner as to 
produce pain? 
The paths through which these sensory stimuli reach the centers have 
been investigated after nerve section by a number of workers (69). 
Kocher (70) had already described cases in which after section of the 
spinal cord in the upper cervical and thoracic regions a diffuse peritonitis 
ran a painless course. The anatomical details of the course of the sympa- 
thetics and the splanchnics in the cord may be found in the papers of 
L. R. Muller (71). From the nerve sections of Kappis, it is probable that 
pain stimuli from the abdominal viscera are transmitted by way of the 
sympathetics and the splanchnics. Frohlich and Meyer after sectioning 
the spinal cord believe it is the spinal fibres which are concerned, a view 
which is opposed by v. Hoffman (72) and which also disagrees with the 
results of Kappis. 
Finally, we do not know how the pain stimuli reach the centers of 
consciousness for we are not certain of the paths in the spinal cord which 
the sympathetic fibres traverse toward the brain. It has, however, been 
shown by the work of Head (73) that there is close contact in the gray 
matter of the cord between the sympathetic tracts coming from the viscera 
and the spinal sensory nerves from the skin. This is the reason for the 
extreme hypersensitiveness of the latter in many diseases of the viscera. 
The area of skin affected is supplied by sensory fibres from the same seg- 
ment of the cord as that receiving the sympathetic rami communicantes 
from the diseased organ (see also the above remarks on the embryology). 
The best known instances are those occurring in injuries of the brain 
(74) and cardiac diseases, in which the hyperesthesias may often be 
extraordinarily severe, but they may also occur in renal and gastrointestinal 
diseases (75). 
In view of all this, it must be said in summary that even if the pain 
from mechanical stimuli arises almost exclusively from the parietal 
peritoneum and mesentery, i.e., indirectly, we are, nevertheless, capable 
of experiencing certain sensations from pathological processes in our 
viscera, by way of sympathetic nerves arising in the organs themselves. 
Lewandowsky also admits that the muscles supplied by the sympathetic 
system possess sensibility. He assumes that certain stimuli normally 
reach only the spinal cord, but when increased they may suddenly speed 
upwards and then be transmitted as pain to the periphery. He compares 
these processes to those in striated muscles from which we ordinarily do not 176 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
receive sensory impulses, but when an abnormally powerful contraction 
occurs, as in the calf, severe pain is experienced. 
The proximal and distal ends of the intestinal tract, together with 
the bladder, have a separate innervation. This will be discussed under 
the particular organs (75). 
The innervation of the diaphragm requires special mention because of 
the well known fact that pain in the shoulder and neck often occurs in 
affections of the upper abdomen, particularly in those around the diaphragm 
(76). The phrenic nerve which supplies the diaphragm carries both sen- 
sory and motor fibres. It should be mentioned, however, that according 
to the investigations of Ramstrom (77) it is only the more central portions 
of the diaphragm which are supplied on its peritoneal surface by the 
phrenic. The lateral parts are supplied by the sensory nerves of the ab- 
dominal wall. As Ohlecker (78) remarks, it should be assumed that there 
is a transmission of sensations in the spinal cord from the ganglion cells of 
the phrenic nerve to other sensory cells in the same segments (third to 
fifth) (see also 79). 
The question of the functions of the great omentum has occupied the 
imagination and powers of observation of many investigators for years (80). 
Since it is known that an organ with no function atrophies and disappears, 
it is obvious that the great omentum has some duties to perform in the 
economy of the organism. Not only is it doubtful if all its functions are 
known, but in the interpretation of those that are, there is a great diver- 
gence of opinion. The fact that a fatty omentum protects the organs 
covered by it from cold is not to be disputed, but even if Aristotle, Galen, 
and others have considered this as the actual use of the organ, it can very 
well be objected, that a thick layer of fat in the abdominal wall would 
perform the same service (Bromann). This “function” alone therefore 
can hardly justify the existence of this organ. 
The great omentum is not a fat reservoir, as the older writers believed 
(Bauhin, Hensing, Stosch, Glisson, and others), because its fat content 
usually parallels that of the rest of the body. Indeed it sometimes 
happens that an obese body has an omentum poor in fat (81), but we are 
unacquainted with the opposite condition. Still less explicable are the 
views of other authors that the function of the omentum is purely 
mechanical. Their ideas have been summed up in the catch word “plug” 
of the abdominal cavity (82) because it is frequently found in pathological 
bulgings of the abdomen, that is, in hernias. This fact in itself shows only 
the mobility of the organ and is evidence of those conditions which will be 
discussed under intraabdominal pressure. No striking “function” may 
be deduced from this, and just as little from the view that it guarantees 
the roundness of the small intestines and thus favors peristalsis (Fran- THE PERITONEUM 
177 
sen). Attempts have often been made to construct a function from its 
anatomical position. Thus Heusner (83) recently reopened the whole 
question by stating that it acted as a support 6r anchor for the stomach 
and the colon. This view, expressed in such a form is not supported by 
fact, and it naturally provoked animated opposition (Witzel, Schieffer- 
decker, Gundermann (84), Bromann). 
Fabricius ab Aquapendente regarded the great omentum as a reserve 
fold of the stomach. The latter organ folded itself between the leaves 
of the omentum so that when filled, it was partly covered with serosa 
belonging to the great omentum. This hypothesis is also mentioned by 
Cuvier. According to Bromann this could occur in the omentum only 
within 5 centimeters of the stomach. He observes that it is pure hypothe- 
sis to suppose that “our forefathers were such gluttons that they needed a 
reserve fold in the great omentum because of the tremendous dilatation of 
their stomachs.” Gundermann (84) could not satisfy himself from animal 
experiments of the correctness of the belief that this folding occurred. 
The view already advanced by Rivinus and Zigerus that the omentum 
is a regulator of the blood supply of the abdomen, has recently been 
revived by Witzel, Schiefferdecker and Gundermann, and Witzel believes 
that the bloody stools after resection of the omentum result from disturbed 
blood regulation. The ulcerations have already been discussed in connec- 
tion with gastric ulcer and were related by v. Eiselberg (85), for instance, 
to retrograde embolism. Friedrich (86) observed multiple simple anemic 
and hemorrhagic necroses in the livers of guinea-pigs, which may be regarded 
as results of portal thromboses after resection of the omentum. According 
to the view of Gundermann such retrograde embolism points to an insuffi- 
ciency of the valves in the veins of the great omentum. Since these valves 
are present in certain species of animals and absent in others, the varied 
experimental results might be explained by these anatomical peculiarities. 
The appearance of bloody stools, however, does not prove that the omen- 
tum regulates the blood supply if such hemorrhages are due to emboli. 
The same phenomenon has been described after extirpation of the spleen 
(see chapter on spleen). 
Gundermann observed the vessels in the omentum of a dog after 
laparotomy both when the stomach was empty and when it was blown 
up by air, and believes he could see dilatation under the latter conditions. 
But the quantity of blood, which accumulates in the omentum, cannot be 
determined in such an experiment, and it is just this factor which must be 
known, if the function of blood regulator is to be assigned to the omentum. 
This view has not been proved by any means. 
For the surgeon, the great importance of the omentum resides in its 
protective power in infections. It walls off the area of inflammation and 178 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
possibly helps in the destruction of organisms. The anatomical studies 
of Bromann have shown that the omentum first appears in mammals and 
that it must be regarded as a lymphatic apparatus. It is also known that 
it is particularly well developed in carnivora, and Bromann’s explanation 
is the necessity for protection against the greater injury from splinters of 
bone contained in their food to the wall of the gastrointestinal tract with 
its resulting greater likelihood of peritonitis. 
The first experimental investigation of the part played by the omentum 
in infection was done by Roger (87). He extirpated the organ of rabbits 
and guinea pigs and after a short time, injected cultures of staphylococci 
into their abdominal cavities. The animals died in two or three days while 
controls who received the same dose recovered completely. This showed 
that the great omentum is an important protection against infection, but 
gave no clue regarding the mechanism. 
The absorptive process of the peritoneum has been discussed above 
from the general standpoint. The special work on that of the great 
omentum may now be added (88). If animals are killed a short time 
(15 minutes) after the injection into the abdominal cavity of carmine, 
india ink, or bacteria (Gundermann), it will be found that the diaphragm, 
especially the central tendon, is intensively stained, while the omentum 
will not as yet have taken up any of the dye stuff. If a longer time, 24 
hours (Heusner, Koch), is allowed to elapse, the diaphragm will show less 
and the omentum will be deeply colored. The latter not only takes up 
dye particles and bacteria directly into its lymph channels, but also 
receives them from cellular elements (macrophages) which engulf the for- 
eign particles and then wander back into its tissues. This may be termed 
indirect absorption (Koch) (for the origin of the phagocytic leucocytes in 
the abdominal cavity, see Weidenreich and Schott (89)). The lymph 
nodules of the .omentum swell and become plainly visible during this 
taking up of bacteria. In chronic inflammations, e.g., after experimental 
injections of tubercle bacilli in rabbits, the omentum becomes congested, 
swollen and rolled up in 24 to 48 hours, while otherwise the serosa is 
smooth and shiny. Whole parts of organs may also be taken up. Pirone 
(90) ligated the vessels of a rabbit’s spleen and observed that the omentum 
wrapped itself around it and completely absorbed it in less than three 
weeks. Rost (91) observed a similar process around pancreatic tissue. 
As is well known, if pieces of pancreas are introduced into the abdominal 
cavity, the animals die of fat necrosis (see under pancreas). If, however, 
the pancreas is wrapped with omentum, its outline remains unchanged 
for weeks, but the tissue is completely destroyed and infiltrated with 
leucocytes (macrophages). In rupture of the liver, Suzucki (92) found 
liver cells and epithelium from the bile passages in the dilated lymphatics 
of the great omentum. THE PERITONEUM 
179 
This organ is also an important part of the lymphatic apparatus of the 
gastrointestinal tract. Koch (88) by laparotomy introduced bovine 
tubercle bacilli into the intestines of rabbits and found that after several 
weeks, the omentum was covered with tubercles but the bowel mucosa 
was intact. Perhaps the staphylococci which Dudgeon and Roos found 
so frequently in perfectly healthy guinea pigs reached the omentum by the 
same route (93). Pirone (94) even believes that the omentum may 
function vicariously for the spleen, because after the injection of sodium 
taurocholate in normal animals, there is a marked “phagocytic reaction” 
in that organ, while in splenectomized animals, an hyperplasia of the 
lymph follicles in the great omentum appears. How far the omentum 
participates in the formation of antibodies has not been settled. 
It has always seemed remarkable to surgeons how well the omentum 
is able to encapsulate inflammatory processes and to close peritoneal 
defects or ruptures of viscera. This property visualizes the importance 
of this structure as the protective organ of the abdominal cavity. It is 
found very frequently in hernial sacs. If the anterior abdominal wall is 
punctured by a bullet or stab wound, the omentum falls forward and 
closes the opening. If the appendix becomes the seat of inflammation, 
it is covered and protected by this “apron” and, at operation, it has often 
been found that the appendix has perforated into this protecting cavity. 
The abscess therefore remains localized and the remainder of the peri- 
toneum shows no changes worth mentioning. Perforations of the bladder 
may also be plugged and closed in this manner (95). Many animal 
experiments relating to this have been performed (96) but they have only 
verified this well-known clinical observation of the activity of the omen- 
tum in encapsulating abscesses, etc. They give no information concerning 
the forces which bring the omentum to the point of danger. The idea of 
Morison that the omentum purposefully searches for these places is, of 
course, only an unproved assertion which was at once opposed by Beattie, 
Burn and Drummond. The omentum possesses no auto-motive power as 
Rubin showed (97), and clinical observations make it seem probable that 
the omentum encapsulates only when the endangered place is in its imme- 
diate vicinity. Thus it is found, for example, in experimental rupture of 
the bladder, that the omentum does not plug the opening in every case 
(Rost). But it is true that our knowledge of whether the omentum 
actually reaches areas of inflammation outside of its immediate vicinity 
is not certain. We know even less of the forces which could move 
it, but that mechanical factors are most important in determining the 
position of the omentum is shown in a communication by Kraske and by 
Bakes (98). The former describes a case in which an omentum weighty 
with fat, fell toward the diaphragm during a Trendelenburg position, and 180 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
caused the death of the patient. The latter observed in an equilibrist, 
whose performance consisted in walking about on his hands, that the 
omentum was covered over the liver and stomach and after the onset of 
an inflammation resembled a tumor. 
Schiefferdecker believes that at first a thread of fibrin forms which 
shrinks and pulls the omentum but this is contradicted by the fact that 
even in the early stages of inflammation before the fibrin can shrink, the 
omentum covers the affected site. Aug. Mayer (99) believes a movement 
of the organs toward the omentum must be assumed, since, after its 
experimental removal he observed that perforations in the lower parts 
of the intestines reached a position under the remaining portion and 
were thus covered. Furthermore, it is known that increased peristalsis 
will displace the omentum and this is probably the most important factor 
in its movements. After all, it must not be forgotten that the omentum 
is very elastic, and is never really very far from the usual inflammatory 
foci—appendix, gall bladder, tubes, etc. and, therefore, the fact that 
the omentum is always at the right place need not greatly astonish us. 
But it is remarkable that the omentum immediately becomes attached 
to any wound in the serosa and plasters over it. The mechanism of this 
property is still entirely unexplained. Even in free transplantations, 
it preserves its tendency of quickly adhering to underlying structures and 
forming a secure closure. In practical surgery, much use is made of this 
plastic property. Suspicious sutures of the intestines are covered by it; 
the stomach is covered by it to prevent displacement by adhesions after 
gall bladder operations; if in injuries of the liver, the hemorrhage cannot 
be controlled, a piece of omentum is sutured into the wound; in brief, 
these useful properties are called into daily surgical practice (100). 
Especially astonishing are the experiments of Benker, Lanz and Rosen- 
stein (101) designed to minimize the danger of gangrene after resections 
of the mesentery by wrapping the intestine with omentum. Lanz first 
separated the mesentery from its attachment to the bowel for a space of 
5 cm., and then wrapped with omentum the segment of intestine which 
showed all the signs of nutritional disturbance. This operation was 
repeated a number of times on the same animal until finally as much as 
50 cm. of small intestine was separated from its mesentery, and remained 
living. That the same thing can occur in man is shown by cases of Lanz 
and Rosenstein, but other operators were less fortunate (author’s obser- 
vation). At any rate, it does not seem advisable as has been suggested, 
to trust to the plastic power of the omentum, and not resect a portion 
of the colon when it is necessary to ligate the middle colic artery. 
With all these important surgical properties of the omentum, it is clear 
that propositions such as that of Carlsson (102) to remove the omentum 181 
THE PERITONEUM 
in order to establish better drainage of the peritoneum, should not be 
entertained. 
Occasionally torsion of the omentum with the clinical picture of intestinal 
gangrene occurs. Although this condition is rare, it is of general patho- 
logical interest, because studies of torsion of other abdominal organs have 
been stimulated by its occurrence (103). The process is presented most 
clearly in the omentum, but experiment and observation have shown that 
the causes even in this organ are multiple. In the first place, as Riedel 
pointed out, it occurs in hernias. The idea has been expressed that the 
omentum is forced into the hernial sac with a rotary movement, similar 
to that imparted to a bullet by a rifled barrel. But cases in which this 
state of affairs occurred are doubtless very rare. Other relations exist 
between a hernia and omental torsion which are probably of more import- 
ance. That portion of the omentum which finds its way into a hernial 
sac often shows inflammatory changes and becomes transformed into a 
mass of inflammatory tissue. In this manner, the specific gravity of 
separate portions varies and such differences in weight of the several parts 
of intraperitoneal organs are very important, as Payr points out. By the 
introduction of the metal magnesium into the abdominal cavity, he 
obtained cysts in the omentum filled with pure hydrogen, and later found 
spontaneous torsion of the organ in a number of his animals. It seems 
very likely that peristalsis played an active part in the production of this 
condition under those circumstances. In other experiments, torsion was 
found after sewing bits of cork, wood, paraffin, etc. into the omentum. 
Thus he could reproduce experimentally the same physical conditions 
which are present in “unequal growth” of the parts of a tumor, or in 
omental clumps. 
According to Payr, another factor which favors torsion of an organ 
is the greater length of the veins as compared to the arteries. If stasis 
occurs, they stretch and twist, but the arteries remain the same in length. 
Payr could actually show by increasing the venous pressure in models 
and cadavers, that torsion of the omentum, as well as of a number of 
tumors, can be produced by such a “hemodynamic” method. This 
explanation is very plausible, especially in connection with torsions of the 
spermatic cord first described by Nicoladoni (104). 
Intraabdominal pressure has been investigated by many authors and 
its importance was undoubtedly much overrated for a long time (105). 
It can easily be demonstrated by frozen sections of the abdomen that a 
free and empty space does not exist between the various organs. The 
atmospheric pressure resting on the yielding abdominal walls, equalizes 
pressure changes within the viscera by allowing the walls to contract or 
expand, as far as this is not regulated by more or less distention of the air 182 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
filled organs. The atmospheric pressure; in other words, the weight of 
the organs themselves, is therefore, as is really self evident, that which 
determines what has been called, somewhat obscurely, “intraabdominal 
pressure.” The unequal weight of the viscera resting on the different 
parts of the abdomen must vary the pressure in the different parts of the 
abdominal cavity (Horrman). The pressure is less than atmospheric only 
in the region of the diaphragm, because here the elastic lungs exert a certain 
pull which, according to Kelling, is 8 cm. of water during expiration, and 
40 cm. during inspiration. The viscera, therefore, show a tendency to 
rise in the abdominal cavity and in injuries to the diaphragm will enter 
the chest (diaphragmatic hernia). If the chest of a cadaver suspended 
in the upright position is opened, the diaphragm sinks downward and 
with it the viscera. But it must be remarked in this place, that we are 
not completely informed of the movements of the diaphragm during 
respiration. 
Furthermore, if the abdominal organs are in such close contact without 
interspaces, it is reasonable that their relative positions are determined not 
only by the ligaments, etc. attached to them, but also by the fact that 
those organs above rest on those below, as on a cushion. Since the specific 
gravity of the viscera is about one, the pressure in the rectum equals the 
height of a column of water which reaches from the highest to the lowest 
points in the abdominal cavity. Generally speaking, the organs lie on each 
other, and, in the upright position, are from 2 to 3 cm. lower than in the 
prone position. This static pressure may also become negative, as for 
example, in the pelvic organs by elevating the pelvis, when air may enter 
the vagina, to escape on resuming the prone position (“garrulitas vulvae”). 
Similarly, air occasionally enters the bladder during catheterization, and 
during operations in the elevated pelvic position, air is heard hissing into 
the abdominal cavity when the peritoneum is opened. According to 
Schreiber (106), a negative pressure occasionally occurs in the stomach, 
especially during attempts at inspiration with the glottis closed (Moritz). 
Since the organs of the abdominal cavity are easily displaced during 
movements of the intestines, it is clear that those with the greater specific 
weight, liver, kidneys, filled stomach, etc. sink downward if there is a 
change in the tensions of the viscera from relaxation of the abdominal walls 
or of the pelvic musculature. 
Like blood vessels, the hollow organs of the gastrointestinal tract have 
a certain pressure of their own, depending on the tonus of the muscula- 
ture, which changes during peristalsis, etc. These varying pressures 
have been observed experimentally, when balloons were placed in different 
parts of the abdominal cavity (107). The development of this indepen- 
dent pressure is favored by the tension of the abdominal wall and this THE PERITONEUM 
183 
in its turn appears orignially because the walls grow more slowly than 
their contents. 
It is not known with certainty if this independent pressure on and in 
the intestines has any relation to their function. Kelling (108) has shown 
that moderate filling of the intestines has no influence on their internal 
pressure, and that it rises only when the filling is quite considerable. It 
is therefore not necessary to forbid entirely the use of fluids after recent 
operations on the stomach, since moderate amounts do not endanger 
the sutures. This independent pressure has often been mistaken for 
“intraabdominal pressure” (Schatz) and this has led to much 
confusion. 
According to Kelling, the pressure in the abdominal cavity is made up 
of the following factors: 
1. Atmospheric pressure. 
2. Static pressure. 
3. Independent pressure of each organ. 
4. Pressure changes from the action of abdominal muscles. 
5. Pressure changes from respiration and heart beat. 
6. Pressure on organs from the special position of the body. 
7. Pathological pressure from overfilling of the abdominal cavity from 
a normal passive tension of the abdominal wall. 
Ordinarily the abdominal walls exert no pressure on the viscera except 
when they are tightly contracted, and vice versa, their tension is increased 
by conditions such as ileus in which the pressure in the intestines is 
especially high. This will be referred to in speaking of ileus. The influence 
of respiration and heart beats need not be discussed. Slowly growing 
tumors, pregnancy, etc. do not lead to an increase of pressure because of 
the elasticity of the abdominal walls (Hormann (105), p. 553). Whether 
the “relaxation hyperemia” of which Wagner speaks is really due to 
removal of the pressure when the abdomen is opened, or whether it is due 
to the inflow of cooler air, is not as yet decided. Nor has it been definitely 
shown that the better results obtained in the treatment of peritonitis by 
closing the abdominal cavity to a small drain, are due to a re-established 
intraabdominal pressure (Notzel (31), Guleke (109)). 
In the origin of enteroptosis, a special importance has been attached to 
this pressure (no). This is undoubtedly justified insofar as the separate 
factors concerned in pressure and tension are able to determine the 
position of the organs. 
The purely mechanical factors in the production of enteroptosis are 
as follows: 
1. General enlargement of the abdominal cavity. The enteroptosis 
in individuals with a pendulous abdomen is viewed by many surgeons 184 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
(hi) as a special form (maternity enteroptosis) and is separated from 
other forms (virginal enteroptosis). Physiologically, such divisions are 
always somewhat arbitrary; but they serve a useful purpose. The im- 
portance of the abdominal walls in maintaining the relative position of the 
viscera may be illustrated under the fluoroscope not only in individuals 
with enteroptosis and lax abdominal walls, but in normals as well, by 
placing a well fitting abdominal binder in position, when the abdominal 
organs will be forced upwards (113). 
Hernias and weakness of the muscles of the pelvic floor are of less 
importance. As a subdivision but more because of its historical interest, 
the view of Glenard (114) through whose work the whole problem of 
enteroptosis was brought to the front may be mentioned. He believed an 
emptyness, i.e., shrinking of the bowel and with it of the entire abdominal 
contents, was especially important in the development of this disease. In 
general, however, an emptyness of the intestines points to a secondary 
and not a primary disease. 
In contradistinction to general enlargement, a second mechanical 
condition in the origin of an enteroptosis is a diminution of one portion of 
the abdominal cavity, that is, of the hypochondrium. A low position of 
the diaphragm as it occurs in emphysema or tuberculosis (115) is accom- 
panied in quite a large percentage of cases by splanchnoptosis even if only 
of mild degree. Thus Bial (116) found splanchnoptosis eighteen times in 
26 cases of emphysema. According to the opinion of most writers, how- 
ever, tight lacing either with a corset, skirt band, or belt is a more import- 
ant factor in this particular type. Tight lacing, first, compresses the 
hypochondrium directly and secondly, it interferes with respiration by 
fixing the thorax, and this is also of importance in determining the position 
of the viscera. 
These injurious mechanical factors just mentioned, unquestionably 
operate in a large number of individuals who show no sign of enteroptosis. 
There is a type of chest, long, narrow, and flat, with which a diminished 
capacity of the upper abdominal cavity is associated and which occurs 
without any kind of lacing. This has led to the opinion that the mechanical 
factors are only secondary influences in splanchnoptosis, and that the 
actual cause is a constitutional weakness of the tissues. Stiller (117) 
describes the “habitus enteropticus” as an individual with long flat chest, 
down hanging ribs, slightly pendulous abdomen, slight build, particularly 
of the skin and bones, potential hernias, tendency to flat feet; in brief, it is 
the type which was formerly characterized as “phthisical.” There is 
undoubtedly a great deal of truth in this opinion that the mechanical 
factors are only secondary, and that constitutional weakness is the primary 
cause. But it must not be forgotten that it is actually in the “habitus THE PERITONEUM 
185 
enteropticus” that all these mechanical conditions which favor descent of 
the viscera are present to their greatest degree. 
The causes, therefore, of enteroptosis should be regarded first as tissue 
weakness, and second as mechanical, and these two may often be combined. 
In certain cases the constitutional cause is the more important; in others, 
vice versa. Just as the causative factors must be judged, so must the 
discomforts be considered from something more than a general viewpoint. 
Undoubtedly, pulling-pains or the sensation of weight in the abdomen can 
be explained by enteroptosis, but the symptoms are usually of a more 
general nature. In this connection, certain experiments of Emma Schulz 
(118) are of interest. Flethysmographic measurements of the arms of 
normals and of individuals with enteroptosis showed that, in the latter, 
there was no increase in the size of the arm after changes in the position of 
the body, perhaps because of venous stasis. A filling of the arm as in the 
normals, could, however, be obtained in the enteroptotics after lifting up 
the viscera. 
In practice, and especially in treatment, the maternal and the virginal 
forms of enteroptosis have always been differentiated (see among others, 
Rovsing (hi)). The mechanical factors will be credited with great 
importance only cum grano salis, in this type, i.e., the enteroptosis with 
pendulous abdomen. Consequently an abdominal binder which supports 
the pendulous abdomen, will often work wonders, as will eventually per- 
haps an appropriate operation (119). In the virginal enteroptosis, on the 
contrary, there is usually a constitutional weakness at work, in which the 
ordinary treatment, fixation of single organs, only influences a symptom 
without curing the disease. The results of therapeutic measures must be 
viewed from this standpoint. A suitable interference is, to begin with, 
not unjustified, but it must be evaluated correctly. 
For the development of hernias and for the positions of the abdominal 
organs, the firmness of the peritoneum, as well as the intraabdominal 
pressure is important. The first investigations in this field were performed 
by Scarpa (120). Moro (121) revived and amplified his experiments by 
testing the resistance of the peritoneum of dogs and cadavers to pneumatic 
pressure, both in situ and after excision. He found that the resistance 
of the parietal peritoneum in man is very high and exceeds in its mean, 
one atmospheric pressure. The elasticity is also very great, indeed 
almost absolute. Experimentally, the membrane tears before it is possible 
to overcome this elasticity. The resistance and elasticity of the peritoneum 
forming a hernial sac are even greater. It cannot, therefore, be accepted 
that a hernia enlarges through stretching of its sac, but either because it 
actually grows, or because additional peritoneum slides in from the abdom- 
inal cavity. This sliding of the peritoneum could not, it is true, be demon- 186 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
strated experimentally by increasing the intraabdominal pressure after 
dissecting free a piece of the membrane from the abdominal walls. But 
that such a process can occur under pathological conditions is shown by 
the so-called slide hernias. Evidently, in patients with this condition, 
the attachment of the peritoneum to its supporting structures is less 
firm than in the dogs used for these experiments. How often such a 
sliding of the peritoneum occurs in ordinary hernias is difficult to estimate. 
It can only be said that there are large hernias which develop very slowly 
(particularly umbilical hernias) in which the union of the hernial sac to the 
hernial opening is so firm that the possibility of a sliding can be excluded. 
The looseness and elasticity of the peritoneum is, in addition, a very 
considerable protection against infection as pointed out by Danielson 
(37). Extraperitoneal abscesses push the serosa forward, and do not 
usually perforate, and an empyema of the gall bladder may stretch the 
serosa covering it many times before perforation occurs. 
Before the most important disease of the peritoneum—peritonitis— 
is discussed, the physiology and pathology of the intestinal tract must be 
considered. 
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19. Nelaton: Des epanchements de sang, These de Paris, 1880, p. 27. THE PERITONEUM 
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37. Danielsen: Bruns Beitrage, 1907, V. 54, p. 458. 
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39. Kuttner: Bruns Beitrage, 1903, V. 40, p. 136. 
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42. Metschnikoff: In Kolle-Wassermanns Handbuch d. pathogenen Mikroorganism, 
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48. Wegner: Arch. f. klin. Chir., 1876, 20, p. 106. 
49. Borst: Das Verhalten der Endothelien bei der acuten and chronischen Entzundung 
usw. Wurzburg, 1897. 
50. Schrader: Deutsche Ztschft. f. Chir., 1903, V. 70, p. 421. 
51. Pal: Jahrbucher der Wiener Aerzte, 1888. Schmid: Pflugers Arch., 1909, 126, 
176-192. 
52. Mall: Arch. f. Anat. u. Physiol., 1892, p. 419. 
53. Meisel: Bruns Beitrage, 1903, V. 40. 
54. Lewandowsky: Handbuch d. Neurologie, 1, p. 308-417. 
55. Langley in Asher-Spiro: Ergebn. d. Physiol., 1903, V. 2, p. 808 and Meyer, Gott- 
lieb: Exp. Pharmakol., 2, Ed. p. 126. 
56. Gegenbaur: Lehrbuch d. Anat., 1899, 2, p. 523. 188 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
57- Strehl: Arch. f. Klin. Chir., 1905, V. 75, p. 726. 
58. Popielski: Arch. f. Anat. and Phys., 1903, p. 338. 
59. Neumann: Mitt. a. d. Grenzgebiete, 1910, V. 13. Kappis: Mitt. a. d. Grenzge- 
bieten, 1913, V. 26. Exner and Jager: Mitt, aus d. Grenzgebieten, 1909, 20, 
p. 645. Buch: Arch. f. (Anat.) u. Physiol., 1901, 197. 
60. Lennander: Zentralbl. f. Chir., 1901; Mitt. a. d. Grenzgebieten, V. 10, 15, 16; 
Deutschr Zeitschr f. Chir., 1904, V. 73. 
61. Lennander und Wilms: Munch, med. Wochensch., 1904; Mitt. a. d. Grenzgebieten, 
V. 16; Deutsche Zeitschrift. f. Chir., 100; Mfed. Klinik, 1911, No. 1. 
62. Ritter: Arch. f. klin. Chir , V. 90. Propping: Bruns Beitrage, V. 63. 
63. Nothnagel: Arch. f. Verdauungskrankheiten, V. 11. 
64. A. W. Meyer: Mittelrh. Chirurgentag, July, 1914 Deutsche Zeitschft. f. Chir., 
i9I9, V. 151. 
65. Franke: Berliner Klin. Wochenschft., 1912, p. 1997. Engelhorn: Zeitschft. f. 
Geb. u. Gynak, 1911, V. 69, p. 66. 
66. Kast und Meltzer: Mitt. a. d. Grenzgebieten, V. 19. 
67. L. R. Miller: Mitt. a. d. Grenzgebieten, 1908, 18, No. 4, p. 614. Kuttner: Ueber 
abdominale Schmerzanfalle in Albus Sammlung zwangloser Abhandlungen aus 
dem Gebiete der Verdauungs. u. Stoffwechsel krankheiten, V. 1, No. 3. 
68. Ortner: v. Volkmanns Sammlung, No. 347. 
69. Frohlich and Meyer: Wiener klin. Wochenschft., 1912, p. 29. 
70. Kocher: Mitt. a. d. Grenzgebieten, 1896, V. 1. 
71. L. R. Muller: Deutsche med. Wochenschft., 1911, Mitt. a. d. Grenzgebieten, 1908, 
V. 18. Arch. f. Klin. Med. 1911, V. 105. 
72. V. Hoffmann: Mitt. a. d. Grenzgebieten, 1920. 
73. Head: Die Sensibilitatsstorungen d. Haut bei Viszeralerkrankungen (August 
Hirschwald, 1898). 
74. Wilms: Mitt. a. d. Grenzgebieten, n, 697. Forderreuther: Ueber Headsche 
Zonen bei Viszeralerkrankungen Inaug. Diss. Heidelberg, 1913. 
75. Zimmermann: Mitt. a. d. Grenzgebieten, V. 20, p. 445. 
76. Nothnagels: Handbuch, V. 14, p. 570. 
77. Ramstroem: Mitt. a. d. Grenzgebieten, 1906, V. 15, p. 642. 
78. Ohlecker: Zentralbl. f. Chir., 1913, p. 852. 
79. Hess: Munch. Med. Wochenschft., 1906. 
80. Brohmann for lit.: Die Entwickelungsgeschiehte d. Bursa omentalis usw. Wies- 
baden., 1904. Bergman. Ders. Ergebn. d. Anat. u. Entwickelungsgeschiehte, 
1905, 15, p. 394. Ders. Hdbch. d. Audt. d. Mensch. v. Bardelebeu, V. 6, 3, 2, 
p. 98. 
81. Schiefferdecker: Deutsche med. Wochenschft., 1906, p. 988. 
82. Fransen: Zeitschft. f. angeu Anat. u. Konstitutionslehre, 1914, V. 1, p. 258-268. 
83. Heusner: Munch. Med. Wochenschft., 1905, p. 1130. 
84. Gundermann: Brun’s Beitrage, 1913, V. 84, p. 590. 
85. v. Eiselberg: Arch. f. klin. Chir., V. 59. 
86. Friedrich: Arch. f. klin. Chir., V. 61. 
87. Roger: La semaine medicale, 1898, 18, p. 79. 
88. Roser: Inaug. Diss. Strassburg, 1907. Koch: Med. Klinik., 1911, No. 51, and 
Zeitsch. f. Hyg., 1911, V. 69. Stuzer: Diss. Petersburg, 1913, Ref. Zentralbl. 
f. d. ges. Chir., 2, p. 635. Heger: Cited by Bromann. 
89. Weidenreich: Anatomkongress 20th. Schott: Arch. f. mikroskp. Anatomie, 1909, 
V. 74. 
90. Pirone: Arch. ital. Biol. F., 1903, 2, (Ref.) THE PERITONEUM 
189 
91. Rost: Unpublished. 
92. Suzucki: Virchows Arch., V. 202. 
93. Dudgeon and Roos: Am. Journ. of Med. Sciences, V. 132, p. 37. 
94. Pirone: Cited by Danielson, Bruns Beitrage, 54, p. 468. 
95. Rost: Munch. Med. Wochenschft., 1917, No. 1. Cornil and Carnot: La semaine 
med., 1898. 
96. Morison: Brit. med. Journ., 1906, p. 76-78. Enderlen- Deutsche Ztschft. f. Chir., 
V._55. 
97. Rubin: Surg. Gynec. and Obstetr., 1911, V. 12. 
98. Kraske: Chirurgenkongress, 1904. Bakes: Arch. f. klin. Chir., 1904, V. 72, p. 70. 
99. Aug. Mayer: Munch, med. Wochenschft., 1912, 59, p. 2497. 
100. Hesse: Brun’s Beitrage, 1, 82. 
101. Rosenstein: Deutsch. Chirurgenkongress, 1909, 1, p. 172. Benker: Inaug. Diss. 
Heidelberg, 1893. 
102. Carlsson: cited in Hygiea, 1898. 
103. Payr: Arch. f. klin. Chir., 1902, V. 68. Deutsche Zeitschft. f. Chir., V. 85, p. 392. 
Pretsch: Bruns Beitrage, V. 48. Riedel: Munch. Med. Wochenschft., 1905. 
Hadda: Bruns Beitrage, V. 48. Lit. see Hochenegg. Wiener klin. Wochenschft., 
1900, p. 291. Finsterer: Bruns Beitrage, V. 68. 
104. Nicoladoni: Arch. f. klin. Chir., V. 31. 
105. Weisker: Schmidts Jahrbucher, V. 219, p. 277. Moritz: Zeitschft. f. Biologie, 
1895, V. 32. R. Meyer: Zentralbl. f. Gyn., 1902. Schatz: Verh. d. Deutsch. 
Gesellsch. f. Gyn., 4. Kongress Leipzig, 1892, 173. Kelling: v. Volkmanns 
Sammlunz klin. Vortrage No. 44. Hormann: Arch. f. Gyn., 1905, p. 527 (lit.) 
106. Schreiber: Deutsch. Arch. f. klin. Med., 1883, V. 33. 
107. Kertecz: Deutsche Med. Wochenschft., 1903, and Berlin klin. Wochenschft., 1904. 
108. Kellung: Arch. f. klin. Chir., 1900, 62, 1, p. 14. 
109. Guleke: Bruns Beitrage, 1908, V. 60, p. 673. 
no. Lit. Burchardt Splanchnoptose in Ergebn. d. Chir., 1912, V. 4. -Also Wiedhopf, 
Deutsche Zeitschrft. f. Chir., V. 128. 
in. Rovsing: Die Unterleibschirurgie, F. C. W. Vogel, 1912. 
113. See Borbjarg and Fischer: Arch. f. Verdauungskrankheiten, 1912, V. 18, No. 4. 
114. Glenard: Les ptoses viscerales, Paris, 1899. 
115. Fleiner: Munch, med. Wochenschft., 1895, No. 42-45. 
116. Bial: Berlin, klin. Wochenschft., 1896, p. 1107. 
117. Stiller: Grundzuge der asthenie, Enke, 1916. 
118. Emma Schulz: Arch. f. klin. Med., 1914, V. 113, p. 402. 
1x9. Wiedhopf: Deutsche Ztschft. f. Chir., V. 128. 
120. Scarpa: Reale Stamperia Milano, 1809. 
121. Moro: Brun’s Beitrage, 1909, 63, p. 208-225. CHAPTER VII 
INTESTINES 
The length of the small intestine varies considerably, with extremes 
of and 8 meters, and according to Dreike’s measurements, a mean of 
about 6 meters (i). In childhood, according to the same author, the 
length of the small intestine is relatively greater than in adults; it is longer 
in men than in women, and in vegetarians than in those who eat meats; 
therefore, the small intestine, generally speaking, is longer in the poorer 
classes than in those more affluent. Beneke (2) states that for every 100 
cm. of body length there are about 387.5 to 389 cm. of small intestine, and 
91.5 cm. large intestine, but these figures do not hold for those races which 
are more purely vegetarian, as examinations of Japanese have shown. 
The intestines are possessed of great vitality. In the experiments of 
Enderlen (3), loops were transplanted into the urinary bladder, etc. and 
Esau (4) who transplanted portions under the skin, found the coats intact 
microscopically even after separation of their entire mesentery. 
Intestinal secretion is studied by means of so-called Thiery’s, Vella’s 
or Pawlow’s fistulse by which a section of the intestine is necessarily isolated 
(5). Even if the true physiological processed of secretion are not maintained 
ideally in such fistulae, approximate knowledge of the mechanism and 
character of secretion is nevertheless gained. It must not be overlooked 
that what is investigated by such methods is not only secretion, but also 
absorption. The two cannot be separated. The net result is that the 
quantity which is actually secreted is not definitely known and this is 
especially unfortunate for comparison with pathological conditions. 
In the intestinal juice, from both small and large intestine, a thin fluid 
secretion is differentiated from a semi-solid slimy material. The first 
carries the enzymes, one of which, the enterokinase, which activates tryp- 
sin, has already been met in discussing the pancreas. Another enzyme of 
the small intestines, the erepsin (6) does not split native albumen, with the 
exception of casein, but reduces the disintegration products of proteins, 
the albumoses and peptones, to crystalline substances. Among others 
may be mentioned arginase (found only in the mucosa and not in the 
secretions), nuclease, lipase, and various carbohydrate splitting enzymes. 
Of the latter, the lactase is particularly interesting, because, according to 
Weinland (7), it is present only during the suckling period, but may re- 
190 INTESTINES 
191 
appear in adult animals if they are fed regularly on milk sugar. Adolf 
Schmidt (8) believes that it is the absence of lactase in adults which is the 
cause of the diarrheas occasionally occurring in individuals who drink 
milk after having been unaccustomed to it for a long time. These individ- 
uals, however, easily reaccustom themselves to this diet. The purely 
diastatic enzymes of the intestines have only very weak powers. 
Secretion takes place only when certain stimuli of mechanical or chemi- 
cal nature reach the bowel wall. During starvation the intestinal mucosa 
produces no secretion; during hunger practically nothing flows from a Vella 
fistula, but secretion starts at once when a tube is placed in the opening, an 
observation not entirely without surgical interest (9). Of chemical sub- 
stances, gastric juice, 0.5 per cent, hydrochloric acid, mustard oil, butyric 
acid, calomel, soaps and many others, stimulate secretion, but a very thin 
fluid, poor in enzymes, is poured out in response. To obtain a fluid rich 
in ferments and particularly rich in enterokinase, it is necessary that 
pancreatic secretion be present at the same time. Provision is thus made 
that the trypsin, inactive as it pours from the pancreas, is activated by 
the enterokinase which is secreted in abundance at the place where the 
splitting of proteins is designed to take place. There are also other ex- 
amples which show the extraordinary purposefulness of the processes of 
intestinal secretion. If a woolen thread is placed in a fistula, a thin fluid 
is excreted; if peas or splinters of glass or similar objects are introduced, 
the fluid becomes much thicker. This,* according to all investigations, 
obviously serves to envelop and glue together solid particles of food, and 
thus protect the mucosa (10). It is possible that the thick fluid also 
checks absorption, similar to the mucoid like factor in medicinal emulsions. 
That the secretion of intestinal juice is also dependent on the nerve supply 
is shown especially well in the so-called “paralytic” secretion. If all the 
nerves which lead to the loop in which a fistula has been made, are severed, 
an enormous secretion begins in a few hours, lasts for about 24 hours, and 
then is gradually abolished. During this paralytic secretion, the blood 
vessels are widely dilated and there is active peristalsis. It is usually 
assumed that inhibitory impulses are eliminated (n), but whether a 
hormonal as well as a nervous stimulus is concerned as in the pancreas, 
has not as yet been determined. 
The secretion oj the large intestine is not only less in quantity (a sixth 
to a seventh) but also less rich in enzymes, particularly in those which 
digest native proteins (in the small intestine there is trypsin and enterokin- 
ase). The fluid from fistulse in the large intestine is therefore much less 
irritating to the skin. The thin portion is quickly absorbed, while the 
thick portion forms the chief part of the feces. Feces, indeed, are not as 
the layman believes, composed of only undigested residue; food remains 192 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
are really only a small fraction, and the chief bulk is formed of secretions 
or excretions of the intestinal canal plus bacteria. Thus in an isolated 
loop, closed at both ends, so much feces collect from secretion of the mucosa 
that rupture finally takes place (Hermann’s fecal ring (12)). For this 
reason, a closed loop of bowel is never replaced in the abdomen if for any 
reason it cannot be resected; but is always sutured into the abdominal wall 
and a fistula established (13). A starving man also forms feces, as can 
be seen daily during certain after treatments in laparotomies. Fr. Muller 
(14) has estimated the amount of feces passed by professional fasters 
during a period of starvation; he found about 4 grams (3.818) to be the 
daily average. The moist feces weighed 22.01 grams. In an individual 
who is taking normal food, the amount is greater because all the glands 
along the intestinal canal, especially the liver and pancreas, are actively 
secreting; to this amount must also be added the residue of food which 
contains much insoluble material, for example, cellulose. But the actual 
amount of remnants depends not only on the kind and quantity of the 
ingested material, but also on individual pecularities of the intestine itself. 
One normal individual may bring the same food material, especially 
cellulose, into solution, better than another (15). The old folk idea of 
“sensitive bowel” is thus confirmed by modern investigations. 
Furthermore, the quantity oj intestinal contents depends on the quantity 
of fluids ingested. If an artificial hyperaemia is produced by large infu- 
sions of saline solution (16), the iatestines will accumulate a fluid feces-like 
material in such amounts that vomiting occasionally occurs. The intes- 
tinal wall will then become edematous. 
Absorption from the bowel is not a simple physical process which can 
be explained solely by filtration or osmosis, but it depends on a “vital” 
activity of the intestinal epithelium. Writers are not agreed as to how far 
intraintestinal pressure influences absorption (17), but the experiments 
of Enderlen and Hotz (18) have shown that it is not increased, but 
decreased when stasis occurs in any portion of the bowel. 
Water is very quickly absorbed in the uppermost portions of the small 
intestine and it is possible to make the stool fluid by saline infusions (15), 
only when large amounts are introduced. 
The elective activity of the epithelium is shown even with salts; 
some are absorbed very easily and some with difficulty or only in minute 
quantities (19). Among food materials, the proteins are absorbed only 
after they are completely broken down to amino acids, or at most peptids, 
which, according to the present day conception, suggests that the body 
does not tolerate foreign proteins in its fluid. When a foreign protein in 
the food is broken down in the bowel, the body constructs from these 
building-stones a protein molecule which is specific for it, and which it INTESTINES 
193 
can utilize, and this synthesis of the specific protein molecule is probably 
begun in the intestinal wall, since thus far it has not been possible to 
demonstrate amino acids or peptids in the blood coming from the intestines 
(20) (see under Liver). Carbohydrates are usually absorbed only in the 
form of monosacharides, fats only when the various fat splitting enzymes 
and the bile have brought them into a soluble form. Fats, such as 
lecithin, which resist this solvent action are therefore not absorbed, but 
fat globules can readily be demonstrated just under the epithelium, a proof 
that the synthesis of fat, that is, the union of glycerin and fatty acids, has 
already been accomplished in this place. 
The absorption of the food is practically completed in the small intestine 
(21) and according to Kaoru Omi (Rohmann), Frey (22) and others, more 
fluids and sugar are absorbed in the jejunum while the ileum absorbs more 
proteins and fats. It is only in over-nutrition or in catarrhal conditions 
which injure the mucosa, that a noteworthy amount of food will pass 
through and enter the colon. This applies, of course, only to food free 
of detritus, not to food rich in cellulose. The latter is hardly touched 
in the small intestine and is split only by the bacteria in the colon. With 
this knowledge, a patient in whom it is necessary to establish a fistula of the 
small intestine will be given food as free as possible from detritus. Chopped 
meat is the best, so that in spite of the fistula he will obtain sufficient 
nourishment without being troubled with excess leakage. The much 
favored barley soup is less useful because, according to Heile’s investiga- 
tions, it forms large amounts of feces. 
In comparison to that of the small intestine, the absorptive power 
of the large intestine is very small. Unchanged protein is not absorbed 
at all. About 20 per cent, of the sugar is taken up and certain amounts 
of split proteins. Water is absorbed in about half its amount, and this 
fact is useful clinically when patients, who cannot drink after operation, 
are given the necessary water by the drop method. Since alcohol is also 
well absorbed, wine and sugar are added to the fluid. Furthermore, the 
colon seems to be of importance in the absorption of alkali, but we are 
not particularly well informed of this fact, especially concerning its patho- 
logical physiological importance. 
The motive power of the intestinal movements lies in the musculature, 
of which there is a longitudinal and a circular layer. Ganglion cells are 
embedded in the former. In the colon, the longitudinal muscle, which is 
arranged tape-like, is differentiated from the circular muscle which 
surrounds the bowel with one continuous layer. Roith (23) assumes 
that the amount of circular muscle becomes greater as the anal end is 
approached but Rost’s planimetric measurements have disproved this 
idea (24). The longitudinal layer is arranged tape-like to the sigmoid 194 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
flexure, and cannot be compared functionally to that of the ileum without 
reservation, since it is, according to Rost, in almost the same state of 
contraction as the circular musculature. The tapes act functionally 
like elastic bands and by their tension keep the bowel shortened and 
cause the formation of those depressions formed between the plicae 
semilunares. 
The following methods have been used to observe the movements 
of the intestines under physiological conditions. First, observation on 
an excised organ or after laparotomy, when it is necessary to cover the 
intestines with Ringer’s or Tyrode’s solution to preserve the approximate 
physiological conditions; second, by means of the #-ray, and third, by 
means of an insert of a transparent celluloid window in the abdominal 
wall, according to the technic of Katsch and Borcher (25). Each of these 
methods has its justification, each has its advantage and disadvantage, 
none is absolutely superior to the other. 
If we study first the movements of the small intestine, exclusive of those 
of the muscularis mucosae, we differentiate a “mixing movement” and 
a so-called peristaltic wave, the latter of which drives the chyme forward. 
The mixing movements which arise from rhythmic contractions of the 
intestinal muscles are of two kinds: kneading, from simultaneous contrac- 
tion and relaxation of the longitudinal and circular muscles (Cannon), 
and pendulum movements from alternate contraction and relaxation of the 
muscle layers of segments of bowel of varying lengths (Starling, Magnus 
(26)). Whether these mixing movements serve as their name implies, 
only to mix the chyme, or whether, as Rieder emphasizes, they are of 
great importance in food absorption by influencing the local blood and 
lymph circulation, has not been decided. Still another form of movement 
has been called Exner’s needle reflex. This consists of contractions and 
relaxations of the muscularis mucosae when the mucosa is irritated by 
a sharp object such as a needle or a splinter of bone. It bulges out and 
attempts to force the pointed end downwards. In its purpose,, this move- 
ment is typical of the general movements and reflexes of all smooth muscle. 
Thus pins, etc., which have been swallowed point downward, are turned 
in the bowel and pass onward, head first. This “marginal current,” 
as it is also called, can be directed either toward the anus or toward the 
stomach, and is independent of the direction of movement of the centrally 
placed intestinal contents, which, of course, are always directed toward the 
anus. It is demonstrable in the stomach as well as in the small and large 
intestines. If corpuscular elements are introduced in an enema, the small 
particles can be carried far upward by this marginal stream, so that 
Grutzner (27) who made these investigations, found lycopodium granules 
which had been injected in an enema, in the stomach. But these findings, INTESTINES 
195 
by no means prove a true anti-peristalsis of the bowel contents. In 
fact, it is possible that the reversed direction of the marginal current in 
Grutzner’s experiments, was due to the sodium in the sodium chloride 
solution, for Nothnagel (28), had observed that the other muscle layers 
of the intestines also showed an ascending wave of contraction if he 
touched the intestine with a sodium salt. Grutzner especially empha- 
sizes that he could demonstrate the lycopodium in the colon and ileum 
only if it was suspended in saline solution; if he used water the granules 
remained in the rectum. 
The peristaltic wave serves to move the bowel contents forward and 
consists of contraction of one segment and relaxation of the next segment 
toward the anus. Like the mixing movements these peristaltic waves are 
stimulated by distention of the bowel; an empty loop lies quiet and motion- 
less. But progressive movement begins only when a certain internal 
tension is reached and is not merely proportional to the state of filling of 
the intestine. This was shown by Trendelenburg (29) who used the 
intestines of guinea pigs, which are particularly well adapted to such 
experiments because the mixing movements and the changes in tonus are 
absent. This principle of filling the bowel is, of course, often used ther- 
apeutically to produce a quicker emptying, for example, when a saline 
cathartic is given, its osmotic pressure prevents the absorption of fluid 
from the stomach and upper intestines, and therefore provides the neces- 
sary filling of the bowel to stimulate peristalsis, and a quicker emptying 
of the small intestines results. Furthermore, the “peristaltic effect” 
also depends, according to Trendelenburg, on the rapidity with which the 
bowel is filled; a fact which explains the well known laxative effect of 
a glass of water, which is taken in the morning on an empty stomach. 
If the filling takes place too slowly, peristalsis frequently does not occur 
at all, but this approaches the pathological. Later, in discussing peritoni- 
tis, it will be seen that the so-called intestinal paralysis is simply a result 
of distention and not its cause. This overdistention must, therefore, 
be guarded against in giving saline cathartics in cases of chronic ileus 
or similar diseases. 
'fhis “classical” form of peristalsis in which the feces are moved for- 
ward step by step, is, according to the general opinion, the usual way in 
which the intestinal contents are transported. There is, however 
another movement—the so-called “rolling movement” or peristaltic 
rush, in which the contents are forced very quickly through longer stretches. 
Some authors believe that this is nothing but an increase of normal 
peristalsis, but this has not been proved. It seems easier to believe that 
in this type of movement a sort of “squirting mechanism” is involved, 
and Albert Muller’s (30) well-known experiments give substantial support 196 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
to this idea. With Hesky and Kondo, he showed that dogs, in which 
large areas of longitudinal and circular musculature of the small and large 
intestine were removed, still had normal fecal evacuation. Removal 
of the longitudinal musculature alone led to a certain resistance in the 
denuded area, but not to absolute obstruction. This fact can be explained 
in but one way, viz., that the segment of intestine above the part devoid 
of muscle is capable of squirting its contents through the immovable 
portion. David’s (31) x-ray studies in which he showed that the masses 
of bismuth slide forward rather rapidly in a tape like manner also seem to 
favor such a theory. 
The much discussed question of “anti-peristalsis” assumes a new mean- 
ing if regarded from this viewpoint. But the anti-peristalsis of the small 
intestine and that of the large intestine must be differentiated. In very 
elaborate investigations, consisting of resections, reversal and reuniting 
of loops of small intestine, a number of workers attempted to solve the 
problem of the actual existence of anti-peristalsis (32). Some of the 
investigators reversed the small intestine throughout almost its entire 
length and found that not only was defecation regular but their animals 
remained in nitrogen equilibrium; therefore, Muhsam, Enderlen and 
Hess concluded that an anti-peristalsis was actually one of the movements 
of the small bowel. Curiously enough, this conclusion was completely 
rejected by Putz and Ellinger on the basis of investigations quite similar 
in principle to those of the former. From the presence of a large amount 
of indican in the urine, from the dilatation of the bowel above the reversed 
loops, and particularly from observations of the intestines in a saline bath 
after the injection of pilocarpine, these authors concluded that a reversed 
movement did not take place. But the fact remains that feces are moved 
forward through the reversed loops and in conjunction with Muller’s 
findings, that defecation is normal in a dog, even after complete removal 
of its bowel muscle, it really seems probable that peristaltic waves are 
not the exclusive agents which move the feces, as has always been assumed. 
Perhaps, as stated above, a squirting mechanism is very important after 
all. Further investigations of this question are very necessary, particu- 
larly x-ray examinations, to show how chyme passes through reversed 
loops. 
It is due to a combination of these different movements that portions 
of small intestines always resume their proper place in the abdominal 
cavity, no matter where they are put. This fact, observed often enough 
at operation, has been studied with the x-ray by Bose and Heyrovsky (33) 
who marked the part in question by suturing birdshot or similar objects 
in its wall. Observations through windows in the abdominal wall have 
shown that the position of the intestines varies with the kind of food 
consumed (Plenge, personal statement). INTESTINES 
197 
The colon, also, is not usually at rest, as is often assumed, but is always 
moving, though slowly. The x-ray examinations of Schwarz (25) show 
that there are two pronounced kneading movements, a bulging out and a 
pulling in of the wall, and displacement of the loop first toward the anus 
and then toward the stomach, usually around a fixed point. These 
alternate with the so-called large pendulum movements designated by 
Raiser (34) as “waving” movements. These “mixing and kneading 
movements” are seen principally in the proximal colon where the feces 
first come to a stop; but they also occur in other segments. 
The second group of movements described move the contents forward. 
These must be differentiated into two forms; first, slow peristaltic con- 
tractions, and second, the so-called great colon movements; both occur, 
doubtless, coincidently in the same individual. A controversy exists only 
as to whether certain of the movements should be regarded as the 
beginning movements of defecation, but this question is of little practical 
importance. This great colon movement, indeed, is the first which has 
been observed in man with the x-ray. Holzknecht (25) saw, in a patient 
with presumably normal bowel, that a bismuth meal, which had filled the 
left flexure, was pushed from the transverse into the descending colon; 
within a few seconds, the constrictions of the transverse colon disappeared 
and rest then supervened. The patient had no perception of this colonic 
movement. Holzknecht later made a similar observation; since then, 
such great colon movements have not been seen, but by serial pictures 
taken at half-hour intervals, it can be satisfactorily shown that such 
movements must have taken place between two exposures. Therefore, 
it is proved, that in normal individuals, independent of defecation, the 
feces are forced forward by this particular form of movement, for a con- 
siderable distance in the colon, in a few seconds of time (25). According 
to Bayliss and Starling (35) the same laws, which apply to the small 
intestine, also apply to the small “regular peristaltic movements” which 
can be seen through the fluoroscope in the descending colon (Rieder (25)). 
By stimulation from within, contraction in this segment occurs with dilata- 
tion in the loop just beyond, and thus the fecal masses are forced forward. 
This is easily demonstrated in the large intestine of the rabbit, whose feces 
form in small hard balls, which fill the distal part of the colon, like a string 
of beads, and each ball is pushed forward individually (Langley and Magnus 
(25)). In man, this form of movement, under normal conditions, progresses 
very slowly (serial pictures of Rieder). 
But in addition to the movements just described there are others which 
propel the feces backward from the anus. As has been explained above, a 
true anti-peristalsis over long stretches cannot be obtained experimentally 
by reversing loops of small intestine, but it does occur in the colon par- 198 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
ticularly in the proximal part. Cannon was the first to show these waves 
by rr-rays of cats, and his findings have been amplified and confirmed in all 
essential points by Elliot and Smith. In man, this anti-peristalsis has also 
been shown conclusively by Stierlin, Bloch, Bohm, Rieder (36) and many 
others. With serial pictures, Rieder could see first an anti-peristalsis 
which rapidly extended over the whole colon from the rectum to the cecum, 
and second, small anti-peristaltic movements confined to the proximal 
colon. 
These intestinal movements are dependent on the nervous supply of 
these structures. Exactly as in the heart, there is, first, an independent 
nervous apparatus in the intestinal wall (longitudinal muscular layer) 
in the form of Auerbach’s and Meissner’s plexus, and second, an extrinsic 
supply through the sympathetic and the cranial or sacral autonomic system. 
The pendulum movements, as well as the peristaltic and anti-peristaltic 
activity are dependent on the presence of Auerbach’s plexus (Elliot and 
Smith (25)), so that this peripheral nervous system must be considered the 
actual motor center which is controlled by stimulating and inhibitory fibres 
from the long nerve tracts. Stimulating impulses come not only through 
the cranial autonomic or the sacral system but also from the vagus or from 
cerebrospinal fibres from the lumbar and sacral segments (N. pelvicus et 
erigens). Inhibitory fibres which reach the intestines by way of the sym- 
pathetic arise in the cceliac ganglion, in the superior and inferior mesen- 
teric plexus, that is, directly through the splanchnics. Stimulation of the 
sympathetic leads, therefore, to a slowing of the movements or a relaxation 
of the intestines. The results of experiments on vagus stimulation, however, 
are not in entire agreement, chiefly because of technical reasons (see Bohm 
(37)), but stimulation of the autonomic fibres always results in tonic con- 
tractions. The experiments on the large intestine have a particular interest 
because they show that stimulation of the vagus leads to a tonic contraction 
of the proximal colon (Bohm), while stimulation of the lumbo-sacral 
plexus produces a contraction of the distal colon (Bayliss and Starling, and 
Elliot and Smith), that is, the large intestine is not a functional unit, 
which fact makes its physiological movements and the disturbances in 
these movements very much more comprehensible. To emphasize this 
functional difference, the large intestine is now divided into a proximal, 
intermediate, and distal part, thus abandoning the old anatomical divi- 
sions (Elliott and Smith). 
Bauhin's valve, under normal conditions, prevents backflow from the 
colon into the ileum. Its action depends first on a ventilator-like arrange- 
ment of the valve leaflets, and second, on a contraction of the annular 
muscle surrounding the valve, the so-called ileo-colic muscle. This 
sphincter is said to be closed when at rest (Elliott, (38)), and it contracts INTESTINES 
199 
firmly when the splanchnic is stimulated and opens on stimulation of the 
vagus, according to Katz and Winkler (39). Section of the splanchnic or 
destruction of the spinal cord leads to a relaxation of the tonus of the 
sphincter. The valve is not competent in the new born and in sucklings, 
and an insufficiency in adults is seen not rarely, especially after enemas. 
Dietlen with the x-ray could find in about every fifth case, a re-entrance of 
bismuth from the cecum into the ileum (40). It seems that in these 
cases of valvular insufficiency there is usually some chronic disease of the 
cecum or its immediate vicinity. Since, however, as stated above, Grutzner 
found lycopodium granules high up in the small bowel and in the stomach, 
after enemas, in entirely normal animals, it is necessary to be cautious in 
the diagnosis of an insufficiency of Bauhin’s valve as recognized with the 
x-ray. Then, too, it is possible that certain substances of special chemical 
nature may have an/ influence on the opening and closing of the normal 
valve from within the cecum. In general, however, the valve prevents a 
back flow from the large intestines, and also remains closed when the 
pressure there is fairly high, as for example, in large intestinal ileus. A 
ballooning of the small intestines is found but seldom in cases of marked 
distention of the cecum. Indeed, according to the experiments of Heile 
(21) it seems that the filling of the colon causes a firmer contraction of the 
sphincter in a way analogous to that of the pylorus, for in experiments 
performed for a quite different purpose, he showed that the introduction of 
a tampon cannula into the colon produced a much slower evacuation of the 
contents of the small bowel through an appendix fistula. This is due to 
an increased contraction of the ileo-colic muscle following the mechanical 
irritation produced by filling the colon. A sudden massive filling, such as 
occurs with the enemas employed by von Genersich and Dauriac (41) 
(from six to nine litres under 100 c.c. water pressure) is necessary to 
spring the valve; 
This valve is interesting from still another viewpoint; as is well known, 
this is the favorite region for invaginations; indeed, an “ileo-caecal invagi- 
nation” is quite commonly found. But Blauel (42) could show that the 
valve itself is not at fault, but that it is more probably due to a bulging 
of the wall of the cecum, and the valve is pulled along with it (see under 
ileus). 
From investigations of Luschka, Henle and O. Krauss (43), it was 
always thought that the layers of muscle in the small intestine divide at 
the junction of the ileum and cecum in such a manner that only the ring 
muscle enters the valve and the longitudinal layer spreads out on the 
surface of the large intestine. Such an arrangement of the muscles 
would, of course, favor the development of an invagination in this region. 
Toldt (44), however, demonstrated that a number of the longitudinal 200 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
fibres also enter the valve and mingle with the circular fibres; with this 
arrangement an invagination of the valve is anatomically almost 
impossible. 
Before we leave this subject, the physiology of defecation and the actual 
evacuation of the feces must be briefly discussed. During this process, 
there is a series of movements of the intestines, abdominal walls and pelvic 
floor, all dovetailing one into the other, so that an evaluation of the 
separate movements is extremely difficult. There is no doubt concerning 
the importance of the pressure of the muscles of the abdominal wall. A 
personal trial is convincing enough. The movements of the large 
intestine shortly before and during defecation are much less understood. 
Schwarz (25) investigated this subject, by stimulating defecation arti- 
ficially, with soap enemas after a bismuth meal. In agreement with 
similar but less normal experiments of von Bergmann and Lenz (45) he 
found first, a “rocking movement,” which mixed the enema and the 
feces, liquefying the latter, and second, the large colon movements already 
mentioned above, that is, those energetic contractions of the transverse 
colon which move its contents forward. Both of these forms may be 
considered the prelude to actual defecation. There then follows the 
important movements of the distal colon, especially those of the sigmoid 
flexure, which occur only when a certain degree of filling exists; in the 
interim, the sigmoid is motionless. This is of especial interest to the 
surgeon, because the periodic activity of the distal portion of the colon 
explains why patients even after complete destruction of the sphincters, 
evacuate feces at intervals and not continuously. The rule was given by 
0. Beiru that the feces collect in the sigmoid before defecation, and do not 
enter the rectum. This has been disputed many times, but was recently 
verified by Strauss (46). In fact, the rectal ampulla is normally empty 
of feces and the passage of feces from the ampulla to the rectum is followed 
by the sensation of a need for defecation. Of course, normally, the stool 
can still be controlled by the sphincters. That many people, especially 
bedfast children, often have the rectum packed with feces, does not 
disprove the rule; this enters the domain of pathology. It will be shown, 
when constipation is discussed, that the sensitivity of the rectum is of 
quite especial importance for regular defecation. If this is completely 
destroyed, as in fractures of the spinal column, it may lead to a very 
grave retention of feces in spite of the relaxed sphincters, and evacuation 
will only take place at haphazard times when the rectum is filled almost to 
the point of rupture. The actual motive power for defecation is supplied 
by the pressure of the abdominal walls and intestinal movements, and 
both are activated reflexly by the desire to defecate, which, in its turn, is a 
result of stimulation of the rectal mucosa. INTESTINES 
201 
The innervation of the distal end of the large intestine is through the 
sacral-autonomic system, that is, from branches of the lumbar and sacral 
nerves. But there are fibres from the inferior mesenteric and the hypo- 
gastric plexuses in addition. Those of the latter supply the mucosa of 
the anus and rectum with sensory and motor fibres (von Frankl 
Hochwart-Frohlich (47)). The sphincters act as a regulating inhibitory 
mechanism. 
The internal sphincter, containing smooth muscle, should be differ- 
entiated from the external sphincter, which consists of striped muscle. 
The latter is assisted by the levator ani and acts in many ways like an 
involuntary muscle. It does not degenerate, for instance, after section 
of its nerves (Goltz and Ewald, etc. (48)). The sphincters normally close 
“independent of the will but dependent on the nervous system” (tonus, 
in the sense of Heidenhain, von Frankl Hochwart). Indeed, the internal 
sphincter can develop considerable tonus, so that operative injury of the 
external sphincter alone does not usually lead to incontinence as, for 
example, in deep incision of an anal fissure (Boyer). Nevertheless, the 
two sphincters are very closely related in man (49), so that the animal 
experiments (von Frankl Hochwart and Frohlich) in which it was found 
that they were completely independent, cannot be applied without 
reservations. 
The activity of the anal sphincters is directed from varied centers. In 
the first place, each contains its own center, which consists of ganglion 
cells located in the musculature. This fact, showing a certain analogy to 
cardiac muscle, is peculiar to the external sphincter which consists of 
striated muscle (50). These ganglion cells gradually bring about a tonus 
of the sphincters even after complete destruction of the spinal cord and 
the sympathetic fibres, and the incontinence which occurs at first is 
replaced by a condition which is much more bearable. Even if these 
patients are not aware of the act of defecation on account of the destruc- 
tion of sensory fibres, the feces, as long as there is no diarrhea, are 
evacuated at intervals, and not continuously (51). This local center is 
governed by a second center situated in the sympathetic ganglion (inferior 
mesenteric). There are also centers in the conus terminalis, in the lumbar 
region of the spinal cord, and one in the cortex, but the position of the 
latter varies in different species of animals (52). The importance of these 
defecation centers should not be underestimated, for even if the sphincter 
tonus is preserved in some animals, when the spinal cord is totally 
destroyed, along with the inferior mesenteric ganglion (von Frankl- 
Hochwart and Frohlich), Roussi and Rossi (53) and others could show 
plainly perceptible disturbances, viz., partial incontinence and relaxed 
sphincters, in dogs and monkeys even five months after the destruction 202 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
of the conus terminalis. The same is observed in patients with injuries 
of the spinal cord, as, for example, after fractures of the vertebrae. In 
addition, an open anus is found when movements of the colon are absent 
and after interruption of the sensory paths, that is, after section of the 
posterior roots of the sacral spinal cord (54). 
By diarrhea is understood a massive evacuation of fluid feces (55). 
Our knowledge of the form of movements of the various portions of the 
intestines in diarrheas is very meager and depends on indirect conclusions. 
For example, it is not at all certain that they are similar to those move- 
ments which occur during catharsis. Observations of the latter condition 
must be used for analogy and may now be discussed. The x-ray examina- 
tions of Stierlin and Meyer-Betz and Gebhardt (56) have shown that 
senna electively increases the movements of the large intestine so that 
the feces hurry through it in from one to two hours. Aloes increases the 
tonus of the musculature of the large intestine, so that this drug gives rise 
to symptoms similar to those of spastic obstipation. Castor oil leads to an 
increase of fluid contents, even in the small intestine; and larger masses of 
fluid, therefore, reach the large intestine. As a result of the stretching, 
there are sudden large movements of the colon, and a fluid stool is evacu- 
ated. Feces remain in the colon after castor oil about as long as after 
senna, but since the senna stool is mushy and the castor oil stool is fluid, 
it appears that castor oil also inhibits the absorption of water in the large 
intestine. Gas bubbles can be seen by the x-ray and with castor oil, may 
fill the entire large intestine. They stretch the walls and incite large colon 
movements. Probably they are an expression of this defective absorption. 
Jalap and the saline cathartics lead to increased secretion in the small 
intestine. At the same time jalap stimulates the mucosa of the colon, 
while the final defecation after saline cathartics is similar to that after 
castor oil. If the latter is given with the intestines filled, the fluid and the 
gas push past the older fecal contents and take but little of it along. The 
bowel is thus not emptied at all. Calomel is the substance which stimu- 
lates both small and large intestine, without leading to increased secretion, 
and all of the contents are pushed forward. 
If we apply the findings in catharsis to the pathological diarrheas we 
must doubtless assume that there is increased activity of the colon, which 
may be of two forms—either an even increase in movements or, so to speak, 
movements in answer to the increased filling from slow aborption, the 
combination taking the form of an explosive evacuation after a few large 
colon movements. As a superimposed reason for this accelerated empty- 
ing of the colon, it must be assumed, as with senna, that there is a stimulus 
to the motor fibres controlling the colon movements, or an indirect stimu- 
lus from delayed absorption and increased secretion which produce a too 
great and too sudden filling. INTESTINES 
203 
What can be the cause of this stimulation of the motor apparatus? 
The simplest conditions probably occur in the ordinary acute diarrheas 
which may appear after a dietetic error. There results one or two semi- 
fluid evacuations, followed by a certain amount of sensitiveness of the 
bowel for another day. Then all disturbances cease. The stimulus in 
this case is undoubtedly the unsuitable food, but it is not because it 
should be expelled as quickly as possible that there is diarrhea, but because 
the food initiates a purely reflex stimulation. The whole affair can perhaps 
be quite well compared to the appearance of an urticaria occasionally 
following the consumption of certain fish. If there is a transudation of 
fluid into the subcutaneous tissues in urticaria, there may also be a similar 
leak into the intestines in these reflex diarrheas (perspiration of the bowel) 
(57). That this increased secretion is actually the cause of the diarrhea 
has been shown by numerous examinations and weighings of the feces; 
and according to the present idea, it takes place in the colon at a time 
when the offending food is still in the small intestine. Delayed absorption 
in the small intestine can hardly play a role in the fluid condition of the 
stool since even in severe diarrhea, it is rarely possible to find in the feces, 
sugar or other substances, which are easily absorbed (Strassburger). 
The diarrheal stool is also quite different, even grossly, from the material 
passed through a fistula of the small intestine. An increased peristalsis, 
therefore, is not the only cause. It is only in the very rare jejunal diar- 
rheas that a stool having the properties of the contents of the small 
intestine is evacuated. In this case, there must be an accelerated 
peristalsis in this part of the bowel. 
It is a fact, well known also to the layman, that certain individuals 
react to various foods with almost certain diarrhea. Furthermore, some 
in the same condition of nutrition, develop diarrhea very readily, and 
others never. A “bowel weakness” is spoken of quite generally, but an 
effort has been made, particularly in the chronic cases, to establish groups. 
Thus, as A. D. Schmidt and Strassburger (58) first pointed out, there are 
patients who develop diarrhea upon consuming any kind'of carbohydrates, 
probably because, according to the present idea, their intestines cannot 
split carbohydrates, especially cellulose. The contents, assisted by 
bacteria, therefore, ferment in the large intestine (fermentation dyspepsia). 
The more or less fluid feces, and especially the gas, lead to accelerated 
peristalsis and to a secondary increase in the secretion of the colon. 
Primarily, however, there is constitutional weakness of the ileum, since 
we have seen above, the splitting of carbohydrates takes place here. 
In another group of cases, carbohydrate digestion is normal, but the 
digestion of muscle and connective tissue is disturbed. This last form is 
often due to achylia of the stomach (59). In the absence of pepsin and 204 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
hydrochloric acid, the connective tissue in meat is not dissolved and only 
roughly comminuted fragments enter the intestine and there decay from 
bacterial activity. These decomposing masses irritate the bowel and lead 
to diarrhea. Intestinal bacteria, therefore, only play an intermediary 
part in this process. It is not a question of the development of certain 
kinds of bacteria, or even an increased virulence of those present, but 
only a purely quantitative increase in number, due to favorable conditions 
of growth. 
Disturbances of absorption in the small intestine may also lead to the 
development of diarrhea, especially when the absorption of fat is hindered 
in the presence of tuberculous mesenteric lymph nodes (tabes mesenterica 
or tuberculous peritonitis). The absence of pancreatic secretion will also 
lead to fatty stools and to symptoms of defective fat absorption. Quite 
peculiar is the hypersensitiveness of some patients to even a small quantity 
of hen’s egg albumen. Schittenhelm and Weichardt (60) believe that the 
intestinal wall of such patients is permeable to unchanged egg albumen. 
As always, when foreign protein is introduced into the blood stream, a 
hypersensitivity to this particular protein develops, and the ingestion of 
even the most minute quantity will lead to a kind of anaphylactic shock, 
expressed in these cases by diarrhea. It has been thought that the diar- 
rheas in non-ulcerative tuberculosis, in exophthalmic goiter, etc. might 
also be explained in this manner, but the ideas are only unproved 
hypotheses. 
Intestinal movements are also dependent to a great extent on the 
nervous system, even in healthy individuals. Diarrheas, from fear or 
excitement or other psychic factors are quite common. Here also the 
question is not of accelerated peristalsis, but of an increased secretion into 
the bowel. 
Thus far, we have discussed only the disturbances of intestinal func- 
tions which show no anatomical changes. If the latter are present, we 
speak of an intestinal catarrh, an enteritis, or a colitis. Intestinal dyspep- 
sias form a basis for understanding the functional disturbances observed 
in inflammatory processes. The differential diagnosis is founded on the 
abundant excretion of inflammatory products (mucous, pus, blood). In 
the etiology, especially of the acute varieties, bacteria (typhoid, para- 
typhoid, and streptococci) play a large part. Furthermore poisons, 
organic and inorganic, whether they enter through the mouth or from the 
blood, are also important exciting causes. Both routes are often combined. 
Mercury poisoning, for example, leads to “an excretion inflammation” 
in the colon; in addition there is occasionally a corrosive action in the 
stomach (61). It is an open question in mercury poisoning whether its 
action is due to the excreted metal or is a result of thrombosis and other INTESTINES 
205 
injuries to the vessels. Many other poisons are also excreted into the 
bowel and may cause severe inflammation of the mucosa in the process. 
The same explanation is given for the enteritis in nephritis, in severe burns 
of the skin, and in general sepsis. How much of a part anaphylactic 
phenomena play in the inflammations following poisons of a protein 
nature (see above), has not been sufficiently investigated. 
In the bacteriological etiology of acute enteritis, the question of non- 
specific organisms, especially colon bacilli, is very important. The 
occasional demonstration of B. coli in the blood, proves that this usually 
saprophytic organism can become pathogenic under certain changed life 
conditions. Whether the advent of a pathogenic colon bacillus is neces- 
sary or whether an organism within the bowel may suddenly acquire 
virulence is still an open question. Both possibilities are reasonable. 
The cause of such a severe enteritis is often not recognizable. This is 
especially true of the colitis which is occasionally observed after operation 
(62). Anschutz (63) has observed them particularly after operations on 
the stomach and believes that they are produced by poorly digested food 
masses entering the intestines which have become hypersensitive through 
fasting, etc. Riedel thinks of mechanical injuries (pressure from intestinal 
contents). Muller (64) denies that they are true dysenteries. According 
to our experiences, these explanations are not sufficient. Patients whose 
intestinal tract was entirely normal, have often been the victims of this 
very grave post-operative acute colitis and at autopsy a destruction of 
the entire mucosa of the large intestine is found. We saw this, for 
instance, in a child, after Forster’s operation, and the impression was 
gained that it was actually due to a chemical poison; but in the cases 
known to me, no such poison could be found, nor did the kidneys show, 
for example, the characteristic changes of mercury intoxication. 
In chronic inflammation, the ordinary chronic infectious organisms such 
as B. tuberculosis, actinomyces, spirochseta pallida, play a part in only 
a few of the cases. The etiology of the majority, especially those suitable 
for surgical treatment, such as the interesting forms of ulcerative colitis, 
is entirely unknown. A good result is occasionally achieved by short- 
circuiting the feces through a fistula or an artificial anus and treating the 
bowel from above by irrigation. The success resulting from such treat- 
ment seems to show that the feces are a continuous source of irritation to 
the ulcerated area. An ulcer once formed, becomes chronic, probably 
because of the poor local conditions for healing, but whether other eti- 
ological factors co-operate, cannot be answered in a way applicable to all 
cases. Sometimes there is a constitutional disease which produces a 
lowered tendency to heal (gout, leukemia and scurvy and others). In 
other cases, a constitutional intestinal weakness, such as has been 206 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
described in dyspepsias, may possibly be operative, but very frequently the 
whole process is one of poor healing of an acute inflammation. For 
instance, cases of gonorrheal proctitis which appear very hopeless and 
have persisted for years, often heal rapidly after the establishment of a 
fistula. 
Those cases of enteritis often associated with extensive ulceration do not, 
however, always show diarrhea—the latter is often absent when the ulcers 
are present in the lower small intestine and in the cecum, while it is present 
more frequently in ulceration of the lower colon. Whether diarrhea is 
present or not in ulcerative processes, depends, according to A. 
Schmidt, on the condition of the mucosa between the ulcers. To produce 
diarrhea, it is necessary to have secretion, and this is absent in the ulcer- 
ated areas. For this reason, a classification of enteritis cannot simply 
be made from the slightest to the most severe, and including finally, 
those with ulceration. Even if such a grouping is jutifiable in isolated 
cases, some pathological physiological peculiarity must nevertheless be 
present when ulcers appear. 
Irritating conditions within or about the rectum lead to tenesmus. 
The explanation of this condition is clear from the statements regarding the 
physiology of defecation. 
Delayed evacuation of the bowels, that is chronic constipation, has only 
recently awakened surgical interest since attempts to eliminate or improve 
this disturbance have been made. 
Although, theoretically, constipation may have its origin in any part 
of the gastrointestinal tract, x-ray investigations have shown that the 
usual reason is disease of the motor apparatus of the large intestine. 
Since the colon is structurally not a unit so far as its innervation and move- 
ments are concerned, it furthermore appears advisable to recognize a 
classification, according to the locality where the stagnation of the 
feces occurs. This can be done by means of the x-ray. It is more impor- 
tant, however, to observe when the shadow of the bismuth appears in a 
certain segment of the intestine than the length of time that it remains 
visible in a higher segment (65). 
The most frequent jorm of constipation is the proctogenic (66). This has 
been known relatively for the longest time since the diagnosis is compara- 
tively simple, that is, can be established by the introduction of the finger. 
About 60 per cent, of all cases fall in this group (67). Among the causative 
factors of this form, are, first, mechanical obstructions in the rectum or in 
the neighboring parts of the bowel. In the case of tumors within or with- 
out the colon, congenital or gonorrheal strictures, loops of the descending 
colon (68), the constipation is only a symptom of an entirely different 
disease. No difficulty in the explanation of the pathological physiological INTESTINES 
207 
processes, is presented in these cases, although frequently a rectal carci- 
noma is treated as simple constipation until it is too late for operation. 
This form of obstruction should be classed with ileus, just as the obstruc- 
tion in Hirschsprung’s disease (69), or the kinking of the sigmoid flexure 
against the rectum which is pathologically physiologically related to 
Hirschsprung’s disease (70). Far more difficult to evaluate, in relation 
to constipation, are- the hypertrophic folds of Houston, that is, the folds 
at the junction of the anus and the rectum which represent the remains 
of the anal membrane (71). Gobel (72) destroyed these folds by means of 
special crushing forceps and obtained good results in this type of constipa- 
tion. They are much discussed as causes of constipation, in English and 
American literature. 
Secondly, the proctogenic type of constipation is found in increased 
tonus, that is, spasm of the sphincter. The primary relation of both 
disturbances is also shown here by the good results from appropriate thera- 
peusis. If the spasm of the sphincter is abolished by dilatation, the con- 
stipation is cured, often permanently (73). That the cause of these 
spasms is usually a painful affection in the region of the anus, especially 
fissures, is probably true from therapeutic results in numbers of cases, but 
the failures show that it is not always such a simple disease. Patients 
with fissure ani, complain chiefly of pain at the moment of evacuation of 
the stool. The fissure is exceedingly painful on rectal examination and 
the sphincter is spasmodically closed. But other patients complain of 
severe pain, also, which begins one to two hours after defecation, but is 
different in type from the local pain at the point of the fissure, although its 
starting point is usually in the sphincter. These after pains sometimes 
persist, even after the fissure should long have been healed by incision 
or stretching, and when the pain, during the actual evacuation of the stool 
is entirely absent. It can hardly be doubted that it bears a certain rela- 
tion to the fissure, since intelligent patients state positively that it began 
with the fissure. To speak of a reflex, is nothing more than to avoid the 
issue and whether there is an analogy to lead colic—atropin usually has 
no effect whatever—is thus far completely unknown. The most probable 
explanation is that there is a more extended spasm of the colon, which is 
possibly responsible for the constipation, also. Locally there is found, 
according to the microscopical examinations of Quenu and Hartmann (74), 
a neuritis of the terminals of sensory fibres, and while the reflex spasm of 
the sphincter is sufficiently accounted for by this finding, it fails to explain 
the after pains. 
The tonus of the sphincter varies very considerably in different 
individuals. Rossolimo (75) made extensive investigations of this 
subject, and found that it is increased in neurasthenics among others, 208 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
and also in certain nervous diseases, particularly those affecting sensory 
paths, the whole having been summed up as rectal neuralgia (76). In all 
such cases, a constipation of proctogenic type may result from this 
increased tonus. 
A third finding often seen in proctogenic constipation and which 
doubtless has an etiological relation to it, is a lowered sensitivity and 
motility of the distal end of the intestine. Although corresponding 
anatomical findings have thus far not been found, there is a certain amount 
of experimental and clinical data concerning severe lesions of the nerves, 
which helps to explain some of the lesser disturbances which we meet in this 
condition. Thus it has been shown experimentally, that after section 
of the posterior roots of the sacral spinal cord no movements of defecation 
can be incited through sensory stimuli (54). Furthermore, constipation 
results from destruction of the lumbar segment of the spinal cord (Goltz), 
either experimentally or from pathological causes (tabes (77)). Since 
there is, of course, interruption of the reflex arc in all these cases, it is 
clinically, very often difficult to decide whether the injury is to the motor 
or to the sensory mechanism. In many cases, not depending on severe 
nervous diseases, there is often a proof of the described disturbance in the 
innervation of the distal end of the intestine by a failure of the reflex 
movement of this portion on the introduction of a proctoscope or after 
distension with air. This is also often encountered in high rectal carcinoma. 
Here the palpating finger finds a wide, relaxed ampulla, and this is actually 
a suspicious diagnostic sign if the tumor is located too high to be reached 
by the finger. 
Finally, among the causes of proctogenic constipation, disturbances 
of the accessory muscles of defecation (diaphragm, levator ani, abdominal 
walls), may be mentioned. Practically, it is often very difficult, in a 
given case, to decide how much is due to this poorly functioning accessory 
apparatus, since weakness of the muscles is only a sign of a general muscu- 
lar weakness; i.e., an asthenia, in the sense of Glenard and Stiller (78). 
Pinkus (79) describes a special form of constipation belonging in this 
group. He calls it “constipatio muscularis sive traumatica mulierie 
chronica,” a constipation due to a weakness of the pelvic diaphragm fol- 
lowing the trauma of childbirth. The statement regarding asthenia 
covers this type. But how small a part weak abdominal muscles actu- 
ally play in regular bowel movements is shown by a case of Hertz (65), 
who observed a child with complete congenital absence of the entire 
abdominal musculature which, nevertheless, had very regular stools. 
That hernia may also occasionally cause constipation is shown by a case 
of Ebstein (80) in which an appropriate operation completely cured the 
constipation. In general, however, hernias have nothing to do with INTESTINES 
209 
proctogenic constipation, and similarly, the numerous sections of the 
phrenic nerves, according to the method of Sturtz and Sauerbruch (81) 
have shown that the diaphragm is not as important in defecation as has 
been assumed. 
Although the designation “proctogenic constipation” covers a variety 
of conditions, nevertheless, the disease pictures correspond insofar that 
in each case the distal end of the bowel is the seat of the obstruction. 
This is unquestionably of importance in treatment, and this classification 
therefore should be retained for the present. 
An attempt has furthermore been made to contrast an “ ascending type ” 
with the proctogenic type (82). This grouping, however, gathers very 
different etiological forms into a seeming unity. Fecal obstruction in the 
proximal colon does not occur only in “weakness” of the cecum in its 
broadest sense, but also when the seat of constipation is in a deeper 
segment of the bowel (73). In this way, the name may be misleading, but 
it is widely used, and has led to resections of the cecum in those more 
severe forms of constipation in which, by the £-ray, the intestinal contents 
were demonstrable abnormally long in that portion of the bowel. If the 
actual seat of trouble in such cases was below the cecum; if, for instance, 
it was proctogenic, where the fecal stasis in the cecum was secondary, the 
resection naturally did not give relief (73). 
The experiments of Bohm (83) have, of shown that constipation 
confined solely to the proximal end of the colon is conceivable and may be 
explained as a consequence of vagus stimulation. He found, indeed, in 
cats, and even better in rabbits, that after vagus stimulation, there was 
increased anti-peristalsis and mixing movements in the proximal colon, 
with tonic contractions at the end of the same structure. We cannot say 
with certainty at the present time, in the absence of anatomical findings, 
that such a form of constipation occurs in man. Some axray pictures seem 
to speak in its favor (84). But then it would be necessary to accept the 
theory of a constipation due to irritability of the large intestine and return 
again to the “spastic constipation” of Fleiner, which has been completely 
refuted (85). 
Other :r-ray findings have, however, taught us the justification of 
Fleiner’s idea that a constipation caused by increased irritability of the 
colon can occur. The tonus of the colon, as shown, for example, 
by enemas, is indeed very varied. Singer and Holzknecht, Schwarz (86), 
Stierlin, and others, have published #-ray reports showing that there 
may be a diminution in the size, indeed, a tape-like pulling together of the 
entire intermediate and distal colon, beginning with the transverse por- 
tion. A “ hyperkinesis ” of the proximal colon was also found in such cases, 
a proof, as far as we may judge at present, that the different forms of 210 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
“spastic” constipation, or if preferable, the “constipation with increased 
irritability of the large intestine,” cannot be sharply separated from each 
other. The cause of these spasms has not been demonstrated. A great 
number may be functional, since they affect youthful persons and quickly 
disappear under suitable treatment, but naturally, in such cures we may 
have removed an external cause such as a change in food, removal of 
parasites (87), etc. In regard to the value of resection of the proximal 
colon, it must be remembered that retention of the feces in this portion of 
the intestine is purely secondary; such a procedure can, at the best, only 
improve the constipation by allowing feces to reach the distal colon in a less 
concentrated form, and this may act favorably on the spasm. The 
improvement shortly after operation is often deceiving, for the follow-up 
investigations of Rost have shown that the permanent results of cecum 
resection in this form of constipation are by no means brilliant. That 
present with gastric ulcer must also be classed as secondary (88). In this 
case, removal of the ulcer improves the constipation, but it returns when a 
new ulcer appears. Even if appendectomy in chronic appendicitis relieves 
the constipation, this also should be considered “ secondary.” 
Furthermore, it has been stated that adhesions and veil-like coverings 
of the colon, especially of the cecum, are a cause of long lasting constipation. 
This condition will again be met in chronic peritonitis. On the proximal 
colon, these adhesions are called Reid’s, Treve’s, Lane’s, Jannessko’s and 
Jackson’s membranes, or collectively, they are known as ligamenta 
varioforma (89). These fold-like formations of the parietal peritoneum 
may occur entirely without symptoms. As Eastmann says, a “large X,” 
an unknown something, must be added in order that these membranes 
become troublesome (90). In some cases a colitis acts as an apparent 
exciting factor; but furthermore, as will be mentioned under chronic 
peritonitis, such veil formations may be the result and not the cause of 
chronic constipation. This can only be decided case by case after the 
results of operation are seen. Schlesinger (91) describes a stasis of the 
contents of the cecum below its junction with the ileum, resulting from 
such peritoneal ahesions. 
Finally, a long lasting fecal stasis, 48 hours or more, in the proximal 
colon results when there is a diffuse atonic form of intestinal movements, 
that is, when the contents of all parts of the intestines are fairly uniformly 
delayed in their onward course. Under the #-ray, the colon is abnormally 
wide and relaxed. We do not know, at present, what disturbances of the 
innervation lead to such an atonic constipation. We are inclined to 
assume with Schmidt and Lohrisch (92) that there is an abnormally in- 
creased power of the colon to split cellulose, but it must not be overlooked 
that these writers found the same increase in the utilization of the food in INTESTINES 
211 
all forms of constipation, including the spastic. This too complete 
utilization can therefore only be a result and not the cause of the 
constipation. 
Why is it that in all of these forms of constipation, the stasis of feces 
should occur in the proximal colon? Its reason, as Rost’s anatomical 
investigations have shown, probably lies in that functional separation of 
the proximal and distal colon which has been discussed under normal 
colon motility. Rost showed by planimetric measurements of whole 
colons, and of the cecum resected on account of constipation, that there 
is no atrophy, but an hypertrophy of the proximal colon and it occurs in 
just those cases in which the feces had stagnated abnormally long in the 
proximal colon and in which this latter structure seemed relaxed and dilated 
(“ typhlatonie ” (93)). This can only be explained by assuming that the 
actual site of constipation was distal to the cecum and the ascending colon, 
and that the intestines functioned against abnormal resistance, if there 
was not actual hyperfunction of the proximal colon in analogy to the 
animal experiments of Bohm, with vagus stimulation. It may be assumed 
further that the proximal colon can at first overcome the resistance, but 
later it must gradually fail. 
To sum up, fecal stasis of long duration in the proximal colon, in the 
different types of constipation mentioned, must on the basis of what has 
been said, be considered purely secondary. This must be taken into 
account in attempts at surgical treatment. 
That form, distinguished by Stierlin (84), as a transverse colon stasis, 
occurs when this portion of the bowel is ptosed and kinked at the splenic 
flexure (see under chronic peritonitis). But stasis occurs without the 
kink, and in these cases the anatomical investigations of Rost have shown 
that an atrophy of the muscle of the transverse colon is present and during 
life this particular form of constipation occurred. It cannot be stated, 
however, whether this atrophy is primary or secondary; it may easily be 
imagined that this transverse stasis is only an end result of a spastic 
constipation. At present, our x-ra.y pictures, are, of course, only isolated, 
and we are by no means informed of the processes involved in the develop- 
ment of constipation. This would necessitate observations of patients 
extending over years. 
Finally a word must be added concerning the surgical treatment, which 
usually consists of the removal of the proximal or the entire colon. From 
the preceding statements, it is easily recognized that the pathological 
physiological conclusions regarding such procedures are not quite as simple 
as they appear. Hertz in speaking of the operation of Lane, who as is 
well known, resects the entire colon, affirms that Lane removes every 
healthy part of the large intestine and leaves behind the diseased portion 212 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
(proctogenic constipation), but it must not be overlooked that patients 
who are in a pitiable condition are often remarkably benefited by this 
operation. The only good explanation at present is that the elimination 
of some sort of toxic substances has been improved. 
This leads us to the difficult and practically unsolved problem of 
chronic intestinal intoxication (see the remarks under ileus). Such 
substantial improvements have been seen after relief of constipation by 
resection of the cecum not only in high grade malnutrition, with its gray 
discoloration of the skin, but in cardiac disturbances, renal difficulties, 
numerous neurasthenic disorders, and changes in the blood picture, that 
it makes pertinent the assumption that absorption of toxic substances took 
place chiefly in this portion of the bowel. Operative procedures for 
constipation should be considered from this viewpoint. 
As a third large division in the pathology of intestinal motility, the 
symptom complex known as ileus must be discussed (94). The four 
cardinal symptoms of this condition are retention of feces, vomiting of 
bile-stained or fecal material, meteorism, and abdominal pain. These 
sketch in rough outline this symptom complex, but to determine its exact 
boundaries has always been and will be its greatest difficulty. 
The classification of those intestinal disturbances, which are collec- 
tively called ileus, is as varied as the viewpoints from which the question 
can be approached. If we adopt the pathological physiological facts 
as the basis of our classification, we must differentiate the obstruction 
due to mechanical causes from that of disturbances of any sort in the 
innervation (dynamic ileus), and we must further distinguish in mechanical 
ileus whether the blood vessels have also been obstructed (strangulation 
ileus or obturation ileus). Mechanical ileus is the easiest to explain. 
That the passage of feces should be impeded or checked completely when 
the lumen of the intestine is obstructed by a constricting carcinoma, or an 
impacted gall stone, etc. is naturally self evident. A stasis of feces 
must occur above the obstruction. Dilatation of the bowel and disten- 
tion result and finally gases are forced back into the stomach and expelled 
by vomiting and eructation. We shall discuss the symptoms in detail 
later. 
The conditions are not quite as simple in strangulation ileus because 
the obstruction to the circulation plays the most important part. On 
this depend all other symptoms of which, first of all, distention and meteor- 
ism must be mentioned. 
In all forms of ileus, the explanation of meteorism has been considered 
easy. Gases and intestinal contents collect above the point of obstruction, 
evacuation cannot take place downward, new material is steadily added 
from above and distention must naturally result, its degree depending INTESTINES 
213 
on how far down the obstruction occurs (95). But clinical experience 
has shown that this explanation of meteorism does not apply to all cases, 
for meteorism not general, but localized and circumscribed, has been 
observed especially in strangulation ileus (96). The extensive experimental 
investigations of Kader (97) have enlightened us on this point, and our 
understanding of meteorism has been considerably improved. We must, 
according to these experiments, differentiate the meteorism in obturation 
from that in strangulation ileus. Every ligation of the mesenteric vessels 
(naturally also thrombosis or embolism), with its resulting stasis leads to 
a local meteorism, which forms quickly, and increases very rapidly. This 
meteorism, resulting from circulatory disturbance, paralysis and distention 
of the intestine, is very much greater than that resulting from simple 
obstruction of the lumen. But as we shall see presently, the paralysis and 
distention occur also in obturation ileus, and just as in strangulation ileus, 
are dependent on circulatory changes. This is of great theoretical interest 
(98), (18). The differentiation of strangulation and obturation ileus, as 
inaugurated by von Wahl, Manteuffel and Kader on the basis of the meteor- 
ism is, therefore, only an expression of gradual differences. In both cases, 
the circulatory disturbances are the essential causes, in practice, neverthe- 
less, the differentiation of strangulation and obturation ileus, according 
to the degree of meteorism present, is quite justified. 
In strangulation ileus, the muscularis of that portion of the intestine, 
the nutrition of which is disturbed, becomes paralyzed in a few hours, and 
the layers of the wall become edematous and hemorrhagic. These changes 
first affect only that portion of the intestine from which the circulation is 
cut off. The other portion, however, is also paralyzed reflexly, so that the 
same vigorous peristalsis is not seen or heard as in obturation ileus. This 
paralysis really corresponds more to that occurring in peritonitis for which, 
clinically, strangulation ileus is often mistaken. 
There are many factors at work in the rapid appearance of meteorism 
after interruption of the intestinal circulation, that is, especially in strangu- 
lation ileus. In the first place, and this seems to be the most essential 
factor, the gas exchange between the blood and the intestines is impaired. 
As is well known, intestinal gases normally are composed of swallowed air 
and a mixture derived from decomposing food. Since carbon dioxide and 
oxygen are quickly absorbed, methane and hydrogen are especially found in 
the lower intestinal segments. These latter, and also nitrogen, are absorbed 
with difficulty. Sulphuretted hydrogen is present in such small quantities 
that its relation to meteorism is unimportant. The investigations of 
Zuntz and Tacke (99) have yielded most astonishing results; namely, 
that under normal conditions most of the gases in the intestines, indeed, 
even large quantities, are eliminated by the lungs after being absorbed in 214 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
the blood stream, and only a very small quantity escapes through the 
anus (proportion io to i). A defective peristalsis, therefore, does not 
impede the elimination of these gases, but according to Zuntz, circu- 
latory disturbances do, and of course in strangulation ileus, there is 
complete interruption of the blood supply. 
However, all these statements do not explain why the gas exchange is 
lowered by passive congestion of the intestinal vessels; probably it is 
ultimately due to changes in the bowel walls themselves, since it cannot 
be assumed that the blood is carried away too slowly for this purpose. 
But it can be seen from extensive investigations (18) that absorption is 
diminished in the beginning of ileus; later it is practically abolished, and 
finally actual extravasation of fluid into the bowel takes place. These 
experimental findings correspond perfectly to clinical observations and 
explain, at the same time, why gases are contained only in that loop in 
which the circulation is impaired and why they do not escape to the adja- 
cent parts of the intestines, which are apparently much less altered, but in 
which, obviously, the absorption is also much diminished. 
As Hotz could show, the degree of paralysis of the bowel in ileus and 
peritonitis has a certain relation to the distention of the viscus. He found, 
when he isolated a loop of bowel, closed the central end and left the 
peripheral end open, that it was only the closed and distended loop that 
was paralyzed after peritonitis had begun, while the loops efferent to the 
section, and which had remained open, were not paralyzed. Furthermore, 
as Kocher (100) showed experimentally, distention of a loop of intestine 
has, in itself, caused circulatory disturbances so that there is a close recip- 
rocal relation between meteorism, paralysis and circulatory disturbance, 
and it is easily comprehensible how one of these pathological processes can 
often influence the other unfavorably. 
According to Pommer’s (18) investigation, meteorism in circulatory 
disturbance of the bowel can result, not only from diminished absorption, 
but in another manner. In a case of thrombosis of the mesenteric arteries, 
he found an extraordinary massing of butyric acid bacilli in the bowel 
wall, which doubtless had found a very satisfactory pabulum in the dis- 
integrating epithelium. Pommer believes that these gas forming organisms 
were responsible for the gases in this instance. 
The paralysis in strangulation ileus finds its anatomical expression in 
edematous saturation of the musculature of the walls. 
As stated above, the explanation of the occurrerfce of distention paral- 
ysis and circulatory disturbance in obturation ileus, must be essentially 
similar to that in strangulation ileus. But there are certain differences 
which are important, especially in the clinical progress of the former disease. 
In obturation ileus, the vascular supply is not so seriously involved in the INTESTINES 
215 
beginning, since the obstruction affects only the lumen of the intestine; 
nor is the distention so great, provided of course that the disease picture is 
not erased by peritonitis. The gases, at first, find areas in the intestines 
in which the absorption is still more or less normal; the dilatation occurs, of 
course, above the obstruction and remains the greatest in this part through- 
out the further progress of the disease. The distention of that portion 
immediately above the obstruction, can be explained chiefly by the 
increased current of fluid passing from the blood into the intestines. This 
increased secretion of fluid from the mucous cells is expressed anatomically, 
and the efferent and afferent bowel segment can be easily recognized 
microscopically from the appearance of the goblet cells (13). 
As stated, the intestinal contents in obturation ileus are chiefly 
liquid (101), at least when the obstruction is of the small intestine; when of 
the large intestine, the gases predominate. This is especially interesting 
because, as we have seen, in discussing diarrhea, liquefaction is demon- 
strable particularly in the region of the colon. The complexity of the 
pathological processes is thus shown. If the obstruction persists, the 
distention may also become enormous; the musculature hypertrophies and 
not a short, but a very large segment of the intestine is dilated. In such 
cases, the difference in size of the afferent and efferent loops is very apparent 
at operation and in resection the suturing is made very difficult. Further- 
more, after resection, such chronically diseased intestines do not recover 
very rapidly as the entire bowel has been affected. It has already been 
shown that circulatory disturbances resulting from the distention, occur 
at this stage. In strangulation, on the other hand, the normal activity 
is usually quickly re-established after resection, since the segments above 
the affected loop are paralyzed reflexly and not as yet from distention. 
This must not be overlooked, even if the disease picture in strangulation 
ileus is otherwise more dangerous because of the quickly supervening 
gangrene. 
It has not been decided whether the meteorism in hysterical individ- 
uals is due to a paralysis of the intestinal musculature, or as Trousseau 
(102) assumes, to a spasm of the diaphragm with relaxed abdominal walls. 
If such a case is operated on, under mistaken diagnosis, it is most remark- 
able to see the meteorism disappear completely during the anesthesia. 
The influence of the nervous supply of the intestines, in relation to the 
appearance of meteorism, is very little understood. Numerous observa- 
tions have shown us, however, that there is a type of distention, which can 
only be considered due to a nervous reflex. Such cases are the intestinal 
distention at the moment of omental strangulation, twisting of the pedicle 
of intraabdominal tumors or organs, the meteorism in renal or biliary 
calculi, retro-peritoneal hemorrhages, mild abdominal injuries (103), and 216 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
many other conditions. The gaseous distention often amounting to 
ileus, which occasionally occurs after all sorts of aseptic laparotomies, 
also belongs to this class (104). It is usually assumed in these cases that 
the splanchnic nerve, that is, the inhibitory nerve of bowel motility, has 
been strongly stimulated reflexly. Whether this idea is correct has thus 
far not been examined experimentally. Reflex meteorism and reflex 
paralysis are only gradual differences of one and the same process. The 
impression is gained clinically, that the severe forms of this reflex paral- 
ysis presuppose a certain nervous disposition, but it must not be for- 
gotten as we have said above concerning hysteria, that our knowledge of 
the actual cause of meteorism in such cases, is still very meager and 
uncertain. 
After blunt trauma to the abdomen, as for example, a kick by a horse, 
the intestines are not usually distended shortly after the injury, but are, on 
the contrary, contracted and pale (Wilms (82), p. 81). Heineke believes 
that it is the tension of the abdominal walls, after intraabdominal hemor- 
rhages or injuries to the intestines, which prevent distention of the latter 
structures. He concludes this from the observation in certain cases that 
marked meteorism was present in mild bruising of the abdomen. In these 
cases, no intraabdominal injury was present. 
The meteorism which is occasionally seen in diseases of the central 
nervous system (tabes, apoplexy and that developing especially after 
fractures of the vertebrae) is generally held to be due to intestinal paralysis, 
but thus far there are no careful investigations regarding degeneration in 
nerves and ganglion cells. If the abdominal walls are also paralyzed 
another factor comes into play. 
The separation of obturation and strangulation ileus relates only to the 
final condition; it often happens that an ileus begins as the obturation 
type and in the further course of events, that is, when the mesentery is 
also pinched, it changes to the strangulation type. The mechanism which 
produces strangulation ileus is not always easy of explanation. If we find, 
for instance, a large number of loops of intestine passed through a com- 
paratively narrow ring, it may, in the first place, be caused by what we 
usually designate as “ elastic incarceration.” Under the pressure of the 
abdominal walls and forcible stretching of the elastic rings, as in an hernial 
aperture, a large segment of bowel is forced through. If the pressure 
within the abdominal cavity is reduced, the ring again contracts and 
incarceration is the result. The size of the incarcerated loop would then 
be proportional to the pressure in the abdominal cavity, and the diameter 
of the aperture. For conditions in a hernia, this mechanism is quite easy 
to understand, because low pressure exists within the hernial sac. This 
term “elastic incarceration” is now generally accepted in this condition, INTESTINES 
217 
especially since Ranke (105) reported a very typical case from Volkmann’s 
clinic. But the conditions are quite different when loops of intestines 
slip through a ring within the abdominal cavity. Wilms (106) points with 
justice to the fact that the so-called intraabdominal pressure cannot be 
involved. There is actually no difference in pressure in the separate 
abdominal spaces, and if Kertecz (107) obtained different pressure readings 
by introducing a rubber ball into various parts of the abdominal cavity, 
it is obvious he was dealing only with measurements of the peristaltic 
power of the intestines. It is the peristalsis which plays the deciding part 
in the incarceration of large loops of bowel through some ring within the 
abdominal cavity. 
All investigations and observations of suitable cases have conclusively 
shown that the further involvement of loops in such a ring is always at 
the expense of the efferent and never of the afferent segments. There is, 
however, considerable difference of opinion concerning the manner in 
which this pulling-in takes place, and this difference is difficult to remove 
because the intestines of the usual experimental animals, for example, 
the rabbit, do not have the peristaltic power of human intestines (106). 
Wilms believes it occurs in this manner: with enlargement, and stretching 
of the loop which is not at first incarcerated, and with a smooth constrict- 
ing ring, more and more intestine from the afferent segment is pulled into 
the ring according to the law of lateral pressure. He attempted to support 
this view by experiments on cadavers ((106), p. 35), in which he pulled a 
loop of bowel through a smooth ring and injected fluids into the incarce- 
rated loop. As a matter of fact, similar conditions occur in the living 
when the afferent segment forces fluids or gaseous contents into the 
constricted loop. Theoretically it can also be conceived that a similar 
mechanism has acted when a large loop of bowel is found pulled through 
a ring in ileus. Naturally it must be supposed that there was no incarcera- 
tion at the beginning. 
But how does the incarceration develop if the ring is wide enough to 
permit loops of bowel to pass through it in this manner? The principle 
is the same, whether the incarceration occurs inside the abdominal cavity 
or outside in a hernial orifice. When years and tens of years pass, and 
large masses of intestines lie in a hernial sac without being incarcerated 
and then suddenly the loops will not return to the abdominal cavity, 
without any stronger pressure having been applied, naturally the above 
mentioned form of elastic incarceration cannot be operative. In such 
cases, the term “fecal incarceration” is used. Many workers have dealt 
with this question experimentally (108). The experiments of Borggreve 
and Hessel, in which they placed a loop of intestines through a gap in 
the abdominal wall and then observed circulatory disturbances which 218 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
finally led to such edema of the bowel that the loop could not be returned, 
cannot be utilized in this connection, because the intestines came in con- 
tact with air. These conditions are entirely different from those occurring 
in ruptures. But the general importance of circulatory disturbances in 
incarcerated hernias must not be ignored on this account. 
In the last century, during the forties, 0. Beirn performed an experi- 
ment which is really basic for all later experimentors. He cut a round 
hole, i.s cm. in diameter, into a piece of pasteboard and pulled a loop 
of bowel through the opening. If he blew air through a catheter into one 
end of the bowel, it escaped at the other end, but if he blew a large quan- 
tity in suddenly, none escaped and the loop of bowel became enormously 
distended. The method which Roser used in his well known and much 
cited experiment was somewhat different, but not new in principle. He 
pulled a loop of intestine through a ring, filled it half full of fluid and then 
attempted to empty its contents by sudden and forcible pressure. He 
did not succeed, even though the ring was fairly large, and Roser believed 
a fold-like formation at the level of the ring acted as a constriction. 
Many others have performed experiments in the same or similar manner 
(109). The results of all were the same, but the interpretation differed 
with the various writers. Thus Lossen believed that the afferent intestine 
would kink off the efferent loop as soon as the former was tightly distended, 
and thus no contents could escape. This idea has been much contested, 
probably with justice, and this mechanism in hernial incarceration prob- 
ably does not play a large part in the living, even though Lossen, from 
these experiments on cadavers, devised a special method of taxis. 
The application of these experiments to the living has always been 
in dispute since the contents of the intestines collected in this manner 
would have to be evacuated quickly into the afferent loop, thus releasing 
the incarceration. As further experiments then showed, a fecal reten- 
tion resulted if in place of one hole, two holes are used through which the 
loop of intestine passes. A pinching off of the efferent through the 
afferent surely cannot take place in this experimental arrangement. 
Busch believed that the efferent loop was kinked off at the constricting 
ring, since, of course, the pressure on the convex side of such an arc shaped 
tube as the loop of bowel simulates in the hernial sac, is greater corre- 
sponding to its larger surface than that of the concave side. Consequently, 
the arc attempts to straighten out because of the increase in the internal 
pressure, and thus the efferent loop is kinked. But fecal incarceration 
results experimentally if the entire loop of bowel is placed in a funnel 
with the afferent ends protruding below. In this experimental arrange- 
ment, kinking is surely avoided. Karpetschenko therefore believes that 
a portion of the loop is occasionally twisted within the hernial ring and this 
leads to fecal incarceration. INTESTINES 
219 
In simplyfying these experiments, new facts were discovered. Busch 
demonstrated that contents cannot pass if a simple section of bowel no 
loop) is passed through a ring and then is distended, or if a segment of 
intestines is slightly constricted at any point, and then suddenly distended. 
Kinking, in the true sense of the word, does not occur in this case and 
Kocher then showed, with a slight alteration in the method, that 
distention of the lumen alone is sufficient to produce occlusion of the 
afferent loop. This occlusion occurs, as can be easily shown, through 
pulling some of the wall of the afferent loop, chiefly the mucosa, into 
the ring. This corresponds to the above mentioned lateral pressure. 
In this manner the entire lumen of the afferent end is occluded. 
To briefly summarize, a so-called fecal impaction results if the bowel 
is constricted at any place by a ring, and quickly distended above this 
narrowed place. These experiments on cadavers have therefore taught 
us the manner in which a stasis of feces is brought about in a hernia. A 
stasis is, however, not an incarceration. The stasis of feces, would neces- 
sarily be relieved when a peristaltic wave relaxed, if other factors were not 
added. But that stasis persists is just the remarkable part of impaction, 
and to explain this, the effect of circulatory disturbances must be brought 
in. These develop in the manner described. We know that a circulatory 
stasis occurs in a short time after irritations of all sorts, and these 
disturbances once begun, naturally increase more and more. They 
probably also cause a simple stasis of feces to finally become an incarcera- 
tion. How much this incarceration depends on circulatory conditions 
after ordinary fecal stasis is seen in the so-called “relaxed incarcerations” 
of old people, which, actually occur only in weakened circulation, as 
Wilms could show. In such cases ordinary fecal stasis persists for a long 
time, and it does not proceed to the incarceration which injures the bowel 
wall. The intestine is often found in such good condition even after 
three to eight days of incarceration that it is not necessary to resort to 
resection. 
Circulatory disturbances therefore belong to the picture of incarcera- 
tion, and they become especially severe when the mesentery also is 
kinked in intraabdominal strangulation ileus, or, if it is present in a 
hernial sac. Kocher, indeed, believes that there is still another form of 
circulatory disturbance possible. His experiments give evidence, though 
they are not conclusive, that distention alone can produce such severe 
circulatory disturbances, that hemorrhage and gangrene finally result. 
But an impeded venous outflow may lead to distention of the bowel, and 
his demonstration, that distention for two and a half hours leads to 
complete and permanent paralysis, is essential for the comprehension of 
the anatomical changes in circulatory disturbances. Paralysis of the 220 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
bowel, distension, and circulatory disturbances are therefore in close and 
causative relation, but thus far it is only known that circulatory distur- 
bances cause all the others, and not vice versa. 
Bands and adhesions in the peritoneum from previous pregnancy or 
from peritonitis, may cause ileus by the slipping of a loop of intestine under 
them; incarceration then results in the described manner. In the classic 
form of knot in the human intestines, such adhesions do not enter into 
consideration. Gruber and Wilms (no) showed that these knots occur 
because of a too long and too movable sigmoid flexure. The work of 
Wilms also goes into detail concerning the different forms which these 
knots may assume, and the conditions are made clear by a model made of 
tubes. 
A most peculiar form of ileus is brought about by so-called retrograde 
incarceration. By this is understood that two loops of bowel find their 
way into a hernial sac without suffering very grave changes, but if the 
hernial opening is enlarged and the connecting loop between the two is 
pulled forward it is often gangrenous. Such cases have been described 
by Hochenegg, Klauber, Lauenstein, Neumann, Sultan, Lorenz (in) 
and many others. The mesentery of the connecting loop was kinked 
in the hernial opening in only a very few of the cases; in the majority, 
there was no compression whatever of the mesentery. As Lorenz, among 
others, showed, the reason for the gangrene is in a peculiar kinking of the 
mesentery of the loop of intestine which is in the abdominal cavity. 
There is a certain similarity to what Wilms has called “twist closure.” 
Lorenz could support his opinion by experiments on models. 
Finally in mechanical ileus, the mechanism of invagination has been 
the object of many experiments. It is not difficult to produce them in 
animals, since small invaginations which usually resolve of themselves, 
are often found accidentally with otherwise quite normal intestines (112). 
That similar conditions occur in children during the agonal period, is also 
well known to pathologists. Nothnagel, Wilms and Knapp stimulated a 
segment of intestine with the faradic current and observed the formation 
of a local point of contraction which was then roofed over by the relaxed 
distal segment, somewhat like an umbrella. Finally, an invagination of 
the contracted portion into the relaxed portion occurred. These invagina- 
tions usually resolve themselves in a very short time. Propping and 
Knapp readily obtained similar invaginations by the injection of physo- 
stigmin. There is, however, still some difference of opinion in regard to 
the manner in which the longitudinal musculature participates, if at all. 
A prolonged invagination, as it occurs in man, cannot be obtained in 
animals, at least, only by complicated methods which correspond little 
to natural conditions (113). If, as Knapp states, these experimental INTESTINES 
221 
invaginations occur through stimulation of the ends of the vagus nerve in 
the intestines, observations of invaginations in individuals with vagotony 
would be of especial interest. That the ileocaecal valve is not the part 
where invaginations begin, as it wras formerly assumed, has been discussed 
under Bauhin’s valve. 
The classical example of “paralytic ileus” that is, obstruction resulting 
from paralysis, occurs in peritonitis. In general, the assumption is made 
that it is a toxic effect on the ganglion cells which lie in the walls of the 
intestine. That this view is too simple has been shown by the investiga- 
tions of Hotz (98), who found that intestinal paralysis in peritonitis 
occurs only in the distended segments, and those which are not distended, 
but which are equally involved in the inflammatory process, retain a quite 
normal motility. According to this, it seems probable that the distention 
and the paralysis are also indirect results of circulatory disturbance in 
this particular condition. Since, according to the investigations of Ender- 
len and Hotz (18), the absorption from the intestine is decreased in the 
early stages of peritonitis and ileus, while later there is considerable more 
fluid excreted into the bowel, we observe, in every pronounced case of 
these diseases an enormous accumulation of fluid in the lumen of the 
intestines, and this, together with the gases, leads to further distention. 
There results, according to the above statements, a severe, and eventually 
irrepairable circulatory disturbance, and later, according to Hotz, pa- 
ralysis. The surgeon, therefore, in operations for ileus or peritonitis must 
assume the task of removing these abnormal fluid and gaseous masses 
which have collected in the bowel. Evacuation is the first consideration 
in the treatment, and an astonishingly quick recovery of an apparently 
paralyzed bowel (for example in incarcerated hernia) is often seen after 
the bowel has been emptied by stripping during the operation. Fistulse 
often act in a similar manner, but are naturally less completely 
effective (114). 
Still more difficulties are presented for pathological physiological 
analysis, by the lighter grades, in which there is no pronounced obstruction 
to the intestine, but only a certain inhibition or irregularity in the peris- 
taltic movements. 
Spastic ileus in which there is obstruction to the passage of intestinal 
contents through prolonged contraction of various segments, presents a 
contrasting picture to the paralytic type. From the pharmacological 
viewpoint a paralytic ileus would correspond to that resulting from adre- 
nalin while spastic ileus corresponds to the action produced by pilocarpin. 
The most important practical example of spastic contraction, resulting 
from poisons, is that due to lead. The spasm observed in the presence 
of ascarides in the intestines, also depends on the action of a poison (87). 222 
THE PATHOLOGICAL PHYSIOLOGY' OF SURGICAL DISEASES 
Those seen with ulcers or fissures are usually considered as reflex. Others 
occurring in the presence of foreign bodies, for example, small calculi not 
obstructing the lumen, are usually placed in the latter category. 
Such contractions rarely produce ileus, but it does occur occasionally 
(for example, in the presence of ascarides (87)). Unquestionably, they 
occur in certain individuals more readily than in others, as we have seen 
under fissures where there is an extensive painful spasm of the entire large 
intestine. A nervous disposition is spoken of, based on the occurrence 
of spasm in hysterias, in which disease they may supposedly be sufficiently 
severe to produce ileus. The difficulties in understanding how contrac- 
ture of a small segment can offer an absolute obstacle to the passage of 
feces or gas, have been emphasized often enough, but it must be remem- 
bered that in circumscribed spasms, we do not know what movements 
this segment and those in its vicinity carry out, or what disturbances 
which cannot be observed fluoroscopically, the other loops of intestine 
undergo, but which may be able, nevertheless, to produce obstruction. 
Something like this occurs in ascaris ileus (Rost). 
Probably the highest degree of spasm is observed in tabes, in which it 
occurs over large areas. Indeed, Schlesinger (91) describes a case in which 
the entire descending colon contracted to a tape-like form at a time corre- 
sponding to a crisis. 
A special form of circumscribed meteorism was first described by Maydl 
and Bayer (115). In this condition, the cecum becomes distended, 
balloon-like, after deep seated obstruction of the bowel. It may reach 
a degree severe enough to produce ulcers from stretching, which finally may 
perforate and cause death from peritonitis (116). An essential in the 
formation of this isolated distention of the cecum, is an air tight Bauhin’s 
valve. Furthermore, the investigations of Anschutz (117) and von 
Greyerz have shown that the thinness of the wall and the relative width of 
the cecum are the causes leading to the greater distention of this part. 
The former illustrates the conditions very well by a schematic investiga- 
tion which has often been confirmed (Greyerz). He tied two rubber 
balloons of unequal size to a “T” tube and blew air through the third 
arm. The larger balloon expands very quickly and bursts before the 
smaller balloon has reached any noteworthy size. Kreuter, indeed, has 
doubted that the interpretation which Anschutz gives to this experiment 
is correct, but the mathematical calculations of A. de Quervain (reported 
by von Greyerz) have shown that “with membranes of equal elasticity, 
the pressure is higher when the radius is smaller; therefore, that degree of 
pressure which will suffice to distend the membrane with the larger diam- 
eter, will not be sufficient for the smaller.” Consequently, it cannot 
very well be doubted that the greater diameter of the cecum, as compared INTESTINES 
223 
to other portions of the colon, is the reason for the exceptional distention 
of this part. Clinical observations also support this view. In rectoscopy, 
for instance, when air is blown from the rectum into the colon, the patients 
usually complain of pain first in the region of the cecum. There must 
be the greatest amount of tension here, of course, since it is the end of the 
tube. Attempts have been made to utilize this pain in the region of the 
cecum as a diagnostic sign in appendicitis (118), but it is naturally not 
pathognomonic and is useful only in isolated cases (see 119). 
The formation of ulcers above an obstruction must be regarded as the 
mechanical result of severe distention. They are usually small and 
rounded and often present in large numbers; their former description as 
“decubitus or stercoral ulcerations” (Nothnagel (112) p. 183) indicated the 
view that they were produced by the pressure of stagnating hardened 
feces. But Kocher (108) has correctly pointed out that thick or solid feces 
are not present in ileus, but fluid and considerable gas, and, therefore, 
the contents of the afferent loop are soft. As a result of his investigations 
in incarcerated hernias, he considers them the result of overstretching. 
The distention of the intestine leads to a disturbance in the nutrition of the 
wall, and this to a circumscribed ulceration and gangrene, both of which 
processes are favored by the omnipresent bacteria. According to the later, 
extensive experiments of von Greyerz and von Shimodeira (120), there is 
a diminution in the arterial blood flow very soon after distention makes 
its appearance. The intestine becomes pale and ulcers may appear even 
at this stage. After the distention is released, the intestine becomes deep 
red in color, a sign of venous stasis. Kocher and Prutz (121) in their first 
paper at least, also consider this venous stasis and its resulting thrombus 
formation and hemorrhage the essential reason for the formation of these 
ulcers; but it is really very difficult to arrive at a certain conclusion. The 
explanation of such anatomical findings, as reported by Prutz, is indecisive, 
because it is never known whether they are primary or secondary. The 
fact that experimental ulcers occur only after four to five days following 
distention with air, as described by Shimodeira, really seems to point to 
nutritional disturbances of the intestinal walls through venous stasis. 
And now paralysis of the intestine may follow the circulatory disturbances 
as has been discussed in detail above. In addition, the absorption of gas 
is limited, and this in its turn, leads to the development of meteorism. 
There is thus created once more a viscious circle, which requires that the 
contents of the intestines be emptied as quickly as possible. 
Further results of distention, as it occurs in ileus, are increases in intra- 
abdominal pressure; from this standpoint the same pathological physiolog- 
cal conditions arise as in ascites. In Hamberger’s investigations of the 
influence of intraabdominal pressure on absorption, the question of 224 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
blood pressure was also considered (17). He increased intraabdominal 
pressure by injecting physiological saline solution and attempted to 
eliminate the elasticity of the abdominal walls by placing a plaster of Paris 
cast around the abdomen of the rabbit. At the beginning of the increase 
in intraabdominal pressure, he observed an increase of blood pressure, but 
when it reached high levels there was a sudden fall in blood pressure fol- 
lowed by death of the animal. Hamberger’s investigations were confirmed 
in their most important parts by Qurin (122), who used air instead of saline 
solutions. Oppenheim (123), who pumped air into the lumen of the intes- 
tines and produced high grade meteorism, also observed a marked failure 
of cardiac action, leading, in certain cases, to quick death. These writers 
interpret the results of their experiments, as follows: “When pressure is 
exerted in the abdominal cavity, the circulation, especially that in the 
veins labors against increased resistance.” The results of this condition 
are first, increase in the blood pressure and second, when the resistance 
becomes too high, complete failure of the heart with a fall in blood pressure, 
and death. But Stadler and Hirsch (124) criticised this interpretation. 
They also determined the blood pressure after increasing the intra- 
abdominal pressure by blowing air into the anus. They obtained a true 
meteorism. They also found the primary rise in blood pressure, but 
demonstrated that it was synchronous with difficulties in breathing from 
elevation of the diaphragm which with displacement of the heart could be 
seen with the In violent dyspnea, a vagus pulse was noted, but they 
never observed the fall in blood pressure which Hamberger obtained. 
This fall was explained by saying that the inelastic plaster cast finally 
caused a complete compression of the large veins and thus the heart 
secured no more blood to pump. The heart fails, therefore, not because 
of an increased resistance, but because it contains no more blood upon 
which to act. But the researches of Hamberger are interesting from the 
standpoint of the surgeon, because severe disturbances in breathing and 
heart action are occasionally observed when large plaster casts are placed 
too tightly around the abdomen, especially when intraabdominal pressure 
increases after partaking of a meal, or in conditions of distention. In 
applying these casts, this should be remembered, and an abdominal pad 
placed in such a position that it can be removed when the plaster has 
hardened. 
The stagnant contents in the paralyzed and distended loops are said to 
lead to an intoxication of the organism {auto-intoxication). This ques- 
tion of auto-intoxication, arising from products within the intestines has 
played a very large part in the literature. Metchnikoff has given this 
question its most popular form in his book on an optimistic world philoso- 
phy, which finally culminates in the recommendation to use Yoghourt- INTESTINES 
225 
milk (sour buttermilk) which by cleansing the intestinal tract, diminishes 
the intoxication and is said to insure long life. We will confine ourselves 
in this discussion to that occurring in ileus, since the conditions are the 
simplest in this disease. The special question to be decided is whether 
death in ileus is actually a result of such an intoxication as is frequently 
asserted. The theory, which unquestionably is very attractive, was first 
put forth by Amussap in 1839, and later by Humtert, Bouchard, Albu and 
many others (125). From the surgical side the practical deduction was 
drawn, that toxic intestinal contents must be removed in ileus through 
enterostomy in the quickest possible time; undoubtedly this was an enor- 
mous step forward in the treatment of ileus (100), (114), (126). Enter- 
ostomy, however, owes its favorable influence to other reasons, as was 
discussed above viz., because it removes the tension in the loops of 
intestines, as Heidenhain pointed out. 
It required many experiments to decide the importance of auto- 
intoxication in ileus; the works of Nikolaysen, Nesbieth, Kukula, Albeck, 
Borszeky and Genersich (127) may be mentioned. The plans of these 
investigations were all more or less similar. The writers produced an 
intestinal obstruction in animals in various ways (a procedure which is 
not always easy), they sterilized the contents by filtration or heat, and 
injected into other animals, either intravenously or intraperitoneally, the 
filtrate or even the gases formed in distended loops. Several also used in- 
testinal contents from human cases of ileus. The investigators then 
obtained, with considerable uniformity, certain signs of intoxication, 
usually followed by the death of the animal, which they emphasize, is 
similar to the death occurring in ileus. The next step was to isolate the 
toxins from the intestinal contents, and this led to the conclusion that they 
were probably of bacterial nature, but other substances, such as sulphur- 
reted hydrogen, phenols, etc., were isolated, which also produced severe 
symptoms. They were evidently not due to neurine, proteoses or peptones, 
substances which might occur to one (128). It was indifferent how they 
were applied, these poisons always produced the same results if the pro- 
portion to body weight was properly chosen. 
The fact must be borne in mind that these experimental procedures 
were not sufficient to decide the question, because they only tell us that 
certain poisonous products are in the obstructed intestinal contents, and 
do not decide that they cause the death of the animal. It must first be 
shown that such poisons do not exist in normal intestinal contents, or 
that they are present in a considerably smaller quantity. But this 
demonstration has not been carried out with sufficient detail in any of the 
works quoted, as Braun and Boruttau (129) point out. Albeck, it is true, 
mentioned that, in his experiments, the injection of normal intestinal 226 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
contents only occasionally, but that of strangulated loops, almost always 
caused death, or at least grave symptoms, but the very careful comparative 
results of Gamier (130) are in contrast to these more or less doubtful 
statements. The latter found on dilution of the stagnating contents, 
that there was no difference in the toxicity of the normal and obstructed 
material. Further experiments of Braun and Boruttau confirmed these 
results, indeed they showed that the injection of similarly large amounts 
of the contents of normal bowel, and strangulated loop would occasionally 
be withstood. A great deal depends on the portion of the intestine from 
which the contents were taken, at least, the studies of Roger (131), 
Magnus-Alsleben, Falloise, Braun and Boruttau, show that the contents of 
the duodenum are by far the most toxic, possibly because of the large 
quantity of enzymes they contain. Conversely, the contents of the colon 
are the least toxic. This corresponds quite well with an observation of 
Clairmont and Ranzi, that intestinal contents lose their toxicity on 
prolonged standing. 
If proof, that stagnant intestinal contents are more poisonous than 
normal is not forthcoming in these experiments, there is nevertheless the 
possibility that the toxins unquestionably present in ileus, are absorbed 
more rapidly than under normal conditions, and may produce their 
damage because the organism cannot keep pace with its splitting of the 
poison. Clairmont and Ranzi have studied the absorptive processes in 
ileus in the following way: an obturation ileus was produced and at 
various intervals laparotomies were performed and iodide of potassium 
injected into the dilated loop; the excretion of the iodide was then deter- 
mined in catheterized urine. They believe these experiments showed that 
there is an increased absorption at first, but later it is delayed. However, 
as Braun and Boruttau emphasize, only the time elements have been con- 
sidered in these investigations, and this gives a false picture of the magni- 
tude of absorption. In place of the potassium iodide, these workers 
therefore, injected a crystalloid poison (strychnin), and then they showed, 
in the first place, that it requires a much larger quantity of the poison, to 
produce convulsions and death, when this substance is injected into a 
distended loop, and secondly, the convulsions and death in ileus occur 
later than under normal conditions. “The intensity and rapidity of 
absorption in ileus are as a rule immediately and increasingly diminished. ” 
Finally Enderlen and Hotz (18) in very extensive experiments, studied the 
same question in both ileus and in peritonitis. They found that absorp- 
tion is diminished quite early in ileus and ceases almost completely soon 
after. In peritonitis, the absorption is unchanged at the beginning, but 
in the later stages it is greatly diminished. 
Furthermore, the question arises, is the experimental disease or its 
course similar to that observed clinically in man? This cannot be INTESTINES 
227 
answered positively. A striking difference is this, the animals in experi- 
mental poisoning from intestinal contents die in convulsions, while this 
symptom, as is well known, is very rare in human ileus. The same phe- 
nomena are observed in animals even when the poison has been injected 
very gradually or in small quantities over longer periods. Furthermore, 
careful examinations of the blood pressure and respiratory curves in the 
ileus animals, and in the animals who have received injections of intestinal 
contents, show that they have not the least similarity (Braun and Borut- 
tau). The statements that the animals die after the injection of intestinal 
contents, with the same symptoms as those observed in ileus rest therefore 
on inaccurate observation. 
McLean (132) has attempted to solve this question in a somewhat 
different manner and by a more suitable method. He removed blood from 
dogs suffering from ileus and injected it into others. Even with this 
procedure, no symptoms of intoxication developed, and he transferred 
almost the entire blood in a number of instances. Thus we may sum up 
by saying that, thus far, there is no proof that the death from ileus is due 
to an intoxication from stagnating intestinal contents. Furthermore, 
Sauerbruch and Heyde’s experiments (133) on animals, which had been 
previously sewed together “ parabiotically ” also have not demonstrated 
the presence of a more severe auto-intoxication in ileus. The fact that 
after ligation of the intestines in one of the animals there was a rise in the 
temperature of both, is too ambiguous, and cannot be used to show the 
cause of death in ileus. 
Another group of authors believe that the clinical course of ileus is a 
bacteremia. We shall discuss the permeability of the intestinal wall for 
bacteria in the paragraphs on peritonitis (paths of infection of the perito- 
neum). Bacteriological examinations of the blood and peritoneum in 
experimental ileus have been made particularly by Albeck, and Borszeky 
and von Genersich (127). As could be expected after what was said in 
relation to peritonitis, no constant success attended their efforts. Bacteria 
could be demonstrated in the blood in only about half of the cases, and in 
the peritoneum, only after quite severe injury to the intestinal wall. 
Clinically, ileus is not a septic process, even though a great number of these 
patients finally die with the same symptoms as those of peritonitis, namely, 
circulatory failure. Death from ileus might therefore be considered 
similar to that from peritonitis, but the question of the fundamental cause 
of the circulatory disturbance must be left open. Pathologically anatom- 
ically, the infection of the peritoneum in ileus is often not very severe, 
but then in peritonitis also, the severity of the symptom complex by no 
means depends on the pathological anatomy. As a matter of fact we do 
not know on what it does depend. 228 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
The clinical course of the disease differs so essentially from that of 
peritonitis that there must be something exceptional. If auto-intoxication 
is not probable on account of recent researches, then it still remains an 
open question what this remarkable something is. The investigations of 
Kirschstein (134) and Reichel (13) are of especial interest in relation to 
this point. They found that if the small intestine is cut through and the 
end closed, it was possible to keep animals living for six weeks without ileus 
developing, the animal’s final death being due to increasing loss of appetite 
and starvation. From these experiments we see that the whole symptom 
complex which we call ileus, that is, vomiting, wasting, liquefaction of 
intestinal contents, etc., is not a simple mechanical result of intestinal 
obstruction. Reichel believes his experiments indicate that there is 
either a reflex action from a strangulated intestinal loop, or peritoneal 
inflammation at the basis of the whole process. 
It is obvious that extraordinarily complicated pathological physiologi- 
cal processes are concerned in this problem and we are still unacquainted 
with the details. 
[Sweet and his collaborators (Sweet, J. E., Peet, M. M. and Hendrix, 
B. M., Ann. Surg., p. 721, 1916) have called attention to the clinical 
similarity, between high intestinal obstruction and acute pancreatis. 
From experiments in which they considered the presence or absence of 
pancreatic juice, they are led to conclude that without its intervention, 
the acute toxemia of intestinal obstruction does not occur. This would 
explain the fact that closed loops of ileum do not give toxic symptoms. 
That is, animals in which a blind end of the duodenum longer than 35 cm. 
from the pylorus is made, live, while if it is less than 35 cm. the animals 
die. Whipple and his associates working on the same problem were 
able to isolate a highly toxic substance of the nature of a protease, from 
isolated loops. They believed it is formed in the intestinal loop, or from, 
or by the mucosa. Sweet believed the proteolytic ferment of the pancre- 
atic juice is concerned in its appearance. Whipple however, has demon- 
strated the presence of toxic proteases in the exudate of peritonitis 
(Whipple, G. H., J.A.M.A., 67, p. 15, 1916).] 
An important diagnostic sign in ileus, is ringing and tumbling noises 
in the intestines which are occasionally somewhat similar to the noise 
produced by the emptying of a bottle. They appear at the end of a colicky 
pain and are caused by the back flow of fluid contents and gases from the 
obstruction. The metallic ring indicates tension, and is due to bubbles 
rising in the fluid contents, or to drops falling back from the wall onto the 
surface of the fluid. They have been studied experimentally by Wilms 
and Leuenberger (135). 
Manipulations of the intestines and of the peritoneum, may lead to 
what we designate as shock. This expression is a collective idea. In the INTESTINES 
229 
first place, the shock of anaphylaxis must be differentiated from so-called 
surgical shock, even though the possibility exists that further investiga- 
tions will show a certain similarity in their clinical symptoms. Experi- 
mentally, anaphylactic shock can be produced by a series of proteins, 
peptones and histamines. The cause in this case is an alteration in the 
blood distribution. As the investigations of Mauthner and Pick have 
shown, there is a constriction of the blood vessels both of the liver and the 
intestines. During the contraction of the liver capillaries, the venous 
blood in the intestinal vessels is choked back (136). A constriction also 
occurs in the capillaries of the lungs. Blood pressure falls because the 
heart receives nothing to pump. 
This fall in peripheral blood pressure is the most prominent sign in the 
shock after abdominal operations. According to the opinion of Crile 
(137), and Mummery (138), the blood pressure sinks because of paralysis 
of the vaso-motor center. But numerous investigations of other writers, 
such as Malcolm (139), Seelig and Lyon, Mann (139), have showm that the 
blood vessels in shock are not dilated but constricted. This applies 
equally to those of the abdomen. There is thus this remarkable similarity 
to the constriction occurring in anaphylactic shock. As stated, unques- 
tionably the fall of blood pressure is the most prominent sign. Its cause 
is not known with any degree of accuracy; that influences which lead to 
shock, act on the central nervous system seems very probable. It is 
possibly not entirely incorrect, to consider with Brown that shock is 
caused at times by the anesthetic and at times by pain sensations which 
reach the nervous system unconsciously, notwithstanding anesthesia (140). 
He considers shock, after operation, a condition of general exhaustion of 
the nerve cells. It cannot be denied that this is a very pertinent idea, 
for it is an old experience that fatigued patients are poor operative risks, 
as for example, soldiers exhausted from severe physical or psychic strain, of 
which Nelson’s surgeon in the naval engagement of Trafalgar has already 
spoken. Ordinary hospital experience also shows how much the post- 
operative course depends on psychic factors, on the energy, and on the 
courage of the patient. But howT these things are related to each other in 
detail is not at all clear. 
Other theories have been proposed to explain the different clinical 
symptoms of shock. Yandell Henderson (141) sees an essential factor 
in carbon dioxide impoverishment of the blood, and he believes that if 
the intestines are strongly stimulated in abdominal operations, breathing 
is more rapid and deep and thus the carbon dioxide of the blood is blown 
off and the natural respiratory stimulant diminishes. Cessation of breath- 
ing is therefore said to be the primary factory in shock. The blood 
pressure would fall later. Among others, Janeway and Ephraim (142) 230 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
subscribed to this opinion, but Short (143) on the other hand, has been 
unable to demonstrate a diminished carbon dioxide during surgical shock. 
Cobbet and Valte (144), in their theory of oligemia, see an increased vis- 
cosity of the blood as the cause of shock. Once again, Short could not 
demonstrate this condition. According to the opinion of Bainbridge and 
Parkinson, the cause of shock is to be found in an exhaustion of the ad- 
renals, but later investigators on this particular question have arrived 
at varying results, although the theory enjoyed fairly extended accep- 
tance. The least that can be said of these last mentioned theories is 
that they were probably too precipitate in their conclusions. It is better 
to first collect a plentiful amount of data, both from observation and 
experiment, and when this is sifted, begin to construct definite disease 
pictures. The future must decide whether surgical shock should be 
considered one or many diseases. 
[Cannon, after considering the results of observations and experiments 
during the war and correlating them with previous knowledge, has 
written a critique which well covers the ground (/. AIM. A. 70, p. 611, 
1917; 70; see also J. Lab. and Clin. Med. Edit. 21, 6, p. 405, 1920]. 
The mechanism of intestinal injuries from the application of blunt 
trauma to the abdomen has been well studied both clinically and experi- 
mentally, so that there is complete harmony in the views of the essential 
points. The magnitude and the direction of the force, as well as the place 
on the abdomen to which it is applied, determine the type of injury. The 
mechanism in both stomach and intestines is quite similar and may be 
discussed jointly under the classification of contusions, ruptures, and tears 
by pulling forces (145). 
An injury from crushing is produced, as Morgagni (146) has described, 
when the anterior abdominal wall is pressed inward with such force that 
the intestine is caught between it and the vertebral column. The abdom- 
inal wall itself is not injured probably because of its anatomical structure, 
on which Longuet and Beck (147), lay particular stress, but even more so 
perhaps, because it is not squeezed directly against the bone, the bowel 
acting as a sort of shock absorber (148). It follows that crushing of the 
intestines is less likely to take place under a tense abdominal wall than 
under one which is relaxed, and actually it is not possible to produce this 
type of injury, by a blow on the taut abdominal walls of a dog tied up with 
his hind legs extended. 
This idea had been forgotten for a long time until Longuet, on the basis 
of an experiment, again formulated and proved its worth. Later investiga- 
tors (149), who worked either on cadavers or animals, found that the 
falling blow must be directed against the vertebral column or the iliac 
fossa; if it was struck over a larger area, only those loops were torn which INTESTINES 
231 
had previously been fastened to a bony base (Curtis). It was not neces- 
sary to hit the median line or the region of the ileum, but the direction of 
the force had to press the abdominal wall against the underlying bone. 
Furthermore it was found, that the loop of intestine must be filled, 
not with air since that is compressible, and tears could be achieved only 
with difficulty (Curtis), but with fluid or hard feces when it is still more 
endangered on account of the greater circumference, thereby differing 
from ruptures, which will be discussed presently. Her tie (150) in his 
studies of the anatomical picture in crushing, found that mild injuries 
tear only the serosa and perhaps the mucosa; the muscularis and the sub- 
mucosa remain intact. More severe trauma tears all the layers, but the 
serosa and the mucosa are usually split over a greater area. 
For rupture to occur, it is necessary that a closed space be formed 
by kinking, displacement or adhesions. The intestinal contents then 
can not escape into an adjacent loop at the moment the force is applied, 
but must exert pressure from within outward when the space is suddenly 
reduced. In the pure cases, therefore, the rupture does not occur at the 
place where the blow falls, but distant from it. This conception has 
given rise to many doubts (151), but Hertle attempted to demonstrate its 
possibility by allowing water to flow through an excised loop of intestine 
and then rupturing it by a blow with his fist. Human findings, appear 
more conclusive, that is, there have been cases reported, though few, in 
which the rupture is distant from the place on which the blow fell, and in 
which a crush can be entirely excluded (Hertle). The opinion of Kempf 
(152), that the air compressed by a blow expands with such power when 
the force is removed, that it ruptures the bowel from within, requires 
considerable experimental support. As a matter of fact, pure rupture is 
probably a rare injury, it is usually combined with crushing, as 
exemplified in the critical references to the cases reported by Petry (153), 
Sauerbruch, Bunge, Hertle and others. By overdistention of the large 
intestine with air, a purely mechanical rupture may be obtained. Clini- 
cally, this may happen when the organ is inflated for diagnostic purposes in 
the presence of ulceration; and such injuries have been described as 
occurring in industries which use compressed air (154) (14 cases of rupture 
of the sigmoid). Anatomical investigations have shown similarly, that 
the serosa and then the mucosa is torn, while the submucosa seems to 
be the most durable and remains intact until the last (Hertle). With 
certain precautions, therefore, conclusions of the type of injury may be 
drawn in a given case, since in crushing the musculature is always torn 
first while the serosa is equal in its resisting power to the submucosa, but 
is much less so in distention. Particular interest has always centered 
around those tears which occur from severe and violent exertion, chiefly 232 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
compression without the application of outside force. Since the pressure 
within the intestine, and that acting on the abdominal wall from the out- 
side, run parallel, a bursting rupture can only occur when there is a 
circumscribed place in the abdominal wall which is elastic, that is, in 
hernias (Bunge). Then a series of events well known to automobilists 
follows; if the casing of a tire is defective at one place and the tube is 
blown up very tightly, the latter first forms a small projection into the 
defect, and finally blows out. The bowel ruptures in a similar way under 
strong pressure, if a portion of its wall can force itself through a hernial 
opening. The peculiar tears of the rectum during violent abdominal 
compression, have also been explained by Bunge’s deductions. Here, 
Douglas’s cul-de-sac, that is, the place through which the rectum passes 
through the levator ani, is the weak point into which the small intestines 
are forced; the rectum stretches, and finally tears. It is a fact, that 
tears in the rectum are found exactly at this place, and loops of small 
intestines often lie in the rectum. Furthermore, such injuries are found 
more frequently when there has been a previous prolapse. 
The mechanism of pulling has been expressed as follows: (Strohl in 
1848) (155), “if an elastic body is to be torn, it must be fastened at one 
end and be pulled away from the place of fixation by some force” (148, 
p. 140). According to A. Neumann (156), the force may be applied either 
perpendicularly or parallel to the axis of the intestines, the difference 
being in the direction of the tear, especially that of the mesentery. Among 
the causes of this form mentioned in the literature, are fall from a height, 
kick from a horse, being run over, blow from a wagon tongue, etc. The 
direction in which the force exerts its action is the important factor in all; 
thus, Sauerbruch produced separation of loops of intestines from their 
mesenteries in cadavers, by delivering a blow against the abdomen from 
the side. Hertle explains the action of pull in being run over, in this 
way; the intestine is caught through the abdominal wall by the wheel 
somewhat like a brake, or the intestine folded against the mesentery 
becomes stretched and tears at its point of fixation. Petry (153) describes 
a case in which he could analyze the direction of the force and its pulling 
effect by the traces left by a hoof on the sigmoid flexure. Anatomically, 
injury from a pull is characterized both by sharp margins which show 
no crushes and by the oblique and transverse directions which the tears 
take. In a fall from a height, a pulling force is exerted on the intestine, 
because similar to the rest of the body, the loops of intestine participate in 
the energy of movement. This momentum is still in action when the 
body strikes the ground, and is brought to rest. A transverse tear is the 
natural consequence, occurring usually at the highest loop of the jejunum, 
near the duodeno-jejunal flexure, which, being fixed, does not yield to INTESTINES 
233 
the pull. In cases of being run over, an occasional result of the pull is 
a circumscribed stripping off of the serosa (Hertle). 
The gravity of the peritonitis following, depends on how high a loop 
was injured, and on the amount of intestinal contents which escape. 
In transverse rupture, only a small amount will be present in the abdomi- 
nal cavity if the patient has not consumed much water, chiefly because 
the mucosa rolls up and plugs the opening (157). 
Apart from the primary peritonitis, hemorrhage and gangrene are to 
be feared because of involvement of the mesenteric vessels. The latter 
may also occur without injury to the intestines (158), as Eichle demon- 
strated experimentally, but little can be added to the statements above 
concerning their mechanism. If the bowel is stretched (bursting mech- 
anism), it may be torn from its mesentery immediately at the point of 
attachment and in a direction parallel to it. These injuries are often 
considered less important than those affecting the intestines themselves, 
but the mortality of unoperated cases, is very high (159). As cases of 
Aldrich and Matthes (160) show, hemorrhage does not always begin at 
once, but may make its appearance days after, although the latter event 
is rare. 
Free hemorrhage into the abdominal cavity is always an indication for 
surgery. That a puncture of the epigastric artery by a stab wound, may 
lead to a pouring out of blood into the abdominal cavity, is not difficult to 
understand. Hematomata readily form in the leaves of the mesentery 
after blunt injuries; if chylous vessels are also injured, a so-called chylous 
ascites develops; a late consequence may be a chylous cyst. These 
hematomata, may, by pressure on vessels, produce secondary gangrene 
of the intestines (161). 
Blunt injuries, that is, crushes, are occasionally produced by attempts 
to reduce strangulated hernias by taxis. Rarely, but still occasionally, 
the mesentery is injured by the application of a Momburg tube. Verth 
(162) among others, reports a case in which, after prolonged constriction, 
there occurred a severe injury to the mesenteric vessels, which was the 
direct cause of death. 
The results of injury to larger vessels in the mesentery cannot be 
separated in their pathological physiological results from thrombosis 
and embolism, since the injuries sustained by the intestines, through such 
lesions, are exactly similar (163). 
Litten’s (164) investigations have shown that ligation of the main 
trunk of the superior mesenteric artery in animals is always followed by 
extensive intestinal infarction, from which the animals die. After the 
ligation, the intestines become bluish red, are saturated with edematous 
fluid, and become thickened. Blood leaves the vessels and enters the 234 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
surrounding tissue, and this increases the discoloration. In other words, 
there is that accumulation of blood in the loops of intestines, which we 
call hyperemia; but why is it that blood accumulates in the loops of bowel 
which have been robbed of their arterial blood supply? Litten adopted 
the same opinion held by Virchow and Beckmann and Cohnheim (165), 
who believed that hemorrhagic infarction after ligation of an artery is a 
result of venous back flow, since no pulsation could be demonstrated 
either in the mesentery or in the bowel, even up until the death of the 
animal. But Cohn, and von Recklinghausen (166) considered this ex- 
planation insufficient, because hemorrhagic infarction was just as pro- 
nounced, or even more so, when the vein, in addition to the artery, had 
been ligated. They believe there is an inflow of arterial blood from the 
margins of the infarct. Litten indeed, had demonstrated that there were 
anastomoses between the inferior and superior mesenteric arteries at the 
margin of the intestines. The superior mesenteric artery is, therefore, 
anatomically, not an end artery, but since such severe nutritional dis- 
turbances result after its ligation, Litten calls it a “functional” end artery. 
A sufficient increase in pressure in the inferior mesenteric artery is not 
developed to fill the collateral channels. But this idea is somewhat mis- 
leading, because the experiments of Bier (167) have shown that a marked 
increase in pressure occurs only when both carotids are ligated, while 
usually the development of a collateral circulation after ligation of any 
artery, is not dependent on an increase of blood pressure. 
The mechanical conditions for forming an anastomosis are more 
favorable in the case of the inferior mesenteric and the celiac arteries. 
Ligation of their trunks, therefore, leads only to a passing hyperemia and 
not to a necrosis of the intestinal wall. 
The whole question entered into a new phase with the observation 
of Sprengel (168), that occasionally, although rarely, an anemic infarct 
may occur in the intestines. Niederstein (169), under Sprengel’s direc- 
tion, studied the conditions under which such an infarct arises. They 
believe that for an anemic infarct to occur, it is necessary that thrombosis 
of the veins be produced in addition to obstruction of the artery. The 
technic, which Niederstein used, in addition to ligation, consisted of the 
injection of paraffin into the vessels. The conclusions, however, are not 
entirely convincing, and objections, such as those of Marek (170) cannot 
be put aside. The latter worked independently and almost at the same 
time as Niederstein, who did not take into sufficient consideration—indeed 
he could not with his technic—how great a part the paraffin played in 
blocking off the arterial anastomoses. Marek, on the other hand, could 
show accurately that to produce an anemic infarct of the bowel, it is 
sufficient to interrupt all the arterial blood supply. According to him, it INTESTINES 
235 
is quite indifferent in the production of an anemic gangrene, whether 
blood coagulation took place in the veins or not. With this, the question 
of why hyperemia occurs, when the mesenteric artery is obstructed, is 
very probably decided. Arterial inflow, through the anastomoses, is 
essential. A venous backflow only increases the results of the arterial 
collateral supply, but can never suffice alone to produce hyperemia in an 
isolated segment of the intestine which has had its arterial supply com- 
pletely interrupted. 
Bier has attempted to explain the reason for the formation of a col- 
lateral circulation after occlusion of one of the main arteries, by stating 
that the smallest vessels in the anemic area dilate automatically, that is, 
independently of the central nervous system, and suck up the blood, as it 
were. There seems also to be a certain selective action, especially among 
peripheral arteries,, in that the vessels are closed to a venous backflow, 
but are open to arterial blood, thus, automatically sucking this nutritive 
blood into their lumena. This faculty of the small vessels, is supposed to 
be developed more poorly in the intestinal vessels than in those of the 
extremities. 
Ligation of the trunks of the mesenteric vein is also followed by hemor- 
rhagic infarction but ligation of isolated branches leads only to stasis, the 
blood quickly flows into the abundant collaterals, and no lasting injury 
results. If, the main trunk of the vein is ligated and collateral circulation 
rendered impossible, the congestion in this area becomes more and more pro- 
nounced, as the artery continually adds blood, until the overloaded small 
vessels rupture and blood escapes into the tissues. Hemorrhagic infarction 
and later gangrene are the natural consequences. In man, ligation of the 
superior mesenteric vein, is always followed by a fatal infarction. The 
contrary statement of Mayo Robson (171), in which he believes that he 
ligated the main branch of the superior mesenteric vein without the death 
of the patient, is doubted by Wilms (172) since, judging by the position 
of the wound in this case, it appears impossible that an injury to the main 
trunk of this vein was produced. It can be reached only behind or above 
the pancreas. Of course, there are occasional anatomical anomalies which 
might permit of sufficient collateral circulation after ligation of this vessel, 
but they must be rare (see 159, p. 221). 
Thrombosis in the mesenteric veins in man usually produces less 
severe results than ligation. It does not obstruct as quickly and therefore 
time is left for the development of sufficient collaterals. Hemorrhagic 
infarction is rare, and occurs only if all the smaller vessels have been 
occluded. There are many accidental causes which produce thrombosis 
and it occurs in all probability almost daily after operative interference. 
Thanks to the well developed collateral circulation and the slow formation 236 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
of thrombi, it is rare to find extensive injury, especially gangrene of the 
intestines (about 50 cases have been described). 
The question of safety after ligation of small vessels in the intestines 
awakened general interest when gastric and intestinal resections were 
first performed. Madelung and later Rydigier (173) performed experi- 
ments on this question. They found it impossible to establish general 
rules as to which vessels of the mesentery of the small intestine could be 
ligated without danger of gangrene. As is well known, the mesenteric 
vessels branch into the so-called arcades. Individual arcades or annular 
anastomoses occur in varying number in the small intestines—about 
three to five. Individual arcades can, of course, be ligated, but the closer 
the ligature is applied to the intestine, the greater the danger, since the 
anastomoses become fewer as that region is approached. The attempt to 
determine metrically at what distance from the bowel the ligation would 
be devoid of danger, has failed completely, since the individual differences 
are too great. In injuries, however, as is easily understood, tears in the 
mesentery parallel to the intestines are always more dangerous than those 
that correspond to the radius of the mesentery. 
The vascular supply of the large intestine is somewhat different; the 
arcades are fewer, and there is really a so-called marginal vessel running 
parallel with the bowel and sending supply branches into that organ. In 
this case, also, the results of injury may easily be deduced from the ana- 
tomical facts. 
The microscopical findings in hemorrhagic infarction of the intestines 
have frequently been studied. It is very important that the injury should 
first affect the sensitive mucosa, which then becomes ulcerated. After 
ligation of one of the main branches of the mesenteric artery, the nutrition 
of the capillaries in the mesentery is also impaired and blood can pass 
through the vessel walls into the tissues, i.e., by diapedesis. Even if 
ligation, injury, embolism or thrombosis, do not lead to an extensive 
gangrene, there may arise conditions of the intestines which indicate 
disturbances in nutrition. Most important are the ulcers, which are 
frequent, probably because of the greater sensitiveness of the mucosa. 
As the experiments of Schloffer (174) have shown, stenosis may occur 
from such ulceration, and possibly without it, and we find it occasionally 
as a cause of ileus. Physiologically, therefore, the most important factor 
in such cases is always the defective blood supply. When, therefore, a 
stenosis is discovered years after a crushing injury, it should not be assumed 
that the intestinal wall itself was injured directly by squeezing, but that 
the mesenteric vessels were involved, and as a result, a small amount of 
intestine became gangrenous. Busse (175) takes the same view in rela- 
tion to tuberculous stricture of the intestines. He believes, on the basis of INTESTINES 
237 
pathological anatomical investigations, that, iii such cases, the ulcera- 
tion itself is not the cause of stenosis, but the injury to the blood vessel 
supplying the diseased area leads to a stricture, similar to those described 
by Schloffer. 
The symptoms, following obstruction of the mesenteric vessels, depend 
on the intestinal infarction. Embolism and thrombosis cannot very well 
be differentiated in their symptomatology, even though their etiology is 
entirely different. Cardiac disease or arteriosclerosis must first be 
considered as causes of embolism, in which also a thrombus may form secon- 
darily and involve the veins. In true mesenteric vein thrombosis, a throm- 
bosis primary in the portal vein which secondarily involves the mesenteric 
vessels may be differentiated from a primary mesenteric thrombosis, but 
both are rare occurrences. 
In view of the many injuries which occur to veins during operation, 
it is really remarkable that thrombosis is not observed more often. Small 
ones, as were studied by Payr (176), actually occur, but as a rule, they 
remain localized and produce very few, if any, clinical symptoms. It is 
only in intestinal obstruction that thrombi carried from the intestines, 
are important. An event observed, not rarely, is increasing infarction in 
a loop of intestine apparently healthy as it is released from a strangulated 
hernia. As is easily understood, this is due to the greater arterial inflow 
from the margin through the anastomoses, and simultaneous occlusion of 
the venous outflow (see above, under “retrograde incarceration”), the 
arterial supply having previously been interrupted because of separation 
or kinking and beginning again after liberation of the constriction. This 
progression of the nutritional disturbances in strangulated hernias is 
well known, and the practical deduction follows, not to resect too little, 
but from five to seven times more than the loop which was contained in 
the hernial sac. 
Less surgical interest is attached to the much discussed “phlebosclero- 
sis,” i.e., primary disease of the walls of veins with which thrombosis is 
associated. Furthermore, changes in the coagulability of the blood are 
also factors favoring mesenteric thrombosis, as the increased coagulability 
found by Schmorl (177) in eclampsia. It may be mentioned, in passing, 
that obstruction of the mesenteric vessels with the formation of aneurysms 
is not an unusual cause of death in horses infested with worms. 
Of all the thrombotic processes in mesenteric vessels, those developing 
in connection with infections in the viscera are the most interesting in 
surgery. In these forms of thrombophlebitis, it is not the intestinal 
infarction which interests us, but the suppurative process in the veins, 
clinically characterized by pyemia, with chills and rigor, and which leads 
to multiple abscesses of the liver. We find this condition following gastro- 238 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
intestinal inflammations and ulcerations, cholelithiasis, occasional infec- 
tions such as anthrax (178), and especially appendicitis flit, see Sprengel 
(179)). If pus once enters the veins, a fatal outcome is almost certain, but 
Wilms (180) succeeded in saving a number of such patients by ligating 
the veins in the meso-colon. Late thrombosis may also occur following 
appendicitis (181), but strangely enough, it is quite rare in typhoid fever 
and dysentery (182). 
Clinically, the severe pain in mesenteric embolism and thrombosis 
(183), which we have already mentioned in discussing abdominal pain in 
general, is very striking; blood appears in the stools from the ulcerative 
processes, and there is a rapid pulse as in all affections of the peritoneum. 
The latter should probably be considered a result of reflexes. 
PERITONITIS 
One of the most important symptoms of peritonitis is the reflex rigidity 
of the abdominal walls, to which Trendelenburg especially called attention 
in the diagnosis of intraabdominal injuries (184). A. Hoffmann (185) 
has studied the conditions under which this rigidity appears by injecting 
irritant substances into dogs and goats—oil of turpentine proved to be 
most effective—first into the musculature of the abdominal wall, then into 
the muscles and nerves adjacent to the vertebral column, then into the 
exposed intercostal nerves and finally into the peritoneal cavity. By a 
suitable operative procedure, he was able to separate the parietal and 
visceral peritoneum. These experiments were intelligently combined 
with section of the sensory roots in the spinal canal, and finally, as a 
supplementary procedure, the irritants were also injected into the pleural 
cavities. As a result, he found that rigidity of the abdominal walls is a 
reflex process running by way of the intercostal and lumbo-sacral nerves. 
It is produced only when the parietal peritoneum is irritated, but may be 
easily produced through direct action on the intercostal and lumbo- 
sacral nerves, as occurs, for example, in kidney injuries, when there is 
inflammation in the region of the spine. These experiments explain the 
frequent observation that abscesses lying centrally in the abdominal cavity 
are not often accompanied by rigidity 
As has been mentioned above, appendicitis in its early stage is almost 
always accompanied by a peritonitis, probably toxic, and this fact explains 
the generalized rigidity. This sign, however, soon subsides, only to 
reappear when the appendix perforates and a purulent peritonitis is 
initiated. The inexperienced are therefore tempted in the beginning stage 
of an appendicitis to make a larger incision than is necessary. Irritation of 
the sensory nerves at their point of exit may also produce rigidity and thus INTESTINES 
239 
lead to diagnostic errors. Many a case of gun shot wound of the kidney 
or of perinephric abscess has been subjected to laparotomy because the 
abdominal rigidity suggested peritonitis or injury to a viscus, and in the 
literature, cases have been described of crushing wounds of the vertebral 
column in which this symptom was present to a high degree (186). Further, 
the experiments of Hoffman give an explanation for it, when it is 
present in pleuritis and pneumonia, for the abdominal muscles became 
very tense after the injection of oil of turpentine into the pleural cavity. 
The surgeon, now and again, sees cases of pneumonia diagnosed as appen- 
dicitis. But whether this is an “irradiation” as Hoffmann calls it, or 
whether it is actually an inflammatory process spreading through direct 
lymphatic channels (187), from the pleura to the region of the appendix, 
is not yet clearly determined. 
Since abdominal rigidity is a reflex process, it follows that it occurs in 
irritations of the parietal peritoneum as long as the short reflex arc is intact, 
i.e., it will occur even after section of the spinal cord in the middle or upper 
thoracic regions. This fact may also have occasional practical significance. 
The most important disease of the peritoneum is acute bacterial 
inflammation (188). In the great majority of cases the primary cause 
lies in one of the viscera, the appendix, gall bladder, stomach or female 
genitalia (see in those chapters); in a small number of cases, the primary 
focus cannot be demonstrated. Corresponding to the great variety of 
intestinal flora, varied organisms are found in the exudate of peritonitis, 
and they are not only of one type, but a mixture of many varieties. It 
has been attempted, of course, to separate from the mixture a specific 
organism on which to lay the blame for the peritonitis, and on the basis 
of such investigations, for example in appendicitis, the colon bacillus has 
often been considered the offending cause. -The fact, however, that a 
certain organism outgrows all others in the culture tube does not neces- 
sarily indicate that this particular bacterium is the cause of the disease. 
Indeed, every one with even a small amount of experience in bacteriology, 
knows that the colon bacillus grows especially easily and abundantly, and 
that it is impossible, or at least very difficult, to isolate other organisms 
from a mixture in a test tube in which this organism is implanted. We 
should only consider a bacterium the cause of a peritonitis in cases where 
it can be demonstrated that the body has developed antibodies toward it, 
such as agglutinins, etc. The work on animals which has attempted to 
establish the pathogenicity of an organism has also a certain value in 
peritonitis; all others are interesting only as illustrative contributions. 
In the compilation of Weil (189), it is found that in the peritonitis 
following appendicitis, colon bacilli were present in 60 per cent, of the cases, 
B. coli and streptococci in 19 per cent. B. coli and other bacteria 4 per cent., 240 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
streptococci in 9 per cent., diplococci in 3.5 per cent., and staphylococci 
in 1 per cent., the remainder was divided among B. proteus, fecalis alkali- 
genes, pyocyaneus and mixed infections without B. coli. The anerobes 
were not considered in these figures. 
But it is just these latter which, according to newer investigations, are 
of particular importance in the etiology of gangrenous peritonitis (Veillon 
and Zuber, Tavel-Lanz, Ali Krogins, Friedrich, Heyde (190). There are, 
of course, different opinions concerning the classification of these anerobic 
organisms, but Heyde found Bac. fusiformis, fragilis, ramosus and anerobic 
staphylococci in his investigations. All of these types are highly toxic 
(toxin formers), and in fact, many of the cases of post-appendiceal peri- 
tonitis show the picture of a severe intoxication and not an actual sepsis. 
The anerobes just mentioned are putrefactive bacteria, hence the pene- 
trating stench of appendiceal pus. Rumberg (191) found the agglutinin 
titer of the blood markedly increased to certain of these organisms, which 
fact is of interest for reasons above mentioned, even though it should not be 
overestimated. 
In a large percentage of his cases of appendicitis, Heile (192) found an 
anerobic, spore bearing bacillus, probably belonging to the group of potato 
organisms, which had, like other anerobes, marked necrotising and toxic 
properties. In severe cases, the agglutinin titer was very high for these 
spore bearers, but unfortunately it was not determined in these investiga- 
tions whether it was also increased for other bacteria. 
For the etiology of post-appendiceal peritonitis, the recognition of the 
importance of these putrefactive organisms is a big step forward, for the 
frequent gangrene of the appendix was not readily explainable from our 
knowledge of those inflammations in which the ordinary pyogenic organ- 
isms were involved. How far the course of a peritonitis is influenced by 
such putrefactive organisms has pot been revealed in detail, but clinically, 
it is not unusual to see very severe cases of post-appendiceal peritonitis in 
which the picture of a severe toxemia is developed. It has been attempted 
to differentiate streptococcus peritonitides from the others (193) but not 
without opposition. The agglutinin titer and the opsonic index have, thus 
far, not been found increased to streptococci (Runneberg), so that proof 
that these particular organisms are the decisive factors in the respective 
cases, is not complete. 
A “chronic” peritonitis may be produced by mechanical irritation 
without infection, as shown by Wegner who repeatedly blew air into the 
abdominal cavity, and by Wieland (194) who introduced sterile foreign 
bodies. 
This leads to the question of how bacteria gain entrance to the peri- 
toneal cavity. In the first place, they may enter from the intestinal INTESTINES 
241 
canal through perforations, not only of the appendix, but also from the 
stomach or any other part of the intestinal tract, as for example, in typhoid 
fever; and the following rule has been enunciated: “the higher in the 
intestine the perforation, the more often are streptococci found in the pus; 
and the lower the perforation, the more frequently are colon bacilli 
present.” It may be mentioned that, according to Cushing and Livingood 
(195), the bacterial flora in the upper gastrointestinal tract is less in 
variety and amount than that lower down. 
The mode of infection of the peritoneum in perforations is not difficult 
to understand, and this is also true in gall bladder and biliary duct infec- 
tions, and those of the female genitalia. Of course, it must not be for- 
gotten that the peritoneum very stubbornly resists suppurative processes 
developing in its vicinity, and as shown in the experiments and clinical 
investigations of Meisel, it succumbs only when there is in addition a 
profound disturbance of its circulation (196). Ordinarily, pus pushes 
the peritoneum ahead of it, or stretches it. We are indeed justi- 
fied in seeing an important protective mechanism in this elasticity and 
displacement of the peritoneum, as when we observe the serosa of the 
gall bladder stretched to two or three times its original size by an empyema 
of that organ. 
It follows that in wounds through the abdominal walls in which there 
are no intestinal injuries, there is no great danger of infection, as numerous 
experiences in the war have shown (see Schmieden (197)). The experi- 
ments of Friedrich (198) show that the incubation time of peritoneal infect- 
ions is about the same as in external wounds, namely from six to eight hours. 
In perforations of the stomach, much depends on whether it was caused by 
ulcer or carcinoma. As Brunner (199) found in animals, gastric contents, 
free of hydrochloric acid, as we often see it in carcinoma, are much more 
dangerous than the normal contents. 
The cases of peritonitis in which no communication between the 
lumen of the organs and the peritoneal cavity can be discovered, are 
far more difficult to explain (200). The question of whether there is 
actually a penetration of the intact intestinal wall by bacteria has been 
examined experimentally from all viewpoints. Many workers attempted 
to find bacteria on the serosa or in the fluid, in incarceration of the intes- 
tines, especially incarcerated hernias. Their results do not harmonize 
entirely, but the differences may be explained by technical errors which 
need not be discussed. To summarize, bacteria were demonstrated 
only occasionally, and it was necessary that the intestinal wall be rather 
severely injured before they appeared in the serous fluid in hernial sacs. 
Ordinarily, the organisms normally present in the intestine do not pene- 
trate its walls, as is taught by our every day experience (201).  THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
242 
The more important experiments are probably those which have 
attempted to show whether foreign organisms, pathogenic to the individual, 
would pass through the intestinal walls, when swallowed. This work 
also led to varying results, but it seems that virulent organisms can pass 
through an undamaged intestinal wall under certain circumstances, and 
lead to a general infection (202). The first researches on this question 
were undertaken by Kocher (203), but his results are not of value, because 
he produced injuries to the legs of his animals at the same time. Karlin- 
ski (204) added staphylococci to the milk of new born animals and found 
a general infection in a goodly percentage of the cases. Of course, the 
objection that the portal of entry may not have been the intestinal tract, 
but the tonsils, for instance, cannot be gainsaid. Neisser and Buch- 
binder (205) could not convince themselves that the intestinal wall 
was permeable to bacteria, but both of these writers have paid too little 
attention to the virulence of their organisms. Clinical and autopsy 
observations of peritonitis arising probably from penetration through a 
diseased intestinal mucosa have been contributed by Langemaak, Len- 
nander and Nystrom, Erkes and others (206). Penetration may also occur 
in the enteritis of children (Escherich, Baginski). 
Among the peritonitides of unknown portal of entry, that due to the 
pneumococcus is of the greatest interest to surgeons (207). Jensen 
(208) could show in two guinea pigs, that feeding with virulent pneumo- 
cocci gave rise to a fibrinous peritonitis; histologically, he found the 
intestinal wall loaded with organisms, although no ulcerations were present 
in the mucosa. Since pneumococcic peritonitis usually begins with diar- 
rhea, Jensen believes it not improbable that the infection arises within 
the lumen of the intestine. This view, however, does not explain the 
fact that in the great majority of cases this disease occurs in girls. It 
therefore seems more logical to believe that the portal of entry is the 
genital tract. But clinically, nothing points to these organs, and at au- 
topsy the tubes, ovaries, etc. are usually normal. But, minute histological 
examinations on the question do not seem to have been made. The 
studies of Krogius (209), Jensen and others show that the pneumococcus 
which is, of course, frequently present in sputum, is also found very often 
in the intestinal tract (for example, in appendicitis). 
In adults, furthermore, pneumococcus peritonitis occurs with equal 
frequency in males (Jensen, author’s observation). An extension of a 
pneumococcus infection from the lungs to the peritoneum, of which, 
indeed, it is tempting to think, is scarcely ever observed, although after 
injury to the pleural endothelium, bacteria may pass through the dia- 
phragm. In animals, also, it is most difficult to obtain a peritonitis from 
an infection of the pleura (210), for according to Jensen, the current_of INTESTINES 
243 
fluids is directed from the abdominal cavity to the pleura and not in the 
reverse direction. 
The work of Peiser (211) especially, is directed toward the possibility 
of infection of serous surfaces, particularly the peritoneum, through the 
blood stream. “The serous membranes as long as they are uninjured, 
are impermeable to bacteria circulating in the blood stream.” Invasion 
takes place only “in the moribund stage of a severe septic process when 
the bacteria at the height of their multiplication enter all the organs.” 
If the peritoneum has been subjected to the action of even a mild irritant 
(physiological saline is sufficient), bacteria will enter the peritoneum 
very quickly. Whether they multiply, i.e., whether a diffuse peritonitis 
results, depends on the virulence of the bacteria and the resistance of the 
individual. The same results were obtained in the pleura. The appear- 
ance of a peritonitis in sepsis is, therefore, the beginning of the end, and 
operation in such a condition is useless. 
In discussing the reaction of the peritoneum to these invaders, Wegner 
has shown that it can protect itself against a certain number of bacteria 
by making use of its absorptive powers (see above). Grawitz (212) 
indeed, on the basis of his experiments, believed that the resistance of 
the peritoneum against bacteria is very high. But Pawlowski (213) 
opposed this view, for he found that pathogenic staphylococci when 
introduced intraperitoneally, always produced a fatal peritonitis; but 
saprophytic organisms were harmless. In spite of this, Grawitz, and with 
him quite a number of other authors, among whom may be mentioned 
Tavel and Lanz (214), (201), continued to hold the view that “primary 
bacterial peritonitis never occurs because this membrane either easily 
absorbs organisms or is entirely invulnerable to them.” They believed 
that the peritonitis which occurred quite uniformly, as, for example, 
after laparotomies in laboratory animals in the older days, developed 
because of extensive injury to the tissues. If this be true, those cases of 
Pawlowski in which peritonitis occurred after the experimental introduc- 
tion of bacteria were really the results of a primary infection of the incision 
or of the stitches. Doubtless, this explanation of Pawlowski’s results is 
far fetched, and Reichel’s observation (215) that it depends to a large 
extent on the virulence of the injected organisms is entirely correct. 
Moreover Walthard (216) introduced staphylococci into the peritoneum 
of an animal after an operative procedure, and a general peritonitis began 
from the places where the serosa was injured, especially by drying, and 
if this latter was prevented, no peritonitis appeared. These experimental 
infections are favored by the presence of such good culture media as blood 
or ascitic fluid, an observation which corresponds very well with our clinical 
experiences. In suppurative peritonitis, no one factor can be considered 244 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
the most important; there is a combination of bacteria, enzymes, toxins, 
resistance of the tissues, etc. 
Surgical experience has taught us first, that a progressive infection of 
the peritoneal cavity from the abdominal walls rarely occurs, but that its 
possibility must not be ignored. Therefore, the warning is enunciated 
not to drain the abdominal cavity through the hernial orifice in strangu- 
lated hernias because of the danger of secondary infection (217). Sec- 
ondly, the peritoneum is not as susceptible to infection as was believed, 
always provided that it has not been injured severely by mechanical 
means. Thus, for example, in the operations not strictly aseptic, such 
as opening the gastrointestinal tract, unavoidable slips in technique are 
followed much more often by infections of the abdominal walls, than by 
peritonitis. The former are therefore more susceptible than the perito- 
neum (217) and for this reason, we drain the incision and not the peritoneal 
cavity. At present, it is impossible to decide whether there has been an 
injury previous to the inflammationin the so-called “spontaneous” types, 
for example, pneumococcus peritonitis, or whether there is an infection 
through an intact membrane. The diarrhea Which has been described 
as a precursor of pneumococcus peritonitis might easily injure the serosa. 
What is the nature of the course run by a peritonitis (218), (214)? 
Experiments have demonstrated that in the first few hours after their 
introduction into the peritoneum, the number of the bacteria diminishes. 
This is brought about first, by absorption, second, by accumulation on 
the walls of the cavity where they are partly free and partly enclosed in 
leucocytes or endothelial cells; and third, by phagocytic destruction. 
There is of course no object in assigning a special importance to any one 
or the other of these processes, as was formerly done to absorption, but 
Notzel (219) could show that animals did not succumb to 100 times the 
minimum lethal intravenous dose when the same organisms were given 
intraperitoneally. On the other hand, animals with peritoneal infection 
may be kept alive by preventing absorption through ligation of the 
thoracic duct even though this does not exclude the possibility that bac- 
teria may be found for prolonged periods in the blood stream. Jensen 
(208) in his experiments on pneumococcus peritonitis at least could detect 
the organisms in the blood in four to five minutes after they were injected 
intraperitoneally, and they remained there during the entire course of 
the disease. He contradicts Bordet’s claim (218) that bacteria enter the 
blood in peritonitis only during the agonal period. This question of 
bacteremia has been frequently discussed in such peritoneal diseases as 
appendicitis. It will be considered more fully under that topic, but it 
might be mentioned here that it often occurs in this condition (Canon (220)). 
But whether Jensen’s opinion, as he expresses it, “the decisive struggle INTESTINES 
245 
in peritonitis takes place not in the peritoneum, but in the circulation,” 
is correct, depends somewhat on the viewpoint. 
Peiser’s (221) experiments show that absorption of bacteria from the 
peritoneum takes place in quantity, only in the first stages of the disease, 
later, absorption is much slower. Even in the cases with all the symptoms 
of peritoneal sepsis, absorption becomes limited, and the increase of the 
bacteria occurs rather in the blood. The fact that the peritoneum absorbs 
substances quickly only at first—as Peiser found in his sodium chloride 
solution experiments—and later, but slowly, to keep pace with the kidneys 
as it were, is a protection for the body against overwhelming amounts of 
bacteria and toxins. If this equilibrium is disturbed by the introduction 
of saline solution into the peritoneum, the animals die a septic death from 
increased absorption, while the controls remain alive. In operative 
cases, it was also occasionally found that death occurred very quickly if 
the peritoneum was irrigated, so that the impression could not be avoided 
that this procedure caused direct damage. But whether the injury 
occurs in the sense of Peiser, or whether in spite of careful technic, it 
occurs because protective adhesions are freed, is difficult to decide in a 
given case. 
But now the parietal peritoneum on account of its smaller surface 
and poorer vascular supply absorbs much less than the visceral layer. To 
this difference Meisel (196) assigns the chief reason for the localization 
of secondary abscesses in peritonitis. In fact, these abscesses occur 
mostly in the peripheries of the abdominal cavity, that is subphrenic, in 
the lumbar region, in Douglas’s cul de sac and in the hollow of the sacrum 
on the right side. Obviously the position of the abscess depends even 
more on the position of the organ in which the infection arose. The pref- 
erence for the right side is related of course to the appendix. But delayed 
absorption on the part of the parietal peritoneum is probably also a factor 
which should not be underrated. 
Another protective mechanism of the peritoneum is the leucocytes 
and their ability to destroy organisms. The fundamental studies of 
peritoneal phagocytosis were made by Metchnikoff (222), on the normal 
peritoneum, using not bacteria but the red corpuscles of the goose 
as objects for phagocytosis. Clairmont and Haberer (223) studying 
the subject under pathological conditions, found in guinea pigs that every 
exposure of the intestines, either moistened or dry, led to a leucocytosis 
which was greater than that produced by the injection of geese erythro- 
cytes into the closed peritoneum. Phagocytosis by these leucocytes was 
very energetic at first but soon ceased, so that in later hours, when that 
in the control animals was at maximum, it had become almost zero in the 
operated animals. According to Metchnikoff (222) there is an increased 246 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
phagocytosis in the exudate of peritonitis. The morphology of the process 
has been studied particularly in relation to bacteria, and it has been 
found that the mononuclear form of leucocyte, which is normally present 
in the peritoneal cavity, is the first cell to engulf the invader. After 
phagocytosis, the leucocytes perish (Metschnikoff (224)), or they deposit 
themselves on the peritoneum. After this period of mononuclear leuco- 
cytosis there is a period of leucocytic diminution, which, however, lasts 
but a short time. In a few hours after the injection, polymorphonuclear 
forms appear in great abundance, and these now take up the struggle. 
At first large numbers of bacteria are engulfed, but this phagocytosis 
soon ceases, and if the pus is examined in the following period, there are 
found but few bacteria enclosed within leucocytes. They seem to undergo 
some unknown change which make them unpalatable, but freshly added 
bacteria, especially if they are of another kind are easily phagocytosed 
(225). This period of diminishing phagocytosis does not continue until 
the death of the animal, but usually increases shortly before, with simul- 
taneous disintegration of the leucocytes. Wallgren therefore believes 
that substances are set free from the destroyed leucocytes which rupture 
the protecting shell of the bacteria and thus render them again susceptible 
to the phagocytic process. 
This is not the only method by which the abdominal cavity is protected. 
The peritoneal fluid under normal conditions has bactericidal properties 
and this faculty of clumping and dissolving bacteria is increased by the 
presence of leucocytes, which on destruction—perhaps also because of a 
secretion—liberate antibodies into the surrounding fluid (226), (202). But 
not only thd leucocytes, but the endothelial cells also produce such agglu- 
tinins, precipitins and bacteriolysins. 
As a prophylactic measure after an operation, when a general peri- 
tonitis is feared, attempts to produce a leucocytosis in the peritoneal 
cavity are made so that antibodies will be brought to the situation where 
they will be needed. This has been done particularly in gynecological 
procedures on the day before operation by the injection of nucleic acid or 
camphorated oil (227). Perhaps delayed absorption after the latter 
substance has been injected also helps. Just as this artificial procedure 
awakens the protective powers, so do the spontaneous suppurative pro- 
cesses stimulate the peritoneum to reaction. According to Moskowicz 
(228), even in the earliest stages of appendicitis, there is diffuse irritation 
of the peritoneum which produces a relative immunization of that mem- 
brane. If the disease progresses, this previous immunization will possi- 
bly prevent or at least hinder the immediate involvement of the entire 
peritoneum. This is said to explain the relatively quick and efficient 
localization in appendicitis and the surgeon practices the rule of not inter- INTESTINES 
247 
fering too much with the adhesions in appendiceal abscesses, but knows 
that draining the abscess cavity alone is sufficient (179). This irritation 
of the entire peritoneum is caused, according to Hagler (cited by Sprengel), 
by the entrance of toxins. It is also possible in animals to protect against 
further infection from the peritoneum by previously injecting cholera 
organisms in small numbers (229). 
Investigations to discover whether the exudate itself has antibacterial 
properties were undertaken by Pansini, R. Stern, R. Pfeifer, Schrader 
(230) and others. Apparently it has none; at least, in Schrader’s experi- 
ments, bacteria grew in the exudate, though not as well as in bouillon. 
It seems however, to possess an inhibiting influence on intestinal organ- 
isms, but the statements of various writers on this point do not agree 
entirely. 
It has already been mentioned that the tendency of the peritoneum 
to form adhesions and to localize infections is another very important 
protective mechanism. 
If the bacteria are highly virulent, they develop, notwithstanding all 
the natural protections. If the infection is mild, and does not lead to 
a fatal issue, the whole course of the disease is slower. Leucocytes begin 
to accumulate only after a few hours have elapsed, and are never so 
abundant as in the severe types. The mononuclears predominate in 
these milder forms and they are also usually in the majority at the end of a 
peritonitis. The bacteria are often not given the opportunity to multiply, 
but are phagocytosed in a few hours. Between these two extremes there 
are all gradations, but the struggle for supremacy always proceeds in the 
same way. 
Unfortunately it is impossible to give a prognosis of the disease from 
the type of organism found in the exudate. Even the discovery of strepto- 
cocci is not necessarily decisive; such organisms not rarely produce a 
peritonitis which runs a very benign course. We have treated several 
cases in which the cause could not be definitely determined, but in which 
streptococcic pus flowed from the abdominal cavity. The patients 
recovered, although in the further course, several abscesses formed and 
were evacuated. But these organisms, and as far as I know other cases 
in the literature, have not been examined for their hemolytic power. 
Furthermore, the severity of the clinical course and the degree of 
pathological anatomical change do not always run parallel. We often 
see only a slight congestion of the serosa, with scarcely any exudate, 
except a few flakes of fibrin, in cases which have run a very severe course. 
The term “septic” has been applied to this type, not a well chosen word, 
because according to our present knowledge, every patient with peritonitis 
is more or less septic. 248 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
This leads us to a discussion of the cause of death in peritonitis. An 
exhaustive review of the older literature is given by Hefnecke (231) who 
has also performed extensive experiments on this problem. According 
to the majority of writers, an intoxication is the cause of death, to which 
factor may be added a sort of shock, not clear, however, in its details or 
action (232). Heineke sectioned the small intestines of rabbits and deter- 
mined the blood pressure by the same methods which Romberg and 
Passler used in the investigation of diphtheria and other infectious diseases. 
The animals'died about 12 hours after operation, and Heinecke could 
demonstrate that the circulatory disturbance in the peritonitis from per- 
foration is due to a paralysis of the vasomotor center in the medulla 
oblongata. Damage to the heart is certainly done in the early stage of 
collapse, but in the later stages, heart action is impaired principally 
because of an insufficient supply of blood resulting from the vasomotor 
paralysis. Respiratory disturbances appear later than those of the circu- 
lation, but respiratory failure precedes cardiac failure. Both may prob- 
ably be considered due to central paralysis of the medulla oblongata, and, 
according to Heinecke, this results from the direct action of bacterial prod- 
ucts, and not reflexly through transmission by the nervous system. 
Friedlander (233) has submitted these investigations and conclusions 
to a rather interesting criticism. He believes it necessary to separate the 
rapidly progressing sepsis as it occurred in the researches of Heinecke and 
Romberg from the slowly progressing actual peritonitis. On account of 
the fact that the pulse rate and temperature are not proportional, he 
believes that reflex influence cannot be entirely ignored. He produced 
a “peritoneal irritation” in animals by ligation or removal of the omentum, 
and then found that the pulse rate was proportional to the temperature if 
the vagi were cut; if they were intact, the pulse rate was higher. Strehl 
(234) could not confirm these results in intestinal obstruction in rabbits 
and cats, and found that there was no difference in the pulse rate when the 
vagi were sectioned at the cardia. Extirpation of the coeliac plexus also 
had no effect on the pulse rate in peritonitis. But even if Friedlander’s 
experiments could not be verified, at least one of his ideas is valuable, 
namely, that peritonitis is not merely a sepsis with quantitative differ- 
ences, but that, in the death from this disease, the complicated nervous 
supply of the abdominal cavity must also be taken into consideration. 
Whether such influences on the circulation and respiration are demon- 
strable, remains for future experiments to decide. Braun and Boruttau, 
and Perthes (235) also found the blood pressure remained normal for a 
long time, and it showed a tendency to fall suddenly, only shortly before 
death. Careful blood pressure determinations in peritonitis have also 
been made by Lichtenberg (236). INTESTINES 
249 
Paralysis of the intestines must also be considered in the causes of 
death from peritonitis, and Askanazy (237) believes the dilatation of 
lymphatic channels around the ganglion cells in the intestinal walls is 
the anatomical basis of the paralysis. This explanation is doubted by 
Walbaum (238), but the anatomical finding has been confirmed byStrehl 
on cat’s intestines which were quickly placed in fixative while still living. 
According to the prevailing opinion, this intestinal paresis is of toxic origin. 
The resulting distention of the abdomen and absorption of decomposing 
intestinal contents, act as injurious and finally destructive factors on the 
entire body. But this general opinion, as it is usually taught, is probably 
incorrect; at any rate Hotz (98) has shown experimentally, that the intes- 
tine, the serosa of which shows peritonitis but no distention, will give 
practically the same motility tracing as the normal bowel. Paralysis, 
therefore, is not demonstrable. For the same reason, the statements 
that meteorism and intestinal paralysis are consequences of inflammation 
of the cceliac ganglion, have thus far not been proved. The distended 
intestine has, however, an entirely different form of movement and the 
question in this case is: What is the cause of the distention? 
The researches of Enderlen and Hotz (18) have shown that, as in fully 
developed ileus, there is a markedly diminished absorption from the intes- 
tine in peritonitis, and in the later stages, there is actually an outpouring 
of fluid into the intestinal lumen. The works of Clairmont and Ranzi 
and of Braun and Borrutau (239) also lead to this conclusion. There is, 
consequently, in peritonitis, the same close relation between distention, 
paralysis and circulatory disturbance that we have studied in ileus. At 
operation in early peritonitis, markedly contracted and markedly dilated 
segments are often seen side by side. Whether this is due to an unequal 
distribution of the injury to the circulation or not, still remains in doubt. 
A symptom of intestinal paralysis in the late stages of peritonitis is 
vomiting. This terminal fecal vomiting must be differentiated from the 
vomiting and singultus at the beginning of peritonitis, just as it must be 
done in ileus. In appendicitis, we often observe these symptoms in the 
very beginning, but, as Sprengel (240) points out, they disappear again 
when an abscess has been encapsulated. Vomiting is very rare during 
the stage of formation of the abscess, but it reappears when rupture takes 
place, and a diffuse peritonitis sets in. It is the irritation to the peri- 
toneum which causes vomiting, and this is present, as stated above, in the 
earliest stages of every appendicitis. This type must, therefore, be 
considered reflex through stimulation of the vomiting center by way of 
sympathetic fibres. More details are given in the pages devoted to 
gastric motility. Since this vomiting is purely reflex, it is easily under- 
stood that it occurs more readily in some individuals, and in others, not 250 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
at all. According to Nothnagel (112, p. 530) singultus does not neces- 
sarily mean that the peritoneal surface of the diaphragm has been affected, 
since the phrenic nerve sends branches to other regions of the peritoneum. 
As stated, the reflex vomiting in the early stage of a peritonitis must be 
differentiated from the fecal vomiting in the late stages. The character 
of this latter is entirely different from the reflex type. The descriptive 
term “running over” has been aptly used to describe it (241) on account 
of the quantity and the absence of associated abdominal compression. 
The fecal odor, however, is not evidence that it comes from lower levels, 
i.e.} large intestine. Decomposition takes place in the small intestine, 
where, on account of paresis, certain bacteria are given free rein (Noth- 
nagel). If the paralyzed intestine now becomes filled with more and more 
feces and fluid, then according to the theory of Haguenot in 1713 (241) 
the abdominal compression forces the contents toward the stomach, and 
it is emptied in the direction of least resistance. The question of whether 
antiperistalsis which has been discussed in detail on previous pages, plays a 
part has caused much controversy. This type of movement cannot be 
of much importance in fecal vomiting which occurs, as stated, only after 
the intestinal muscle is paralyzed, and when it no longer reacts to stimuli. 
With this theory of Haguenot, it is necessary to assume, furthermore, that 
the pylorus remains open; an assumption thus far not proved, and which 
really contradicts that which we otherwise know of the act of vomiting. 
Like all the other general symptoms of peritonitis, vomiting has also 
been considered due to an “intestinal intoxication.” This question has 
been discussed more in detail under ileus where the conditions are clearer. 
In all probability we may safely conclude from the investigative results 
recounted that “intoxication” is not very important, first, because the 
intestinal contents are not so poisonous in fecal stasis, and second, absorp- 
tion is diminished in peritonitis and ileus (18). Moreover, vomiting is 
not observed after the experimental injection of stagnant intestinal con- 
tents (239). Finally, it must not be overlooked in considering Haguenot’s 
theory, which ignores the vomiting center altogether, that it is not entirely 
clear why certain animals, e.g., rabbits, do not vomit at all after being sub- 
jected to the same mechanical conditions in the experimental production 
of an ileus. 
Occasionally, although only in a very small percentage of the cases, 
hematemesis occurs in peritonitis. This has been called “vomito negro,” 
as in yellow fever. The theories concerning gastric hemorrhage have been 
discussed under gastric ulcer and parenchymatous gastric hemorrhage, 
and these sections may be consulted for details. Doubtless, the infection 
plays a very important part in the hematemesis of peritonitis, at least, 
it is usually found only in the most severely septic cases. INTESTINES 
251 
In the treatment of acute peritonitis, the question of drainage is 
encountered in addition to the primary evacuation of the pus. 
In the literature a distinction is not always made between tamponade 
and drainage, probably because of the idea that the tampon, i.e., the strip 
of gauze, would also help in evacuating the fluids. This was combated 
by Chrobak and Volcker (242) who pointed out that the meshes of the 
gauze are quickly filled by the thick flowing viscid mass, and thus it is 
changed to a practically solid body. The experiments with solutions of 
dyes cannot be compared to the conditions in patients (see (243)). A wick 
acts better in drawing off, if care is taken to prevent compression by the 
edges of the wound. In the experiments of Rotter (244) such a wick led 
off in the first seven hours as much fluid, and probably more, than a 
drain. But as we shall presently show, after twelve hours, no more pus 
finds exit even through a rubber tube introduced into the abdominal cavity, 
so that there is no difference in this respect to a strip. If a strip is packed 
too tightly into a wound, or if it is compressed by sutures in the abdominal 
wall, it acts only as a “tampon,” i.e., like a cork, and does not drain. 
For these reasons, a drainage tube is used if it is desired to evacuate 
pus, and tampons are used if hemorrhage cannot be controlled, or if it is 
advisable to stimulate adhesions, e.g., to help in the encapsulation of an 
abscess. The foreign body is such an effective stimulus to the formation 
of adhesions that a pus focus will be walled off from the remainder of the 
abdominal cavity in twelve hours (Volcker). It is easy to understand 
that a tampon may occasionally be used to close a fistula or fill up an 
empty space (Volcker). Now these adhesions which develop so quickly 
around a strip of gauze, no matter how well the technic is carried out, 
make it impossible to drain the entire peritoneal cavity. Indeed, even 
such a mild irritant as a rubber or glass tube stimulates the formation of 
enough adhesions to prevent the evacuation of pus except from the sinus 
through which the drain passes. If there are other abscesses, they may 
not be influenced at all by the original drainage. A recognition of these 
principles in surgery and gynecology was acquired quite early, but broad 
drainage usually accompanied by tamponade, was combated at first, 
and then later, drainage in ordinary so-called aseptic or half septic ab- 
dominal operations. Even today, there is a divided opinion on drainage 
in peritonitis (245). 
But the point accepted by all is that the whole abdominal cavity 
cannot be drained in this disease; it is only a question of whether it is 
possible and advantageous to drain those regions, which experience has 
taught us are sites where abscesses localize. Rehn and his school (246) 
are of the opinion that during and after peritonitis, the pus tends to collect 
almost exclusively in Douglas’s cul de sac, therefore after irrigation, they 252 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
place a drainage tube there and lead it through the operative incision; 
e.g., in appendicitis this would be to the right, at the level of the spine of 
the ileum. Otherwise, the abdomen is firmly closed and Rehn believes that 
the pus is forced out by the viscera which sink downward toward the 
pelvis in conformity to the laws of communicating tubes. This opinion 
has aroused opposition, particularly from Rotter (244) who has investi- 
gated the subject both experimentally and at the bedside. He placed a 
loop of intestine in a vessel containing water and found that one half of 
the loop sank, which was natural since its specific gravity is one, and that 
the water rose in the drain, which may be considered as a lateral leveling 
tube, only as high as its level in the vessel. There was no sign of a forcing 
out of the fluid through this tube. It can take place only when the fluid 
is under a certain tension, which may occur in peritonitis as long as the 
intestines are markedly distended or when a gas containing abscess is 
formed in a space firmly closed by solidly adherent loops of bowel (Prop- 
ping). That the exudate will be forced out through a drain in the cul de 
sac by the sinking of the intestines is, therefore, an erroneous idea. The 
law of communicating tubes cannot be evoked in the case of the abdominal 
cavity because bodies of different physical states are present (solids and 
liquids), one of which floats on the other. Rehn in his theory did not 
consider the “upward pressure.” Furthermore, he assumes that all, 
or the greatest part of the exudate formed, flows continuously into the 
cul de sac. This assumption is also incorrect, as Rotter showed, because 
after twelve hours, almost nothing drains from the tube, and separation 
from the free abdominal cavity must have occurred. The fluid which 
reappears later comes probably from the granulations of the drainage 
tract. By forcing water into the canal under pressure, Rotter also showed 
that the drainage tract ceases to communicate with the free abdominal 
cavity, since all the water returned freely around the tube. But that all 
drainage should be considered illusory because the openings in the tubes 
occasionally become plugged with omentum or intestines, is also incorrect. 
If the operation in peritonitis is confined to simple incision without 
irrigation, nothing at all flows from the drain in the cul de sac, because 
the amount of pus is not sufficient. That which is evacuated in the first 
twelve hours in cases treated by Rehn’s method, is chiefly the water from 
the irrigation, which Rotter advises removing by dry sponging. After 
mopping, Rotter closes the abdominal cavity tightly, provided that the 
cause of the suppuration is removed and no necrotic bits or other sequestra 
remain. This is an extremely important point; the abdomen is not closed 
completely if, for example, the appendix had been covered and enmeshed in 
dense adhesions. The clinical results by this procedure are said by Rotter 
to be equally as good as those treated by drainage (Rehn’s method; see also INTESTINES 
253 
(247))- English and American authors, many of whom had already closed 
the abdomen before Rotter, have reported very good results by this 
method (248). Nevertheless, as Chrobak expresses it, “an active pro- 
cedure always excites more favor than inactivity” and thus the closure 
of the abdominal cavity advocated by Rotter on such reasonable grounds, 
is followed by few surgeons. Douglas’s cul de sac may be drained better 
through the vagina or rectum as Friedrich (190), Bordenheuer (247), 
Wilms (248) and others have advised, than by Rehn’s drainage. The 
latter method is, however, better than drainage through the lumbar 
region (Rotter). But none of these methods is effective for prolonged 
drainage because of reasons made clear above. The vaginal or rectal 
route has long been in use, of course, for the evacuation of secondary 
abscesses. 
By chronic peritonitis is meant a process which does not begin with 
suppuration, but one in which the anatomical picture is dominated by 
“thickenings and adhesions of inflammatory origin” (112). Naturally, 
the etiology of this disease will be varied, even though tuberculosis is 
a frequent cause of these diffuse inflammatory conditions. In those of 
local nature, a slowly progressing appendicitis, salpingitis, diverticulitis, 
etc. and organisms similar to those producing acute inflammations will 
come under consideration. The type is not difficult to understand, and 
is of great importance in the causation of ileus. But the question of 
whether such chronic adhesive forms of peritonitis arise without previous 
bacterial inflammation, has not as yet been solved. We have found through 
the many laparotomies that are performed daily, that a “pericolitis” 
is by no means rare. It has been described by Rokitansky and a number 
of French and English writers. Virchow (249) was familiar with it, 
and in addition to those in individuals with a “rheumatic tendency,” 
he believed it resulted from trauma and diseases of “intraabdominal 
channels.” Today we cannot add to this excellent definition. The 
meaning of “trauma” in the widest sense of the word, may be studied 
daily in laparotomies. And it was these observations, especially in patients 
who had been operated several times, that showed the special tendency of 
certain individuals to the formation of adhesions (250). The cause of 
this “connective tissue energy” is unknown (251). But that certain 
humans and animals respond more readily than others with connective 
tissue formation, under the same stimulus, is proved by clinical observa- 
tion and animal experimentation. When Virchow speaks of a “rheumatic 
peritonitis,” this statement only shows that he occasionally found exten- 
sive adhesions without adequate reason in the history and the findings. 
If we speak at present of “predisposition” it shows only that we observe 
these things from an altered viewpoint. Unfortunately our actual 254 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
knowledge of the reason why one organism shows a greater tendency to 
form adhesions than another has not been increased since Virchow. 
Although an individual may form connective tissue with the greatest 
readiness, nevertheless, some external stimulus which causes this forma- 
tion must always' be present, and thus in chronic adhesive peritonitis the 
question arises, is this stimulant bacterial or not? We know very little 
regarding this. Bittorf (252) has observed true primary pericolitis in 
conjunction with pneumonia. In such cases it is, of course, perfectly 
natural to think of bacterial infection, either a slight general peritonitis 
or a spread of the infection through the lymphatics, as assumed by Franke 
(187). According to Virchow, the most frequent cause is constipation, 
an opinion which is generally accepted even today (Rosenheim (253), 
Bittorf, Payr). But it must never be overlooked in these cases that 
pericolic adhesions are also very frequently the cause of constipation and 
not its result (254). It is not clear how constipation causes pericolitis, 
but from the experiments mentioned above, it might be assumed that 
bacteria wander through the congested intestinal walls, although according 
to our experience to date, this only occurs with very virulent bacteria, 
and then rarely. It is also not known whether toxins penetrate the 
intestinal wall in constipation. Both conceptions are possible, but 
nothing is proved. Actual fecal stasis is by no means the rule in constipa- 
tion (see section on constipation), and the pericolitis may only be the 
consequence of purely mechanical irritation. As stated above, Wieland 
could demonstrate its development experimentally after mechanical 
stimulation. At any rate, further investigations, especially bacteriologi- 
cal, are necessary in this problem. 
The consequences of chronic peritonitis, and its resulting adhesions, 
can be seen in the mechanical interference with defecation (255). 
We shall deal later with the formation of bands, and the ileus caused by 
them; but will speak of the two places in the intestines at which more 
serious difficulties arise from diffuse adhesions, i.e., at the junction of the 
ileum and the cecum, and at the splenic flexure. Payr has perforrtied 
exhaustive work on this latter form of chronic stenosis of the colon. Gas 
blocking may be caused by such surface adhesions about the splenic flexure, 
and with the distention by gas the same discomfort is caused as in colonic 
ileus, i.e., periodic severe pain with every contraction of the gas filled 
segment. Even normally, the splenic flexure is a difficult spot for £he 
passage of contents (23); it is so firmly fixed by the phrenico-colic liga- 
ment to the diaphragm and to the abdominal wall, that an acute angle 
forms in the concavity of which the intestinal wall lies as a fold. It is 
possibly due to this angular kinking of the splenic flexure that, as Roith 
states, feces are usually found in the ascending and transverse colon in INTESTINES 
255 
the cadaver, while the descending colon is, as a rule, empty. That fluids 
and feces can pass through this narrow region more easily than gas, has 
been shown by Quenu, who caused water to pass easily under only m. 
pressure even with the most pronounced kinking to an acute angle. There- 
fore the stenoses described may justly be considered gas-blocking, e.g., as it 
is frequently seen in our irrigator tubing. 
Polyserositis occupies a special position among the forms of chronic 
peritonitis. We understand thereby a disease which manifests itself 
suddenly with ascites or peritoneal irritation, then it runs a gradually 
ensuing chronic course which points to congestion in the regions drained by 
the portal vein. This congestion in the portal circulation can be caused 
by a narrowing of the inferior cava in the pericardium (Pick’s pseudo-cir- 
rhosis of the liver) or by occlusion of branches of the portal vein within 
the liver due to perihepatitis (Zuckergusleber). The actual acute stage 
of the inflammation of the serous membranes, winch affects the peri- 
cardium in addition to the peritoneum, has probably no uniform etiology; 
it seems that all types of infection may be causes. The second stage of 
portal vein congestion is of greater surgical interest. In addition to fre- 
quent paracentesis, the other operations discussed under ascites have 
been tried, including decapsulation of the liver. As far as I know, the 
pericardial adhesions in this disease have been left alone; but Rehn (257) 
has performed a splitting of the sternum in juvenile adhesive pericarditis 
with supposedly good results. 
Of all ulcerative diseases of the bowel, appendicitis or epityphlitis is 
of the greatest surgical interest, since it is the disease which is the most 
frequent cause of acute diffuse peritonitis. Without doubt, the physi- 
ological importance of the appendix is not especially great, at least no ill 
consequences which might seem to have arisen from its absence have been 
observed following the numerous appendectomies. Comparative anat- 
omy shows that an appendix is present in anthropoid apes, in lemurs, 
and in the opossum, as well as in man (258). The dog also has 
an appendix well differentiated from the cecum. 
The abundance of lymphoid tissue in the appendix is anatomically 
most remarkable; and it is reasonable to suppose that this lymphoid 
tissue has a certain functional importance in the economy of the organism 
(259). A protein splitting and a carbohydrate splitting enzyme have been 
found in the appendices of fistula dogs (260), and it is demonstrable that 
the intravenous injection of appendiceal secretion causes active peristalsis 
in the intestinal tract of the rabbit (261). But we know that all intestinal 
juice shows a similar action, and great caution is necessary to avoid 
erroneous deductions regarding the importance of this particular intestinal 
secretion. Furthermore, Heile could trace certain relations of the 256 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
appendix to the ileocolic muscle which is situated at the valve of Bauhin, 
insofar as a meso-appendicitis, or novococain injections, led to a relaxation 
of the sphincter. It is advisable to be cautious in evaluating these 
findings also, since it is naturally conceivable that the sphincter itself 
becomes affected by this injection or inflammation. At any rate, it has 
not as yet been proved that removal of the appendix or its mesentery 
causes insufficiency of the ileocolic muscle. 
Now the inflammations of the appendix show anatomically a fairly 
uniform picture (262). According to the undivided opinion of all authors, 
the first change, i.e., that due to a slight attack which may be easily repair- 
ed, is a lesion of the epithelium in the appendiceal crypts, and in its place 
we find a membrane consisting of leucocytes and fibrin. If the inflamma- 
tion progresses, the epithelial defect enlarges, the whole appendiceal wall 
thickens and becomes infiltrated with pus, thus forming a true phlegmon. 
This condition, which can be reached even in the first 24 hours, may also 
regress, but it generally leaves a narrowing of the lumen which favors a 
new attack, as we shall see presently. The third stage is characterized by 
progressive destruction of the wall, either from penetration of the super- 
ficial mucosal ulcers, or from rupture of the abscesses. This leads to 
perforation, peri-appendicitis, and finally peritonitis, with all the reactions 
of the serosa as described above. 
It is remarkable how these anatomical changes may be repaired. It 
always produces astonishment when an appendix is removed about one- 
fourth year after a large abscess has been opened. 
The question arises, what are the conditions under which this ana- 
tomical picture develops? What causes this destruction of the wall from 
within outward? In the first place, it must be remembered that infection 
is one of the most essential factors in appendicitis, but this factor must not 
be overemphasized. It has been shown by numerous investigations 
(263), (190), (193), (191), that colon bacilli, streptococci, staphylococci, 
pneumococci, influenza bacilli and many other organisms, including 
numerous anaerobes, may be the sole or predominant organisms. But a 
specific organism for appendicitis does not exist, nor can deductions be 
drawn from the bacteriological findings as to the course of an appendicitis. 
Although Haim claims that he has seen an especially malignant form 
from the streptococcus, there are so many contradictory observations on 
record that this statement has no general application. It is to be 
remarked that many authors found in the peritoneal exudate in appendi- 
citis, bacteria differing from those normally in the intestine (191): Never- 
theless, according to our pathological physiological conceptions, it is 
impossible that the organisms found should be the only causative factors in 
this disease. It would indeed be most peculiar if such bacteria should only INTESTINES 
257 
show a predilection for the appendix and ignore the other portions of the 
intestines, with the possible exception of the diverticuli (Meckel’s, sigmoid 
flexure). All things considered, we are forced to the conclusion that an 
important factor is the appendix itself, i.e., its anatomical singularity. 
First of all we must discover how bacteria enter the wall of the appen- 
dix. Obviously, this may take place either through the blood or from the 
lumen of the organ. Certain clinical considerations, i.e., the sudden 
attack, the rapid destruction of the wall, the early general involvement of 
the whole body, as seen, for example, in the increase of leucocytes, etc., 
suggest an hematogenous infection, but in the later stages there is 
not always anatomical pathological uniformity. In many organs, e.g., 
kidney, parotid gland, prostate, an inflammation in the sense of an 
excretory inflammation has been demonstrated, which means epithelial 
destruction without demonstrable change in the blood vessels, from direct 
hematogenous infection. This fact naturally has theoretical importance 
in relation to appendicitis. Kretz (264), for instance, believes that 
his findings in a number of severe and quickly fatal cases point to embolism 
as the causative factor, but this interpretation has been assailed. 
Attempts have been made to decide the source of infection by experimental 
means (265), (263). The results show in the first place, that it is possible 
to obtain embolic foci with inflammation and necrosis of the wall,*by 
intravenous injection of almost any bacteria, although those are best 
which had been grown from spontaneous appendicitis in animals of the 
same type. But embolism was found also in other organs. Secondly, 
experimental appendicitis can be evolved from the mucosa, if steps are 
taken to occlude the lumen against the cecum as may be easily done by 
the introduction of a foreign body (paraffin, etc.). Ligation with silk 
thread gave variable results. 
But these experiments do not satisfactorily decide the question in 
point. Both groups of investigations have only this practical interest 
for the surgeon, they prove that the appendix can be destroyed either by 
hematogenous infection, or by infection direct from the bowel. The route 
must be decided in each case by a combination of clinical observations 
and pathological anatomical investigations. This method will show us 
that cases such as were reported by Kretz, i.e., severe embolic destruction 
of the appendix, are really rarities, and when irregular circumscribed 
perforating ulcers of the size of a lentil, are seen in cases with sudden onset, 
they are probably of embolic origin. But in the majority of cases, the 
infection comes most likely from the bowel, and as stated, the possibility 
is deducible from the anatomical structure of the appendix. Being a 
terminal organ it empties itself of feces which enter it, in spite of the valve 
of Gerlach, with more difficulty than any other intestinal segment (266). 258 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
To this must be added that its position is often very unsuitable for dis- 
charging its contents, e.g., it may be retrocolic, or kinked by adhesions, or 
by position changes of other organs, as the cecum. In the appendices 
of adults the emptying is made still more difficult because former slight 
inflammations have left scars which narrow the lumen. At least, these 
scars found so frequently, are considered to have this etiology at present, 
while formerly there was a tendency to conclude from them that the human 
appendix was an organ showing retrogressive changes. This difficulty in 
discharging its contents causes a more marked decomposition of the feces 
(“vas clos” after Dieulafoy (445)), not in the sense of a bacterial increase, 
but on the contrary, the number of bacteria decreases as shown both-in 
humans and animals, but, according to Heile, probably more in the sense 
of increased toxicity of its contents. Experiments of Klecki (268), 
Dieulafoy (240), Hartmann and Mignot (240) have shown that the viru- 
lence of the bacteria increases if the appendix is closed, or the wall is 
injured by ligation of vessels (Klecki) and their toxins supposedly destroy 
the mucosa. 
It is quite plain that the weakest point of the enterogenous theory 
lies here, if it depended solely on bacteria, it is difficult to understand why 
other intestinal segments, e.g., the cecum, should be immune from such 
destructive infection. For this reason, it is impossible to completely 
ignore the condition of the appendiceal vascularization if we wish to abide 
by this theory. This has been recognized by many (269) and a number of 
mechanical factors which may influence its blood supply have been sought. 
Klauber (270) is of the opinion that displacements and strangulations of 
the mesoappendix cause nutritive disturbances, and that, therefore, the 
conditions are similar to those in strangulated ileus. Other authors 
believe that tension of the walls caused at first by catarrhal swelling of the 
mucosa, or from inflammatory hydrops behind an occluding fecal concre- 
tion, will produce deficiency in the appendiceal blood supply. But we 
must bear in mind that appendicitis is rare in catarrhal enteritis, and nurs- 
ing babies who develop catarrh of the bowel in its purest form, very rarely 
develop appendicitis. Fecal concretions have also been held responsible 
for compression of blood vessels, but probably erroneously, because it is 
certain that gangrene of the wall does not always begin where the fecal 
concretion is located but rather directly distal from this place. Atrophy 
of the mucosa as a possible consequence of the pressure of a fecal calculus, 
has been frequently described. It is often claimed that the concretion is an 
inflammatory product, but this is difficult to prove. Since animal 
experiments, described above, have shown that appendicitis can only be 
obtained if the lumen is closed, and since in man the inflammatory process 
is observed remarkably often distal to a fecal concretion occluding the INTESTINES 
259 
lumen, or from a scar narrowing it, it seems quite justifiable to assume a 
certain causative relation between the occlusion of the lumen and the 
appearance of the inflammation in the sense spoken of above. The fact 
that the most destructive cases of appendicitis usually show a fecal con- 
cretion (Sprengel), can also be very easily interpreted that the calculus is 
formed of cast-off mucosal cells. 
But according to Brunn (271), the blood supply may also be affected 
by a spasm in the fine capillaries which supply the mucosa and this may 
be induced by bacterial toxins. The conditions would be quite similar to 
those in gastric ulcer. Brunn, in order to support this very tempting 
viewpoint, searched for relations between vascular distribution and inflam- 
matory changes, and actually found that gangrene always begins where 
one of the vertical side branches springing from a main branch, enters the 
wall of the appendix. His microscopical findings emphasize the im- 
portance of the vascular supply. In appendicitis there always exists a 
combination of “inflammatory stasis, and hemorrhagic infarction” in 
the vessels, i.e., the same process as found in gangrene of a loop of small 
intestine. If the interruption of the vascular supply in the small intestine 
is of but short duration we first find, as stated above, nutritional distur- 
bances in the mucosa. It is only when this interruption is prolonged that 
the other coats also become necrotic. The process is probably similar in 
the appendix. The ultimate cause of this supposed vessel spasm is 
unknown, but it might be due to increased toxicity of contents produced 
by partial or complete closure of the appendix, and possibly the nutrition 
also plays a certain role (see below). This view is naturally hypothetical, 
and many details must still be investigated both experimentally and 
clinically, especially as regard the vasoconstricting effect of confined 
intestinal contents, but the doubts which made it . difficult to consider 
appendicitis an enterogenous infection from the clinical view point, have 
largely been dissipated. 
There is a strong belief, that diet and general habits of living are the 
causes of the frequent appearance of appendicitis. 
And indeed it is remarkable, as McLean (272) points out, that in 
certain peoples, especially the Chinese, appendicitis is practically un- 
known, while Germans or Englishmen living there are affected as fre- 
quently as at home. As a matter of fact, appendicitis has undoubtedly 
increased in the last few decades, even if erroneous diagnoses are consid- 
ered. But whether nutritional factors are at fault is difficult to say. 
It has also frequently been stated that appendicitis became more rare 
during the war, and this was supposedly due to vegetarian food. But it 
must not be overlooked that before the war, appendicitis was very frequent 
in a section of the population which did not eat meat to excess (Germany). 260 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
For the present, all these hypotheses must be accepted with caution, and 
can not be verified by impressions, but only by statistics. An example 
of one of these can be presented thus: according to Aschoff, appendicitis 
is quite frequent in young folks of our civilization but is relatively absent 
in people living closer to nature because the intestines of the latter children 
are more resistant, having longer natural nutrition. But this is also 
merely a vague hypothesis. 
Perhaps our whole viewpoint in appendicitis is too much confined 
to the local process. Just as we show a tendency today to consider peptic 
ulcer more and more as a symptom of a general disease, Hoenck (273) 
has attempted to build up a similar theory for appendicitis. Little is 
gained by his observations inasmuch as the diagnosis has not been con- 
firmed by operative evidence in even one case. But on the other hand, 
it has been justly pointed out (Sprengel 240, p. 209) that removal of the 
appendix in the early stages of inflammation certainly puts an end to the 
disease, forcing upon us again and again, the conception that it is a local 
condition. 
Above all, the invariable increase of leucocytes, points to a general 
reaction of the body, and while this leucocytosis and the shifting of 
Arneth’s blood picture is considered by Sonnenburg (274) an answer of the 
body to peritoneal irritation, he nevertheless observes that leucocytosis 
also appears in closed appendiceal empyema, i.e., without peritoneal 
involvement. Furthermore, in other forms of peritonitis, e.g., pyosalpinx, 
the leucocytosis is not so marked, which proves that it cannot be con- 
sidered as the simple consequence of peritoneal irritation. 
Some of the clinical symptoms deserve short discussion. Kafemann 
(275) has described in detail the pain sensations in his own case of perfo- 
rating appendicitis. At first the patient complains of pain of varying 
intensity over the entire abdomen, especially in the epigastrium; perfora- 
tion is described as “the sudden plunging of a saw tooth knife into the 
abdomen, and the repeated twisting of the weapon within the belly.” 
The explanation of this pain must be practically similar to that in “indi- 
gestion and peritonitis” as described above. Thus the diffuse pain at 
the beginning of the disease is due probably to the presence of free peri- 
toneal exudate. It is a common observation, noticed in other diseases 
also, that abdominal pain is frequently localized in a place distant from 
the seat of trouble, especially in the epigastrium. It is usually assumed 
that at the beginning of peritonitis, there is increased intestinal motility 
and this is responsible for localized pain (Wilms). But there is much 
uncertainty, and the reason why abdominal pain should always be epi- 
gastric, has not been found. The pain in the right side of the lower abdo- 
men is probably due simply to irritation of the parietal peritoneum, but INTESTINES 
261 
Sonnenburg (274, p. 102) believes that “appendicular colic” is produced 
by the attempts of the appendix to expel its contents. The extent of 
involvement of the regional nerves or lymph vessels is uncertain in the 
well known sensitiveness to pressure at McBurney’s point. This pain 
on the right side is also seen in pneumonia and one of these two routes 
must surely be affected. On the basis of his anatomical investigations, 
Franke (187) thinks that it is due to continuation of the inflammatory 
process via the lymphatics. But it is not quite so easy to explain why 
there should be such severe pain at the moment of perforation, for the 
peritoneum, which is destroyed during perforation, is the visceral layer 
which is supposed to be insensitive. We must assume that the escape of 
even minute quantities of air, feces, etc., are sufficient to exert a very severe 
irritative effect on the parietal peritoneum. But it is still very remarkable 
that perforation of the stomach or appendix should produce such severe 
pain at the moment of its occurrence, while traumatic ruptures or stab 
wounds are not necessarily painful, at least, not at first. The only 
assumption that can be made is that the preceding inflammation has made 
the peritoneum especially sensitive. It is still an open question whether 
vascular changes also are involved in producing these pains (276). 
As a further evidence of the above statement, that even a slight appen- 
dicitis can not be explained from the view point of a local process alone, 
is the fact that such patients are quite sick from the very beginning. 
Kafemann, like most patients, thus describes it: “In the evening, perfectly 
well, only to wake up in the morning with marked sensation of illness.” 
Until further knowledge, we must consider the impairment of general 
well being, which is usually more acute than in other intestinal conditions, 
as a septic or toxic process, although as stated, a bacterial examination 
of the blood is usually negative. The presence of albumen in the urine is 
probably also of toxic origin; likewise icterus, which, however, is rarely 
seen. 
It must be remembered, furthermore, that in the later stages of 
appendicitis, there is often infection of the retroperitoneal tissue in addi- 
tion to that of the peritoneum. This explains occasional differences in 
the usual course of peritonitis, e.g., the often dangerous “septic” process 
with its rigors and pulmonary emboli (Sonnenburg 274, p. 130). All 
these symptoms point to the fact that in appendicitis the essential factor 
is not bacterial invasion of the wall of the appendix, but the defense, 
successful or otherwise, which the body sets up throughout the infection. 
If appendicitis were only a local disease there should be more similarity 
to gangrene of the bowel, as, e.g., in strangulated hernia. 
Another question, very complicated, and thus far not generally solved 
is this: Why are some forms of appendicitis so malignant, while others 262 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
are readily encapsulated? There is no special tendency for encapsula- 
tion in the appendicitis of youthful individuals; on the contrary, we quite 
frequently see the very severe forms of peritonitis in children. The other 
ordinary factors must of course count, as bacterial virulence, bodily resist- 
ance, extent of necrosis, etc., but the details of the conditions are not 
quite clear. 
It is, moreover, rather difficult to find an acceptable explanation of 
why appendiceal abscesses which are not opened by operation, show a 
tendency to rupture through the abdominal wall, i.e., actually through the 
thickest part of the abscess wall, and less frequently into the bowel. This 
is probably due, in the first place, to anatomical conditions, as a retrocecal 
position of the appendix, etc., but also to the fact, as pointed out by 
Sprengel, that the abdominal wall forms the side of the abscess which is 
least able to yield to pressure, while the intestines are more free to move. 
It must further be considered if nutritional conditions also are involved, 
they are certainly better in the intestinal wall than in the wall of the 
abdominal cavity. Altogether, however, this problem is by no 
means solved. 
Chronic appendicits, so called, merits special discussion and as a disease 
conception has acquired an especially great importance in French litera- 
ture (274), (240). Doubtless very different things are understood by the 
name of chronic appendicitis, and careful differentiation and separation 
are necessary to obtain insight into the question. If we begin with the 
anatomical picture, we know of certain appendiceal changes not related 
to an acute attack, but which present a cicatrizing process in the widest 
sense of the word. To this class belong appendiceal obliterations and 
adhesions to surrounding organs, including the changes in the blood vessels 
which are described in detail by v. Redwitz (276). The congenital ano- 
malies in position are, of course, not included here. 
Whether obliterative appendicitis is an involution process or is the 
result of chronic or acute inflammation has been discussed for a long time 
(277). But so far as a decision from anatomical evidence is possible, 
the investigations of Miloslavich and Namba (278) have demonstrated 
that in young individuals it is due chiefly to inflammation, while in older 
persons, sclerosis of the submucous and mesenteric arteries might also be 
responsible. That these latter changes can be inflammatory also, has 
been shown by the investigations of v. Redwitz. Therefore the anatomical 
changes may be caused by some form of a slow chronic process or by acute 
attack. In the former it is proper to speak of “chronic” appendicitis. 
In the second case these changes are only the end result of an acute 
attack, and the disturbances should be regarded as due to adhesions and 
pulling, or to inflammatory vascular and nerve changes. INTESTINES 
263 
The therapeutic results in chronic appendicitis show that differentia- 
tion of the otherwise similar anatomical findings, according to the clinical 
viewpoint, is entirely justified. Because, as the reinvestigations of Mel- 
chior and Loser have shown, in the operations of those cases in the second 
group, i.e., the so-called “interval operations,” 94 per cent, of the patients 
are cured, while in all such cases not preceded by acute appendicitis, only 
60 per cent, of cures are effected by removal of the appendix. Further- 
more, operative results in group one are satisfactory only if actual gross 
changes are found in the appendix. Aschoff (270) and others believe that 
all appendiceal changes are due to a former acute inflammation and not 
to a chronic process. It must, however, be stated that cases are known 
in which this form of pathological anatomical change is found, without 
a history of any previous acute attacks (pressure atrophy of the mucosa 
from fecal concretion (280)). This must suffice for the present, although 
it can not be denied that light attacks may have been overlooked. Since 
the anatomical picture only shows conditions as they are, it is impossible 
to state from it alone, whether the changes observed actually demonstrate 
a previous attack. 
Thus far, we are on fairly secure ground, v. Redwitz sees in vascular 
injury the reason for the attacks of pain induced by chronic appendicitis. 
They resemble arteriosclerotic changes very markedly and therefore, 
like these, can produce colicky pain. 
But especially in the French literature, a chronic appendicitis is recog- 
nized even if the changes in the appendix are so minute that, according 
to our conception, with due regard to the pathological anatomical view- 
point, we can not find in them a sufficient explanation for the subjective 
suffering. Cases are known to every surgeon in which a diagnosis of 
“chronic appendicitis” is made on account of illy defined abdominal 
pain, and an appendectomy is performed. These are probably included 
in the above mentioned tabulation given by Melchior and Loser with 
about 60 per cent, of cures. The fact that appendectomy gave no relief 
in 40 per cent, of the cases shows that the appendix was not the only cause 
of the trouble. 
But conversely, cases are also known and frequently reported in the 
literature, in which recovery followed, even though the pain did not 
implicate the appendix alone, but gastric and general abdominal pains, 
etc. were also present. This brings up the question: is there any known 
relation of the appendix to other organs, in the sense that discomforts 
localized in other organs are actually incited by changes in the appendix 
itself? Such relations have frequently been assumed. Payr (281) 
states that gastric fissures and ulcerations are due to emboli resulting from 
chronic appendicitis, and Moynihan (282) also emphasizes that the symp- 264 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
toms of chronic appendicitis can resemble most markedly those of gastric 
or duodenal ulcer and even hematemesis may be observed. Hyper- and 
hypochlorhydria, “dyspepsia,” etc., have been frequently described 
(283) French authors speak of an hepatic form of chronic appendicitis 
(284) accompanied at times by icterus, and believe there are toxic and 
infectious factors at work. Renal, vesical and pulmonary disturbances, 
the latter partly masked as asthma or tuberculosis, are cured by appendec- 
tomy (284). Even a symptom complex called “pseudotuberculosis” 
has been created. It is not quite just to refute all these descriptions as 
errors of observation without more ado, although sometimes a little more 
critical examination seems desirable. But the final conclusion that the 
appendix should be the cause of all these different disturbances, seems 
erroneous. With these symptomatic differences, the disease of the 
appendix could either be only a part of a causative general disease wdiich 
must yet be found (see gastric ulcer), or it is secondarily involved in other 
diseases, as was explained in constipation. Recovery, following the 
removal of the appendix, at any rate, does not prove that it was the cause 
of the disease, for it must be remembered, that with this operation and the 
after treatment, many possible factors are added which may lead to the 
disappearance of the symptoms. 
In this symptom complex of chronic appendicitis, it is easy to dis- 
tinguish those disturbances which have been described more in detail in 
the chapter on constipation, and which have their cause in affections of 
the colon, especially of the cecum (motile cecum, typhlatony, etc.). But 
that nonspecific acute inflammatory processes are occasionally observed 
in the cecum also, has been proven by the anatomical investigations of 
Jordan and Seek, and also by the reports of Fischl (285). 
In resections, the length of intestine which must be removed depends, 
generally speaking, on the extent of the disease or injury and not on the 
actual free will of the operator. Nevertheless, the questions of how much 
can be removed, and what disturbances result, are of great interest, since 
they have considerably enlarged our knowledge of the physiological im- 
portance of the different parts of the intestine. 
The most extensive intestinal resections carried out on man were done 
successfully by v. Brenner, 540 cm., Ghedim, 534 cm., Nigrisoli, 520 cm., 
Axhausen, 475 cm., Pauchet, 400 cm. (286). All these patients, to whom a 
large number of others might be added, stood the operation very well, and 
although they showed some nutritional disturbances at first of which we 
shall speak presently, they afterwards lived and ate like normal individuals. 
But nearly all died a short time afterwards, as Denk (287) discovered by 
inquiry, although only the patients of Brenner and Pauchet died from the 
actual intestinal disturbance; the others from inter current diseases and INTESTINES 
265 
also from recurrence of ulcers. It must be agreed with Denk, that the 
resistance of the patients is lowered by extensive intestinal resection. From 
the large number of published cases, an idea can be gained of the length 
of intestine which can be removed from an individual without directly 
jeopardizing his life. Since the length of the intestines varies in different 
individuals, as stated above, the ratio of the part removed to that of the 
part remaining must, always be considered. These reports have shown 
that one-half and slightly more of the small intestine can be removed, 
without endangering life. If the removed part amounts to 80 per cent, or 
more, grave symptoms are observed practically always and death ensues. 
These numerical proportions in length are very similar in animals, especially 
in the dog. 
The disturbances in metabolism and intestinal digestion which follow 
such extensive resections have been studied in numerous experiments and 
by observations on man. Trzebicki and Monari (288) made simple 
estimations of weight and found that seven-eighths of the small intestine 
could be resected without causing loss of weight, while after resection of 
eight-ninths to nine-tenths, although the animals remained alive, they 
lost one-third of their weight permanently. 
In the extensive resections in humans, it was with few exceptions the 
ileum which was removed. Various authors have tried to determine 
whether resection of the jejunum is more dangerous. Trzebicki, Albu, 
and Blayney, believe, on the basis of their experiments, that removal of 
the jejunum is less well tolerated than that of the ileum, while according 
to the statements of Diliberti-Herbin (289), Takayasu, Soyesima, Monari 
a.o., no difference exists. With these opposed results, it may surely be 
said that the difference between the two resections can not be great. The 
investigators who emphasized the danger of jejunal resection assumed that 
this part of the intestine was an especially important region for the absorp- 
tion of nutritive substances. This view is erroneous, because Lieblein’s 
(290) studies have shown the absorptive power of two loops of equal length 
of jejunum and ileum to be equal (see also above under “absorption”); 
indeed in fat absorption, the ileum is even more important. London (291) 
found in fistula dogs, that the ileum absorbed abundant protein; and Sivre 
emphasizes this point particularly. 
But large resections of the small intestine are procedures which always 
cause considerable disturbances of the digestive processes immediately 
after the operation. Diarrhea, loss of weight, sometimes bulemia and 
thirst, are the symptoms uniformly described, and it has already been 
mentioned that the intestine remains “sensitive” for a considerable time 
afterward. Nevertheless, a certain, even almost complete equilibrium is 
created, and the question of how it is brought about and which part of the 266 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
intestine establishes this balance in each case has been answered in the 
experiments of Stassoff (292) on fistula dogs. After resection of 164 cm. of 
ileum not only does an increased secretion of gastric juice occur, but gastric 
digestion lasts two hours longer than normally. Intestinal movements were 
slowed in the jejunum above the place of resection, cleavage of the chyme 
progressed further, and more was absorbed, so that only half of the chyme 
now appeared at the fistula which was situated close above the resection. 
In the following months this state of compensation failed and the animals 
died with diarrhea and general loss of strength. Therefore, according to 
these investigations, the stomach, duodenum and jejunum substitute for 
the resected ileum, while it was found in other experiments, where the 
colon was removed later, that this part of the intestine does not participate 
in these compensatory processes. 
Conditions are different after jejunal resection. Stassoff removed 132 
cm. of this portion of the intestine and found that the reflex causing the 
flow of bile excretion and pancreatic juice which is incited from the duo- 
denal and jejunal mucosa, was not diminished by removal of the 
jejunum; on the contrary, more pancreatic juice was It was 
shown by experiments in which one fistula was established in the duo- 
denum, and a second just above the valve of Bauhin, that after jejunal 
resection, the chyme when it reaches the colon is less digested than before 
operation, and also that less protein, carbohydrates, and fats, are absorbed 
in the small intestine. The degree of protein digestion remains almost 
unchanged, but that of carbohydrates is diminished. Thus the colon 
must compensate for the resected jejunum, but as far as fats are concerned, 
the task is somewhat beyond its powers (288). 
The alterations in the digestive activity, as shown in these fistula dogs, 
must affect the general metabolism, at least after those resections which 
are on the border line of the possible. Metabolism determinations have 
been made in large numbers on men and animals, and show, with con- 
siderable uniformity, that the utilization of carbohydrates is good, that 
of proteins, although sufficient, is much impaired, while fat utilization is 
the poorest of all (286), (287), (289), (293). From these findings, Lieblein 
has drawn very interesting practical deductions for the nutrition of such 
patients. Accordingly, to compensate for the insufficient absorption of 
proteins, abundant food rich in nitrogen must be supplied, and meat is 
the best, since animal nitrogen is more easily assimilated than vegetable 
nitrogen. It is inadvisable to increase the intake of fat for purely 
mechanical reasons, because excess of fat makes the action of the digestive 
juices on proteins more difficult and those fats which are easily absorbed, 
or what is the same, most easily liquefied, as olive oil, goose fat or lard, INTESTINES 
267 
must be preferred to those which liquefy with difficulty. Carbohydrates 
may be given abundantly, especially since they spare proteins (294). 
The anatomical results of these compensatory processes were studied 
in animals by Monari, Nagano, Flint (295) and others, and hypertrophy 
and hyperplasia of the mucosa were found. But Trzebicki, Evans and 
Brenizer (296) in animals, and Barker (297) and Denk in man, could not 
demonstrate any anatomical changes which might be considered due to the 
resection. For the present, these anatomical findings are quite uncertain. 
Prolapse of the rectum,, i.e., protrusion of the rectal mucosa after every 
bowel movement, is a condition which has its origin in various anatomical 
and physiological factors. In about 70 per cent, of the cases children are 
affected, middle age is rarely touched, while in advanced age it again 
appears more frequently (298). The prognosis in children is favorable, 
less so in adults. From these facts, it must be concluded that an essential 
etiological factor is present in the condition of the tissues, i.e., in their 
tonus. This increases in children, but in adults after a certain age limit, 
it decreases. This diminished tissue tonus and the relaxation of the 
pelvic floor is readily demonstrable in patients with rectal prolapse (299), 
and Ludloff (300) found microscopical degeneration of muscle fibres and 
hypertrophy of the connective tissue in this neighborhood. Only in 
very rare cases will it be possible to discover the reason for these changes. 
Without quoting single cases, Beresnegowsky (301) states that typhoid 
fever, repeated childbirth, etc. will cause such muscular weakness. Bell 
and Hirschberg (302) describe rectal prolapse after trauma. In both 
cases, the prolapsus and the primary muscle weakness developed possibly 
from hemorrhage into the spinal canal, i.e., of central origin. 
But how does a weakened pelvic floor lead to prolapse of the rectum? 
Pathologically anatomically, prolapsus of the mucosa must be differen- 
tiated from actual prolapse of the rectum. The latter is a true hernia. 
In the earliest stage, Douglas’s cul de sac and its content of intestines, 
bulge into the anterior wall of the rectum, which does not necessarily 
extend to the outside. It is only gradually that this invaginated portion 
passes through the anal opening. The perineal part, i.e., that part of the 
rectal mucosa which in the male begins at the prostate, and which is very 
closely attached to its surroundings, remains at first fixed in its position 
(prolapsus recti), but in a later stage this also becomes loose and everted 
and thus an “eversion fold” in its ordinary sense ceases to exist (prolapsus 
ani et recti). The modern conception of the pathogenesis of prolapse is 
based chiefly on the anatomical investigations of Waldeyer (303), and was 
further amplified by Ludloff, who also added clinical evidence. The 
older opinion, subscribed to by Esmarch (304), is that the prolapse of the 
perineal part is primary, and that only in the progress of the disease a 268 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
prolapsus of the other tissue layers of the rectum occurs. This 
opinion may still be correct in the prolapse of children, although system- 
atic investigations are lacking. At any rate, a pure anal prolapse is more 
frequent in childhood. It is probably only accidental that Ludloff found 
but 3 cases in his compilation of ioo from the literature. True 
prolapse of the rectum, i.e., where a true transition fold still remains, 
while the perineal part has not yet been everted, is without doubt, a 
rare occurrence (4 cases in 100 according to Ludloff). 
But if we consider the classical prolapsus ani et recti, i.e., the type 
which includes 87 per cent, of all such cases, the low level of Douglas’s 
cul de sac must be considered the chief predisposing factor (305). We find 
from the investigations of Zuckerkandl and Trager that in children the 
cul de sac of Douglas is always lower than in adults. In the male it 
reaches to the upper margin of the seminal vesicles; in the new born, to the 
lower margin of the prostate; in children to the level at which the ureters 
enter the bladder. The investigations of Napalkow (301) and Beresneg- 
owsky show that its low level is an absolute necessity for the development 
of a rectal prolapse. Experimentally, they produced a rectal prolapse on 
cadavers of children first by filling the pleura with plaster of Paris to fix 
the diaphragm, and then pumping formol solution into the abdominal 
cavity under a pressure of one-half to two atmospheres. After prolapsus 
was established, the bodies were hardened by intraarterial formol injec- 
tion and freezing; and it was found that the floor of the peritoneal sac was 
always below the line which connects the coccyx with the lower border 
of the symphysis. As long as the floor of the pelvic peritoneum was not 
below this line, no prolapsus occurred. In all cases of prolapsus, the 
coccyx had assumed an almost vertical position, and this is a further very 
essential factor. Physiologically, the coccyx is always more vertical in 
children than in adults, and this change to the vertical position supposedly 
occurs in adults if prolapsus recti develops. But it is not quite clear 
whether we are dealing with a causative factor, or more probably with a 
sequel. Actually, the direction of the intraabdominal pressure is changed 
by the vertical position of the coccyx, for ordinarily it is directed against 
the sacral hollow, meeting its resistance in the bone (306). But if this 
hollow is absent, as it is in the vertical position of the coccyx, the rectum 
instead of presenting its concave surface from behind forward assumes a 
straight direction, and thus the pressure on the bowel, and on the soft 
parts of the pelvic floor, is undoubtedly increased. Mummery, wfith this 
point in mind, has advised that children who show a tendency to prolapse 
should attend to their stool with legs strongly adducted, he attempts by 
these means to direct intraabdominal pressure more strongly towards the 
sacrum. INTESTINES 
269 
Apart from the weakness of the pelvic musculature, it was also believed 
that ligamentary attachments of the rectum had become loose if prolapsus 
occurred. This relaxation was thought somewhat similar to that in 
sliding hernia. Jeannel (307), who advanced this theory, points out 
that with perineal rupture or section of the sphincter, no prolapsus occurs, 
while the strongest sphincter cannot prevent the protrusion of a loosened 
bowel. Jeannel uses a very effective simile when he says that the bowel 
is like a chained prisoner. The cell might be left open, but as long as the 
chain holds, the prisoner cannot escape. With the chain broken, the 
closed door might still prevent the flight of the prisoner but he would 
escape as soon as the door opens, and Verneull, in defence of this much 
assailed opinion of Jeannel, continues: “and the door opens during 
every bowel movement.” Jeannel’s opinion contains a kernel of truth, 
but its author presented it one-sidedly, and thus encountered considerable 
opposition (308). It cannot be denied that in consequence of his theory 
his advice to perform colopexy has been followed by good results. In 
animal experiments (Ludloff (300), p. 760), it has indeed been shown that a 
prolapsus does not continue in the dog even if the rectum has been loosened 
far enough that it can be pulled easily through the anus, provided that the 
musculature of the perineum and the sphincter is not injured. But 
these experiments prove little in opposition to the opinion of Jeannel; 
they only show how important a good perineal musculature is, and explain 
why attempts at improving its tonus should be made by massage. 
The factors mentioned, namely, weakness of the pelvic muscles, 
low position of Douglas’s cul de sac, vertical position of the coccyx, too 
loose fixation of the bowel, all favor the development of a prolapse, but 
they do not cause it. To these must be added the intraabdominal pressure 
which first invaginates Douglas’s cul de sac, i.e., the anterior wall of the 
rectum into the rectum, thus forming the perineal hernia. The greater 
this abdominal pressure and the oftener it operates, the easier it is for 
the rectum to be everted, and this explains why constipation favors a 
prolapse, exactly as it is favored by diarrhea and catarrh of the intestine. 
Therapy has taken all these details into consideration, and there are 
a large number of methods for operative treatment. After all that 
has been said above, it is natural that no preference can be shown to one 
method, but that according to the various causes and favoring factors, 
often a combination of several treatments must be applied. 
LITERATURE TO INTESTINES 
1. Dreike: Deutsche Ztschft. f. Chir., 1895, V. 40, p. 43. 
2. Beneke: Deutsche Med. Wochenschft., 1880. 
3. Enderlen: Deutsche Zeitschft. f. Chir., 55, p. 419. 270 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
4- Esau: Bruns Beitrage, V. 60, p. 508. 
5. Lit. see Babkin: “Die aussere Sekretion der Verdauungsdrusen,” Verlag Springer, 
1914. 
6. Cohnheim: Zeitschft. f. physiol. Chemie, 1901, V. 33, p. 451. 
7. Weinland: Zeitschft. f. Biol., 1898, V. 38 and 40. 
8. Adolph Schmidt: Klink. d. Darmkrankheiten, Wiesbaden, 1912, V. 1, p. 33. 
9. Scheponalnikow: Diss. St. Petersburg, 1899. 
10. Glinski: Diss. St. Petersburg, 1891. 
xi. Molnar: Deutsche Med. Wochenschft., 1909. 
12. Pflugers Arch., 1890, V. 46. 
13. Reichel: Zentralbl. f. Chir., 1896 and Deutsche Zeitschft. f. Chir., 1893, V. 35. 
Justi: Mitt. a.d. Grenzgebieten, 1902, V. 10. Narath: Arch. f. klin. Chir., 
V. 52. Baracz: Zentralbl. f. Chir., 1894 and Arch. f. Klin. Chir., V. 58. 
14. Fr. Miller: Virchows Arch., 1893, V. 131, Suppl. 
15. Ad. Schmidt: Darmkrankheiten 1, p. 41, also more of composition of feces here. 
16. Cohnheim: Virch. Arch. 1877, V. 69. 
17. Hamburger: Arch. f. (Anat. u.-) Physiol, 1896, p. 332. 
18. Enderlen and Hotz: Mitt. a. den Grenzgebieten, 1911, V. 23. 
19. Ury: Arch. f. Verdauungskrankheiten, 1909. 
20. See Abderhalden: Lehrbuch d. physiol. Chemie, 2nd. Ed., 23. 
21. Heile (Roehmann): Mitt. a. d. Grenzgebieten, 1905, V. 14. 
22. Kaoru Omi: “more fluid and sugar is absorbed from the jejunum than the ileum,” 
Pflugers Arch. f. Physiol., 1909, V. 126. Frey: Pflugers Arch. f. Physiol., 1908, 
V. 123. 
23. Roith: Anatomische Hefte, 1903, V. 20, p. 64-65. 
24. Rost: Arch. f. klin. Chir., 1912, V. 98. 
25. Stierlin: Ergebn. d. inneren Med., 1913, V. 10; Klinische Roentgendiagnostik d. 
Verdauungskanals, Wiesbaden, 1916, for further lit. Rieder: Fortschr. auf. d. 
Gebiete der Rontgenstrahlen, 1911, V. 18, p. 99. Schwarz: Munch, med. 
Wochenschft., 1911, p. 1489, 1624, 2060. Holzknecht: Munch. Med. Wochen- 
schft., 1909, No. 47. Borchers and Klatsch: Zeitschft. f. exp. Pathol, u. 
Therapie, 1913, V. 12, p. 221-295; Deutsche med. Wochenschft., 1913, p. 1294. 
Elliot and Smith: Journ. of Physiol., 1904, V. 31, p. 272. Cannon: Am. Joum. 
of Physiol., 1902, V. 6, p. 251. Langley and Magnus: Journ. of Physiol., 1905, 
V. 33, p. 34- Magnus: Pflugers Arch., 102,103,108, 111. Bayliss and Starling: 
Journ. of Physiol, 1899, V. 24, p. 99 and 1901, V. 26, p. 125. 
26. Starlin: Ergebn. d. Physiol., 1902, p. 455. Magnus: Ergebn. d. Physiol., 
1908, V. 7, p. 41. 
27. Grutzner: Pflugers Arch., 1898, V. 71, p. 492 und Deutsche med. Wochenschrft, 
1894, No. 48, u. 1899, No. 15. 
28. Nothnagel: Handbuch, V. 17, p. 6. 
29. Trendelenburg: Deutsche med. Wochenschft., 1917, p. 1225 and Arch. f. exp. 
Path. Pharm., 1917, 81, p. 55. 
30. Albert Muller: Arch. f. d. ges. Physiol. V. 116 and Mitt. a.d. Grenzgebieten, 1911, 
V. 22. 
31. David: Mitt. a.d. Grenzgebieten, 1919, V. 31. 
32. Muhsam: Mitt. a.d. Grenzgebieten, V. 6, p. 451. Prutz andEllinger: Arch, f. 
Klin. Chir., V. 67, p. 970 and V. 72, p. 415. Glassner: Wiener, klin. Wochen- 
schft., 1904. Enderlen and Hess: Deutsche Zeitschft. f. Chir., 1901, V. 59, 
p. 240. INTESTINES 
271 
33* Bose and Heyrovsky: Arch. f. klin. Chir., 1909, V. 90, p. 587. 
34. Raiser: Inaug. Diss. Giessen, 1895. 
35. Bayliss and Starling: Journ. of Physiol., 1900-1901, V. 26, p. 107. 
36. Bloch: Med. Klin., 1911 and Fortschr. auf d. Gebiete Roentgenstrahlen, 17. 
Boehm: Fortschr. a.d. Gebiete d. Roentgenstrahlen, 8 u. 18. Stierlin Rieder: 
Deutsche Zeitschft. f. Chirurgie, V. 106; Zeitschft. f. klin. Med., 70; Munch. Med. 
Wochenschft., 1910 u. 1911. 
37. cf. Boehm: Arch. f. exp. Pathologie and Pharmak., 1913, V. 72. 
38. Elliot: Journ. of Physiol., T904, V. 31, p. 159. 
39. Katz and Winkler: Beitrage z. exp. Pathol., 1962, p. 85. 
40. Grodel: Fortsch. r. d. Gebiete d. Roentgenstrahlen, 1913, V. 20, p. 162. Dietleu: 
Fortschr. a.d. Gebiete der Roentgenstrahlen, 1914, V. 21, p. 23. 
41. Genersich: Progr. medic., 21. Dauriac: Progr. medic., 21. 
42. Blauel: Brun’s Beitrage z. klin. Chir., 191c, V. 68. 
43. O. Krauss and Henle: Arch. f. klin. Chir., V. 44, p. 410. 
44. Toldt: Sitzungsher. d. Kais. akad. Wissensch. Wien, 1894, V. 103, 3, Div. 
45. v. Bergmann andLenz: Deutsche Med. Wochenschft., 1911, p. 1425. 
46. Strauss: Therapeutic Monatshefte, 1906, p. 373. 
47. v. Frankl-Hochwart-Frohlich: Pflugers Arch., 1900, V. 81, p. 455. 
48. Goltz and Ewald: Pflugers Arch., 1896, V. 63, p. 381. 
49. Matti: Deutsche Zeitschft. f. Chir., V. 101. 
50. Goltz: Pflugers Arch., 1874, V. 8, 479. 
51. L. R. Muller: Deutsche Zeitschft. f. Nervenheilkunde, V. 21, p. 86. 
52. see Cohnheim: Nagels Handbuch f. Physiol., V. 2, p. 642. 
53. Roussi and Rossi: Compt. rend. Soc. Biol., 1908, V. 64, p. 604. 
54. Merzbacher: Pflugers Arch., 1902, V. 92. 
55. Lit. see Schmidt: Darmkrankheiten, 1912; Strassburger im Handbuch d. inneren 
Medicin, V. 3, 2 part. 
56. Stierlin: Munch. Med. Wochenschft, 1910, No. 27. Meyer-Betz and Gebhardt: 
Munch, med. Wochenschrift, 1912, No. 2 ,33-34. 
57 Ury: Arch. f. Verdauungskrankheiten, 1908, V. 14, p. 506. 
58 Ad. Schmidt and Strassburger: Arch. f. Klin Med., 1901. V. 69, p. 570. 
59. R. Schutz: Arch. f. Klin. Med., 1908, V. 94. Oppler: Deutsche med. Wochen- 
schft., 1896, No. 32. Einhorn: Arch. f. Verdauungskrankheiten, 1896 u. 1898, 
V. 1 u. 3. 
60. Schittenhelm and Weichardt: Deutsche med. Wochenschft, 1911, No. 19. 
61. see Kaufmann: Spez. pathol. anatomie, 3, Edit., p. 439. 
62. Riedel: Chirurgenkongress, 1912, p. 256; Deutsche Ztschft. f. Chir. V. 67, p. 422. 
63. Anschutz: Naturforscherversammlung Breslau, 1904. 
64. Muller: Chirurgenkongress, 1912. 
65. Hertz: Constipation and allied intestinal disorders, London, 1909, p. 118. 
66. Straup: Therap. Monatshefte, 1906, p. 373. 
67. Gant: Constip. and Intest. Obstruc., London, 1910. 
68. Groedel and Seybert: Ztschft. f. Roentgenkunde, V. 13, 4 to 5. 
69. S. Perthes: Arch. f. klin. Chir., 77. Konjetzny: Brun’s Beitrage, 1911, V. 73. 
70. Hertz, Axtel: cited in Chir. Kongr. Zentralbl., 1913, 3, p. 595. 
71. Pennington: J. A. M. A., 1900, V. 35, p. 1520. Gant: Krankheiten d. Mast- 
darms u. Afters. Deutsch von Rose. 
72. Goebel: Med. Klink., 1910, p. 1771. 
73. Rost: Mitt. a. den Grenzgebieten, 1915, V. 28. 272 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
74- Hartmann and Quenn: Chirurgie des Rectums, 1897, Paris. 
75. Rossolimo: Neurolog. Zentralbl., 1891, p. 557. 
76. Albu: Berliner Klin. Wochenschft., 1907, p. 1649. 
77. L. R. Muller: (destruct. of lumbar spinal cord means constipat.), Zeitschft. f. 
Nervenheilkunde, 1901, V. 21, p. 86. 
78. Stiller Glenard: Die asthenische Konstitutionskrankheit, 1907, Stuttgart. 
79. Pinkus: v. Volkmanns Sammulung klin. Vortrage, 474-475. 
80. Ebstein: “Die chronische Stoolverstopfung Stuttgart, 1901, p. 18. 
81. Sturtz und Sauerbruch: Munch, med. Wochenschft, 1913, V. 60, p. 625. 
82. Stierlin: Deutsche Ztschft. f. Chir., V. 102, p. 426 and ergebn. d. inn. Med., 1913, 
, 10, p. 471. 
82. Wilms: Verh. d. Deutsch. Ges. f. Chir., 1911. 
83. Boehm: Munch, med. Wochenschft., 1912; Deutsches Arch. f. klin. Med., 1911, 
V. 102 and Arch. f. exp. Pathol, and Pharmak., 72,p. 1. 
84. Stierlin: Klin. Roentgendiagnostik d. Verdauungskanals, 1916. 
85. Boas: Med. Klinik., 1908, p. 1685 and Arch. f. Verdauungskrankheiten, V. 15. 
Mathieu: Arch, de maladie de 1’ app. digest., 1908, No. n. Pflanz: Pragermed. 
Wochenschft, 1908, No. 50. Fleiner: Berl. Klin. Wochenschft., 1893, P- 60. 
Albu-Kretschmer: Med. Klinik., 1908, No. 52. 
86. Schwarz: Munchner. med. Wochenschft., 1911, No. 28 and 1912. Holzknecht 
and Singer: Munch. Med. Wochenschft., 1911, No. 48 and Deutsche med. 
Wochenschft., 1912. Singer: Die atonische and spast. Obstipat. in Albus Samm- 
lung etc. in V. 1, No. 6; Wien. kl. Wochenschft., 1909. 
87. Rost: Deutsche Zeitschft. f. Chir., 1919, V. 151. 
88. V. Redwitz: Deutsche med. Wochenschft., 1919, p. 931. 
89. Jackson’s and other ligaments of the proximal colon: Arch. des. med. de 1’ app. 
dig., 1913, V. 7. Rjesanoff: Chirurgia, 1913, V. 33, p. 326. 
90. Eastmann: J. A. M. A., 1913, V. 61, Discussion. 
91. Schlesinger: Deutsche med. Wochenschrift, 1918, V. 37, p. 515. 
92. Schmidt und Lohrisch: Deutsches Arch. f. Klin. Med., 1903, V. 79, p. 383. 
93. Fischler: Munch, med. Wochenschft., 1911. 
94. Nothnagel: Lit. and discussion, Nothnagels Spec. Pathol., V. 17, p. 180; Wilms: 
Der Ileus in Deutsche Chir.; Leichtenstein in Ziemssens Handb., V. 7, 2 part. 
95. Leichtenstern: v. Ziemssens Handbuch d. spez. Path. V. 7. 
96. Zoge von Manteuffel: Arch. f. Klin. Chir., 1892, V. 41. v. Wahl: Arch. f. Klin. 
Chir., V. 38 and Zentralbl. f. Chir., 1889. 
97. Kader: Deutsche Ztschft. f. Chir., 1891, V. 33. 
98. Hotz: Mitt. a.d. Grenzgebieten, 1909, 20. 
99. Zuntz and Jacke: Deutsche med. Wochenschft., 1884, p. 717 and Tacke: Inaug.- 
Diss. Berlin, 1884. 
xoo. Kocher: Mitt. a.d. Grenzgebieten, 1899, V. 4. 
101. Talma: Ztschft. f. Klin. Med., 1890, V. 17. 
102. Trousseau: cited Deutsche Med. Wochenschft., 1884, p. 717. 
103. Heineke: Arch. f. klin. Chirurgie, V. 83. 
104. Olshausen: Ztschft. f. Geburtshilfe and Gynak., V. 14. 
105. Ranke: cited by Albert, Lehrbuch d. Chir., 1882, V. 3, p. 234, 2nd Ed. 
106. Wilms: Rupture, Deutsche med. Wochenschft., 1903, p. 81, u. 369; Arch. f. klin. 
Chir., 1913, V. 69. 
107. Kertecz: Deutsche med. Wochenschft., 1903, No. 23 and Berlin, klin. Wochen- 
schft., 1904, No. 52. INTESTINES 
273 
108. Kocher: Deutsche Ztschft. f. Chir., 1877, V. 8. Lossen: Arch. f. Klin. Chir., 
1874-1876, V. 17 u. Bd. 19. Busch: Arch. f. Klin. Chir., 1875, V. 19. Roser: 
Zentralbl. f. Chir., 1875, 1886, 1888, Arch. f. Heilkunde, 1864. Further lit. 
Schmidt: Underleibsbruche Deutsche Chir., 1896, V. 47. Borggreve and 
Hessel: Diss. Marburg, 1856. O. Beirn: cited by Albert, Lehrbuch, V. 3, 
p. 227. 
109. Roubaix-Karpetschenko: cited by Albert, Lehrbuch, p. 234. Hofmokl: Wiener 
med. Presse, 1876 and Zentralbl. f. Chir., 1876. 
no. Wilms: Arch. f. Klin. Chir., V. 69. Gruber: Virchows Arch., 1869, V. 48. 
in. Sultan: Zentralbl. f. Chir., 1907. Klauber: Deutsche med. Wochenschft., 1906. 
Neumann: Deutsche Ztschft. f. Chir., V. 91. Lorenz: Deutsche Ztschft. f. 
Chir., V. 102. Lauenstein: Deutsche Ztschft. f. Chir., V. 77; Zentralbl. f. 
Chir., 1907. 
112. Wilms: Der Ileus. Deutsche Chir., 46 g. Northnagel: Handbuch d. spez. Pathol., 
1895, V. x7- Propping: Mitt. a.d. Grenzgebieten, 1910, V. 21. Knapp: Inaug. 
Diss. Heidelberg, 1915. 
113. Propping: Dieterichs cited in Chir. Kongresszentralbl., 3, p. 873. 
114. Heidenhain: Arch. f. Klin. Chir., v. 55, p. 211 and Deutsche Ztschft. f. Chir., V. 
43- 
115. Maydl: Ueber Darmkrebs Wien., 1883. Bayer: Arch. f. Klin. Chir.; 1898, V. 
57, P- 233- 
116. Weiss: Arch. f. Klin. Chir., 1904, V. 73, p. 839. v. Greyerz: Deutsch Ztschft. 
f. Chir., 1905, 77, p. 57. Kreuter: Arch. f. Klin. Chir., 1903, V. 70. 
117. Anschutz: Arch. f. Klin. Chir., 1902, V. 68, p. 195. 
118. Dreyer: Munch. Med. Wochenschft., 1912, No. 34. 
119. cf. Rost: Munch. Med. Wochenschft., 1912, No. 38. 
120. v. Greyerz and Shimodeira: Brun’s Beitrage z. Chir., 1911, V. 22, p. 229. 
121. Kocher-Prutz: Arch. f. klin. Chir., 1900, V. 60. 
122. Qurin: Arch. fr. klin. Med., V. 71, p. 79. 
123. Oppenheim: Deutsche med. Wochenschft., 1902. 
124. Stadler and Hirsch: Intraabd. pressure Mitt. a.d. Grenzgebieten, 1906, 15, p. 448. 
125. Albu: Ueber die Auto intoxikationen des Intestinaltraktes, Berk, 1895, Lit. 
126. Sick: Deutsch Ztschft. f. Chir., V. 100. 
127. Borsieky and Genersich: Bruns Beitrage z. klin. Chir., V. 36, p. 448. Nikol- 
aysen: Studien over Aethiologie og. Pathologien of Ileus, 1895. Nesbieth: 
J. Exp. Med., 1899. Kukula: Arch. f. klin. Chir., V. 63, p. 773. Albeck, 
Ileus Arch. f. klin. Chir., V. 65, p. 569. 
128. Magnus-Alsleben: Hofmeister. Betr. z. chem. Physiol., 1904, V. 6, p. 502. Fall- 
oise: Arch, intern, de Physiol., 1907, V. 5, p. 159. 
129. Boruttau and Braun: Deutsche Ztschft. f. Chir., 1908, 96, p. 544. 
130. Gamier: Compt. rend. d. 1. soc. de Biol., 1905, V. 57, p. 388. 
131. Roger: Compt. rend. d. la soc. de Biol., 1906, V. 58, p. 666, p. 675. 
132. McLean: Ann. of Surg., 1914, 59, p. 407. 
133. Sauerbruch and Heyde: experim. Ileus. Ztschft. f. exp. Pathol, u. Therapie, 1909, 
V. 6. 
134. Kirschstein: Deutsche Med. Wochenschft., 1889, p. 1000. 
135. Wilms: Munch, med. Wochenschft., 1910, No. 5. Leuenberger: Munch, med. 
Wochenschft., 1910, No. 14. 
136. Mauthner and Pick: Munch. Med. Wochenschft., 1915, p. 1142. 
137. Crile: Revue de chir., 1914, No. 1, and J. A. M. A., 1913 and 1916. 274 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
138. Mummery: Lancet, 1907; Brit med. journ., T908. 
r39. Mann: Surg. Gyn. and Obst., V. 21, No. 4. Seelig and Lyon: J. A. M. A., r909, 
July. Malcolm: Lancet, 1907. 
140. Brown: Practitioner, 1910. 
i4r. Yandel Henderson: Berlin, klin. Wochenschft., r9r3, V. 50, p. r938 u. 1989. 
r42. Ephraim and Janeway: cited in Chir. Kongresszentralbl., 3, p. 2. 
143. Short: Brit, journ. of Surg., r9t3, V. r, p. rr4 and Lancet, r9T4, t86, p. 731. 
r44. Cobbet and Valte: cited by Short, Lancet, T907. 
r45. Moty: Revue d. chirurgie, r890, p. 878. 
146. Morgagni: De sedibus et causis morborum, Lit. sr. 
T47. Longuet: Bullet, d. la soc. anat. de Paris, 1875, p. 799. Beck: Deutsche Ztschft. 
f. Chir., r879, V. n, u. V. 15. 
148. Sauerbruch: Mitt. a.d. Grenzgebieten, T903, V. r2, p. 93. 
149. Ferrier and Adam: Franz. Chir. Kongr. Lyon., r894. Eichel: Brun’s Beitrage 
z. klin Chirurgie, r898, V. 22, p. 219. Curtis: Am. Journ. of Med. Science 
r887, V. 44. Thommen: Arch. f. klin. Chir., r902, V. 66. 
150. Hertle: Bruns Beitrage z. klin. Chir., r907, V. 53, p. 257, Lit. 
T5T. Bunge: Brun’s Beitrage z. klin. Chir., 1905, V. 47, p. 771. 
152. Kempf: Deutsche Ztschft f. Chir., 1908, V. 93, p. 524 (lit.). 
rs3- Petry: Bran's Beitrage z. klin. Chir., r896, V. t6, p. 555. 
rs4: Andrews: Surg. Gyn. and Obst., V. r2. 
T55. Strohl: Soc. de med. de Strassbourg: Gaz. med. de Strassbourg, r848. 
r56. A. Neumann: Deutsche Ztschft. f. Chir., 1902, V. 64, p. rs8. 
r57- Chaput: Bull, et mem. de la soc. de chir. de Paris, 1895, p. 230. 
r58. R. Neumann: Brun’s Beitrage, V. 43, p. 676. 
159. Pratz: Deutsche Chir., 46, K. 
160. Matthes: Zeitschft. f. med. Beamte, r904, V. 17, p. 837. Aldrich: Annal. of 
surg., T902, p. 343. 
r6r. Me Cosh: Med. and surg. Rep. Presbyt. Hosp., 1902, N. Y. 
r62. Zur Verth: Munch, med. Wochenschft., r9ro, p. 169. 
r63. Rech: Ergeb. d. Chir., i9r3, V. 7. Lit: s. bei Neutra. Zentralbl. f. d. Grenzgeb., 
r902, V. 5. Prutz: Deutsche Chir., 1913,46. Zesas: Zentralbl. f. d. Grenzgeb., 
rpro, T3. 
r64. Litten: Virchows Arch., 1875, V. 63. 
165. Virchow: Ges. Abhandlungen, 1856, p. 420, etc. Cohnheim: Untersuchungen 
ueber d. embolischen Prozesse, Berlin, r872. 
r66. v. Recklinghausen: Deutsche Chir., r883. Cohn: Klinik der embolischen Gefass- 
krankheiten, i860, Berlin. 
167. Bier: Virchows Arch., V. 147 u. 153. 
168. Sprengel: Deutsch. Chirurgenkongress, 1902 and Arch. f. klin. Chir., 1902, V. 67. 
169. Niederstein: Arch. f. klin. Chir., 1906, V. 85, p. 410 u. 1909, V. 98, p. 188. 
r7o. Marek: Deutsche Ztschft. f. Chir., 1907, 90. 
171. Mayo Robson: Brit. med. Journ., 1897, 2, 77. 
172. Wilms: Munch. Med. Wochenschft., 1901, No. 32. 
173. Rydigier: Berlin, klin. Wochenschft, 1881 und Deutsche Ztschft. f. Chir., V. 21, 
p. 546. Madelung: Arch. f. klin. Chir., 1882, V. 27, p. 277. 
174. Schloffer: Mitt. a.d. Grenzgebieten, 1900, V. 7, p. r and 1905, V. 14, p. 2sr. 
175: Busse: Arch. f. Klin. Chir., V. 83. 
176. Payr: Zentralbl. f. Chirurgie, 1904 and Deutsch. Chirurgenkongress, 1907. 
177. Schmorl: Path. anat. Untersuch ueber Puerperaleclampsia, Leipzig, 1893; 
Gynak-Kongress, 1901, Arch. f. Gyn., V. 65. INTESTINES 
275 
178. Bouisson: Arch, de med. exper., Nov., 1889, p. 843. 
179. Sprengel: Lit. Deutsche Chir., 1906, 46 d. 
180. Wilms: Zentralbl. f. Chir., 1909, p. 1041. 
181. Koerte: Freie Ver. d. Chir., Berlins, 1909. 
182. Koester: Deutsche med. Wochenschft., 1898, p. 325. 
183. Mattes: Med. Klin., 1906, p. 397. 
184. Trendelenburg: Deutsche med. Wochenschft., 1899. 
185. A. Hoffmann: Bruns Beitrage, 1910, V. 69, p. 701. 
186. Baum: cited by Weil in Ergebn. d. Chir., V. 2. 
187. Franke: Deutsche Zeitschft. f. Chir., 1912, V. 119. 
188. Lit. see Sprengel: Deutsche Chir., 1906, No. 46 d.; Koerte im Handbuch d. pract. 
Chir. Weil, Ueber akute frei Peritonitis, Ergebn. d. Chir., 1911, V. 2, p. 278. 
189. Weil: Die akute freie Peritonitis im Ergebn. d. Chir., 1911, 2, p. 308. 
190. Heyde: Med. Klin., 1908; Bruns Beitrage, 1911, 76. 
191. Runeberg: Studien uber die bei perit Affekt. append. Ursprunges vorkommenden 
Bakterieformen, Berlin, 1908. Friedrich- Arch. f. klin. Chir., V. 68. 
192. Heile: Mitt, aus d. Grenzgebieten, 1911, 22, p. 58. 
193. Haim: Arch. f. Klin. Chir., 1906, 78, p. 82. Cohn: Arch. f. klin. Chir., 85. 
194. Wieland: Mitt, aus d. Kliniken d. Schweiz, 1895, V. 7, 2 R. 
195. Cushing and Livinggood: cited by Koerte in Handbuch d. prakt. Chir., 1913, V. 
3, p. 48. 
196. Meisel: Bruns Beitrage, V. 40, p. 529. Danielsen: Bran’s Beitrage, V. 54. 
197. see Schmieden: In'Borchard-Schmieden Lehrbuch d. Kriegs chirargie, Leipzig, 
19x7. 
198. Friedrich: Arch. f. Klin. Chit., V. 95. 
199. Brunner: Brans Beitrage, V. 40, p. 51. 
200. Zesas, Denis: Ueber kryptogenetische Peritonitiden, v. Volkmanns Sammlung 
klin. Vortrage, 1912, No. 515. 
201. Bonneken: Virchows Arch., V. 120. Engstrom: Ztschft. f. Geb. u. Gyn., 1897, 
V. 36. Rovsing: Zentralbl. f. Chir., 1892, No. 32. Schloffer: Bruns Beitrage, 
1895, V. 14, p. 813. Ritter: Diss. Gottingen, 1890. Ikonnikof: Annal de 
’1 inst. Past. 23, p. 921. Tavel-Lanz: Mitt, aus Kliniken usw. d. Schweiz, 
1893, U Part 1. Garre: Fortsche d. Med., 1886, p. 486. Arnd: Mitt, aus 
Kliniken usw. d. Schweiz, 1 Reihe, Part 4. 
202. Bail: Arch. f. Hyg., 1897, V. 30, p. 348. 
203. Pansini: Zieglers Beitrage, 1893, V. 12. Kocher: Arch. f. klin. Chir., 23. 
204. Karlinski: Prager med. Wochenschft., 1890. 
205. Neisser: Zeitschft. f. Hyg., 22, p. 12. Buchbinder: Deutsche Ztschft. f. Chir., 
V. ss, p. 458. 
206. Erkes: Zentralbl. f. Chir., 1918, p. 97. Lennander: Nystrom Ztschft. f. klin. 
Med., V. 43. Langemaak: Bran’s Beitrage z. klin. Chir., V. 37. 
207. Rohr: Mitt. a.d. Grenzgeb., V. 23, p. 659. 
208. Jensen: Arch. f. Klin. Chir., 1903, V. 69 and 70, p. no, Lit. 
209. Krogius: v. Volkmanns Sammulungen Klin. Vortrage, No. 467-468. 
210. Burchhardt: Brans Beitrage, 1901, V. 30, p. 731. 
2ix. Peiser: Brans Beitrage, 1907, V. 55, p. 484. 
212. Grawitz: Charite Annalen 11, Jahrg., 1806, p. 770 and Virchows Arch., 1889, 116, 
p. 116. 
213. Pawlowski: Virchows Arch., 1889, 117, p. 469. 
214. Wallgreen: Lit. Zieglers Beitrage, 1899, 25, p. 206. 276 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
215. Reichel: Deutsche Zeitschrft. f. Chir., 1890, 30, p. 1. 
216. Walthard: Arch. f. exp. Pathol., 1891. 
217. Voelcker: (second infect, in infect, hernia), Bruns Beitrage, 1911, V. 72, p. 647. 
218. Pfeiffer-Kolle: Ztschft. f. Hyg. u. Infect-Krankh., 1896, 21, p. 203. Isaeff: 
Zeitschft. f. Hyg. u. Infect. Krankh., 1894, 16, p. 287. Bordet: Annales de P 
institut. Pasteur, 1897, 1, p. 177. 
219. Notzel: Arch. f. klin. Chir., 1898, V. 57, u. 81. 
220. Canon: Deutsche Ztschft. f. Chir., 1908, V. 95, p. 21. 
221. Peiser: Brun’s Beitrage, z. klin. Chir., 51, p. 681. 
222. Metschnikoff: Immunitat bei Infectionskrankheiten Deutsche v. J. Meyer, 1902 
und die Lehre von d. Phagozyten usw. in. Kolle Wassermanns Handbuch der 
pathog. Microorganismen., 1913, V. 2, 2nd Edit. 
223. Clairmont and Haberer: Arch. f. klin. Chir., 1905, 76, p. 41. 
224. Metschnikoff: Annales de 1’ institut Pasteur, 1895, 369. 
225. Bordet: Annales de 1’ institut Pasteur, 1897, n, p. 177. 
226. Haukin: Zentralbl. f. Bact., 1892, 12, p. 777 u. 809 u. 1893, V. 15, p. 852. Schat- 
tenfroh: Arch. f. Hyg., 1897, V. 31, p. 1. Buchner: Munch, med. Wochen- 
schft., 1894, p. 717. 
227. Glimm: Deutsche Ztschft. f. Chir., V. 83. 
228. Moskowitz: Arch. f. klin. Chir., 1904, V. 72, p. 773. 
229. Pfeiffer and Wassermann: Ztschft. f. Hyg., 14, p. 46. 
230. R. Stern: Ztschft. f. klin. Med., 1891, V. 18. Schrader: Deutsche Ztschft. f. 
Chir., 1903, V. 70, p. 421. R. Pfeiffer: Ztschft. f. Hyg., V. 16, 18, 20. 
231. Heinecke: Arch. f. Klin. Med., 1901, V. 69, p. 429. 
232. Bauer: Krankheiten d. Peritoneum in Ziemssens Handbuch, V. 8. 
233. Friedlander: Arch. f. Klin. Chir., 1904, 72, p. 196. 
234. Strehl: Arch. f. klin. Chir., 1905, 75, p. 711. 
235. Perthes: Chirurgenkongress, 1900, p. 112 f. 
236. v. Lichtenberg: Ueber die Kreislaufstoerungen bei Peritonitis Wiesbaden, 1909. 
237. Askanazy: Verhandt. d. Deutsch. Pathol. Gesellschaft, 3. 
238. Walbaum: Wiener med. Wochenschft, 1902, V. 37. 
239. Braun und Boruttau: Deutsche Ztschft. f. Chir., 1908, V. 96, p. 544. Clairmont 
and Ranzi: Deutsche Ztschft. f. Chir., V. 33, p. 52. 
240. Sprengel: Die Appendizitis Deutsche Chir., Lief., 1906, 46 d. 
241. Henle: cited in Nothnagel’s Handbuch, V. 17, p. 204. 
242. Volcker: Lit. see Volcker, Bruns Beitrage, 1911, V. 72, p. 633 and Kroher: 
Deutsche Ztschft. f. Chir., 1915. V. 134. Chrobak: Wiener klin. Wochenschft, 
1906. 
243. cf. Iselin: Zentralbl. f. Chir., 1911; Mitt, aus d. Grenzgebieten, V. 23 and Bruns 
Beitrage, 1916, 102. 
244. Rotter: Arch. f. klin. Chir., 1910, V. 93, p. 1. 
245. Wells: cited by Proot, Geschichte d. Drainage, 1884. Nussbaum: cited in Proot. 
Geschichted. Drainage, 1884. Olshausen: Ztschft. f. Gyn., 1902,48. Mikulicz: 
Sammlung klin. Vortrage, 1885, 262-264. 
246. Propping: Arch. f. klin. Chir., 1910, V. 92. Rehn: Arch. f. klin. Chir., 1902, V. 67. 
Noetzel: Brun’s Beitrage z. klin. Chir., 1905, V. 46 u. 47 u. Arch. f. klin. Chir., 
1909, V. 90. 
247. Torek: Med. Record, 1906. Buchanan: Med. Record, 1911. Scheidtmann: 
Deutsche med. Wochenschft., 1912. Morris: Med. Record, 1902. Clark: 
lit. see Kroher, Deutsche Ztschrft. f. Chir., 1915, 134. INTESTINES 
277 
248. Wilms: Munch, med. Wochenschft., 1916. 
249. Virchow: Virchows Arch., 1853, V. 5, p. 339. 
250. Payr: Naturforscherversammlung Wien, 1913 (chir. Sect.). 
251. Rost: Deutsche Zeitschft. f. Chir., V. 125 u. 127. 
252. Bittorf: Grenzgebiete, 1909, V. 20, p. 150. 
253. Rosenheim: Ztschft. f. klin. Med., 54 u. Deutsche med. Wochenschrift, 1909 
254. Mylard: Brit. med. Journ. March, 1907, p. 484. 
253. Zeidler: Mitt. a.d. Grenzgebieten, V. 5, p. 606. Riedel: Arch. f. klin. Chir., 1898, 
V. 47, Chirurgenkongress. Payr: Arch. f. klin. Chir., 1905, V. 77, p. 671. 
Terrier: Bull. et. mem. la soc. de chir. de Paris, 1902, p. 467. Lequeu: 
Gaz. des hopitaux, 1895, P- 1328. Quenu-Walter-Routier: Bull et. mem. de la 
soc. de chir. de Paris, 1902, p. 712. Poirier: Bull, et mem. de la soc. de chir. de 
Paris, 1902, p. 472 (discussion). Brunn: Deutsche Ztschft. f. Chir., 1905, V. 
76. v. Bergmann: Arch. f. Klin. Chir., V. 61, p. 921. Berard and Patel: Revue 
de chir., 1903, p. 590. 
256. Collective References: Isler Zentralbl. f.d. Grenzgebiete, V. 12, 18-19; Pick, 
Ztschft. f. klin. Med., 1896, V. 29: Esau, Deutsche Ztschft. f. Chir., V. 125. 
257. Rehn: Handbuch f. prakt. Chir., 1913, V. 2, p. 932. 
258. Corner: Annals of surg., 19x0. 
259. Corner: Brit. med. Journ., 1913, p. 325. 
260. Funke: cited by Sprengel, Appendicitis, Deutsche Chir., 46 d. p. 49. 
261. Robinson: Compt. rend. hebd. des seances de l’acad. des sciences, 1913, V. 107, 
p. 790. Heile: Brun’s Beitrage, V. 93. Chirurgenkongress, 1914, p. 247. 
262. Appendicitis: Lit. Lanz: Brun’s Beitrage, 1903. Klein: ibid., 1904, Adriau, 
Grenzgebiete, 1902, V. 7; v. Hartsemann, ibid., 1903, Sommenburg, Pathol- 
ogie u. Chir. d. Perityphlitis, Leipzig, 1905; F. C. W. Vogel; Sprengel: 
Deutsche Chir., V. 46. Aschoff: Die Wurmfortsatzentzundung. Jena, 1908, u. 
Ergebn. d. inneren. Med., 1912, V. 9. Meisel: Bruns Beitrage, 1903, V. 40. 
Schrumpf, Grenzgebiete, 1907. Blinddarmanhanges, Jena, 1910. V. Brunn, 
Ergebn. d. Chir., 17. Kretz ibid.; Noll, ibid. Winkler, Die Erkrankungen 
d. u. Orthop, 1911, V. 2. 
263. Tavel-Lanz: Rev. de chir., 1904. Heile: Chirurgenkongress, 1909. 
264. Kretz: Wiener klin. Wochenschft. 1900; Verh. d. Deutsch. pathol. Ges. 1906, 
Mitt. a.d. Grenzgebieten, 1907 and 20, 17; 1909; Ztschft. f. Heilkunde, 1908, 
V. 28. 
265. Muhsam: Deutsche Ztschft. f. Chir., 1900, 55. Winkler: Erkr. d. Proc. vermi- 
formis. Jena, Fischer, 1910. Stoeber and Dahl: Mitt. a.d. Grenzgebieten, 24. 
Ribbert: Deutsche Med. Wochenschft., 1885. Roux-Roger-Losne: Rev. de 
med., 1896, V. 16. Charrin: Compt. rend. Soc. de Biol., 1897. Anghel: These 
de Paris, 1897. Beaussenat: Bull, de la soc. anat. de Paris, 1897. Paine: 
Lancet., 1911, Brit. med. Journ., 1911. Adrian: Mitt, aus d. Grenzgebieten, 
1901, V. 7,9. 
266. Ten Horn: Arch. f. Klin. Chir., 109, Part 2. 
267. Dieulafoy: Acad. de. med., 1896. 
268. Klecki: Annales de 1’ inst. Pasteur, 1895 u. 1899, 9 u. 11. 
269. Meisel: 33 Deutsches Chirurgenkongress, 1904. 
270. Klauber: Munchener med. Wochenschft., 1909, p. 451. 
271. Brunn: Mitt. a.d. Grenzgebieten, 1909, V. 21. 
272. McLean: Mitt, aus d. Grenzgebieten, 1909, V. 21. 
273. Hoenck: Ueber die Rolle d. Lymphathicus bei Erkrankung d. Wurmfortsatzes 
Jena. Fischers Verlag, 1907. 278 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
274- Sonnenburg: Perityphlitis 1913, p. 108, 7 edit., F. C. W. Vogel. 
275. Kafemann: Deutsche med. Wochenschft, 1911. 
276. v. Redwitz: Brun’s Beitrage, 1913, V. 87. 
277. Rippert: Virchows Arch., 1893, V. 132 and Deutsche med. Wochenschft., 1903, 
inflammation is accepted. Zuckerkandl: Anat. Hefte, 1894. Schmorl: Mun- 
chener med. Wochenschft., 1910, V. 17, p. 936. Oberdorfer: Grenzgebiete, 
1906, V. 15. 
278. Miloslavich and Namba: Grenzgebiete, 1912, V. 24. 
279. Aschoff: in Deutsche med. Wochenschft., 1906, p. 985. 
280. Riedel: Arch. f. klin. Chir., 1902, 66. 
281. Payr: Arch. f. klin. Chir., 1907, V. 84. 
282. Moynihan: Brit. med. Journ., 1910, p. 241. 
283. Paterson: Lancet., 1910, p. 708. 
284. Silhol: 24th French surgical congress, 1911. Ewald: 28 Deutscher Chirurgen- 
kongress, 1899, p. 685. 
285. Sick: Zeitschrift. f. Chir., V. 70. Jordan: Arch. f. klin. Chir., V. 69. Fischl: 
Prager med. Wochenschrift, 1904. 
286. Ghedini: La Clin, chir., 1905. von Brenner: Wiener klin. Wochenschft., 1907. 
Extensive Resect, of ileum collected by Kukula: Arch. f. Klin. Chir., 1900, 
V. 60, p. 912. Nigrisoli: Nuovo Raggogl. med., 1902. Pauchet: Gaz. med. 
de Picardie, 1905. Axhausen: Mitt, aus d. Grenzgebieten, 1910, V. 21. 
287. Denk: Mitt, aus d. Grenzgebieten, 1911, V. 22. 
288. Trzebicki: Arch. f. klin. Chir., V. 48, p. 54. Monari: Brun’s Beitrage z. Klin. 
Chir., 1896, V. 16. 
289. Blayney: Brit. med. journ., 1901. Soyesima: Deutsche Ztschft. f. Chir., 1911, 
V. 112. Diliberti Herbin: Gaz. med. ital., 1903. Albu: Mitth. a. d. Grenz- 
gebieten, 1909, V. 19 and Berlin, klin. Wochenschft., 1901. 
290. Lieblein: Mitt, aus d. Grenzgebieten, V. 23, part r. 
291. London: Zeitschft. f. physiol. Chemie, V. 49. 
292. Stassofif: Bruns Beitrage z. klin. Chir., 1914, V. 89. 
293. Ziesch: Deutsche med. Wochenschft., 1909, p. 739. Riva-Rocci: Gaz. med. di 
Torino, 1896. Nagano: Bruns Beitrage, z. Klin. Chir., V. 38. Erlanger 
und Hewlett: Am. J. of Physiol., 1901, V. 6. Albu-Lexer: Berliner, klin. 
Wochenschft., 1901, p. 1248. 
294. Brugsch: Ztschft. f. klin. Med., 58, p. 518. 
295. Flint: Bull, of John Hopkins Hosp., 1912. 
296. Evans and Brenizer: Bull, of John Hopkins Hosp., 1907, p. 477. 
297. Barker: The Lancet., 1905. 
298. Bauer: Ergebn. d. chir., 1912, V. 4, p. 573. 
299. Rost: Munch, med. Wochenschft., 1918, No. 5. 
300. Ludloff: rectal prolapse, Arch. f. klin. Chir., 1899-1900, V. 59 u. 60. 
301. Beresnegowsky: Arch. f. klin. Chir., 1910, V. 91, p. 627. 
302. Bell and Hirschberg: Berlin, klin. Wochenschft., 1894, No. 14. 
303. Waldeyer: Lehrb. d. topogr. chir. Anat., 1899. 
304. Esmarch: Deutsche Chir., V. 48. * 
305. Ziegenspeck: Arch. f. Gynakol, 31. Trager: Arch. f. Anat. (u. Physiol.), 1897. 
Wenzel: Deutsche Ztschft. f. Chir., 1905, V. 76, 19. Waldeyer, Zuckerhandl: 
Deutsche Ztschft. f. Chir., 1891, V. 31, p. 590. 
306. Mummery: Brit. med. Journ., 1907, p. 2439. 
307. Jeannel: Legons. de clinique chir. faites a’ 1 Hotel-Dieu de Toulouse, 1897. 
308. Lenormant: Le prolapsus de Rectum These de Paris, 1903. CHAPTER VIII 
KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
In unilateral renal disease, it is always very important to make sure 
that the other supposedly healthy kidney is really functionally efficient. 
To determine this, methods are frequently used which depend on the 
appearance of foreign substances in the urine after they have been admin- 
istered through various routes to the patient (i). These methods pre- 
suppose that endogenous and foreign substances are eliminated by the 
same anatomical part of the kidneys, and also that the different chemical 
substances all pass through the same place in the renal system. Since 
this supposition is incorrect, all the kidney functional tests which depend 
on the elimination of foreign substances, colors, salts, etc., have only 
comparative values although this does not condemn their practical 
usefulness. 
But what do w6 actually know of the 11 microscopic” junction of the 
kidneys, i.e., of the locality and the manner in which the elements of the 
blood are excreted? The theory of Ludwig and that of Heidenhain still 
hold the center of interest. Ludwig claimed that renal function is a pure 
filtration process consisting of the formation of urine from the blood by 
filtration through the glomeruli. Heidenhain believed that urine is a 
product of secretion of the renal epithelium, especially of the convoluted 
tubules. The numerous investigations of the last decades (2), have shown 
that neither of these theories can claim absolute correctness; the forma- 
tion of urine is an exceptionally complex process, and the excretion of the 
different substances which constitute it probably occurs in different parts 
of this glandular organ. Perhaps even part of the water excreted is again 
reabsorbed in the uriniferous tubules, but all these factors are not as yet 
clear (3). 
[In passing, it may be useful to consider the so-called “ modern theory ” 
of renal secretion. The details may be found in the monograph by 
Cushny. The substances of the blood are divided into two classes in 
reference to their excretion by the kidney, the threshold and the no- 
threshold bodies. That is, there are substances which are excreted as long 
as any are left in the blood, in other words, in proportion to their absolute 
amount in the plasma. Others, the threshold bodies, are excreted when 
their amount in the blood exceeds a certain threshold value. An example 
of a no-threshold body is urea, but while it cannot be proved directly 
279 280 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
for this substance, because it is continuously replaced in the blood, it 
nevertheless resembles in its excretion, other substances which can be 
demonstrated to be no-threshold bodies. Dextrose, chloride .and 
sodium are at the other extremity, and when their amount in the plasma 
falls below a certain threshold, they cease to be excreted. 
The recent advances in physical chemistry have shown that Ludwig’s 
theory cannot account for kidney function, mainly because the known 
physical force, i.e., the blood pressure, is not adequate to filter off a 
urine of greater osmotic pressure from the blood plasma. The blood 
pressure can, however, filter off the constituents of the plasma with the 
exception of the proteins to which the capsular membrane is impermeable, 
and therefore, what amounts to a deproteinized plasma can pass through. 
This is very different from the final urine, for the proportions of the solids 
have changed. This is accounted for by assuming that in its passage 
through the tubules, water and certain other of its constituents are 
absorbed by the living epithelium. To put it briefly: The threshold 
bodies are taken up by the vital activity of the epithelium and returned to 
the blood in the proportion determined by their normal values in the 
plasma, while the no-threshold bodies are allowed to proceed further and 
be excreted. 
The known physical forces are therefore supplemented by the neces- 
sary addition of this unknown force which discriminates and returns to 
the blood, substances which ensure its normal composition. 
It might be mentioned that the evidence for reabsorption has been 
entirely indirect until the recent work of Wearn has given direct data. 
He has succeeded in introducing a very fine capillary pipette into the 
capsular space of a frog’s kidney under indirect illumination and direct 
vision. Glucose was found in seven instances in glomerular urine and not 
in bladder urine. The same was true of chlorides in four frogs. The 
results are offered as proof of reabsorption in the tubules and as strong 
evidence of glomerular filtration (4)]. 
It would be of the highest practical importance if the salts, colors and 
other substances, including water, used for functional tests, could be grouped 
according to the part of the kidney from which they are excreted, for by 
investigating the elimination of a member of each group, it would be possi- 
ble to obtain a true picture of the functional ability of a kidney. Attempts 
have frequently been made to classify renal diseases in this way, hoping 
primarily, to define clearly the different forms of Bright’s disease. The 
excretion of these various substances was measured in vivo, and later 
controlled by autopsy to discover which part of the kidney was especially 
affected. It was supposed that by reasoning backward, the particular part 
of the tubular system in which these different substances were excreted could KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
281 
be found. This idea seems reasonable, but nevertheless, it has not helped 
to mold a uniform opinion. Quite to the contrary, while.Koranyi and his 
pupils think that the excretion of water and sodium chloride takes place 
in the glomeruli, while nitrogen excretion is assigned to the convoluted 
tubules, Fr. Muller, and Monakow (5), believe the reverse. Schlayer 
(6) attempted to solve this question by systematic experiments. He 
produced nephritis in animals by various poisons and believed that two 
forms occur. The first, “ vascular nephritis,” primarily affected the 
vessels, and led to a complete suspension of the secretion of water, for 
instance, after arsenic and cantharidin. The second, a “tubular” form, 
first injured the epithelium, and soon showed diminution of sodium 
chloride and potassium iodide elimination, but the excretion of water was 
not diminished; on the contrary, polyuria was present. The excretion of 
milk sugar was not impaired, and he believed, therefore, that a delay 
in milk sugar excretion would suggest vascular injury. Many objections 
which cannot be detailed here were raised to these experiments (see 
Gross (3)), particularly to their application to human pathology. Vol- 
hard ((2)p. 1182) concluded that glomeruli and tubules excrete the same 
substances, although in different concentrations, and that the specific 
action of the glomeruli consists in dilution, while the specific action of the 
tubules consists in concentration. 
Topical function tests of the kidneys seem almost hopeless, and 
practical surgery has been content to use methods which give an idea 
of the total excretory ability of a kidney, without considering a possible 
affection of separate parts. The usefulness of most of these functional 
tests is, as already stated, based merely on the “sum total” of practical 
experience. Those methods are useful which consider the specific activity 
of the glomeruli and the tubules, testing, therefore, whether the renal 
concentrating power is sufficient, and whether the kidney is able to elimi- 
nate water quickly when given in excess (Gottstein (1)). 
The drink test first advised by Albarran (7) is now little used in surgical 
renal diseases. The reasoning is this: with a dry diet, the specific gravity 
of urine quickly increases; and it is a sign of renal insufficiency if the 
kidneys cannot eliminate concentrated urine. But in addition to changes 
in concentration, we often consider polyuria itself a sign of renal insuffi- 
ciency; and as an example, the polyuria in patients with prostatic hyper- 
trophy need only be mentioned. 
Other methods attempt to determine the functional ability of each 
separate kidney in an even more general manner. It has been proposed 
to examine the secretion of the separate kidneys to discover if equal 
quantities of urea or chlorides are excreted under the same experimental 
conditions. The functional ability of a single kidney may also be tested 282 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
by determining whether colors, which are usually administered to the 
patient intramuscularly, reappear in the urine in a certain time and in 
a certain quantity. Phloridzin injections have been used, after which 
a healthy individual excretes sugar, as is well known, and this constitutes 
a true renal glycosuria. The diseased kidney excretes less sugar or its 
excretion is delayed. Finally, in unilateral renal diseases, it may be nec- 
essary to determine only whether the total ability of both kidneys is 
sufficient. For this purpose, the molecular concentration of the blood is 
determined by the lowering of the freezing point or by other physico- 
chemical methods. This is exceptionally constant under normal conditions 
and rises only if the excretion of certain urinous substances becomes impaired. 
The activity of the kidneys, like that of other glandular organs, can 
be much influenced by their nerve supply; and they, like other glands, 
possess a double innervation: the major and minor splanchnic nerves 
and the vagus (8). (In regard to the ramification of the renal nerves see 
Disse, Smirnow, Renner (9)). There are also sympathetic ganglion cells 
in the kidney itself, which explains why urine is secreted, and why the 
kidney shows a certain adaptability to every possible functional stimulus 
even after all afferent nerves are severed, as shown for example, by Loben- 
hofer (10) who succeeded in suturing the vessels of one kidney to the 
splenic vessels. But the afferent nerves are not altogether without 
influence. Although cutting and stimulation of the vagus have not given 
constant results, Meyer, Jungmann and Eckhard (11) found that section 
of the splanchnic nerve caused polyuria; while irritation was followed by 
alterations in urine secretion (12); a statement verified by other workers. 
These sympathetic branches pass to the celiac ganglion, and this is prob- 
ably the first station, where reflex stimuli can be transferred from one 
side to the other. Another station can be demonstrated in the spinal 
cord, but the further course of these tracts toward the cerebrum is not 
known in detail. Gaetani’s (13) statements that unilateral renal extirpa- 
tion in the rabbit leads to demonstrable changes in both anterior 
columns of the spinal cord as far as the cerebral base require further 
investigation. 
Eckhard showed that polyuria can be induced by puncturing the 
medulla, somewhat lateral to the area used for the Claude Bernard sugar 
puncture, and Jungmann and Erich Meyer have found in addition that 
a tremendous increase of sodium chloride elimination results from this 
medullary lesion. For this reason they speak of a “salt-puncture.” But 
it is not quite clear at present whether these phenomena are caused 
by some form of direct nerve stimulus (Jungmann, Meyer), or indirectly, 
by activation through some hormone, i.e., adrenalin or hypophysin, which 
in'its turn stimulates the kidneys through the blood (see Volhard (2)). KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
283 
The question whether the nerves described should be accepted as 
secretory nerves, or whether they influence urinary secretion indirectly by 
vasomotor activity is decided by microscopical anatomical investigations 
showing that the kidney is probably supplied by secretory nerve fibres, 
in addition to its abundant vasomotor nerves (9). The kidney capsule, 
the pelvis and also the renal connective tissue, contain sensory nerve fila- 
ments according to Meyer and Jungmann, while the musculature of the 
pelvis contains motor fibres. The kidney becomes painless after cutting 
the spinal cord at the eighth to ninth dorsal level, while cutting the 
splanchnic nerve has no influence on its sensitivity (14). 
It is not certain that the attacks of pain in different renal affections 
are due only to pulling of surrounding tissue as stated by Wilms (15). 
Even if the patient does not feel the introduction of the ureteral catheter, 
he usually feels a stabbing pain when the wall of the pelvis is touched (see 
also (16)), and this pain can become very severe if, for instance, the pelvis 
is filled for pyelography. For this reason it must be assumed that these 
sensory nerves transmit pain sensations. The stimuli are frequently 
transferred to spinal nerves which explains the “radiation” of the pain in 
renal colic. 
This nerve supply is of particular interest because it forms the founda- 
tion for studying reflex anuria, which occurs not rarely in surgical renal 
and ureteral diseases. Such reflex anuria is observed chiefly when a 
calculus obstructs an ureter; and according to Goetzl and Israel (17) it is 
caused by an increase of intrarenal pressure. In the animal experiments of 
Goetzl, anuria was rare; and this has been confirmed by other workers 
(18). But Cohnheim and Roy (19), by irritation of the sciatic nerve, and 
Masius (19) by vagus irritation, obtained anuria. In both cases, accord- 
ing to general opinion, this is due to a reflex vessel spasm. But nothing 
certain is known in the matter; and a spasm would hardly explain an 
anuria of some duration; Ghiron (20) also, who observed the living organ 
under a light cone, could not demonstrate vessel spasm, but he found a 
delayed coloring of the striated border after injection of aniline blue. 
Meyer and Jungmann (21) produced reflex anuria fairly regularly by 
irritating the bladder and ureter, after previously cutting the splanchnic 
nerve. Jenckel (22) reports a very interesting case, appropriate in this 
connection, in which after unilateral nephrectomy a complete anuria 
developed which could not be explained at autopsy even microscopically. 
In interpreting all these so-called reflex disturbances of renal function, 
it is important to know the quantity, quality and time of normal secretion. 
Cystoscopic data is always somewhat uncertain because the instrument 
acts as a renal irritant, and because ureteral catheters never fit closely 
enough to prevent the escape of urine around them. Animal experiments 284 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
relating to this question have been made by Kapsammer (23), Pflaumer 
(8) a.o. They hardly give an accurate picture of the normal conditions, 
however, since in all these experiments considerable manipulation is 
unavoidable. The observations made in cases of exstrophy of the bladder, 
reported by Luter, and Meyer, also Allard (24) are more useful. Accord- 
ingly, the urine usually escapes alternately from the two ureteral orifices; 
it is only during more marked diuresis that the flow proceeds irregularly. 
The quantity poured out by each ureter is not the same during short 
periods of observation; during longer periods, the differences diminish. 
The same is true of the composition of both urines. But if the kidneys 
are functionally severely taxed, i.e., by copious water drinking, the differ- 
ences in the quantity and composition of the urines become greater. 
Changes in posture influence renal activity (25) (8). During an upright 
position the kidneys secrete less than when prone, and lying on the side 
also seems to have its influence. It has not been determined how much 
of these postural variations are due to reflex influences. In addition, the 
ureteral movements may be influenced reflexly. In Allard’s patients, a 
mere touch of the ureteral opening, was sufficient to interrupt their 
rhythmic action for minutes. The urine in the mean time collected in 
the pelvis, and after this pause, was discharged all the more quickly. 
Pflaumer, in his experiments on animals, obtained somewhat different 
results. There was an increase in ureteral activity and in water secretion 
after touching the ureter with alcohol. 
The more the bladder fills, the more the ureters contract; but water 
secretion diminishes and this decrease of urine formation does not depend 
on stasis in the ureter, but must be considered as a vesico-renal reflex (8). 
Increase in water excretion (polyuria) which occurs normally after an 
abundant intake of fluids, and also after a diet especially rich in nitrogen, 
is observed in the most varied conditions. It is usually divided into an 
indirect, neurogenous, or reflex form, and into a hematogenous or nephro- 
genous form. Polyuria from a contracted kidney, in which of course the 
greater number of the glomeruli is destroyed, is a nephrogenous polyuria, 
and is a symptom of a certain type of renal insufficiency. From this, Fr. 
Muller (5) concluded that the secretion of water in the kidney must 
occur not only in the glomeruli, but also in the convoluted tubules. 
In surgical kidney disease, it isjpften very difficult to distinguish these 
two groups and, e.g., the polyuria in tuberculous nephritis (26), the so- 
called “clear” polyuria, is considered by some as evidence of renal insuffici- 
ency, and by others as pollacissuria, and, therefore, a purely reflex process. 
According to Guyon, a voluntary increase in the quantity of urine can be 
produced by frequent urination. Conversely “if convivial drinkers at 
long sessions abstain from the first voiding, they are able to retain the urine KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
285 
without pain for considerable time,” but after the first voiding, a flow of 
urine takes place which necessitates repeated urination (27). It has 
already been stated that a “sugar- or salt-puncture,” i.e., injury of the 
central nervous system produces polyuria, a fact which forms the experi- 
mental basis of our knowledge of the diabetes insipidus occasionally seen 
following head injuries. 
The influence of peripheral innervation on the quantity of urine has been 
shown in the experiments of Rohde and Ellinger (12) in which polyuria 
occurred after tearing the renal nerve supply apart. The older experi- 
ments of Eckhard (n) and Knoll (11) also produced polyuria in the dog, 
by sectioning the splanchnic nerve. Purely reflex polyuria is occasionally 
caused by ureteral catheterization (n), (23). By this method of investi- 
gation, however, it is necessary to be cautious in drawing far-reaching 
conclusions from the quantity of urine excreted. 
The production of urine during retention is always of special interest, 
not only for purely experimental reasons, but also because the polyuria 
in prostatic hypertrophy belongs to this group. Related experiments 
were made by Cohnheim, Albarran, Ponfick, Steyrer, Filhene and Rusch- 
haupt, Allard, Schwarz, Pfaundler a.o. (for further lit. see under “Hydro- 
nephrosis” (27)). They served in part to study the changes occurring 
in hydronephrosis, and in part to discover whether a reabsorption of 
urine actually took place in the uriniferous tubules; finally, this method 
of approach seemed the least disturbing in attempting to produce a 
graduated renal lesion. This latter viewpoint also interests the surgeon, 
i.e., the question of the effect on function of a slight but chronic retention 
of urine. Unfortunately the writers have not obtained similar results. 
Some observed polyuria with urine of low specific gravity, others, a 
decrease of quantity and diminished nitrogen and sodium chloride excre- 
tion. A number of these records relate to investigations on man, but 
here also there is no uniformity in the findings. According to the very 
careful observations of Allard on a patient with exstrophy of the bladder, 
it seems that in unilateral obstruction, the other kidney can compensate 
and secrete a much larger quantity, while the test kidney produces less 
urine than normal. Styrer a.o., obtained similar results. But undoubt- 
edly in most cases of hypertrophy of the prostate, the quantity of urine 
is greatly increased, even at a time when there is only a slight dilatation 
of the renal pelvis (28). Whether the frequency from vesical irritation 
which is usually present in the early stages of this condition, has led to 
marked polyuria, is not certain, but possible. As a whole, these contra- 
dictory findings have not been cleared up, but the impression is gained that 
the kidney responds with extraordinary sensitivity to any stimulus, and 
changes the quantity and composition of urine. Therefore, the end 286 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
results of our more or less clumsy experimental and operative interferences 
are not always uniform. The duration of the observations must also be 
considered. 
If this chronic retention has gradually distended the pelvis, and thus 
diminished the amount of kidney tissue which is functioning, a condition 
arises somewhat analogous to the experimental renal atrophy, studied 
by many workers (29). As a rule polyuria was found, but we can only note 
the fact, the reasons for polyuria of whatever type, are completely 
unknown. The supposition of Schlayer from findings in his animal experi- 
ments, that it is due to a hyperirritability of the vessels, can not, according 
to Volhard, be accepted as a generalization. 
Furthermore, in chronic retention, the concentrating ability of the 
kidneys is much disturbed (30); considerable storage of residual nitrogen is 
avoided by the abundant flow, but mineral constituents accumulate in the 
blood and lead to a lowering of the freezing point. Veil has shown that 
even in normal individuals the molecular concentration of the blood is 
increased after copious drinking, perhaps because the tissues are rinsed out 
more thoroughly. The blood concentration must increase all the more if 
the kidneys on account of chronic retention have lost the power to excrete 
concentrated urine. The net result of such a washing out is that 
the patients feel more thirsty and drink still more, thus forming a vicious 
circle, which finally leads to a marked desiccation quite characteristic of 
patients with hypertrophy of the prostate, or chronic retention from any 
other cause. 
The question now arises, how is this disease complex related to uremia? 
Uremia means an accumulation of substances in the blood, which are nor- 
mally excreted in the urine. The purest form should then be caused either 
by extirpation of both kidneys, or by mechanical prevention of the outflow 
of urine. The clinical picture is usually described as though it were a 
suddenly appearing condition of coma and epileptiform convulsions. But 
if we observe a patient with functional insufficiency, or one in whom 
nephrectomy has been done when the other kidney was absent, we see 
quite a different picture. It corresponds perfectly to what was formerly 
called “chronic uremia:” “The patients complain of dull headache, or 
a confused feeling in the head, the eyes become dim and expressionless, 
the lines of $he face sag; they are indifferent, forgetful and fatigued. 
Then deep lethargy follows, and finally a few terminal convulsions ”(31). 
The epileptiform or eclamptic convulsions generally considered as charac- 
teristic of uremia are usually absent. Is this merely due to degrees or 
time differences in the course of the disease? Most decidedly not; because 
it cannot be conceived how a more complete and quicker accumulation of 
urinous substances can take place in the blood than in bilateral neph- KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
287 
rectomy. It follows, as was first pointed out by Ascoli (32), that every 
acute disease accompanied by epileptiform convulsions cannot be a result 
of the accumulation of urinous substances in the blood, but that these 
convulsions are due to some other toxins. Ascoli, who thinks of decom- 
position products derived from the diseased kidney itself (nephrolysins), 
calls this symptom complex “kidney wasting.” We shall presently return 
to these questions. 
At any rate, we must distinguish in these pathological conditions, 
those which are actually due to accumulation of urinous substances in 
the blood (“urinary toxemia” according to Ascoli), and those described 
above in the words of Frerich. Most surgical kidney cases die of the former 
of these disease complexes, i.e., hydronephroses, pyonephroses, cystic 
kidneys, nephrectomies, etc. Although very many investigations and 
experiments have been conducted by numerous authors, no definite one 
of the urinous substances can be said to cause the symptom complex (33). 
Of practical importance is the fact that there is an increase of residual 
nitrogen in the blood in all these forms of true uremia, i.e., to repeat it 
again, a uremia due to poisoning by urinous substances. It is not certain 
that this residual nitrogen contains the “toxic” substance, but it is not 
improbable; and this leaves the question open, of whether it is the urea or 
some other organic body which produces the toxic action. From the 
surgical viewpoint (34) it has been stated on the basis of suitable experi- 
ments, that there is a certain similarity between uremia and the toxemias 
produced by introducing burned tissue subcutaneously into animals. 
But at present, it is entirely unknown how the toxemia resulting from such 
protein decomposition products has anything in common with uremia, 
directly or indirectly. 
It has also been thought that uremia could be produced indirectly 
only through the liver (35). 
Whether there are still other factors, alone, or in combination, is en- 
tirely Unknown at present, although Sauerbruch and Heyde (36) conclude 
from their para-biosis research, that retention of urinous substances alone 
cannot be responsible for the death of the animals, for they found that the 
removal of both kidneys of one animal, linked para-bioticaly to the 
other, caused the death of both. Consequently the animal with kidneys 
did not excrete sufficient toxins. 
Jehn, Birkenbach, and Morpurgo (37) arrived at identical results with 
similar methods. But for the present, too far reaching deductions should 
not be made from these experiments, since we do not know from residual 
nitrogen determinations, how much of these urinous substances was 
carried through to the unoperated animal. 
Opposed to this chemical conception of the toxic action of urinous sub- 288 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
stances is the physical theory of Koranyi and Lindemann (38), according 
to which the increased osmotic pressure of the blood serum is responsible 
for the clinical disturbances described. 
The symptoms thought by Ascoli to be the result of “kidney wasting,” 
must be sharply differentiated from this true uremia. The term is not a 
happy selection. It is intended to describe conditions, which, asVolhard 
expresses it, may occur withou t renal insufficiency, and which are, therefore, 
not directly dependent on an accumulation of urinous substances in the 
blood. The uremia of acute nephritis is of this type. Without doubt, 
the retention of urinous substances is a factor in this disease, but the 
characteristic attack with coma and convulsions, vomiting and headache, 
is not a result, since it does not occur with nephrectomy or ureteral liga- 
tion. Volhard (33) in particular points out that this triad, headache, 
vomiting, and slowing of the pulse, to which may be added convulsions, 
reminds us more of a space reducing process within the skull, and the 
high pressure found at lumbar puncture bears out this idea. Traube 
(39)> years ago, thought of edema of the brain as a cause of uremic seizure, 
and if this belief was ignored for decades, it was only because no difference 
was recognized at that time between the different symptom complexes of 
“uremia.” Traube for this reason considered all forms of uremia includ- 
ing that following kidney extirpation, due to edema of the brain, which was 
incorrect. But that it is actually present in the uremia accompanied by 
convulsions is shown by the pictures of Volhard. Zangemeister, by 
trephining (33), has actually been able to show the edema of the brain 
in vivo in a case of eclampsia. The same condition has been demonstrated 
repeatedly at operation during the convulsive attacks of epilepsy which 
show similarity to those of uremia. 
It is naturally very difficult to say which is cause and which is effect. 
Volhard believes the edema of the brain in uremia is from congestion, 
assuming an ischaemic contraction of the cerebral arteries, with wide open 
veins. He supports this idea by the eye-ground findings in acute nephritis, 
in which there are tightly contracted arteries with dilated veins. The 
permeability of the vessels is also supposedly abnormal. 
These vascular changes, especially the increased vasomotor irritability, 
always play a considerable role in the symptom complex (see “Hyper- 
tension Theory in Eclampsia”-—Osthoff, 1886), and explain the enormous 
increase in blood pressure and hypertrophy of the heart found in such 
patients. The theory of Cohnheim-Traube that the blood pressure 
increase is a result of increased resistance in the kidney, has been generally 
abandoned. But it must again be emphasized that these vasomotor 
disturbances are not usually encountered in surgical uremia (nephrectomy, 
ureteral ligation, etc.), although it is possible that the picture may be KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
289 
complicated; especially in chronic cases (hypertrophy of the prostate) and 
naturally also in the presence of arteriosclerosis. 
No positive explanation of the etiology of this “tendency to edema” 
and the vasomotor disturbances is, as yet, possible. Since the clinical 
picture gives the impression of an acute poisoning, it is natural to look 
for some toxic substance, and in drawing analogies, the acute uremic attack 
resembles most markedly the picture of anaphylaxis. For this reason 
the idea of a protein toxemia was frequently expressed, but the theories 
concerning the mechanism are most varied (40). Brown-Sequard and 
his pupils thought of the disappearance of an internal secretion of the 
kidneys. H. Pfeiffer draws analogies between uremia and anaphylactic 
shock, and believes he demonstrated an anaphvlatoxin in the urine (33). 
Other writers, such as Biedl, content themselves with proving that renal 
extracts, especially from those organs showing nephritic changes, possess 
peculiar properties, i.e., marked lymphagogue action, and the ability to 
increase the permeability of the vessels, phenomena which are also ob- 
served in uremia. When theories are carried too far, they are only 
misleading. It is indeed conceivable in uremic attacks, that certain 
decomposition products of renal origin enter the circulation and incite the 
attack, but this has not been proved. In fact, the process may be quite 
different, and far more complex than is imagined. It seems necessary 
to make extensive investigations of the blood of patients during uremic 
attacks, because it is in this fluid that we must search for the toxins. 
Schlayer (41) and Straub (41) did determine the acidity of uremic blood 
and believe it is increased, a statement disputed by some, and confirmed 
by others (41). 
[In regard to the term “anaphylaxis,” it should be remembered that 
many conditions are grouped under this heading in the literature and that 
great confusion has resulted. Wells (Physiol. Reviews, 1, p. 44, 1921) has 
clearly given the criteria in which the term should be used and suggested 
that “anaphylactoid” should be the name for conditions simulating true 
anaphylaxis. The criteria are: 
1. The toxicity must depend on sensitization, i.e., must not produce 
similar symptoms in non-sensitized animals. 
2. They must be characteristic of anaphylaxis. 
3. Passive sensitization with the serum of a sensitized animal must be 
demonstrable. 
4. The bronchial spasm in guinea pigs must be relieved or prevented 
by atropin or adrenalin. 
5. Capillary thrombosis or embolism must be excluded. 
6. After recovery from anaphylactic shock, desensitization should be 
exhibited. 290 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
The acid-base equilibrium, according to present ideas, may be summed 
up as follows: the reaction of the blood and of the tissues as a whole remains 
remarkably constant. The factors determining it are, of course, the rela- 
tive amounts of acids and bases present. Since direct measurements 
determine the hydrogen ion, i.e., the acid radicle, the results of determina- 
tions are expressed in terms of the concentration of these ions, and in order 
to simplify the expression, the symbol Ph,or Ch, with a minus logarithm 
as exponent is used. 
The “total” acid may be said to be composed of two varieties, the 
volatile, namely carbon dioxide, excreted by the lungs; and the fixed, 
such as are bound with phosphates, chlorides, proteins, etc., excreted 
mostly by the kidneys. During life there is constant production of acid, 
and a constant oscillation between acid and alkali, but so delicately 
balanced that the “total” amount of acid, i.e., the H ion concentration, is 
kept within very narrow limits. For example, the fixed acids may be 
increased because of either overproduction as in diabetes, or failure of 
excretion as in nephritis. To keep the “total” amount of acid constant, 
it is necessary that the carbon dioxide be reduced in amount per cubic 
centimeter of blood. An estimation of its quantity will therefore discover 
a smaller amount. This has been termed “compensated acidosis.” 
“Uncompensated acidosis” results when the increase of fixed acids is so 
great that the carbon dioxide cannot be sufficiently reduced per cubic 
centimeter of blood to maintain life. In other words, the “total” H ions 
are increased. In either of the two cases, since each unit of blood carries 
less carbon dioxide, it follows that to rid the body of this substance, if its 
production is not diminished, the individual must breathe more rapidly, or 
the circulation rate must be increased, or both. Hence, we have dyspnea 
without cyanosis. 
But if by overventilation, an excessive amount of carbon dioxide is 
breathed off, it leaves the blood more alkaline, and it is thought that 
alkali is transferred from the blood to the cells and that other shifts in 
acid and basic salts take place. At any rate, it is clear that there are 
nine possibilities, the carbon dioxide of the blood may be high, low or 
normal, and the H ion concentration may be high, low or normal. The 
only condition which is normal, is where both carbon dioxide, and H ion 
concentration are within normal limits (see Van Slyke, D. D., /. Biol. 
Chem. 48, 153, 1921). It follows that accurate information of the condi- 
tion of a patient at any given time must involve the determination of both 
the carbon dioxide and the H ion concentration of the blood. 
But it must be emphasized that “acidosis,” a name used very loosely, 
is but a symptom of an underlying cause which can oftimes be recognized. 
If it is desired to treat an uncompensated acidosis, -per se, the use of an KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
291 
alkali is indicated, but an overdose is to be avoided. Alkalosis has not 
received as careful study as the opposite condition, but there are indica- 
tions that it is also harmful. The proper dose of sodium bicarbonate may 
be calculated to within sufficiently narrow limits by the use of the formula 
devised by Palmer and Van Slyke. Assuming that sodium bicarbonate is 
absorbed from the gastro-intestinal tract and is distributed equally 
throughout the body fluids, the amount of carbon dioxide yielded from one 
gram of sodium bicarbonate, namely, 267 c.c., will be distributed among 
the fluids of the body (about 700 c.c. per kilogram of body weight) in 
volumes per cent., according to the formula where W = the 
weight in kilograms. If g grams of the alkali are given the rise in volumes 
38 g 
per cent. = Whence g, or the amount necessary to raise the carbon 
CW 
dioxide by C volumes per cent. = G = (see also J. Biol. Chem., 
46, p. 493> 1921). 
Finally, it might be remarked that this acid-base equilibrium is so 
intimately dependent on other factors that L. J. Henderson has been 
enabled to construct a diagram on which he plots the values of the free 
and combined oxygen, the free and combined carbon dioxide, or carbonic 
acid, the serum chlorides and the hydrogen ions of the blood. If the 
value of any two are properly determined in a given sample of blood, the 
values of the others can be unequivocably placed, a fact from which the 
conclusion that all these six variables are involved in a single physiochemical 
equilibrium, can be deduced. In other words, the manner in which acids 
and bases are shifted, oxygen is combined or dissociated, carbon dioxide is 
combined or dissociated, chlorides are distributed between cells and 
fluid, and oxygen influences hemoglobin to be either a weak acid or a 
weak base, all depend one upon the other (see Henderson, L. J., Blood 
as a physicochemical system: J. Biol. Chem., 46, p. 411, 1921). 
The work, especially of L. J. Henderson, Van Slyke, and Y. Henderson 
can be consulted for details (42).] 
Now decapsulation of the kidney has been suggested as a surgical treat- 
ment for uremia and it would perhaps be interesting to discuss the effects 
of this procedure (43). In that form of uremia which represents the final 
stage of renal insufficiency, i.e., hydronephrosis, cystic kidney, etc., it is 
self evident that no result can be expected from this operation. Unger 
(44) implanted the kidney of a monkey in a case of this kind, but could not 
prevent death. According to the reports of some writers, renal decapsula- 
tion seems to have yielded good results in a few cases of anuria (45). On 
the other hand it is not astonishing that many operators report bad results. 
Naturally an old contracted kidney cannot be saved by decapsulation and 292 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
from all that has been written, success seems to depend on the type of 
anuria for which the decapsulation is done. 
In attempting to discover how improvement can occur, investigators 
found there was a difference in the amount of urine excreted if the decapsu- 
lated kidney was made diuretic by saline infusions, etc. Some secreted 
more during diuresis, i.e., as a response to increased demand, others less 
(46). The blood flow, even after corrosive sublimate poisoning, was 
always better (47). Ferrarin (48) could obtain no success from this opera- 
tion in experimental uranium poisoning. But very few deductions for 
decapsulation may be drawn from these experiments, because we do not 
yet know with certainty what produces the anuria in acute nephritis. 
If there is actually vascular spasm, it is necessary to assume with Volhard 
(33), that decapsulation forced this spasm to relax, through injury of the 
ganglion cells of the hilus. 
But we also know of good results from nephrotomy in anuric conditions 
(49). Conversely, it has been assumed, furthermore, that the kidney of 
acute nephritis required expansion on account of vascular congestion 
and edema, but was prevented by the unyielding capsule. This would 
lead to compression of the capillaries—“ glaucoma” of the kidney—and the 
often described “bulging,” which is observed during decapsulation, seems 
to support this view. 
These conditions are by no means clear. The most necessary data, 
are accurate observations on patients. Only really pronounced cases will 
prove anything, because experience shows that such anurias often 
disappear spontaneously. 
Decapsulation was advised not only for acute anuria, but also for 
chronic nephritis (Edebohl (50)). The conception on which he built his 
theory was that after decapsulation, not only would collateral circulation 
develop, sufficient to remove toxins and other substances noxious to the 
kidneys, but this improved vascularization would help in the healing of the 
inflammation. A disproportionately large number of investigators has 
attempted to demonstrate whether this collateral circulation is actually 
evolved from the renal cortex (51). Its extent was observed either in injec- 
tion preparations (partly by x-ray pictures), or by observing if decapsulation 
is completely or partially capable of preventing the circulatory disturbances 
which follow ligation of either the renal artery or the renal vein. In a 
number of cases, the kidney was imbedded in omentum to assist in the 
formation of this circulation (Bakes). A new capsule formed very quickly, 
probably starting from the torn vessels. A certain, although superficial 
collateral circulation seemed to form when the kidney was enveloped in 
omentum, but that this became abundant enough to permit the ligation 
of the renal artery without producing the usual total necrosis, as has been KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
293 
reported by some writers (Parlavecchio, Lobe, Katzenstein), is only an 
experimental error. In the dog, as Liek has shown, there are, normally, so 
many collaterals and side-branches that the renal artery may be ligated 
without decapsulation. Thus the assumption that this procedure brings 
about circulatory improvement by collaterals is purely hypothetical, since 
what follows is merely a process of cicatrization on the renal surface. 
Furthermore, Bright’s disease is not always a process due to deficient 
blood supply, but may be primarily cell degeneration, with secondary vas- 
cular atrophy. Finally, the whole conception of the elimination of toxins is 
equally vague. Taken all in all, the attitude of aloofness of the majority 
of surgeons in relation to this operation is quite intelligible (52), (49) and 
the good results reported by Edebohl himself, have been destructively 
criticized by a number of authors (53). In many cases, Rovsing’s objection 
is justified; they were not cases of Bright’s disease at all; in other cases, the 
reports were made after only a very short time had elapsed. How the 
good results in the remaining cases are to be explained, cannot be decided 
at present. According to Zondek (54), the capsular vessels have valves to 
take care of the great physiological blood pressure fluctuations in the 
kidney, thus decapsulation robs the kidney of a very essential protective 
apparatus. 
But the decapsulation experiments have unearthed an important fact, 
viz., that the renal artery itself is not an end artery but that anastomoses 
and collaterals are especially well developed in some species of animals. 
That, in the dog, for instance, is so complete, that even bilateral ligation 
of the renal arteries does not cause death. The artery divides at its 
entrance to the kidney into an anterior and a posterior branch, and as 
Zondek’s (55) investigations have shown, the level at which these two 
vessels divide does not lie in the same plane of section, but 0.5 cm. behind. 
For other details concerning the renal vascularization, Albarann (56) may 
be consulted; moreover, the transplantation experiments show that the 
kidney can support interruption of its circulation for some time (57), (10). 
Compression can be withstood, without causing clinical symptoms, for 10 
or 20 minutes (58). But that compression of the renal vessels for but a 
short time may lead to albuminuria, is shown by the appearance of this 
substance in the urine after palpation (Schreiber), a fact of diagnostic 
importance, if the origin of a tumor in this region is not clear from palpa- 
tion (59). Cohn (60) studied this matter experimentally. 
Ritter (61) recently advised ligation of the renal veins in the treatment 
of bilateral tuberculosis of the kidneys. Necrosis does not usually result, 
but there is always a tremendous lasting hyperemia. Buchwald and 
Litteu, Weissgerber and Peris (62) subjected this proposition to animal 
experimentation. Small hemorrhages appear in the renal parenchyma, 294 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
and gradually a contraction of the whole organ takes place with hyper- 
trophy of the other kidney; the renal function, however, remains perma- 
nently unimpaired in spite of the ligation. Consequently, there must be 
collaterals, although restricted in numbers. But whether ligation of the 
veins can exert, a curative influence on tuberculosis will be shown only by 
further experience, and comparisons of the favorable influence of atrophic 
processes in the lung in pulmonary tuberculosis are not possible without 
reservations. The experiments of Isobe show that ligation of renal veins 
is by no means a harmless procedure; for he lost all the animals in which 
he performed a unilateral nephrectomy and then tied off the vein of the 
other kidney (63). 
The effect of venesection in uremia is also difficult to explain. Once 
again, a true uremia must be differentiated from so-called pseudo-uremic 
symptoms. The experiments of Becker have shown that venesection 
does not constitute a detoxifying process; on the contrary, the amount of 
retained nitrogen in the blood as well as that in the tissues, increases. 
The statement that is frequently made, viz., that dilution of the toxins and 
washing out of the tissues take place, is, therefore, incorrect. In fact, 
venesection does not help in true chronic uremia, but its influence on the 
headaches, spasms and convulsions is often remarkable, that is, on those 
symptoms which are summed up as pseudo-uremic, as stated above. In 
this condition, the beneficial influence of venesection is expected primarily 
from its action on the circulation. In healthy individuals, the blood 
pressure remains practically normal after the removal of small or medium 
amounts of blood, because the vessels contract and a current is quickly 
established from the tissues into the blood; in arteriosclerotic and uremic 
patients, considerable lowering of blood pressure is observed, because the 
regulative contractibility of the smaller vessels is impaired (64). Whether 
this decreased blood pressure, and the lowering of venous tension, which 
is also demonstrable, have any influence on cerebral circulation or in any 
other way, is still in hypothetical regions. 
The question of whether disease or injury of one kidney is detrimental 
to the function of the other kidney, has often been raised, i.e., whether 
there are relations between the two kidneys, somewhat similar to those 
between the two eyes. 
Isobe (65) investigated this problem by ligating the vessels of one 
kidney, either the vein alone, or both artery and vein; and examining the 
other after some weeks had elapsed. He always found parenchymatous 
changes in one after severe injury to the other, and he correlates these 
changes with absorption of decomposition products formed by the injured 
kidney (nephrolysins (45)). KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
295 
Hyde (66), after displacing both kidneys of rabbits under the skin of the 
back, found no trouble in the remaining kidney after the removal of the 
other, but squeezing one produced oliguria and death. Fiori (67) reports 
experiments in which ligation of one ureter, was followed by lesions in the 
other kidney. Clinically, cases are known in unilateral renal tuberculosis, 
in which albuminuria from the sound kidney ceased as soon as the tubercu- 
lous kidney was removed (Kummell a. o.). Meaugedis (68) gives a similar 
report in unilateral renal calculus. 
But how much of a “specific” correlation there is between the kidneys 
in all these investigations and observations is not certain. As is well 
known, they respond with nephritic symptoms to all kinds of diseases and 
injuries to the rest of the body, and it is not surprising when one kidney 
is removed, or its function impaired, that the remaining one should be 
affected in a greater or less degree. An increased sensitivity of one kidney 
to injuries affecting the other, cannot be deduced from the findings in the 
experiments described, but the hint that in unilateral renal disease the 
other kidney is also in grave danger, is of great practical importance. 
Human kidneys occupy such exceptionally protected positions under 
normal conditions that an explanation of how blunt injury can reach them, 
causes some difficulties. As experiments of Maas (69) have shown, it is 
easy to grasp the kidney of a rabbit between the abdomen and the back 
and to crush it between the fingers. But in man such a mechanism can- 
not operate, because the force required would have to be so powerful, 
not only because of the distance between the abdominal wall and the back, 
but also because of the tension of the abdominal walls, and injury to the 
intestines could not be avoided. Furthermore, as Kuster (70) points out, 
renal tears running diagonally into the pelvis, as is usually the case, can- 
not be due to direct crushing. They can only result from hydraulic 
pressure, and in suitable experiments, Kuster could show that kidney tears 
similar to those observed clinically, can be obtained if the renal veins 
in a cadaver are ligated, the kidney filled with wrater through the artery, 
and a blow struck against it. This is especially effective by reason of the 
movable lowest ribs. The direct consequence in patients is first, hemor- 
rhage, and then cessation of renal activity—anuria. In the traumatized 
kidney, it is probably the injury to the vessels which causes anuria; but 
the other intact kidney also fails at times. This is spoken of as “reflex 
anuria,” which will be discussed later. 
The healing oj renal wounds of all types has been studied many times 
both experimentally, and in man (71), (69). It was necessary to show 
first, how wounds of the kidney heal, and what histological processes may 
be observed, and secondly, whether a true regeneration of the glandular 296 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
elements takes place. At the same time data accumulated, which showed 
how much kidney tissue could be removed without endangering the life 
of the animal. 
The kidney heals readily. As in every wound, at first we find necrosis 
of the tissue adjacent to the surface of the cut; the convoluted tubules 
disintegrate in a remarkably short time, but the glomeruli are more 
resistant. The lesion fills with serum and fibrin (72) and after even a 
few days, the tear is filled with a delicate, highly cellular connective tissue. 
There is growth of the epithelium, but functioning gland tubules are not 
found; the growth is somewhat irregular and the tubules are merely solid 
buds of epithelial cells. 
The connective tissue soon contracts, so that according to Windboltz 
(73) only a small scar remains after nephrotomy. But Langemak and 
Hermann (74) obtained larger lesions after longitudinal section of the 
kidney, and they advise the less injurious transverse section. This 
difference in results depends on the vascular architecture, so that Sim- 
monds found a scar only of the thickness of the back of a knife two years 
after nephrotomy (75). The remaining part of the kidney enlarges, 
similarly to the hypertrophy of the other kidney after unilateral 
nephrectomy. 
Enderlen (76) has studied the histological changes in the remaining 
kidney after the latter operation. It is now practically proven by the 
experiments of Barth and Wolf, that enlargement is due only to hyper- 
trophy, and not to the formation of new renal substance. New growth of 
functioning kidney tissue does not take place, especially is there no new 
formation of glomeruli, as was formerly asserted. 
The ability oj the remaining kidney tissue to junction after experimental 
operative interference does not, generally speaking, depend on the amount 
of tissue removed, for after the removal of one kidney, portions of the other 
amounting to one-third to one-half of its original weight may be sufficient 
to prevent any impairment of function as shown by the ordinary tests. 
On the other hand, animals have died of uremia, when much less kidney 
substance was removed, but at short intervals. Therefore, kidney func- 
tion does not depend merely on the anatomical lesion. But in spite of 
this, it must be concluded from the polyuria in cases of kidney shrinking 
(see later), that operative reduction of kidney mass is followed by dimin- 
ished function, even though we may not be able to demonstrate it by the 
ordinary methods. The hypertrophied kidney after extirpation of one 
organ or after injury, is especially liable to functional changes in the 
beginning, as observed by Wossidlo (77). He showed that the epithelium 
is increasingly permeable after carmine ingestion, so that the filtering 
power of such a kidney might fail in a short time when extraordinary KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
297 
burdens are laid upon it. The normal permeability is reestablished only 
gradually. 
Even though the proper functioning of the adrenals is essential and a 
regular undisturbed excretion of adrenalin is necessary for surgical suc- 
cesses, nevertheless, they are seldom interfered with operatively. The 
few experiments which have been done from the surgical point of view, 
have been confined to the possibility of transplantation or to the demon- 
stration of the changes the glands undergo after operations in their vicinity, 
especially after kidney operation. 
Suprarenal glands were either transplanted at a distance from their 
original site, or imbedded in the kidney substance with or without pedi- 
cles (78). It was hoped that hypernephromata would arise from these 
transplants, but all the experiments failed. Indeed it is very question- 
able whether the so-called Grawitz hypernephroma has anything in 
common with misplaced adrenal rests; possibly it is a tumor, originating 
from the renal tubules themselves (79). 
Nakahara (80) found changes in the chromaffin cells of the adrenal 
medulla after operations on the kidney, but they were so variable that 
they can be considered purely a result of contusion, and quite unrelated to 
influences from the kidney. Since one of the adrenals can be removed 
without endangering the organism, no special precautions are required in 
kidney operations. 
Of much greater pathological physiological interest than severe trau- 
mata, are the disturbances frequently considered the result of very slight 
“trauma” and grouped under the name of 11 orthostatic albuminuria” (81). 
By this is understood, a disease picture, in which periodically, with no 
subjective knowledge on the part of the patient, a considerable amount of 
albumen is excreted. Usually it is preceded by unusual physical exertion; 
but it is often found after merely arising from bed and it quickly disappears 
if the patient is kept in a prone position. But Posner, Senator (82) 
a.o., have shown by their investigations, first, that the urine of every 
normal individual shows faint traces of albumen with especially sensitive 
reagents, and secondly, if a normal individual engages in exceptional 
physical labor, this output of albumen is increased to such an extent that 
it can be demonstrated by the boiling method. Such studies have been 
made after all sorts of athletic contests. But the albumen excreted never 
approaches the quantity found in this so-called orthostatic albuminuria, 
in which it appears after “physical exertion,” which like merely arising 
from bed, does not deserve this name. Therefore, we must assume that 
there is a special inferiority of the kidneys, and an exceptionally marked 
permeability to albumen in such individuals. The cause for the albumi- 
nuria must reside in the patient himself, while the different external causes 298 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
(“trauma”) must be regarded merely as accessory factors. This renal 
inferiority may be a temporary condition, only present in adolescence and 
disappearing later. 
From many studies of the external causes, a large amount of interesting 
data is available which cannot be correlated; for example, there were 
patients who showed no albumen or only a slight trace after the fatigue 
incurred by a mountain trip, but it reappeared after much less trying 
exertions. In these cases it cannot be the degree, but the type of physi- 
cal activity which is responsible. According to Jehle, it is the exercise in 
which patients bend their lumbar spinal column sharply to the lordosis 
position (83). Such patients usually have a natural tendency toward 
lordosis and Jehle speaks of a “lordotic albuminuria.” But this can only 
be considered, after the previous statements, an external cause in a 
predisposed individual. There are youthful patients with quite marked 
lordosis, e.g., in juvenile muscular atrophy, who show no pathological 
elimination of albumen (84). Therefore, lordosis with orthostatic albu- 
minuria is probably to be considered a sign of tissue weakness. Jehle 
points out that to assume the upright position from the ordinary quad- 
ruped position must at first have necessitated a lordosis, as is seen now in 
anthropoid apes. But in man, with a muscular development suitable to the 
upright position, lordosis of the lumbar spine has been diminished. In 
addition to albuminuria, such patients show a cylindruria, and a dimin- 
ished secretion when albumen appears. To this are added certain dis- 
turbances in the chemical composition. 
At present, it is thought that lordosis produces an effect on the kidney 
through circulatory disturbances. It is not clear whether other factors 
also play a role—the innervation for instance. At any rate, albuminuria 
ceases, even in an upright position, if a corset corrects the lordosis. Bunge 
(85) has recently shown that mechanical pressure on the normal kidney will 
cause albuminuria and he has suggested a special position for renal 
operations. 
Massive hemorrhage into the bed of the kidney must also be considered 
one of the lesser traumatic injuries (86). It must not be confused with 
injury caused by a blow, and while Ricker (87) obtained hemorrhage in 
the capsular region after ligation of the renal veins of animals, such hemor- 
rhages were only occasionally observed in the kidney itself. Therefore, 
congestion must be a necessary factor in producing this peculiar symptom. 
With Ricker we can easily imagine, that the sudden filling of a hydro- 
nephrotic sac, or change of position, as may occur in a floating kidney, may 
lead to stasis in the renal vein. But stasis alone does not explain this 
disease complex; even experimental hemorrhage from ligation of the 
renal vein is insufficient. Something else must be added to account for KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
299 
the premeability or increased hemorrhagic tendency of the vessels, and 
present data seems to indicate that these massive hemorrhages into the 
renal bed have developed mostly in those kidneys altered by chronic 
inflammatory changes. Possibly they are the cause of the tendency, but 
in seeking its source, we encounter the difficulty of determining whether 
it comes from the kidney itself, or from a vessel outside the kidney. To 
assume a capillary bleeding is somewhat unsatisfactory, considering its 
amount and its sudden onset. 
Normally the fixation of the kidney is not rigid but only relatively so. 
Although, according to anatomists, a connective tissue thickening desig- 
nated as renal fascia gives support to the kidneys, it is not these bands, 
but the support supplied by the mutual interaction of the different tissues 
of the body, which is the deciding factor in renal fixation. Tissue tonus 
and its changes are responsible for the positions assumed by the abdominal 
organs. No one has a better opportunity of observing the importance of 
this tissue tension and tissue firmness than the surgeon, who must daily 
take it into account in his operations. Even the beginner knows the 
“poor” fascia in hernia for which no explanation can be found as a local 
condition, and which can be correlated only by the conception, at present 
very hazy, of some general physical condition. ' 
We have touched upon all these things in discussing enteroptosis 
including its relation to the physical type (habitus asthenicus, Stiller). 
It must be remembered that ptosis of the kidney almost never occurs alone, 
but that it is only one of the symptoms of general enteroptosis. Of 
course, the disturbances caused by such a kidney may predominate to 
such a degree that the ptosis of other viscera is entirely overlooked. For 
this reason, it is often forgotten in the chapter on floating kidney that 
it is only one symptom of a general body condition which is not necessarily 
congenital. Sudden loss of weight (88), pregnancy, etc., may lead to 
ptosis, just as “disposition,” as was mentioned above in discussing 
maternal enteroptosis. 
Nevertheless, mechanical factors force themselves on our attention, 
because, as Kuster points out, floating kidney occurs mostly in women and 
then chiefly on the right side (89). Direct injuries of the kidney region 
must be named first among “mechanical influences,” but in addition, the 
more chronic injuries may also be considered, e.g., riding in a side saddle. 
According to investigations of v. Fisher Benzon (90), (Heller), tight lacing 
causes lateral displacement of the right kidney from pressure transmitted 
by the liver. The much quoted anatomical investigations of Wolkoff 
and Delitzin (91) offer certain supporting points in explanation of the 
facts that the right kidney is more often floating than the left; and that it is 
more common in women. These investigators showed with plaster casts 300 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
that the kidney beds resemble niches, and that these niches are deep and 
funnel shaped in man, while in woman they are flatter and cylindrical, 
and in floating kidney this flattening increases. Furthermore, they found 
the right niche more shallow than the left. At present, the indication for 
operative fixation in renal ptosis, depends chiefly on the temperament of 
the surgeon in question. This is shown by the fact that some busy sur- 
geons do not operate for floating kidney for years, while others in the same 
length of time see fit to operate hundreds of cases. This statement also 
shows how little is known of the whole question. The fact remains that 
few operations are performed at present, which means that the results 
are not very brilliant. In other words, it has been recognized that a 
large part of the disturbance blamed on the floating kidney (as backache, 
etc.) is not due to this condition, but is a sign of the peculiar general 
nervous constitution of such individuals. But sudden and very severe 
attacks of pain combined with collapse, meteorism, rigidity of the ab- 
dominal walls, in fact all the symptoms suggestive of renal colic, are 
sometimes encountered. Since Dietl’s (92) time, this is spoken of as 
renal incarceration, and although it is very questionable whether the cases 
seen by Dietl were not acute cholecystitis, there is no doubt that such 
attacks of pain occur from kidney conditions. For the present, it is not 
certain how they are to be explained, and possibly several factors con- 
tribute. Thus far there is hardly any operative experience recorded 
during the acute attacks, but Borzeky (93) reports a case of torsion of the 
kidney pedicle. The attack of pain in this case was produced by the 
circulatory disturbance and this is a hypothesis which plays a great role in 
the explanation of “renal incarceration” since Landau (88) emphasized it. 
A sudden kinking of the renal pedicle is supposed to take place and the 
venous outflow is obstructed and the result is a swelling of the kidney 
which can be palpated during the attack. Atrophy and contraction have 
also been accepted as the late results of such circulatory disturbances, and 
these have occasionally been found at autopsies of patients with old 
floating kidney. Other writers (94) believe that the pains must be inter- 
preted as hydronephrotic, since it is well known that hydronephroses can 
occasion such pain. We will speak later of the conditions resulting from 
floating kidney. 
The tissue surrounding the kidney has abundant nerves originating 
from the lumbar spinal cord,, and thus every pull and position change, or 
stretching of the pelvis, must be painful (15). But it has not been 
decided whether the pelvis has its own sensory sympathetic fibres (see 
above). In many abdominal affections we often find an incongruity 
between the subjective pains and the actual findings, and it is, therefore, 
not justifiable to expect a pronounced anatomical condition in so-called KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
301 
“renal incarceration.” Israel considers a pull on the renal attachment 
and on the perirenal nerves quite sufficient to explain the pain. Con- 
versely, Riedel in his explanation of all the disturbances in floating 
kidney, saw extensive adhesions, but only during laparotomy. We must 
admit that it is impossible to judge at present how the pain is produced. 
It may be in the kidney itself, for such attacks have been known to occur 
in nephritis, and floating kidneys showing nephritic changes have often 
been found, but the details are unknown. Since slight trauma (palpation) 
affects the kidney, producing albumen excretion (see above); and since 
this trauma is in a sense repeated innumerable times in floating kidney, 
this may be supposed to lead finally to nephritis. But then we should only 
obtain a unilateral chronic parenchymatous nephritis, and the question of 
whether it actually is unilateral in such cases, is still very problematical 
(45)- 
As stated, a number of writers believe that the acute painful attacks 
are related to stasis of urine in the pelvis, from kinks of the ureter where 
it emerges from the pelvis. Then in the course of the disease, or after 
repetition of this sudden kinking, enlargement of the pelvis results; i.e., 
an hydronephrosis. In experiments made by Tuffier and Hildebrand and 
Haga (95), these changes have been followed in animals by producing a 
hydronephrosis after the establishment of an artificial floating kidney 
and ureteral kinking. 
It is not difficult to understand that mechanical factors play such an 
important part in the development of hydronephrosis. Abnormal vas- 
cularization, renal incarceration, scar tissue within the ureters, are all 
known causes. A very extensive pertinent literature has been built up, 
and experimental studies dealing with the results of ureteral ligation are 
also available in large numbers (96). All the mechanical obstructions 
affect the ureter itself, from its point of emergence from the pelvis.' 
But hydronephrosis also occurs in hypertrophy of the prostate, phimosis, 
hypospadius, etc.; i.e., in cases in which the obstruction makes it difficult 
to empty the bladder, and in which a backflow of urine through the ureters 
into the pelvis might take place. Numerous investigations and observa- 
tions have shown that the oblique entrance of the ureter into the bladder 
is no absolute protection against backflow (97). Normally, the ureteral 
orifice opens periodically, probably under the influence of ganglion cells 
situated within its walls. But if, for instance, the filled bladder contracts 
at the moment when the ureter opens, urine may flow backward and reach 
the pelvis, as Levin and Goldschmidt showed by manual pressure on the 
bladder. It is obvious that this organ contracts more often, and more 
suddenly in inflammations and thus more frequent opportunity is given 
for this backflow. If the normal ureteral openings are no absolute pro- 302 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
tection against backflow, it follows that the pathological orifices are still 
less so, and by cystoscopic examinations, they are found wide open after 
the passage of calculi, in tuberculosis, etc., but even if the obstruction is 
more peripheral, e.g., in hypertrophy of the prostate, they are also found 
gaping. In such cases it must be assumed that the ganglion cells have 
finally failed. If the ureteral orifice is open, the backflow of urine is 
unimpeded, and hydronephrosis is the inevitable result. After the injec- 
tion of collargol into the bladder, x-ray examinations show both ureters 
and renal pelvis filled with the substance (Rost (97)). 
Still other factors favoring the development of hydronephrosis are 
disturbances in the activity of the ureter itself, exclusive of its orifice. 
Peristaltic waves normally travel at irregular intervals from the pelvis to 
the bladder, and are controlled by numerous ganglion cells in the walls 
of the ureters (98). If the ureter is cut through transversely, the peristal- 
tic waves go only as far as the incision (99) and for this reason the removal 
and replacement of a section of the ureter is unsuccessful. Hydro- 
nephrosis develops in all such animals (100). Similarly it is very rare for 
a peristaltic wave to pass over a constriction. Furthermore, such dis- 
turbances in the ureteral motility can be produced by loosening it over 
extensive areas (101), for when its vessels and nerves are stripped, the 
ureter ceases to move. The result is hydronephrosis, and if bacteria 
enter the bladder, pyonephrosis. Such extensive loosening is done if the 
ureters are conducted through the skin of the loin after total extirpation 
of the bladder, when infection of the pelvis always follows, but in man it 
develops after a longer interval than in animals (102). On the other hand, 
the investigations of Lorin (103) have shown that the ureter which has been 
cut through, without having been loosened, as in nephrectomy, retains its 
motility for two to three years after which it becomes obliterated. In the 
experiments of Aksne the stump of the ureter showed antiperistaltic 
waves. As can be seen in the cystoscopic field, the orifice also moves for a 
long time after cutting through the ureter above. 
Ureteral function can also be disturbed as a result of inflammation 
alone. Thus Primbo (104) obtained inhibition of motility in the ureter 
of guinea pigs by applying bacillus coli toxin to it. 
The consequence of such urinary retention in all such cases is dilatation 
of the pelvis. 
Polyuria caused by urinary retention, has been discussed. If the 
ureter is ligated, as may happen in gynecological operations, disten- 
tion of the renal pelvis ensues with a gradually increasing pressure atrophy 
of the renal parenchyma. The glomeruli are preserved longest (105). 
But ureteral ligation for a short time is more interesting to the surgeon. 
The investigations of Rautenberg (96) show that injuries caused in this KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
303 
way are quite lasting, for progressive parenchymatous atrophy developed 
after occlusion of the ureter for 14 days and more. If the obstruction 
was removed the parenchyma recovered slowly, and extensive regenerative 
changes appeared, leading to the formation of apparently perfectly normal 
urinary tubules. Scott (106) confirmed this result. But such regenerated 
tissue is not viable, it slowly breaks down, and the atrophy continuing in 
spite of the regenerative interruption, leads gradually to death. It is 
shown clinically by permanent albuminuria. The experiments of Boetzel 
(107), in which he stained rabbits intravitally after ureteral ligation, and 
later observed the distribution of the granules, give an idea of the changes 
in the cells. 
In incomplete obstruction, the dilatation of the pelvis is less marked, 
and its variability has been recognized only since the application of col- 
largol injections, with subsequent x-ray observation (108). 
In the past, the interest of investigators was attracted to the result of 
injection of fluid into the pelvis by the subsequent finding of air embolism; 
although Marcus (109) afterwards showed in reinvestigations, that it 
occurred only if small tears were made in the mucosa. Recently, all 
kinds of accidents have happened during the injection of collargol (no) 
and the question of whether it causes injuries, was again raised (Wossidlo 
(iii)). It was shown that under great pressure, collargol not only pene- 
trates into the lymph spaces and renal tubules, and thus injures the 
kidney, but may directly enter the circulation through injured vessels. 
Disturbances which must be explained similarly are occasionally seen in 
lithotrity, when fluid mixed with air is driven into the bladder from the 
aspirator under too great a pressure. 
The degree of hydronephrosis depends, of course, on the resistance 
offered to the outflow of urine. In minor obstruction, e.g., phimosis or 
hypospadias, decades may pass before renal insufficiency appears. In 
such cases the pelvis may be found but little distended, and renal insuffi- 
ciency is probably a result of the parenchymatous atrophy. 
To what degree injuries, especially progressive ones, are caused by 
milder forms of hydronephrosis is not easily determined, since the latter 
could be diagnosed with certainty only after the introduction of pyelog- 
raphy. At any rate, the relation of hydronephrosis to degenerative neph- 
ritic processes is most important, because the dangers of hydronephrosis, 
and the often accompanying pyelitis are frequently underestimated (112) 
and thus far, have received very little direct study. It is hardly justifiable 
to assume that dilatation of the pelvis in man is always accompanied by 
progressive renal degeneration, as it is in animals, because an enlarged 
renal pelvis is found in 30 per cent, of all pregnant women, according to 304 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
data from the autopsy records of Hirsch (113). Certainly not that 
number of women have progressive renal disease. 
Since stagnation of urine favors the development of bacteria, a hydro- 
nephrosis may readily become a pyonephrosis, and as we have just seen, 
stagnation of urine due to toxic paralysis of the ureters is always increased 
by inflammation. Thus another vicious circle may be established. 
There are three ways by which infectious organisms may reach the pelvis, 
and probably all are used; by way of the circulation, through the lymph 
channels, and from the bladder through the ureters (114). Ordinarily 
the route can be recognized only on the merits of the particular case. In 
advanced cases in which the whole kidney is destroyed, it is probably 
impossible to decide by what'route the infection entered. 
The type due to vascular infection shows the multiple abscesses of 
pyaemia, but when the disease is complicated by a toxic nephritis, only the 
presence of pyogenic organisms (usually cocci) will prove its existence 
(115) These multiple abscesses are very easily and consistently obtained 
after the injection of bacteria into the circulation and Brewer produced 
them unilaterally if he traumatized one kidney previous to the injection 
(116) In man, very large unilateral abscesses occur in greatly swollen 
kidneys where a preceding suppurative inflammation in some other situa- 
tion points to embolic infection. Why a multiple dissemination of small 
abscesses should occur in one case and a single large abscess in another, is 
not known. Since small abscesses appear oftener in severe septicemia and 
single abscesses occur more often in furunculosis, infected wounds, etc., the 
number of bacteria carried and their virulence must play a part. Koch 
(117) who took virulence into consideration, found chiefly medullary foci 
with almost intact cortex after injecting weakened cultures; after injecting 
virulent organisms, more of the cortical foci were seen. Hematogenous 
unilateral suppuration can also be obtained experimentally (118), (117). 
A very important surgical question in such suppurative nephritis is 
whether the pelvis is involved or not; a hematogenous abscess may dis- 
charge into the pelvis, and lead to pyelitis, but such infections are usually 
not severe (119). But the reverse may happen, i.e., the pelvis is first 
infected and by ascending, the process infects the kidney. Consequently, 
there may be a smooth transition from the mildest pyelitis to the most 
severe pyonephrosis. This latter condition is one of the commonest of 
surgical renal affections, and the organism is found to be bacillus coli in 
most of the cases. 
The route by which the infection reaches the pelvis has provided a 
field for speculation and experimentation. In cases in which severe cysti- 
tis is coexistent, as in the pyelitis of children (120), and in cases with diffi- 
cult urination, as in pregnancy or hypertrophy of the prostate, there is KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
305 
dilatation of the pelvis, open orifices of the ureters and backflow of urine, 
so that it is probably quite natural to think of an ascending infection. 
Even if we assume that the pelvis is secondarily involved from a cystitis, 
nothing can be said as yet in regard to the route by which ascending 
infection took place. It is not without reason that doubts have again and 
again been expressed as to the apparently logical assumption, viz.; that 
bacteria are carried through the ureters to the pelvis, infecting it thus. 
The question is not so much how bacteria may reach the pelvis by this 
route, but why the few organisms which happened to be suspended in the 
urine could give rise to inflammation of the mucosa of the pelvis, when, 
as stated above, a renal abscess, discharging myriads into the pelvis, 
affects it only slightly. But an infection may also be carried from the 
bladder to the pelvis by the lymph route. Sakata and Bauereisen (121) 
have described such lymph channels surrounding the ureter, and Sugemura 
(122) demonstrated that the lymph channels constantly showed inflamma- 
tory changes in cystitis. Lever Stewart (123) transplanted the ureters 
into the bowel and then found extensive infection of the blood and lymph 
vessels surrounding the ureters. 
Why is it that the colon bacillus is the usual infective agent in the 
urinary tracts, while other organisms are rarely found in this group of 
inflammations? It cannot be an infection entering from without; and 
unquestionably the most logical idea is that an individual infects his 
urinary tract with his own colon bacilli; and this is now the generally recog- 
nized view. 
These bacteria can reach the urethra from the anus, and then ascend 
to the bladder. This form is probably the principal one in female children, 
and as proof of the correctness of this supposition, nearly 90 per cent, of 
the children affected with pyelo-cystitis are girls (120). This form of 
infection is frequently assumed to occur even in adult female patients, 
but this seems somewhat forced. 
But bacteria confined to the intestinal tract can reach the urinary 
tract in other ways than through the urethra. First, it must be demon- 
strated that they are able to penetrate the bowel walls under normal 
conditions. This has been discussed on page 240. In the experiments 
quoted there, the essential point was to demonstrate whether bacteria 
could reach the peritoneum through the walls of the bowel; here the ques- 
tion is to discover if intestinal bacteria can enter the lymph channels of 
the intestines. The result of these different investigations and the present 
viewpoint are found in the works of Selter, Conradi, Rogoczinsky, 
Hornemann, Nocard, Posner and Cohn (124), a.o. 
Accordingly, it may be accepted that colon bacilli are almost always 
present in the mesenteric lymph nodes, and from these same investigations 306 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
it may be said that even in freshly butchered animals, bacteria are found 
in all the organs. This fact is of wide interest to the surgeon, because it 
is often necessary to face the question in the medico-legal side of accident 
cases, whether a given limb wras, or might have been infected through some 
injury. Often it is necessary to assume that bacteria circulate in the blood 
or remain in organs from which they may easily enter the circulation at 
any time. As has been stated, this assumption is supported by the experi- 
ments described. 
The anatomical investigations of Francke (114) give information 
concerning the route by which colon bacilli reach the lymph nodes from 
the colon, and from there to the kidney. He could show, by Gerota’s 
method, that lymph channels run from the caecum to the right kidney, 
and similar channels go from the descending colon and the sigmoid to the 
left kidney. Since the permeability of the bowel wall is increased con- 
siderably by even slight catarrh, such a process may be an occasional 
causative factor in producing an infection of the pelvis of the ureter. 
The reports of Wasserthal, Epstein, Roubitschek (125), a. o. show that 
the relation of intestinal diseases to renal diseases is often still more 
complex, as e.g., when albumen and cylindroids appear in the urine after 
the constipation produced by opium. Writers consider this due to reflex 
congestion in the renal region. It is not known whether bacteria appear 
in the urine in such albuminurias, but Brunn (126) demonstrated focal 
necrosis in the kidney in cases of ileus, and could also confirm this finding 
experimentally. Aseptic abdominal operations per se were followed by no 
such necroses, but in cases of peritonitis they could frequently be found. 
Colon bacilli can also enter the urinary tract from the rectum through 
the tissue situated between it and the bladder, but this form of infection is 
rare, at least a correlated cystitis is found but seldom even with perianal 
abscesses. Without doubt, such bacterial invasion is more frequent in 
animal experimentation, although under conditions rarely observed in 
man. Thus Wreden (127) obtained cystitis in the rabbit after injuring 
the upper rectum and Faltui (128) who repeated these experiments, 
obtained it only if he injured the bladder also. Here too belong the 
investigations of Posner and Lewin (129) who proceeded from another 
viewpoint, but ligated the anus in rabbits and then obtained cystitis 
and pyonephrosis. The animals succumbed quickly. Marcus (130) who 
imitated these experiments, thinks that in those of Posner, the escape of 
bacteria from the bowel was only possible on account of the extensive 
injury of the surrounding tissue, and that the bladder and renal affections 
were due to Posner’s experimental methods. If the bacteria once reach 
the lymph nodes, it is not difficult to understand how they enter the 
circulation. KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
307 
It is not certain whether a B. coli bacteremia is present in pyelocystitis. 
A true coli-septicaemia is quite rare; and it could only mean a local or 
quickly passing infection of the blood. Probably bacteria which have 
penetrated the kidney substance from the blood route may pass through 
(see Orth’s nephritis papillaris bacterica (131), (117)). 
In what manner do bacteria reach the kidney substance from the renal 
pelvis, in other words, how does a pyonephrosis develop from a pyelitis 
(132) After injecting bacteria into the renal pelvis, a suppurative 
infection of the kidney tissue can be produced only when complete reten- 
tion and active congestion is caused by ligation of the ureter. A. Muller 
(133) has critically reviewed the different experiments in this direction, and 
amplified them by his own pathological anatomical investigations. He 
concludes that in the vast majority of cases, the extension of pelvic 
inflammation to the renal parenchyma occurs through the lymph channels, 
i.e., in the tissue surrounding the urinary tubules. It is only under 
exceptional experimental conditions, seldom found clinically (e.g., ligation 
of the ureter), that an ascending inflammation in the urinary tubules 
occurs. 
In speaking of hematogenous infections of the kidney, it must also be 
mentioned, that conversely, bacteria easily reach the circulation from the 
urinary tract. Thus Bertelsmann and Man (134) demonstrated that in 
the so-called catheter-fever, i.e., the often observed rigor and fever follow- 
ing immediately after catheterization, bacteria are found in the blood with 
great regularity. 
Suppurative inflammation of the kidney may lead to an infection of 
the perirenal tissue (paranephric abscess), since in this region blood and 
lymph vessels are in the closest relationship to the kidney (119), (135). 
The perirenal tissue, undoubtedly, has a special tendency toward suppura- 
tion, but it is not very certain why this should be. Inflammatory 
processes from the lung may localize here, as well as infections through 
hematogenous sources. Schnitzler has obtained such metastatic perine- 
phritis in the rabbit by the injection of staphylococci into the circulation 
and later contusion of the renal region. But it must be decided in each 
individual case by which of these routes the perirenal tissue was infected. 
At present the general tendency (136), is to assume that in the majority of 
cases, small pus foci were situated under the kidney capsule from which 
the inflammation spreads. The presence of such foci is deduced from 
the finding of isolated leucocytes in the urine. It is now a well known 
fact that in numerous infectious diseases, bacteria are discharged in the 
urine (bacteriuria) and this is of especial importance in typhoid 
prophylaxis. 
As in suppurating renal inflammations, the question of whether 308 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
tuberculosis ascended from the bladder or entered by way of the blood or 
lymph channels, was discussed pro and con for many years (137), (26). 
Pathological anatomy could not decide the question because at autopsy 
only end results were seen in which the bladder is always much changed. 
Clinical observations, especially by means of cystoscopy and operation, 
showed whether renal tuberculosis can exist without tuberculosis of the 
urinary bladder. Of clinical investigative methods the most certain proof 
of renal tuberculosis would seem to be the finding of tubercle bacilli in 
the urine. But urinary examinations made by Foulteron and Hillier, 
Roily, Jousset., Kielleuthner (138) have shown that tubercle bacilli 
are excreted in the urine in severe phthisis, when no tuberculous foci can 
be found in the kidneys at autopsy. Kielleuthner produced proof that 
the tubercle bacilli did not enter the urine from the testes in such cases, but 
that they actually pass through the kidneys without forming colonies. 
Thus the presence of tubercle bacilli in the kidney does not constitute 
renal tuberculosis; something else must be added to encourage the bacteria 
to settle in the renal parenchyma and to destroy it. In the first instance, 
it is natural to think of traumatic causes in the widest sense of the word, 
and correlated experiments were made by a number of workers (139). 
The kidneys were contused, or injured by means of temporary ligation of 
the vessels, and tubercle bacilli were then injected into the ear vein of the 
animal with the result that the injured kidney showed more abundant 
tubercles than the healthy one. But these lesions were different in type 
and localization than those seen in human renal tuberculosis, as will be dis- 
cussed later. Statistics show (140) that a corresponding trauma can be 
traced in but few human cases. For this reason search was made for all 
possible diseases or renal lesions which might favor this infection, such as 
pyelitis, hydronephrosis, renal calculi, floating kidney, and malformations. 
Generally speaking, these accidental findings are of no value in regard to 
its pathogenesis, but under certain circumstances, and not as a rule, 
injuries may favor infection. In animals, a kidney, made artificially 
hydronephrotic, becomes more easily tuberculous than an uninjured 
organ, which is due, according to Meinertz, to the venous stasis usually 
present (141). This view, that circulatory changes, especially congestion, 
active or passive, may favor the growth of tubercle bacilli in some way in 
an organ, will be repeatedly encountered, e.g., in tuberculous orchitis. 
There is a difference between experimental tuberculosis, and that 
found in man, insofar as in the animals there is only a miliary dissemination 
of the tubercles, and that chiefly in the cortex, while in human tuberculosis, 
the infection begins with isolated tubercles in the medulla. Because of 
this primary lesion in the medulla, it was assumed at first that renal 
tuberculosis is an ascending infection, i.e., from the bladder. But the KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
309 
experiments of Pels Leusden (142) have shown that the injection into the 
renal artery of a few, mildly virulent tubercle bacilli suspended in oil, 
gives rise to unilateral tuberculous foci in the medulla. Thus we may 
have a distribution of tubercle bacilli in a manner similar to that of 
pyogenic organisms (117). It also seems to show that unilateral renal 
tuberculosis in man and its localization in the medulla does not depend 
on single bacilli, but on tissue fragments containing tubercle bacilli which 
enter the circulation. 
The complete acceptance of a hematogenous origin which is at present 
practically general, meets nevertheless with other difficulties. In uni- 
lateral involvement, the other kidney is often infected later, while no new 
tuberculous foci appear elsewhere in the body. Why does not bone 
infection, etc. occur? French writers (Albarran (143) and Cathelin) 
believe that transmission occurs through a blood vessel which they have 
demonstrated passing from one kidney to the other, but it is easier to 
think of the lymphatics. Tendeloo (144) is of the opinion, on the basis of 
some autopsies in which he found pulmonary tuberculosis with pleural and 
diaphragmatic adhesions on the same side and also tuberculosis of lymph 
nodes and kidney, that renal tuberculosis is altogether mostly lympho- 
genous, an opinion which has found but few followers. 
Furthermore, it has been assumed that the kidneys of patients who 
have acquired tuberculous nephritis always were especially susceptible to 
this infection. This is an opinion very difficult to prove at present. In 
discussing osteomyelitis we will again touch upon this question and it 
should not be ignored. Many cases of this disease give the impression 
that the bacteria have an affinity for certain tissues of the body, or con- 
versely, that the tissue shows a special predisposition to the particular 
infection. Israel, among others (26), also thinks that tubercle bacilli 
grown in the kidney have a special affinity for renal tissue and that, there- 
fore, the other kidney is more easily infected. 
Tuberculous infection of the bladder is secondary to the kidney, 
and for this reason, the first ulcerations are usually at the ureteral orifice 
of the diseased kidney. Since they are very persistent even though the 
diseased kidney is removed, the question arises if the healthy kidney can 
be infected by an ascending route from the bladder. That it could 
was formerly the prevailing opinion (145) as already stated. 
Attempts to produce experimental infection by introducing tubercle 
bacilli into the bladder with ligation of the urethra, were made quite 
early, but without success (146). It was only after tubercle bacilli were 
injected into the ureters or into the pelvis with obstructed ureter, that the 
desired result was obtained (147). But recently, Wildbolz was successful, 
after causing a backflow of urine into the pelvis by sudden pressure on the 310 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
bladder filled with tubercle bacilli, in imitation of the above cited experi- 
ments (pyonephrosis) of Lewin and Goldschmidt (109)- In human 
pathology, such sudden pressure increase occurs in the inflamed bladder 
from contraction, especially when there is the added factor of rigidity of 
the ureteral orifices infiltrated with inflammatory products. The experi- 
ments of Wildbolz were confirmed by Sawamura, and thus the possibility 
of an ascending tuberculosis cannot be doubted. Rovsing (148) as 
further evidence, has reported some interesting cases. Thus, it is clear 
that care must be exercised in the cystoscopy of such patients. It seems 
natural in all these experiments in which bacteria enter the pelvis after 
sudden pressure on the bladder, that the injury to the pelvis observed 
by Marcus (132) must favor the invasion of the organism. 
In males, tuberculosis of the generative organs is in close relation to 
renal tuberculosis. Remarkably often (43 per cent, of the cases according 
to Simmonds (149)) a combination of testicular-vesical tuberculosis with 
vesical-renal tuberculosis is found, and Wildholz considers the higher 
mortality in males from tuberculous nephritis due to the frequent combina- 
tion of this disease with tuberculosis of the genital organs (150). The 
actual cause of the combination is unknown. The opinion of Kramer 
(151) that congenital infection of the fetal kidney may occur, can only 
be applied in rare exceptions. In isolated cases, i.e., those described by 
Rovsing, the connection is plainer, although such cases also are exceptions. 
Generally speaking, only isolated facts can be noted, e.g., occasionally 
in testicular and renal tuberculosis, the bladder is not infected. Of course, 
this does not exclude the possibility that bacteria may reach the bladder 
from the testes, and then ascend to the kidney. But according to the 
statements made above, this is rare. The reverse route is also conceiv- 
able, viz., that urine containing tubercle bacilli in flowing over the orifice of 
the vas deferens may have led to an infection of the seminal vesicles and 
testes. 
The results of investigations of Baumgarten and Kramer (151) are 
in conflict with this conception, although they occasionally obtained a 
tuberculosis of the base by injecting tubercle bacilli in the bladder of 
a rabbit. Testicular infection was never produced, while primary testic- 
ular tuberculosis always led to an infection of the prostate. Baumgarten 
concludes that the nonmotile tubercle bacilli cannot move against the cur- 
rent of secretion, and that, therefore, tuberculosis of the epididymis is a 
primary hematogenous infection. But it is always dangerous to draw 
conclusions in relation to human pathology from negative animal experi- 
ments, and the theory of primary infection of the epididymis has 
by no means been generally accepted by clinicians and pathologists 
(i49)- KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
311 
Baumgarten and Kramer (151) do not dispute that tuberculosis 
of the prostate and seminal vesicles can develop secondarily from the 
passing urine, or as an extension from the base of the bladder, but admit 
the possibility of infection from the blood. At any rate, not rarely, 
isolated cases of tuberculosis of the prostate and seminal vesicles are 
seen without involvement of the testicle. But that tuberculosis of the 
seminal vesicles cannot invade the epididymis is disputed by Teutsch- 
lander (152) on the basis of a large amount of autopsy material, very 
carefully examined. He points quite logically to the fact, that all of the 
secretory currents may be completely changed if the seminal vesicles 
are inflamed. It is naturally quite clear, that if abscesses are present, 
the pressure of the pus overcomes the secretory pressure, and thus leads 
to a spreading of the organisms towards the testes. This also would be 
true, if it is assumed that tuberculosis extends from the testis towards the 
urethra; here also, the secretory pressure would play no part, because the 
tubules swell on account of the inflammation and atrophy. Even if a 
primary tuberculosis of the testis is assumed, it is the pressure of the pus, 
and not the secretory pressure which determines the further extension of 
the bacilli. 
Loeb (153) was the first to demonstrate by electrical stimulation of the 
hypogastric nerve, that antiperistaltic movements may occasionally occur 
in the vas deferens and the seminal vesicles. Oppenheim and Loew (154) 
repeated these experiments, and by means of electrical stimulation of the 
vas deferens and the injection of pyogenic organisms into the bladder, they 
obtained an epididymitis in their animals. In acute inflammations, in 
which it is generally assumed that extension occurs through the vas 
deferens to the epididymis, antiperistalsis may play a certain role, but in 
chronic inflammations, the explanation of Teutschlander appears more 
acceptable. In addition to this, Baumgarten (155) and Kappis found that 
if the vas deferens were ligated by a thread which had been saturated 
with bovine tubercle bacilli, the infection spread in the vas deferens 
towards the testis, without reaching the epididymis. Although the 
writers themselves drew certain deductions regarding the influence of 
the secretory current in the spread of the disease, the results appear more 
like a pretty proof of the opinion of Teutschlander. 
We cannot discuss all the opinions for and against primary tuberculo- 
sis of the epididymis, but a simple clinical reflection may be mentioned. 
Inflammations known to be metastatic always attack the testicle first, 
not the epididymis (see orchitis in mumps). Kramer believes that 
infection of the epididymis is a peculiarity of chronic infections, since it 
also occurs in leprosy. This reasoning is not convincing, especially since 
we find tubercles in the testes, in the metastatic distribution of miliary 312 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
tuberculosis, and since Janis and Nakarais (156) found tubercles in the 
healthy testes of phthisical patients. 
Tubercle bacilli travel interstitially from the epididymis, or by way 
of the lymph channels to the testis (Simmonds). According to Ash 
(150) experimental injection of tubercle bacilli or tuberculin into the 
internal spermatic artery causes a fibrous inflammation of this organ, with 
proliferation of the cells of the spermatic tubules. Whether the periods 
of erotic excitement in so many consumptives are actually related to this, 
as Asch thinks, does not at present seem proven by these experiments. 
Previous trauma favors the development of testicular tuberculosis. 
Thus Simmonds observed the condition in a rabbit after contusion of the 
testis and intravenous injection of tubercle bacilli. It is also very remark- 
able that it practically always develops during the reproductive period. 
It is not very certain how this is to be explained. Dette Santi (157) 
thinks that engorgement with blood is of importance. He obtained a 
tuberculous orchitis in guinea pigs by the injection of tubercle bacilli 
into the urethra after having ligated the spermatic vein, but in this experi- 
ment, “trauma” to the testis is unavoidable, and it proves little in relation 
to the influence of hyperemia. 
The whole question of the pathogenesis is of great interest for thera- 
peutic reasons. If it is a primary disease of the testis, its removal prom- 
ises much better results than if the seminal vesicles and prostate are 
involved. Conversely, attempts to decide whether the testicle alone 
was diseased have been made from the results of castration. All the con- 
clusions, however, appear to be problematical, because it is only in 
certain isolated cases that we suppose, merely with a certain probability, 
that there is tuberculosis of the seminal vesicles; accurate diagnosis is 
impossible. 
Renal and vesical calculi are diseases which have a certain geographical 
distribution (158). Renal calculi are rare in Germany, only in Wurtten- 
berg and Altburg they are, or were, more frequent (159). The reason for 
this regional difference is, of course, not known with certainty. But since 
their formation is rare in countries of high culture, the supposition is 
that primitive hygienic conditions, especially an unbalanced diet during 
childhood, are the cause of their formation (Schlagintweit, Kuttner). 
In Egypt (160) where vesical calculi are often found even in children, 
the frequent entrance of parasites through the urethra into the bladder 
(bilharzia), is supposedly the cause of their formation (161). 
[The impressive statistical fact has been reported by Osborne, Mendel 
and Ferry that of all rats fed on experimental rations deficient in fat 
soluble vitamin there was formation of phosphatic calculi in every case 
(162).] KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
313 
It has already been mentioned in discussing gall stones, that their forma- 
tion in the human body is a problem in colloid chemistry (163). This 
applies as well to urinary calculi. The urine cannot be considered simply 
as a salt solution (crystalloids), it contains various colloids also. Accord- 
ing to Schade, “the relations of both may be pictured as a salt solution 
suspended in the spaces of a more or less connected scaffold, consisting of 
a very diluted jelly.” It holds more salts than a corresponding amount 
of water could dissolve; and it is due to the colloids present, that the salts 
are not precipitated. Even larger quantities of crystalloids may be 
suspended in such a solution; and the conception which held sway for 
some time (164) that their formation depends on an increased formation 
and excretion of uric acid—the uric acid diatheses or other salt—and that 
it is in close relationship to gout, cannot now be accepted (165). Ebstein 
(166) had already called attention to the fact that there are diseases with 
markedly increased uric acid excretion without calculus formation, e.g., 
leukemia. But precipitation of these crystalloids and colloids takes place 
when “the stability of this system” is disturbed (Lichtwitz). A deposit 
of mucus and crystals is, of course, frequently seen when urine is allowed to 
stand, but such a mixed-deposit of crystalloids and colloids never forms 
a calculus even if it is permitted to dry out, but remains a friable grumous 
mass which can easily be redissolved. It differs from a urinary calculus 
in that the latter is laminated, i.e., layers of colloids and crystalloids 
alternate; furthermore, the colloid will not dissolve, i.e., it is 
“irreversible.” 
Schade, by using an irreversible colloid-fibrin-succeeded in producing 
experimental, laminated calculi, which showed great similarity to urinary 
calculi. Since fibrin is added to the urine in inflammations, this latter 
process must be considered a factor favoring calculus formation; and 
Studensky (167) actually obtained calculi after introducing a foreign 
body into the bladder of the animal, but only after a catarrh of the mucosa 
developed. If inflammation did not occur, no deposit whatever was 
formed on the foreign body. A foreign body per se, therefore, favors 
calculus formation not by becoming a nucleus of crystallization, but only 
insofar as it causes inflammation. The fact that the calculi are found 
massed around the foreign body can be explained by the relatively great 
surface tension at the contact points of foreign body and urine (Schade). 
It must not be assumed from the foregoing experiments that there is 
a demonstrable and regular connection between the formation of urinary 
calculi and inflammations of the urinary tract, since we find far more 
urinary tract inflammations without calculi than with them. It is not 
every kind of inflammatory process which leads to this characteristic 
precipitation of colloids and crystalloids. 314 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Fibrinuria may be present without any inflammation in the urinary 
tract, e.g., with suppurating processes elsewhere in the body (168). But 
the colloid involved in the precipitation does not necessarily need to be 
fibrin, for other colloids have this same property (Schmidt). Ebstein 
and Nicolaier (169) consistently obtained renal calculi in animals by 
feeding oxamid for several weeks, and Tuffier and Rosenbach (170) a.o., 
repeated and amplified these experiments with similar success. Since 
oxamid feeding leads to an injury of the renal epithelium, the above 
mentioned essentials for the formation of calculi are obtained. Their 
presence in osteomalacia and other bone destroying processes is perhaps 
a certain, although loose analogy, and we may assume in these diseases 
that the salts derived from bone destruction favor their formation in a 
manner similar to that in oxyamid feeding (171). 
Therefore, we speak nowadays of a precipitation of irreversible col- 
loids and crystalloids in the formation of urinary calculi. But this is 
only an amplification of the fact discovered by Ebstein, that each calculus 
consists of an organic scaffolding which encloses crystalline salts, and that 
all these calculi grow by further deposits of salts and organic substances. 
This finding has often been verified (172). Chemical analysis has shown 
that the crystalloids consist for the most part of calcium oxalate and uric 
acid, although pure uric acid calculi are rare (173). 
How they act as foreign bodies, and cause all kinds of injury to the 
kidney, especially to the pelvis, has been studied experimentally by 
Kumita (174). His experiments are not very enlightening, since the 
damage from operative trauma, urine retention, infection, etc. cannot be 
differentiated, although they do imitate the findings in calculous nephritis. 
There are the combined influences of the presence of foreign bodies, reten- 
tion of urine, and infection, all of which necessitate operative interference, 
not for the calculus itself, but for relief of its sequelae. 
It might be mentioned that calculi are occasionally crushed spontane- 
ously in the bladder by its contraction (175). 
The nerve supply of the urinary bladder has again awakened consider- 
able interest both on account of the numerous gun-shot wounds of the 
spinal cord with paralysis of the bladder, and because of the increase in 
the most diversified functional bladder disturbances, especially enuresis, 
appearing during the war. 
It is very similar to that of other internal organs (176). Numerous 
ganglion cells which exhibit a pronounced independence are present in its 
walls. Zeissl showed that the bladder will continue contracting periodi- 
cally when all afferent nerves have been cut, and O. B. Meyer (cit. by 
Muller (133)) observed an animal’s bladder which was removed, empty 
itself by contraction after it was filled through the ureter. This indepen- KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
315 
dent function is regulated by afferent nerve fibres, however, and as in 
other internal organs, the innervation is double, their functions being 
opposed. They are first, the sympathetic hypogastric plexus coming 
from the lumbar cord, and secondly, the sacral autonomic pelvic nerve, or 
erigens, from the sacral end of the cord. Both nerve groups not only 
supply the musculature of the bladder but also the internal sphincter; 
while the external sphincter receives separate twigs from the pudendal 
nerve. Ganglion cells are located in the hypogastric, and in the pelvic 
plexuses, and altogether, the more minute ramification of these nerves 
is very complex. 
Stimulation of the hypogastric plexus causes closure of the internal 
sphincter and relaxation of the bladder (detrusor muscle), and conversely, 
stimulation of the pelvic nerve or erigens causes dilatation of the internal 
sphincter and contraction of the bladder. This peculiar condition, when 
stimulation of a nerve causes contraction of one muscle, and relaxation 
of another is called “crossed innervation” (Busch). The nature of this 
is not very certain. 
The hypogastric nerve is controlled from the lumbar cord, and the 
pelvic nerve from the sacral cord (177). Thus, as Muller now emphasizes 
emphatically, there are two separate centers for the bladder which are 
united partly directly, partly indirectly, through reflex relations with all 
the sensory tracts of the body surface. This explains the urgency of 
urination in patients, especially children, from painful sensations such as 
operations, dressings, etc. Furthermore, there must be relations between 
the brain and the bladder centers, although their course is at present as 
little known as the location of the bladder centers in the brain itself. 
Kleist and Forster {tit. by Muller) have indeed reported the interesting 
observation that in bullet wounds of the brain, difficulty in urination is 
present in those cases in which there is a bilateral paralysis of the feet 
present at the same time. This suggests that a bladder centrum exists 
in the temporal apex, and only bilateral destruction wrill produce symptoms. 
Disturbances of bladder function have also been described in focal soften- 
ings in the large root ganglia (178); and in animal experiments, bladder 
contractions have been elicited by stimulation of this area (179). In 
short, a number of facts are known which indicate that we may expect 
bladder disturbances in cerebral disorders, especially injuries, but thus 
far, very little interest has been shown in this question from the surgical 
viewpoint. 
Apart from the disturbances in the motor tracts, there are also dis- 
turbances in the sensory tracts which lead to changes in bladder emptying. 
That the urethra is very sensitive to pain can be quickly shown by cathe- 
terization; it is also sensitive to temperature differences. The sensitivity 316 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
extends throughout the urethra, but it is not known whether it is present 
everywhere to the same degree, both qualitatively and quantitatively. 
In regard to the sensitivity of the bladder itself, the opinions of writers 
differ considerably. R. Zimmermann, prompted by Muller (180), made 
experiments on himself, and found that the touch of a metal catheter was 
only perceived at the vesical sphincter, and that the bladder was unable 
to distinguish between ice water and water at 45°C. Other authors 
such as Frankl-Hochwart-Zuckerkandl, assert that the bladder is very 
sensitive to temperature differences and also to electrical stimuli. Muller 
believes that sensation is elicited only by contraction of the musculature. 
My own observations during cystoscopies, have shown that many patients 
with a normal bladder do not feel the touch of the ureteral catheter at 
all, while others react immediately. Systematic investigations are 
necessary to clear up this question. In numerous operative cases, in 
which the high frequency current was used for its heat effect alone, pain 
was felt only if isolated areas were exposed for some time. This would 
support the opinion of Muller. But these findings cannot be considered 
decisive. Muller was able to elicit neither touch nor temperature sensa- 
tion in vesical exstrophy. With this uncertainty in regard to the simplest 
facts of vesical sensitivity, it is natural, that we have even less informa- 
tion concerning the factors causing spontaneous sensations in the bladder. 
We know that filling causes no sensation whatever at first, and only after 
it has reached a certain degree, is the impulse to urinate perceived; severe 
pain is felt later. Even in this, it is absolutely unknown whether the 
pain is a result of bladder distention, or due to attempted muscle contrac- 
tions (Muller). 
It is also uncertain how the desire to urinate is brought about. Posner, 
Finger (181), a.o., are of the opinion that when the bladder has reached a 
certain degree of fullness, urine is forced into the prostatic part of the 
urethra, and this distention of the posterior urethra, which is, of course, 
still closed by the external sphincter muscle, causes the desire to urinate. 
Other authors believe that the distention of the bladder itself is felt and 
this incites the desire to void; others think that sensation is roused by the 
contraction of the vesical musculature. None of these theories can be 
seriously entertained, until our knowledge of vesical sensitivity in general 
is more definite. Naturally, it is indisputable that certain sensations 
which influence the voiding of urine arise within the bladder. 
Frohlich and H. H. Meyer (182) have studied the route by which these 
sensations are carried to the spinal cord and to the brain; and according to 
them, they are transmitted by the pelvic nerves, because after cutting 
through the posterior roots of the sacral cord, the bladder becomes insensi- 
tive to the faradic current. The sphincter area contains sensory fibres KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
317 
from the pudendal nerve. Finally, according to their experiments, the 
hypogastric plexus has nothing to do with sensitivity. ' 
It is obvious that most diversified vesical disturbances can be caused 
by changes in this complex nerve supply, but thus far, these have been 
only partly analyzed. 
The internal sphincter usually maintains a certain tension—tonus—- 
which, as is well known, persists in the cadaver (Rehfisch) and, for this 
reason the bladder is usually found filled at autopsy. This intermediate 
tonus is also quite sufficient to retain the bladder contents in the living. 
Stimuli for the opening of the sphincter internus are, as already stated, 
carried by way of the pelvic nerve or erigens. If the stimulus is absent, 
or the internal sphincter fails to react, retention of urine is the consequence. 
From the preceding, it is easily seen that no abnormal resistance to the 
introduction of the catheter need exist in these cases. This form of 
retention is not very rare in children (183). By anesthetizing the pudic 
nerve separately from the sympathetic and the sacroautonomous fibres, 
which are only met with in the prostatic region, it can be decided in such 
cases whether the innervation of the internal or of the external sphincter 
has been disturbed (Rost). This form of retention corresponds to that 
obtained by bilateral section of the pelvic nerves; cutting of the hypo- 
gastric nerves does not cause any noteworthy disturbance (Muller). 
According to Zollner, a similar difficulty in voiding is also found in 
sensory disturbances within the area of distribution of the pudic nerve. 
But thus far, these findings, which are of general interest in the physiology 
of urination, have not been verified by other authors. It should not be 
difficult to confirm this observation by anesthetizing the pudic nerve. 
It is, therefore, possible to examine sphincter function to a certain 
degree by the use of separate anesthesia of the pudic nerve and of nerves 
surrounding the prostate. The power of the detrusor can be estimated 
by means of manometric investigations of the urine pressure, but unfor- 
tunately the abdominal pressure cannot be quite eliminated in these tests, 
and this plays considerable role in restless patients (184). The hyper- 
tonicity of the detrusor can also be diagnosed with some degree of cer- 
tainty from the presence of a trabeculated bladder, which, therefore, is not 
merely a sign of difficult urination. 
Schwarz has investigated a large number of cases of spinal cord injury 
by these methods and found all conceivable combinations of detrusor 
conditions on the one side, and sphincter conditions on the other. The 
level of the injury had no recognizable influence on the type. In the 
majority of cases it was found, clinically, that “automatism of the blad- 
der,” as it has been called, was present, i.e., the bladder emptied itself 
periodically, without the intention or knowledge of the patient. There 318 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
had often been a previous total urinary retention. It is known that the 
bladders of patients with spinal cord injuries usually contain residual 
urine, a symptom which is characteristic also of other diseases, e.g.> 
prostatic hypertrophy. Its cause is unknown, but according to Schwarz, 
there are two possibilities; either the bladder does not feel small quantities 
of urine as a stimulus to urination, the detrusor then contracts only as 
far as its threshold; or some anatomical changes prevent complete evacua- 
tion. Thus far no certain differentiation can be made. 
The absorptive power of the bladder and urethra was investigated by 
Treskin, Maas and Pinmer (185), apart from the older works of Segalas, 
Orfila, Demarquai, Brown-Sequard. According to these studies in which 
different substances such as iodine, pilocarpine, strychnine were used, it 
has been proved that certain of them are absorbed by the bladder and 
introduced into the circulation, but according to Treskin, no absorption 
of water takes place. It is especially important for modern surgery 
to know that local anesthetics, such as cocaine and eucaine, are absorbed, 
and may lead to severe toxic symptoms if they are permitted to remain 
in the bladder after an endo-vesical operation. Urethral absorption is 
perhaps even more active, as various observations regarding cocaine 
poisoning have shown, but it must not be overlooked that the anesthetic 
is greatly diluted in the bladder, which is not the case in the urethra. 
These deductions are therefore permitted with the described reservations. 
The normal bladder is free from bacteria, but with the onset of inflam- 
matory changes bacteria are present in the majority of cases, the usual 
organisms being the colon bacillus; staphylococci are rarer (186). Excep- 
tions to this rule occur on both sides. Thus E. Becker, and Strauss 
(187) have recently described cysto-pyelitis observed during the war, 
with urine rich in leucocytes, but sterile. On the other hand, bacteriuria 
is found without inflammatory changes in the bladder. As already men- 
tioned in discussing pyelitis, a change in the bladder and pelvic mucosa 
can be obtained in animal experiments only when retention is produced 
at the same time, or if the bladder mucosa is traumatized, as in the work 
of Bumm (188). 
The mucosa of the bladder and of the pelvis which is normally free 
from bacteria, possesses, therefore, a protection to infection, and injuries, 
usually traumatic, must be added in order that catarrh develop. Gyne- 
cologists frequently observe post-operative cystitis if the bladder has been 
stripped for some distance from its adjacent organs (188), and the cystitis 
appearing after childbirth may also be considered secondary to traumatic 
injury of the bladder walls. But cystitis due to retention is more difficult 
to understand. It is, of course, assumed that the bladder mucosa is irri- 
tated by the decomposition products of urine, such as the ammonia formed KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
319 
from urea (189). Rovsing actually differentiates between bacteria which 
split urea, and those which do not. According to Leube the urea of normal 
urine cannot be decomposed except by bacteria, and Musculus, accepted 
this statement for some time. But possibly the vesical mucosa may be 
irritated by various other chemical substances. 
Pollakisuria, or increased desire to urinate, so generally observed 
during the war, is probably the slightest form of such irritation. Its 
cause is by no means clear. If pollakisuria is combined with polyuria, 
then increased salt content of the food and increased intake of fluids 
must be held responsible for the latter, but perhaps the food also 
contains other diuretically acting substances (Strauss). In some cases 
of pollakisuria, ammoniacal fermentation is assumed to occur (190), or it 
is explained by an old cystitis, psychical factors, colds, etc. (Strauss). 
But all these things can be only occasional factors. Why could not some 
chemical substance, derived from the food, and excreted in the urine, 
cause vesical irritation? It does not absolutely refute the possibility 
of the presence of such a chemical stimulant, that pollakisuria causes no 
anatomical changes in the bladder; the wide spread prevalence rather 
supports it. The vesical catarrh caused by drinking recently brewed beer 
must be similarly explained, but we know very little of the nature and 
chemical composition of such irritating substances. Comparatively 
speaking, we are best informed of those irritations of the bladder mucosa 
due to the chemical substances used in the anilin industry (191). There 
is no basic difference simply because in these cases, it may finally lead to 
carcinoma, or that the cystitis itself may almost disappear. The fact 
remains that workers in anilin plants are subjected to a chronic irritation 
of the bladder mucosa, due to the excretion of a chemical substance, 
(Leueberger supposes this to be a hydroylated aromatic amide compound). 
It is often evidenced only after years; carcinoma frequently appears when 
the workers have not handled the dangerous substance for a long time 
(Oppenheimer). 
We know even less of other injuries to the bladder mucosa than we 
know of the urine soluble chemical substances which irritate it. “Cold,” 
of course, plays a large part and especially a local cold acting on the 
vesical regions. It is known that women acquire cystitis after very cold 
douches; and patients with prostatitis suffer frequently from retention 
after sitting on a cold stone, for example. But it is entirely unknown 
whether in these two cases a cystitis is at fault, or a functional disturbance 
of the sphincter (Rochet). 
Injuries to the urinary bladder, apart from those due to bullets and 
stab wounds, are, in the great majority of cases, caused by an abdominal 
blow striking the filled organ. The physical and physiological aspects 320 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
of rupture have been studied by numerous workers. Houel, Dittel, Ull- 
mann and v. Stubenrauch first investigated the pressure required to 
rupture the viscus by filling with fluid (192). v. Stubenrauch found that 
“the average weight required to just tear a strip of bladder wall 1 cm. 
broad, without considering its thickness, approximated 1.5 kg.” If the 
pressure which just ruptured the bladder was estimated by filling it with 
water the figures were' somewhat less constant. On the average, 
it amounted to 0.5 kg. with a minimum of 0.15 kg.; in the same way, the 
quantity of fluid required to fill the bladder sufficiently to cause rupture, 
also varied (from 300 to 5000 c.c.). These figures show that in practice, 
it is hardly possible to say how far the bladder may be filled without 
danger. Stubenrauch also investigated the elasticity of the bladder in 
relation to traumatic rupture, but he himself is of the opinion that the data 
obtained in the cadaver proves nothing for the living. Berndt imitated 
natural conditions more closely; instead of causing rupture by filling the 
bladder through the urethra, as in the experiments described, he filled the 
bladder to a certain degree and then delivered a blow against the abdom- 
inal wall of the cadaver. As he correctly emphasized, the important 
practical question is, why does the bladder rupture not only on its posterior 
and upper part where it lies free and is struck, but also quite frequently 
through its anterior and lower walls even if the blow strikes the bladder 
from above? As a result of these experiments, Berndt concludes that the 
internal pressure of the bladder is increased by a blow against it, and that 
the bladder tears where its surroundings offer the least resistance. With 
a very full bladder, the upper and posterior parts are torn; when it is 
partly filled, those parts are torn close to the yielding tissues in the pelvic 
floor. Pressure against the promontory and other bones in the vicinity 
is probably not as important as was thought (Bartels). The direction of 
the tear is usually longitudinal, which Berndt, as well as v. Stubenrauch 
considers due to the arrangement of the musculature, but Bartels states 
that the direction of the tear varies. It is usually from within outward, 
and, therefore, incomplete tears are often found, i.e., tears of the mucosa 
only, which naturally have a more favorable prognosis. 
It is also important in the treatment to discover whether the perito- 
neum is torn or not. In the first instance the urine pours into the abdom- 
inal cavity and the bladder is empty. A remarkable symptom in these 
patients is the strong desire to micturate and it has been mentioned above 
that we do not know any details of the cause of this desire. At any rate, 
in such cases an inflow of urine into the prostatic urethra is probably not 
responsible (Posner), but we do not know how soon after injury this 
urgency appears, or if it depends on the position of the tear. In injuries 
involving the peritoneum there is considerable absorption of urine, as KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
321 
investigations of Oehlecker and Rost (193) have shown. In animal 
experiments, Rost found by the retention of nitrogen in the blood, that 
the animals died of uremia after intraperitoneal vesical rupture, before 
peritonitis developed. This fact is of practical value, inasmuch as it 
seems unwise to delay operation, in this condition until peritonitis develops. 
The results of these animal experiments hold good in man. Peritonitis 
develops only if the urine contains organisms or is infected by later cathe- 
terization. Uremia from absorption of urine is the condition to be feared 
in these cases, as shown in the patients of Oehlecker, by an increase in the 
freezing point of blood. 
Wounds oj the bladder heal very quickly, and the regenerative power of 
the urethra is also exceptionally great. Virgli (194) who systematically 
investigated experimental vesical wounds could scarcely find the scars 
after a few months, and it is on account of this exceptional ability to heal, 
that other tissues such as omentum or bowel can be used so successfully 
in closing openings in the bladder (195). In dogs, Rost repeatedly saw 
rapid healing of cuts large enough to establish wide communication 
between the bladder and the abdominal cavity, without having attempted 
to provide a closure operatively. That the urethra also quickly and 
completely regenerates, is well shown in the healing of the defects, several 
centimeters in length, produced by prostatectomy. Ingianni (196) found 
that not only epithelium, but the corpora cavernosa can close this gap in 
a short time by budding, but the musculature does not regenerate. The 
new formed epithelium consists first of one layer and later of several. 
The function of the sphincters must be discussed in some detail. The 
external sphincter consists of striated muscle fibers', i.e., it is under the 
control of the will, and is innervated by the pudic nerve. After the work 
of Rehfisch (197), it is now the general opinion that it only serves to retain 
up until the last instant the urine which has passed into the prostatic 
urethra. It is supposedly not involved in the actual emptying of the blad- 
der. Rehfisch assigns a special importance to the internal sphincter, 
which is placed annularly around the bladder orifice. As stated above, he 
recognized that this sphincter is kept closed by an inherent tonus, and 
opens voluntarily only during the act of micturition. Naturally, it is of 
the utmost practical importance to know in operations near the sphincter, 
e.g., prostatectomies, whether or not the control of the bladder depends 
more or less entirely on this one muscle bundle, the internal sphincter. 
Now Lendorf (357) showed by examinations with Goldschmidt’s urethro- 
scope, that not only the internal sphincter, but the whole of the prostatic 
urethra participates in the closure of the bladder. Indeed, the closing 
power of the internal sphincter is weak and its resistance is more easily 
overcome by the catheter, than that of the external sphincter. Lendorf 322 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
repeatedly observed an open internal sphincter in patients perfectly 
continent after prostatectomy (198), and he explains the observation of 
Freyer (Allen) that after prostatectomy ejaculation occurs not outside, 
but into the bladder, by this open position of the sphincter. In great 
urgency (Lendorf), or in those symptom complexes such as prostatism 
or functional retention of urine in children (183), in which there is over- 
filling of the bladder, it is found that the internal orifice is not firmly 
closed and ring-like, but the bladder continues funnel shaped into the 
prostatic urethra. It is easily understood that an infection of the bladder 
is favored by such conditions. 
As Lendorf could see with the urethroscope, the internal orifice assumes 
a triangular shape with the apex anteriorly when the sphincter opens. 
He deduces from this that the internal sphincter not only opens actively, 
but that there is a simultaneous pull by the detrusor fibres which enlarges 
the opening. 
The disease which is probably the most frequent cause of distur- 
bances in the activity of the sphincter, particularly in producing 
greater difficulty in micturition, is hypertrophy of the prostate (199). In 
spite of the many theories which have been advanced to explain its cause, 
the subject still has its original difficulties. It may be stated, however, on 
the basis of careful pathological anatomical investigations that the inflam- 
matory processes found in hypertrophied prostatic glands are probably 
secondary (Runge, in contradistinction to Rothschild (200)). According 
to Loeschke, the hypertrophy does not develop, as assumed by Marion 
and Lendorf (201) from the periurethral glands, but it begins in the 
muscular portion and forces the muscle bundles apart. Loeschke narrows 
down the old opinion of Guyon, that it is a result of general arteriosclerosis, 
by showing that only those branches of the prostatic artery which belong 
to the portion undergoing hypertrophy, show arteriosclerotic changes. 
We are somewhat better informed of the mechanism of difficult 
micturition in this disease. Of course, it is quite natural to assume that 
enlargement of the organ diminishes the lumen of the urethra, somewhat 
like a stricture. But this idea is incorrect, as shown by the fact that even 
a thick catheter will pass easily if it has the right curve, and the difficulties 
in catheterization are, therefore, not avoided by the use of a thin catheter. 
The different theories which relate the retention of urine in this disease 
to all sorts of mechanical peculiarities of the vesical orifice or the urethra, 
such as valve formations, etc., only hold in single cases. The plaster casts 
of the bladder and urethra made by Reerink (202) have shown with 
certainty that the prostatic urethra is not narrowed, but enlarged [in 
hypertrophy of the prostate, and therefore, the obstruction to urination*is 
evidently not at the exit of the bladder. The opinion of Lendorf, generally KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
323 
speaking, seems well taken, viz., that the function of the internal sphincter 
in producing micturition by active opening, is impaired because a swelling 
develops between the muscular layer and the urethral mucosa, separating 
the musculature from the mucosal tube. Then the sphincter of the 
bladder acts only as a closing muscle—not as dilator. But the difficulties 
in micturition do not always begin as slight difficulties which gradually 
increase to complete retention, but retention may develop with astonishing 
rapidity and may continue for years or permanently, after a single cathe- 
terization. We do not know what causes this complete retention. A 
failure of detrusor action caused, for example, by overfilling of the bladder 
from an unusual intake of fluids (203) is usually assumed. Conversely, 
other authors consider the sphincter the cause of the acute disturbances 
(204), and speak of an inflammation or swelling of the gland which pre- 
vents the sphincter from carrying out its task, i.e., the opening of the 
vesical orifice. 
As has been mentioned above, hypertrophy of the prostate does not 
lead to a uniform enlargement, but to an adenomatous tumor-like forma- 
tion within it, and especially in its muscular part (Loschke). In prosta- 
tectomy, we shell out these tumor nodules, and the closing power of the 
bladder can be, and is, repaired by means of the remaining prostate and 
muscular layers. So-called continence develops, however, in the majority 
of cases, even after complete removal of the prostate, e.g., in carcinoma. 
Whether in such cases certain muscle bundles of the bladder assume the 
function of a sphincter is not known (see also p. 321). 
Resection of the vas deferens or castration was formerly much in use, 
in the treatment of hypertrophy of the prostate, although it is rarely 
employed at present (205). These so-called “sexual operations” were 
based on a not very well understood relation between prostate and testes. 
In regard to the physiology of the gland, we know, in addition to the 
above discussed function of vesical sphincter, that it adds a watery secre- 
tion to the seminal fluid which activates the motility of the spermatozoa 
(206). Notwithstanding the work devoted to studying a supposed inter- 
nal secretion, nothing has been proved (207), although we know from 
autopsies of eunuchs, human and animal, that early removal of the testes 
in adults as well, leads to atrophy of the prostate and seminal vesicles (lit. 
see 207). But whether this is caused by the absence of the external testic- 
ular secretion and function, or by the absence of an internal secretion of the 
same organs, is not known. Deductions have frequently been carried very 
far, and in particular, the improvements in the disturbances of prostate 
patients after operative treatment, have been compared to the atrophic 
processes in the normal gland. But this does not seem correct, because 
hypertrophy of the prostate is a new growth and cannot simply be regarded 324 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
as an enlargement. The fact remains that in no case that could be investi- 
gated by autopsy, was shrinking of an hypertrophic prostate demonstrated 
after castration or vasectomy (Schlange). Probably the relief of patients 
operated by these methods is due only to a subsidence of a swollen pros- 
tate and not to a shrinking of the actual tumor. A fresh specimen will 
show that these hypertrophic prostates are remarkably “adenoma like.” 
These considerations apply equally as well to animal experiments in 
which attempts are made to bring about reduction in the size of enlarged 
prostates by .v-ray treatment of the testes. The illogical deductions 
result from the mistaken analogy between the prostate and the uterus; 
and hypertrophy of the prostate and uterine myomata (208). Embryo- 
logically the prostate is entirely different from the uterus. And after 
the negative results of treatment, enlargement of the prostate cannot be 
compared to uterine myomata. Of course, all these considerations are 
not intended to discuss the value of the sexual operations, but are only 
directed against mistaken pathological conceptions and the conclusions 
derived from them. 
In connection with the influence of castration on the prostate, a few 
words must be added in regard to the general results of this procedure (207). 
According to the statements in the literature, removal of both testes on 
account of tuberculosis, causes very few symptoms from abolition of 
function, psychical disturbances in particular are very rare (209). The 
reason for the inconspicuous symptoms is due not alone to the fact that the 
individuals castrated for tuberculosis are mostly adults, but the sequelae 
are masked by other disease symptoms. Perhaps, however, special 
investigations would discover some symptoms due to the loss. On the 
other hand, in castration for injuries, all kinds of symptoms, especially 
psychic disturbances, develop. Lichtenstein (210) reports a very care- 
fully observed case in which melancholia and depression, disturbed sleep, 
cries during sleep, etc., were present, and Bauer (84, p. 97) describes 
certain peculiarities in a man castrated at the age of 25. There is no doubt 
that the temperament changes after operation; the patient becomes more 
sedate and phlegmatic; a fact utilized since olden times for pastoral 
purposes especially in horse and cattle raising. Sexual impulses arising 
in the brain are supposedly undisturbed by castration; but according to 
Tandler and Gross (211) all statements made by castrated individuals 
with regard to impotence must be accepted with great caution. At any 
rate, observation shows (Lichtenstein) that all sexual functions are 
completely suspended after castration. 
It is, of course, of the greatest practical interest to know whether 
these symptoms due to the loss of organic function are consequences only 
of the loss of internal, or also of the loss of external testicular secretion. KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
325 
This question has been studied very often. Hunter demonstrated that 
roosters lose their male characteristics after castration (capons), but 
retain them if the testes are implanted elsewhere in the body. These 
experiments he repeated in various forms with similar results (cit. by 
Lichtenstein). Steinach (212) carried out such experiments on a large 
scale with rats and showed that disturbances due to castration, e.g., 
atrophy of genitalia, will not occur if the testes are implanted in the 
abdominal musculature. From his experiments, it may be accepted that 
many specific sexual properties are the results of the activity of the 
internal secretion of the reproductive glands and that at least in animal 
experiments, it is possible to produce changes. Lichtenberg who drew 
practical deductions for human pathology from them, implanted an unde- 
scended testis removed from another man, directly into the abdominal 
musculature of a patient, who had suffered considerably from psychical 
and genito-functional symptoms, due to the loss of both testes (trauma), 
with the result that the psychical disturbances disappeared and sexual 
power returned. If, as Rohleder (213) advises, this transplantation has 
other uses, e.g., treatment of the homosexual to reestablish heterosexual 
desires, cannot be decided at present. 
The disturbances are especially pronounced in individuals who are 
castrated in youth; a custom in vogue among some people and religions 
(Tandler and Gross (211)). Physically, the abnormal obesity is note- 
worthy, and points to changes in metabolism. Examination has shown 
these changes are due to decrease in oxidative processes, but we are little 
informed of other details, especially of the metabolism of salts. The 
excessive obesity affects certain portions of the body, especially the hips, 
the breasts, etc. and domestic animals are castrated that they may be 
fattened. Bone growth is increased, but it is not clear whether it is a 
direct result of castration, or indirect, through the influence of the thymus, 
since the involution of that structure is, as will be discussed later, closely 
connected with the development of the testes. But notwithstanding its 
size, the body of the eunuch remains in an infantile stage, especially the 
larynx. The voice remains high pitched. The growth of hair on the 
body is absent, while that on the head is abundant. 
As already stated, these symptoms just described are rarely seen, 
after operative castration, because this is usually done on adults. But 
constitutional changes of the type described, are known, and justify the 
assumption of a hypoactivity of the testicle. Of course, as in most dis- 
eases of the ductless glands, in such cases it is not merely the absence of 
the testes, but involvement of other endocrine glands, especially the hypo- 
physis cerebri, which adds to the complexity of the disease picture. The 
hypophysis in such cases is said to supply insufficient secretion (hypo- 326 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
function). According to Bauer (84 p. 95), in so-called “eunuchoidism/’ 
two very different types must be differentiated—the eunuchoid tall type, 
with graceful physique and long limbs must be distinguished from the 
eunuchoid obesity. Often the wrinkled condition of the face is very 
pronounced, giving the patients a senile appearance (geroderma). 
The reverse, i.e., a sexual precocity, has repeatedly been described in 
children with testicular or ovarian tumors, e.g., carcinoma of the testicle 
(Sacchi, cited by Bauer). Thus, in a nine year old boy, a beard, masculine 
voice, hair on the trunk, libido, etc. developed, and all these symptoms 
disappeared after removal of the tumor. In other cases, this precocity 
is not connected with the sex glands, but is possibly related to changes in 
other endocrine organs, especially the pineal gland. We deduce a retarding 
influence of the pineal gland on sex development, from the fact that its 
destruction by tumors in boys causes sexual precocity and marked growth 
in height, growth of hair, etc. (214). These clinical observations corre- 
spond with experimental results (see Biedl (384)). The pineal gland has 
thus far not been of surgical interest. Since it is a question only of hypo- 
activity of the organ in all the diseases thus far recognized, operation 
could only deal with removal of brain pressure symptoms; we can do 
nothing surgically for its functional failure. 
It is quite otherwise with the second endocrine gland situated within 
the skull, viz., the hypophysis (207). Surgery is the chief method which 
has increased our physiological knowledge of this organ within the last 
few years (215). The hypophysis cerebri is divided both histologically 
and physiologically into three completely separated parts, the anterior, 
the central, or pars intermedia, and the posterior lobes. In the organ 
extracts offered commercially under the names of hypophysin, pituglandol, 
pituitrin, etc., the material consists of a part of the central lobe and the 
posterior lobe. They act essentially by increasing blood pressure and by 
stimulating unstriped muscle tissue such as that of the uterus and 
intestines to contract. For this reason they are used in obstetrics. They 
are also diuretics. As further examinations have shown, the action de- 
pends only on the central lobe, and extracts from the posterior lobe are 
inactive. Nothing is known at present of the function of the latter which 
consists of nerve elements, but it does not appear to be in any relation to 
the known diseases of the hypophysis. The central lobe supplies the 
secretion, the action of which has been described. Colloid droplets can 
be demonstrated in the central duct, and they pass through the posterior 
lobe during excretion. It is assumed that the secretion enters the cere- 
brospinal fluid, but it is not known that this fluid shows an increased 
activity from the presence of hypophysis extract. 
Extracts from the anterior lobe, apart from a brief lowering of blood KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
327 
pressure, probably not specific, have no recognized experimental action. 
But as shown in extirpation experiments, and by observations on patients, 
the anterior lobe is of great importance in the growth of young individ- 
uals, and in metabolism in general, for complete removal of this organ in 
young animals, leads to hypophyseal cachexia and early death. Its 
extirpation checks growth, and the epiphyseal lines are retained dispro- 
portionately long. 
It is now generally assumed that the excessive growth in length after 
castration does not depend on the testes, but on hyperfunction of the 
anterior lobe of the hypophysis. In pregnancy also, certain histological 
changes are found in this gland. Such excessive growth in the long axis 
of the limbs with underdevelopment of the sexual glands, and secondary 
hypersecretion of the anterior lobe of the hypophysis lead to giantism. 
Since the hypophyseal changes are secondary, the treatment of diseased 
reproductive glands need not include treatment of the hypophysis (see 
Biedl). 
Most interesting to the surgeon are the diseases of the hypophysis 
which are related to disturbance of growth. In acromegaly, that extra- 
ordinarily characteristic disease in which only the ends of the limbs, i.e., 
hands and feet, nose and chin, develop enormously, an adenoma of the 
anterior lobe of the hypophysis is found in the great majority of the cases. 
Thus far, the long continued controversy, whether there is an increased, 
decreased, or altered secretion, is by no means cleared up, but is now laid 
aside on account of the success of operative procedures. Since Hochen- 
egg, we know that acromegaly can be cured by the extirpation of the hypo- 
physeal adenoma, therefore, a “too much” is surely present, but whether 
it accomplishes its pathological action directly or indirectly, we do not 
know. In the same way it is quite uncertain how far the edematous condi- 
tion of the subcutaneous tissue in acromegaly is related to a disturbance 
in the thyroid gland. Just as in the other diseases of the hypophysis, 
there are also changes in the reproductive glands in acromegaly (207). 
The menopause is one of the early symptoms of the disease in women. But 
on account of therapeutic results, changes in the sexual sphere in acro- 
megaly must be considered as secondary. 
Another disease complex related to the hypophysis is that form of 
obesity, known as adipose genital dystrophy (216). In this disease, we 
have an abnormal fat development in certain parts of the body with 
uniform underdevelopment of the genitalia. Usually, a tumor of the 
hypophysis is found, but not an adenoma which increases the functional 
activity of the hypophysis, as in acromegaly, but cysts, carcinoma, sar- 
coma, etc., i.e., tumors which destroy the hypophysis. For this reason, 
it is now generally assumed that the obesity is caused by hypoactivity of 328 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
the hypophysis, an assumption which corresponds perfectly to the findings 
in animal experiments. A case reported by Madelung (217) offers a 
beautiful proof for the correctness of this opinion; obesity developed 
after a bullet wound in the brain, and the .v-ray picture showed that the 
bullet occupied the exact situation of the hypophysis. Operative treat- 
ment of adipose genital dystrophy gives good results, but they are not 
progressive (215), (218). After some improvement, the condition 
remains about the same, from which Biedl concludes, that opening a cyst, 
or the removal of a tumor removes pressure, which permits of better secre- 
tion. This is not to be considered as proof that this form of obesity is 
due to hyperfunction, but on the contrary, to hypofunction of the hy- 
pophysis, especially of the central lobe. For this reason, after relieving the 
pressure, treatment which hypophysis extracts gives very good results. 
It has already been mentioned that the hypophysis extracts prepared 
chiefly from the middle lobe, act as diuretics. It is, therefore, logical to 
assume that diseases characterized by polyuria, e.g., diabetes insipidus, 
are related to changes, i.e., hyperfunction of the median lobe. Frank 
(219) observed a case of diabetes insipidus which developed after a 
bullet wound in the head and in which the missile was situated close to 
the hypophysis. He assumes that the bullet acting as a constant irritant 
to the gland, caused hypersecretion. Simmonds (220) describes a case 
in which the metastasis of a carcinoma involved the sella turcica. The 
polyuria which was present, he supposed to be due to irritation of the 
pars intermedia. Conversely, other authors consider diabetes insipidus 
due rather to a hypoactivity of the hypophysis (see 84), because treat- 
ment with pituitrin has repeatedly given good results. All these ques- 
tions, including the relations of the pituitary gland to dwarfism, especially 
to chondrodystrophy (Biedl) are still unanswerable. We require much 
more precise information in all directions. 
The internal secretion of the testes discussed above is due to the inter- 
stitial cells, according to our present opinion. Very instructive in this 
relation are the experiments of Tandler (221) who exposed the testes of 
fallow deer to £-rays, obtaining, thereby, complete destruction of the sperm 
cells while the interstitial cells remained intact. In the animals so treated, 
the antlers grew normally after having been shed; although castrated 
fallow deer as controls, grew a misshapen pair of antlers, the so-called 
perugue antlers. 
The sperm cells are far more sensitive to injury than the interstitial 
cells. This applies especially to nutritional disturbances and the testicular 
blood supply with the results of its interruption have been the frequent 
object of experimental investigations (222). It was found that after 
ligation of the internal spermatic artery, a hemorrhagic infarct of the KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
329 
testis develops very quickly, while the epididymis, which is supplied by 
the deferential artery, is less injured. According to investigations of 
Enderlen, the testicle tolerates the ligation of the spermatic cord, i.e., 
all the vessels, including the veins, for about 16 hours, without showing 
microscopical lesions. This is important in the prognosis of torsion of 
the testicle. The organ recovers even after longer ligation, but spermato- 
genesis suffers, and subsequently a gradually increasing atrophy of the 
organ takes place. 
The testis is just as sensitive to injuries as it is to interruption of its 
blood supply. As observed from experiments of Kocher, Steiner, Jacobson 
(223), scars are prone to occur, and atrophy of the whole gland, usually 
from secondary inflammation, often takes place. An injury of the testis, 
comparatively very slight, however, is seen in operative incisions. Thus 
J. E. Schmidt (224) showed in animals, that a testis with such an incision 
forms only a very superficial scar, of no practical importance. Progressive 
atrophy does not appear after these operative cuts either in the longitud- 
inal or transverse axis, because the anastomoses are fairly complete. 
Many workers have investigated the displacement, and possibilities 
of transplantation of the testis (225). It was found that the organ trans- 
planted in childhood develops in an apparently normal manner at first. 
But as soon as spermatogenesis begins, involution starts, ending in 
atrophy. These experimental results correspond with the findings 
obtained in cases of undescended testicle in man. Thus, in cryptorchitis 
in the young, the testis is often of normal size, but it is always small and 
atrophic in adults. Schmidt thinks that pressure changes exerted by the 
intestines on the testis situated in the abdominal cavity is the cause of 
this atrophy and he offers, as an interesting proof of his assertion, the fact 
that in scrotal hernia, the testis is often small and atrophic. In this case 
a change in pressure from the entering and retreating intestine is present. 
In a similar way, spermatogenesis is lost, if the testis is transplanted 
beneath the abdominal skin, even if the vascular supply is perfectly 
intact. The testis seems to require for its perfect function the loose, half 
suspended position which it normally occupies. These experimental 
investigations are of the greatest importance in the treatment of cryptor- 
chism. They show that it is quite indifferent, whether the testicle in 
cryptorchitis is pushed back into the abdominal cavity or is localized under 
the skin, spermatogenesis will be lost, while the interstitial cells, and with 
them the internal secretion, remain intact. But the resistance of sperma- 
togenesis against occlusion of the efferent channels is most remarkable. 
Posner demonstrated living spermatozoa in the testis after an occlusion 
of the epididymis or vas deferens for 10 years and more. Thus, theo- 
retically, there is the possibility that removal or short circuiting of the 330 
THE PATHOLOGICAL PHYSIOLOGY OP SURGICAL DISEASES 
cicatricially occluded part of the efferent ducts which is practically always 
due to gonorrhea, will reestablish the emptying of normal semen. Unfor- 
tunately, thus far, the practical results have been very poor for technical 
reasons in spite of the numerous animal experiments, and operations on 
man (lit. see Schmidt). Probably a successful end has never been reached 
by implantation of the vas deferens into the testis and similar methods, 
although Bogoljuboff (226) showed in animals, that such an anastomosis 
is possible. 
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48. Ferrarin: La clinica chirurgica, 1903. 332 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
49- Israel, a. o.: Chirurgenkongress, 1904 (discussion). 
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88. Landau: Die Wanderniere der Frau, Berlin, 1881. 
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95. Hildebrano and Haga 3 (hydronephrosis): Deutsche Zeitschft. f. Chir., V. 49. 
Tuffier: Annales des maladies des organes genit. urin., 1894. 
g6. Rautenberg: Mitt. a.d. Grenzgeb., 1906, Vol. 16. Strauss and Gernout: Arch, de 
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97. Rost: Munch, med. Wochenschft., 1919. Levin and Goldschmidt: Virch. Arch. 
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98. Engelmann: Pflugers Arch. V. 2, p. 243. 
99. Aksne: Folia urologia, 1908. 
100. Enderlen: Munch. Mittheilungen. 
101. Stewart and Barbes: Ann. of surgery, 1914, No. 6. 
102. Schischko: Chirurgenkongress-Zentralbl., 4, p. 179. 
103. Lorin: Chirugen Kongress-Zentralbl., 4, p. 854. 
104. Primbs: Zeitschft. f. urol. Chir., V. 1, p. 600. 
105. Kavasoye: Zeitschft. f. gyn. Urol., V. 3. 
106. Scott: Chirurgen-Konkress Zentralbl. 3, p. 486. 
107. Boetzel: Zieglers Beitr., 1913, V. 57. 
108. Voelcker: Chirurgenkongress, 1912. 
109. Marcus: Wiener Klin. Wochenschft., 1903. Lewin and Goldschmidt: Deutsche 
Med. Wochenschft., 1897, p. 601-a., No. 52. 334 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
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112. Fr. Muller: Naturforscherversammlung, 1906. Fromme: Verein der Aerzte in 
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113. Hirsch: Dissert. Munchen, 1910. 
X14. Franke: Mitt. a.d. Grenzgebieten, 1911, V. 22; Berliner klin. Wochenschft., 1911; 
Ergebn. d. Chirurgie, V. 7. 
115. Scheidemantel: Wurzburger Abhandlungen, 1913, V. 13. 
116. Rippert: Deutsche Med. Wochenschft., 1899. Sittmann: Deutsches Arch. f. 
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exp. Path. u. Pharm., V. 39. Pernice and Scagliosi: Deutsche med. Wochen- 
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26. 
117. Koch: Zeitschrift. f. Hyg. u. Infectionskrankheiten, V. 61. 
118. Israel: Chirurg. Klink. der Nierenkrankheiten, Berlin, 1901. 
119. Jordan: Chirurgenkongress, 1899-1905. 
120. Goppert: Ergebn. d. inn. Med., 1918, V. 2. 
121. Sakata: Arch. f. Anat. (u. Physiol.), 1903. Bauereisen: Zeitschrift. f. Gyn. Urol., 
V. 2. 
122. Sagimura: Virch. Arch., V. 206. 
123. Lever Stewart: cited in Franke, 114. 
124. Selter: Zeitschft. f. Hyg., 1906, V. 54. Rogoszinsky: Zentralbl. f. Chir., 1902, p. 
757 (lit.). Conradi: Munch, med. Wochenschft., 1909, p. 1318. Cohn: 
Berliner klin. Wochenschft., 1900. Hornemann: Zeitschft. f. Hyg , 69. 
125. Wasserthal, Epstein: Berlin, kl. Wochenschft., 1909. Roubitschek: Berliner 
klin. Wochenschrift, 1910. 
126. Brunn: Arch. fr. Klin. Chir., V. 65. 
127. Wreden: Zentralbl. f. Chir., 1893. 
128. Faltin: Zentralbl. f. d. Krankh. d. Harn and Sexualorgans, V. 12. 
129. Posner and Lewin: Zentralbl. f. d. Krankheiten d. Harn u. Sexualorgans, V. 7. 
130. Marcus: Wiener klin. Wochenschrift, 1901, No. 1. 
131. Biedl and Kraus: Arch. f. exp. Path. u. Pharm. 3. 
132. Lewin: Arch. f. exp. Path. u. Pharm., V. 40. v. Wunschheim: Zeitschft. f. 
Heilkunde, V. 15. Marcus: Wiener Klin. Wochenschft., 1903. Schmidt- 
Aschoff: Pyelonephritis in anat. u. bakt. Bezichung, Jena, 1893. Savo: 
Wiener Klin. Wochenschft., 1894. Albarran: These de Paris, 1889. 
133. A. Muller: Arch. f. Klin. Chir., 1912, V. 97. 
134. Bertelsmann and Man: cited by Suter von Mohr-Stahelinschen-Handbuch, 
3, p. 1768 
135. Paranephritic Abscesses. Lit by Wurster: Diss. Wurzburg, 1910. 
136. Kummell: Handbuch d. prakt. Chir., V. 4, p. 514. 
137. Lit. see Frank: Zentralbl. f. d. Grenzgebiete, V. 14. 
138. Foulerton and Hillier: Brit. med. Journ., 1901. Kiellcuthner: Fol. urol., 1912, 
V. 7. Roily: Munchener med. Wochenschft., 1907. Jousset: Arch. med. 
exp., 1904. 
139. Seeliger: Zeitschft. f. Urol., 1909. Orth: Berlin, klin. Wochenschft., 1907. 
140. Kuster: Chirurgie d. Nieren. Deutsche Chir. 
141. Meinertz: Virch. Arch., V. 192. Hansen: Annal. des. mal. des org. gen-urin., 
1903. KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
335 
142. Pels Leusden: Arch. f. klin. Chir., V. 95. 
143. Albarran: Assoc, franc, d. urol., 1904. 
144. Tendeloo: Munch, med. Wochenschft., 1905. 
145. Guyon: Lecons cliniques sur les maladies des voies urinaires, Paris. 
146. Baumgarten: Arch. f. Klin. Chir., V. 63, p. 1019. Sawamura: Deutsche Zeit- 
schft. f. Chir., 1910, V. 103. 
147. Bernard and Salomon: Compt. rend, de la soc. de biol., 1905. Kappis: Arb. 
a. d. Gebiete d. pathol. Anat. u. Bacteriol. Tubingen, 1906. 
148. Rovsing: Zeitschft. f. Urol., 1909, Vol. 3. 
149. Simmonds: Deutsche med. Wochenschft., 1915. 
150. Voelcker: Lit. see Voelcker, Chir. d. Samenblasen, Neue Deutsche Chir., V. 2. 
151. Kramer: Arb. auf. d. Gebiete d. pathol. Anat. u. Bakt., V. 4 u. Kramer: Deutsche 
Zeitschft. f. Chir., 1903, V. 69. 
152. Teutschlander: Beitr. z. Klinik. d. Tuberculose, 1906, V. 3 and 5. 
153. Loeb: Diss. Giessen, 1866. 
154. Oppenheim und Loew: Virch. Arch., V. 182. 
155. Baumgarten: Berlin. Klin. Wochenschft., 1905. 
156. Janis and Nakarais: Zeitschft. f. Urol., 1909, V. 3, p. 712. 
157. Dette Santi: cited in Handb. d. prakt. Chir., V. 6, p. 1064. 
158. Treindlsberger Schlagintiveit: Deutsche Ges. f. Urol. 4, Kongr., 1913; Beiheft d. 
Zeitschr. f. Urologie, 1914. Hirsch: Historisch-geograph. Pathologie, 1886, V. 
3, Stuttgart. 
159. Kuttner: Bruns Beitrage, V. 63. 
160. Condrey: Journ. d’ urol., 1913. 
161. Goebel: Ergeb. d. Chirurgie, V. 3. 
162. Osborne, T. B., Mendel, L. B. and Ferry, E. L.: J. A. M. A., 19x7, 49, 32. 
163. Schade: Munch. Med. Wochenschft., 1909, 1 u. 2, 1911, Med. Klin. Lichtwitz: 
Zeitschft. f. Urol., 1913. 
164. Kleinschmidt: Die Harnsteine Berlin Springer, 1911. 
165. Posner: Deutsche Ges. f. Urol. 4 Kongr., 1913 (disc.). Brugsch: Klemperer 
Munchener med. Wochenschrift, 1908. 
166. Ebstein: Deutsche Zeitschrift. f. Chir., V. 7. 
167. Studensky: Deutsche med. Wochenschrift, 1908, No. 32 (literature). 
168. Quincke: Deutsches Arch. f. Klin. Med., 1902, V. 9. 
169. Nicolaier and Ebstein: Exper. Erzeugung von Harnsteinen Wiesbaden, 1891. 
170. Rosenbach: Mitth. a. d. Grenzgebieten, 1911, V. 22. 
171. Langendorff and Mommsen: Virch. Arch., 1877, V. 69. 
172. Posner: Zeitschft. f. klin. Med., V. 16. Pfeifer: Verhandl. d. Kongr. f. inn. 
Med., 1886. 
173. Kahn: Arch, of int. med., 19x3, V. 11. 
174. Kumita: Mitteil. a. d. Grenzgebieten, 1909, V. 20. 
175. Klauser: Bruns Beitrage, 1914, V. 94, p. 98. 
176. S. v. Zeissl: Pflugers Arch., V. 53, 55, 89. Rehfish: Virch. Arch., V. 150. v. 
Frankl-Hochwart-Zuckerkandl: Nothnagels Handbuch Lief., 1906, 19. 
Muller: Deutsche Zeitschft. f. Nervenheilkunde, 1902, V. 21 u. Deutsch. Arch, 
f. klin. Med., 1918, V. 128. Frohlich u. Meyer: Wiener klin. Wochenschrift, 
1912. Rost: Munchener med. Wochenschrift, 1918, No. 1. Langley: Journ. 
of physiol., V. 29. Elliot: ibid., V. 35. Schwarz: Mitt, aus d. Grenzgeb., 
1917, V. 29. Metzner: in Nagels Handbuch d. Physiologie, Adler. Grenzge- 
biete, V. 30. Debaisieux: Chirurgenkongress-Zentralbl., 2, p. 278. 336 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
177- S. also the schematic illustr. of Pflaumer Zeitschr. f. Urol., V. 13. 
178. Homburger: Therapie d. Gegenwart, 1903. 
179. Karplus und Kreidl: Arch. f. Physiol., 135. 
180. R. Zimmermann: Mitt. a. d. Grenzgebieten, V. 20, p. 455. Muller: Mitt. a. d. 
Grenzgebieten, V. 18, p. 633. 
181. Posner: Diagnostik und Therapie d. Harnkrankheiten, Berlin, 1894. Finger: 
Wiener allg. med. Ztg., V. 38. 
182. Frohlich and H. H. Meyer: Wiener klin. Wochenschft., 1912, No. r. 
183. Rost: Munchener med. Wochenschrift, 1918, No. 1. 
184. Schwarz: Mittheil. a. d. Grenzgebieten, V. 29. Adler: Mitt. a. d. Grenzgebieten, 
V. 30. 
185. Treskin: Pflugers Arch., V. 5. Mass and Pinner: Deutsche Zeitschft. f. Chir., V. 
14. 
186. Rovsing: Klin, and exper. Untersuchungen uber die infekt. Erkrankungen d. 
Harnwege, Berlin, 1898. Melchior-Suter, a. o.: Zeitschft. f. Urol., V. 1 (lit.). 
187. Strauss: Zeitschrft. f. Urol., 1919, V. 13. 
188. Bumm: cited by Stoeckel Handbuch d. prakt. Chir., V. 4, p. 843, 4 edit. 
189. Leube: Virch. Arch., V. 100. 
190. Freudenberg: Munch, med. Wochenschft., 1918, p. 277, disc. 
191. Leueberger: Bruns Beitrage, V. 80, lit. Rehn: Arch. f. klin. Chir., V. 50. Oppen- 
heimer: Munch, med. Wochenschft., 1920, No. 1. 
192. Wallney: Diss. Greifswald, 1866. Ullmann: Wiener med. Wochenschrift., 1887. 
Rivington: Lancet, 1882. Stubenrauch: Arch. f. klin. Chir., V. 51. Dittell: 
Wiener med. Wochenschft., 1886. Bartel: Arch. f. klin. Chir., V. 22. Brand: 
Arch. f. klin. Chir., V. 55. v. Beck: Deutsche Zeitschrift. f. Chir., 19. Howell" 
These de Paris, 1857. 
193. Rost: Munchener med. Wochenschrft., 1917. Oehlecker: Deutsche med. Woch- 
enschrft., 1912. 
194. Virgli: Chirurgenkongress-Zentralbl., 4. 
195. Nagano: Bruns Beitrage, V. 38. v. Brunn: Deutsche Zeitschrift. f. Chir., V. 73. 
Enderlen: Deutsche Zeitschrift. f. Chir., V. 55. 
196. Ingianni: Deutsche Zeitschrft. f. klin. Chir., 1900, V. 54. 
197. Rehfisch: Virch. Arch., 1897, V. 150. 
198. Lendorf: Arch. f. klin. Chir., 1912, V. 97. 
199. Frisch: see Frisch im. Handbuch d. Urol, heraus g. v. Frisch Zuckerkandl. Hirt. 
Ergebn. d. Chir., V. 1; Schlange im Handbuch d. prakt. Chir., V. 4. 
200. Rotschild: Fol. urol. Deutsche med. Wochenschft., 1909, No. 33. Runge: Mitt. 
a. d. Grenzgebieten, V. 20. 
201. Marion: Fol. urol., V. 5. Loeschke Naturhist. med. Verein. Heidelberg, 1919. 
Lendorf: Arch. f. klin. Chir., 97, p. 467. 
202. Reerink: Deutsch. Chirurgenkongress, 1903-1904. 
203. De Quervain: Chirurgische Diagnostik., F. C. W. Vogel, Leipzig, 3 Edit., p. 429. 
204. Wilms: Munchener med. Wochenschrift, 1916. Schlange: Handbuch d. prakt. 
Chir., V. 4. 
205. Rovsing: 36th Chirurgenkongress. Grunert: Munchener med. Wochenschrft., 
1907. Koenig: Munchener med. Wochenschrft., 1906. 
206. Furbringer: Nothnagel’s Handbuch d. inn. Med., V. 19. 
207. cf. Biedl: Innere Sekretion, 2 Edit. 2 part, p. 341. 
208. Wilms-Posner: Munchener med. Wochenschrft., 19x1, No. 36. 
209. v. Bramann-Rammstedt: Handbuch d. prakt. Chir., V. 4, p. 1066, 4 edit. KIDNEYS, BLADDER, MALE GENITALIA, HYPOPHYSIS 
337 
210. Lichtenstern: Munch, med. Wochenschft., 1916, No. 19. 
211. Tandler and Gross: Arch. f. Entwickelungsmech, 27, 29, 30 and Wiener klin. 
* Wochenschrft., 1907, 1908, 1910. 
212. Steinach: Pflugers Archiv., 1894, V. 56; Zentralbl. f. Physiol., V. 24 u. 27. 
213. Rohleder: Deutsche med. Wochenschrft., 1917. 
214. Frankl-Hochvvart: Weiner med. Wochenschrift, 1910. 
215. Melchior: Lit. Ergebn. d. Chir., V. 3. v. Eiselsberg: Wiener klin. Wochenschft., 
1907. Horsley: Brit. med. journ., 1906. Hochenegg: Chirurgenkongress, 
1908. 
216. Frohlich: Wiener klin. Rundschau, 1901. Bartels: Zeitschft. f. d. Augenheilk, 
1906, V. 16. 
217. Madelung: Arch. f. Klin. Chir., V. 73, p. 1066. 
218. Cushing: J. A. M. A., 1909, V. 53, p. 249. 
219. Frank: Berliner klin. Wochenschrift, 1910. 
220. Simmonds: Munchener med. Wochenschft., 19x3, p. 127. 
221. Tandler: Arz. d. Wiener Akad., 1910. 
222. Tomsa: Jahresbericht d. Ak. d. Wissenschaften, 1862, Wien., V. 46. Miflet: 
Arch. f. klin. Chir., 24. Enderlen: Deutsche Zeitschft. f. Chir., V. 43. 
223. Steiner: Arch. f. Klin. Chir., V. 16, p. 187. Jacobson: Virch. Arch. 75, p. 349. 
224. J. E. Schmidt: Bruns Beitrage, 1912, V. 82. 
225. Posner: Berliner klin. Wochenschrft., 1905. Stilling: Ziegl. Beitr., 1894, V. 15. 
Matsuoka: Virch. Arch., 1903, V. 18c. Steinach: Zentralbl. f. Physiol., 1910, 
V. 24. Hanau: Pflugers Arch , 1897, V. 65. Goebell: Zentralbl. f. Path., 
1898. Berthold: Arch. f. Anat., 1849. 
226. Bogoljuboff: Arch. f. klin. Chir., V. 70 and 72. CHAPTER IX 
THE THYROID GLAND 
The attitude with which surgery has regarded the thyroid gland and 
its diseases has undergone a tremendous change in the last few decades, 
and the many surgical operations on the thyroid have contributed not a 
little toward directing our knowledge of the normal and the pathological 
physiology of this organ into the proper channels. 
In the beginning, it was chiefly the mechanical interference with 
breathing and circulation from enlargements of the thyroid, “goiter,” 
which led to operative interference. For cosmetic reasons, also, removal 
was desired. At first, the gland was usually removed in toto, but it 
was soon observed (i) that grave general disturbances followed this 
procedure (cachexia strumipriva, or thyreopriva). These unlooked-for 
occurrences showed that the thyroid has an important place in the econ- 
omy of the body, one which should be investigated and analysed (2). 
The older views concerning the functions of the thyroid are admir- 
ably discussed by Horsley (3) in the dedicatory volume to Vir- 
chow. Now, it can be definitely said that the thyroid is chiefly an organ 
of internal secretion even though the actual secretion has not as yet been 
demonstrated in the venous blood leaving the gland. Since ligation of 
all the veins leads to red infarction, this procedure is ineffectual in decid- 
ing the question of whether the secretion leaves by way of the blood or the 
lymph channels (4). From the gland substance itself, Baumann (5) 
isolated iodothyrin, an iodin-containing protein, which according to the 
investigations of Oswald (6) is only a decomposition product, while the 
actual secretion is iodothyreoglobulin, also an iodin-containing protein. 
According to the latter, this iodothyreoglobulin “possesses all the physio- 
logical peculiarities of the thyroid gland itself,” which is not true of the 
iodothyrin (7). Thus it favorably influences the cachexia strumipriva 
following extirpation as well as the myxedema of adults which results 
from failure of function. Furthermore, it increases the general oxidative 
processes of the body and acts on cardiac and vasomotor nerves. Finally, 
according to Koch (6), it increases the resistance of the body to methyl- 
cyanide, and has, therefore, a detoxifying activity also. In addition to 
the iodothyreoglobulin, cholin was found and a nucleoprotein was isolated 
(Oswald), which together with the iodothyreoglobulin represents the 
colloid of the anatomists. That the symptoms exhibited in man and ani- 
338 THE THYROID GLAND 
339 
mals in whom the thyroid has been removed or is functionless, are made 
to disappear in greater or less degree by the administration of iodothyreo- 
globulin indicates that the most obvious function of the thyroid is to 
secrete this substance, but the possibility that it has other duties to per- 
form should not be entirely forgotten. 
[Kendall’s isolation of a substance from the thyroid to which he has 
given the name “thyroxin” probably marks the final step in the purifica- 
tion of the active principle of the gland. As is well known, it has the 
physiological activities of the dried gland itself (8).] 
It has been mentioned that the thyroid was suspected of having some 
sort of detoxifying action (9) and it is possible that those manifestations, 
which are regarded as the result of extirpation of the gland, may be a 
poisoning by substances which ordinarily are rendered harmless. 
Undoubtedly, this question is extraordinarily complicated. It is known 
that thyroidectomized animals have little resistance to certain inorganic 
poisons such as bichloride of mercury (10). But on the other hand, 
Gottlieb (n) showed that such animals actually have an increased 
resistance to poisoning by morphine because they are better able to 
decompose it. 
Reid Hunt (12) found that white mice which had been fed with thyroid 
substance could withstand much better than normal animals acetonitril 
which acts as a cyanide in the body. He, however, does not conclude 
that these experiments show a detoxifying function of the thyroid. Tren- 
delenburg (13) believes such a power is indicated by experimental results 
from somewhat different methods. He fed his white mice, not with thy- 
roid substance, but with the blood of thyroidectomized cats. These 
mice were also able to withstand acetonitril better than the controls. 
Trendelenburg believes that there are substances in the blood of thyroidec- 
tomized animals which may be regarded as toxic products of cell metab- 
olism and that normally these are collected by the thyroid and rendered 
harmless. If this conclusion is to be adopted, however, it would be 
necessary that the blood of these cats contain lasting and always increas- 
ing amounts of these substances. This was not the case in Trendelen- 
burg’s experiments, the results were positive only when the blood was 
taken from 48 to 72 hours after the glands were extirpated. It must be 
admitted that none of the experiments to date have sufficiently proven 
that the symptoms following thyroidectomy can be regarded wholly or 
in part as the result of “poisoning” with substances which the thyroid 
normally destroys. The possibility, of course, should not be entirely 
forgotten. 
Investigations (14) have shown that changes in the sense of chronic 
or subacute inflammatory processes are found in the thyroid in infections 340 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
and intoxications, but how far the term “function’’may be applied in these 
conditions is not as yet known. 
Still less supported are other theories of the functional importance of 
the thyroid, particularly the one which regards it as a regulator of the 
blood supply of the brain. Some theories, such as its importance in 
blood formation and in the development of the sexual organs, can be 
explained sufficiently from the standpoint of internal secretion. They 
are undoubtedly based on correct observation, but the interpretation is 
usually somewhat one-sided. 
The nerve influencing secretion is the superior laryngeal. This was 
prettily demonstrated in the experiments of Asher and Flack (15) in 
which they found that stimulation increased the irritability of the vagus 
and depressor nerves, which otherwise occurs only after the injection of 
thyroid substance, moreover, these experiments are the only ones up to 
the present, which offer direct proof that thyroid secretion normally enters 
the blood stream. The rich nerve supply of the thyroid is shown in the 
anatomical investigations of Andreson (16). 
Even if it is assumed that the thyroid gives its secretion direct to the 
blood, it is still difficult to understand the manner in which it produces 
its effects on the body, for it increases the function of one organ and inhibits 
that of another, which facts point to an indirect rather than a direct action. 
The thought of some sort of a ferment has occurred. Mikulicz has used 
the pithy term “multiplier,” which means that this substance increases 
the general irritability and metabolism of the body. It is not known 
whether the effect is exerted through the nervous system or on the body 
cells themselves. 
It was the effect of total thyroid extirpation which was the principal 
stimulus to interest in the functions of the gland. The acute symptoms 
(tetany) are, of course, as later experiments showed, results of the removal 
of the parathyroids. A chronic cachexia thyreopriva is the only effect 
which can be considered due to thyroidectomy (1). The symptoms in 
children and adults are not entirely identical. In the former there are 
disturbances in growth and the general body development; the growth 
in height is particularly interfered with by defective ossification of the 
epiphyses; the genital organs remain small; puberty, if it occurs at all, 
is late. After extirpation of the gland in adults, menorrhagia in women 
and impotence or sterility in men have been observed. The skin mani- 
festations are peculiar and similar in all cases. It becomes doughy and 
edematous, and pale in color. Eppinger (17) showed that physiological 
saline solution is absorbed more slowly from the subcutaneous tissues 
in myxedema, but the cause of their dough-like consistency is not definitely 
known. A difference in the ability to distend has been spoken of (Biedl THE THYROID GLAND 
341 
io, p. 165). The hair becomes prematurely gray, dries and falls out. The 
general metabolism is decreased, the appetite is poor. In the beginning, 
according to the studies of v. Bergmann (18), there is an increase in weight, 
since there is a positive nitrogen balance. Gradually, loss of weight fol- 
lows with progressive emaciation and weakness, and death occurs not later 
than seven years after operation. At the same time there is a pronounced 
decrease of intelligence, and the patients gradually become total idiots. 
At autopsy, in addition to the emaciation, etc. the hypophysis is found 
enlarged from increase in the cellular elements and from hyperemia (19). 
This is found so consistently after failure of the thyroid that it indicates 
some relation between these two glands. In regard to the other endocrine 
organs, there is a decreased weight of the thymus in addition to the 
diminution in size of the genitalia. 
Animal experiments designed to study the effects of thyroidectomy 
give the same general results as in operative human cases (10), (20). 
In such experiments, it is better to use herbivorous animals because the 
parathyroids of carnivora are in such intimate contact with the thyroid 
that it is very difficult to remove it completely, without injuring or remov- 
ing the parathyroids (10), (21). But when the operation is successful, the 
results in carnivora are quite similar to those in herbivora with differences 
only in the details. Thus Biedl’s dogs showed very large thymus glands 
at autopsy while it is usually found diminished in size, as stated before. 
Furthermore, no psychical changes were observed in dogs, but these 
appear in herbivora just as in man. Young animals show disturbances 
of the growth in length similar to those in humans. The blood picture 
in both man and animals shows a decrease of erythrocytes and of hemoglo- 
bin and a coincident leucocytosis (22). Blood coagulation is delayed at 
first, but later the formation of coagula is abundant, with the fibrin appar- 
ently increased (10). These changes, suggestive of metabolic disturbances, 
have not been explained. 
With the removal of the thyroid in the young not only is the bone 
growth changed, but cellular growth in general becomes somewhat slug- 
gish. Fractures heal more slowly and the formation of callus as well as 
the reabsorption of it, is delayed (23). Marinesco and Minea and F. H. 
Walther (24) observed a markedly delayed degeneration and regeneration 
in crft nerves. Ordinary wounds in soft parts are supposed to heal more 
slowly (25). Furthermore, it has been found that certain disturbances 
occur in other internal secretory glands, as in the pancreas and in the 
chromaffin system; but these questions are still in the formative stage (26). 
The pure form of results and after effects of thyroidectomy are seen 
best in experimental removal of the gland and after the radical operation 
in man, for in the diseases considered sequellae of the failure of thyroid 342 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
secretion, there is always a complicated symptomatology because the 
lengthy absence of the thyroid brings into involvement other organs, 
especially the endocrine glands. Of the diseases which we relate to the 
absence of thyroid secretion, myxedema must be named first. In both 
cases, although the thyroid is absent or much atrophied, a differentiation 
between that of adults and the congenital type must be made. The 
clinical symptoms correspond perfectly with those of experimental thy- 
roidectomy. In children who are perfectly normal at birth and in whom 
the symptoms develop with increasing age, the predominant signs are 
mental dullness and defective bony development. In adults, the increas- 
ing dullness of intellect, and idiocy are the most prominent signs. Less 
severe cases often begin with lassitude and somnolence and mental inabil- 
ity. That all of these clinical symptoms result from the abolition or 
decrease of thyroid function is proven by the fact that the myxedema of 
adults is practically certain to improve or disappear after treatment with 
thyroid substance or by implantation of the gland (27). But the results 
of thyroid implantation in animals are not quite uniform. Enderlen 
(28) believes that the supply of colloid from the implanted gland is insuffi- 
cient, while Cristiani arrived at an opposite opinion and proved with 
Kummer that these glands actually enlarge and form a kind of new 
thyroid. 
In the myxedema of children the results are less satisfactory, which is 
due, according to the general view, to the marked involvement of the other 
endocrine glands which has taken place previous to the time treatment is 
begun. Indeed, it is quite possible that the myxedema of children is not 
merely a result of the absence of the thyroid, but that primarily other 
ductless glands are defective. First of all, absence or insufficiency of the 
thymus gland must be considered, because not only is the clinical course 
markedly different from that in adults, and from cachexia thyreopriva, 
but it shows many analogies to experimental thymus extirpation (29). 
Another disease complex considered due to thyroid insufficiency is 
endemic cretinism (30). By this is understood a mental deficiency disease 
of endemic form, with body changes corresponding to those described in 
myxedema. But cretinism is differentiated from myxedema by the 
fact that it is practically always, or in the majority of cases accompanied 
by goiter, and for this reason the problem is closely bound up with the 
goiter problem, and often simply identified with it. To what extent this 
is justified by our present knowledge, will be discussed later. Further 
marked differences between myxedema and cretinism can be found in the 
progressive character of myxedema, leading finally to death, while the 
cretin lives to a practically normal age. The retardation of bone growth 
also shows differences in the two diseases. In cretinism, it is irregular THE THYROID GLAND 
343 
with both a delay in bone building, and a premature ossification (Ewald 
(30)). That the thyroid function is defective in the myxedema of adults 
as well as in cretinism, is shown by the improvement in both diseases 
after treatment with the extract. Of course, this does not prove that the 
thyroid gland is necessarily the most essential factor in this pathological- 
physiological process; this can be stated positively only when we acquire 
better knowledge of the etiology of both diseases. Kutschera (27) classes 
as cretinism everything of a physical and mental underdevelopment which 
appears in the endemic area and is caused by the cretinogenic “influence,” 
justifying his viewpoint, from the fact that various disturbances in the 
endemic area are often simultaneous, especially in children of one family. 
He also emphasizes that cretinism does not exist without goiter, which is 
recognized now by practically all authors. But there is also an injury of 
the nervous system which probably is not dependent on the goiter, but 
is of equal importance. According to Kutschera again, the condition 
might possibly be an injury, arising from an infection, which acts primarily 
on the nervous system and this in its turn compels the thyroid gland to 
produce less secretion. This defective function may now produce new 
injuries to the nervous system and so on. 
At any rate, these statements show that goiter and cretinism are 
closely related. Or with reservations, a certain type of goiter must be 
etiologically considered together with cretinism, but whether the state- 
ments regarding its etiology hold good in the other goiters to be discussed, 
is difficult to say at present. The goiter problem has been approached 
thus far from only the endemic viewpoint and it remains an open ques- 
tion whether other goiters have a different etiology. 
Practically everything known in general pathology as a cause of disease, 
has been held responsible for the development of goiter, a sure sign that 
our actual knowledge in this matter is very meager. The difficulties 
begin when even a definition of goiter is attempted. It is, of course, 
generally understood that this implies an enlargement of the thyroid, and 
naturally that all pathological anatomical details are carefully investi- 
gated. But even, if we wish to draw conclusions of the type of anatomical 
and functional change in a gland from its microscopical preparation, 
insuperable difficulties are encountered, consisting chiefly of our inability 
to recognize the route and the degree of excretion from the gland. We 
cannot say whether an increased formation of secretion or excretion takes 
place, or if it is stored up; in other words, we do not know whether the 
picture in a given case is an expression of hyperfunction, or should be 
interpreted in the sense of tumor formation. In all probability we will 
not progress very far until the etiology becomes clear. The solution of 
this question is paramount. The pursuit has been along two roads, 344 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
viz., the production of goiters experimentally, and the study of their 
epidemiology. 
It is an ancient belief, shared by Hippocrates, that the drinking of 
water from certain wells caused goiter, but only recently have attempts 
been made to verify this by animal experimentation (31). At first, 
results seemed successful, but the more numerous the investigations, the 
more evident it became that conditions were far more complicated than 
had been imagined. In the first place, it was found that in those regions 
where goiter is endemic, animals develop them spontaneously. Experi- 
mental results obtained in these geographical localities cannot, therefore, 
be accepted without reservation. Animals kept there often showed actual 
endemics, although they received untainted water (for instance in Zurich). 
It was found that some of these animals occupied quarters formerly occu- 
pied by goitrous animals, and, moreover, that a newly arrived animal with 
goiter, “infected” the whole kennel. Possibly the lack of cleanliness 
and food soiled with feces (Bircher (31)) might have been the cause of such 
transmission, but control investigations proved that this conclusion was 
also erroneous. Grassi and Munason (10) kept their dogs in cages cleansed 
daily with disinfectants. The food and water was sterilized, but since 
they experimented in goiter regions, their animals developed enormous 
goiters. The same experiments undertaken in goiter free regions not only 
gave negative results, but showed that imported goitrous animals became 
goiter free. This is observed in man quite often. Furthermore, the fact 
that no goiter developed in animals if a trace of iodine was added to their 
water, gave rise to the belief that the lack of iodine caused goiter forma- 
tion, but neither this theory nor similar ones suggesting special chemical 
properties of goiter water, could be proven. 
Epidemiological investigations have given no better support to the 
“water-theory.” These were made chiefly by H. Bircher (32) who because 
of its prevalence in Switzerland supported the opinion that goiter w’as related 
to special geological formations. Supposedly it does not occur in volcanic 
formations, jura or chalk, or in rain water deposits, but is found with marine 
sediments of the palaeozoic, trias and tertiary ages. Kocher (33) pointed 
out that this classification could not be strictly maintained. Some authors 
such as Lobenhofer (34) thought they could strengthen Bircher’s theory 
by investigations in other goiter areas. But Hesse found that goiter 
free inhabitants in Switzerland lived among the same rock formations 
as those in Saxony who had much goiter, and vice versa (35). Bircher’s 
view, therefore, has no general value. Schittenhelm and Weichardt (36) 
also found that in Bavaria similar geological formations sometimes show 
goiter and sometimes not. Furthermore, the very accurate reinvestiga- 
tions of Dieterle, Hirschfeld and Klinger (37) over the same territory THE THYROID GLAND 
345 
investigated by Bircher, could not prove that the presence of goiter 
depends on such geological formations and their differences, when all of the 
population was examined. Furthermore, Bircher’s evidence for the 
water theory in a mass experiment which consisted of showing that a 
locality completely filled with goiter, became goiter free after switching 
the water supply from one to another geological formation, could not be 
confirmed by these re-investigations. It was found that part of this new 
water supply did not have its origin in primeval rocks, but came from 
marine deposits. Finally, a careful examination of all the population 
showed that the decrease of goiter in these localities was by no means as 
remarkable as it appeared from the military draft lists. 
Kutschera (27) working in Styria found that although certain houses 
were supplied by water from the same source, some of their inhabitants 
had goiter, and others none. He could also show how little the water 
theory applies, by other very interesting examples, as for instance, in his 
investigations of the “Tostenhuben” in Karnten. These are isolated 
houses in which, according to century old history (v. Fradeneck), all 
children and adults were cretins, having goiter also. Kutchera found that 
two of these Tostenhuben which had burned down in the meantime, and 
were rebuilt, harbored no more cretins. In one, it could be shown that a 
child born before the fire was a cretin, while all children born afterwards 
were normally developed. From a third, goiter disappeared after it had 
remained empty for 40 years. In all these cases the water supply had 
always remained the same. From those and other investigations carried 
out with remarkable accuracy Kutchera concluded, probably correctly, 
that goiter depends not on the water supply but on the social community, 
in other words, that it must imply infection from man to man, but from 
very close contact. Kutschera offers very interesting leads to this 
thought; for instance, Kostel reports that in former times the nobility 
in Wallis raised only their first born at home, and intentionally turned over 
the children born later to their cretin servants that these younger children 
might become cretins, and thus prevent scattering of the property. If 
children born of a cretin mother were removed and raised in a goiter free 
neighbor’s home, they developed normally. Kutschera could bring proof 
of his opinion even in animal experiments. He observed that a cretinous 
village pauper had great affection for dogs. Those dogs slept with her in 
a filthy bed consisting only of woolen rags, and were pronounced cretins. 
Kutschera took these dogs from the woman, giving her successively, 
several healthy young dogs to be cared for. These latter eventually 
became cretins and developed goiters. The rest of the same litter, 
which he kept himself, were normal. 
Unquestionably these careful investigations of Kutschera strengthen 346 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
the theory that goiter is an infectious disease, but no infectious factor 
has been demonstrated. Naturally, even less can be said of the place 
and mode of entrance of the infection. All statements, for instance, that 
infection arose in the intestines somewhat like the formation of a toxin, 
which the thyroid gland supposedly detoxified, or that it was only from a 
special mixture of intestinal bacteria, possibly influenced by special food, 
are still in the clouds. In Brazil, a trypanosome has been discovered as 
the cause of a special type of goiter (Chaga’s disease). 
Oswald’s finding, that in 84 per cent, of the inhabitants of Switzer- 
land, the thyroid gland has a greater weight than in regions free from 
goiter, will doubtless be of future value in the etiological study of the 
goiter problem. At present it cannot be properly interpreted. 
Mansfeld and Fr. Muller (38) concluded that a deficient oxygen supply 
may result in a functional change in the thyroid, because they found a 
decreased nitrogen elimination in rabbits which had been thyroidectomized 
and permitted to breathe for some time, in an atmosphere of diminished 
oxygen content. Normal rabbits, breathing the same atmosphere, 
conversely, showed increased nitrogen elimination. Surgically, these 
experiments are interesting since it might be concluded that mechanical 
obstruction to respiration, e.g., goiter, would suffice to stimulate hyper- 
function of the thyroid gland. But the work of Reich and Blauel (39), 
who produced tracheal stenosis in rats, has shown that such stenosis, on 
the contrary, leads to degenerative processes in the thyroid, and these 
experiments seem to justify the assumption that hypofunction and not 
hyperfunction is a result of respiratory resistance as we find it in goiter. 
Differences in thyroid function would occur according to the length of 
time respiration has been impeded. 
In contradistinction to diseases caused by hypofunction of the thyroid 
gland, are those which have recently been considered as due to excessive 
function, or hyperthyroidism (40). It is still undecided whether the 
disease complexes differentiated in this discussion are actually different 
forms, or only stages of one and the same disease, but knowledge of them 
has been considerably increased by operative treatment. The surgical 
point of view has been influenced by both the operative improvement in 
large numbers of cases of Basedow’s disease, and by the poor operative 
results in other cases; and finally, by the sudden death which sometimes 
occurs after operation. The beneficial results seemed to offer proof for 
the correctness of the theory of hyperthyroidism. The poor results and 
the deaths taught us that the problem is far more complex than was 
imagined. 
If we attempt to begin our study from the results of experiment, we 
find that little has been discovered (41). A healthy individual or an THE THYROID GLAND 
347 
animal may be fed with thyroid gland without developing exophthalmic 
goiter. In the common, and in the endemic goiter also, thyroid feeding 
leads very rarely to actual hyperthyroidism. Only one symptom appears 
at all consistently in these feeding and injection experiments and that is 
tachycardia. Iodine is more dangerous, if fed or injected, than thyroid 
gland-juice itself (42). It is often used in goiter, but it was found that this 
medication frequently leads to the disease complex usually called thyroid- 
ism, the chief symptoms of which are palpitation of the heart, tachycardia 
and general nervous excitement; furthermore it results in a decrease of 
the lymphocytes. Since surgeons show a tendency to consider these 
conditions as mild or incomplete forms of Basedow’s disease, it is some- 
times spoken of as an “iodine Basedow’s” (43). 
[The experimental work which has been performed with iodine has 
led to the brilliant results of Marine and his coworkers in the prevention 
of simple goiter in man. Working with the school children in Akron, 
Ohio, many of whom were either beginning to have, or would have devel- 
oped goiter according to the probabilities, they succeeded in not only 
reducing the ordinary incidence to practically negligible numbers, but in 
actually causing the goiter to disappear in one-third of the already devel- 
oped uncomplicated cases. The method is simple and consists merely 
in giving 2 grams of sodium iodide in small doses, twice yearly, at the 
age of puberty. The prevention of fetal and maternal thyroid enlarge- 
ments may be accomplished in a similar manner. The authors suggest 
that the first problem is essentially one of the public health, while the 
second more properly is a responsibility of individual physicians 
(44).] 
The action of iodine presumably causes an increased secretion of the 
gland, but we have no direct proof for this belief. At any rate, it must be 
emphasized especially that healthy individuals, and as stated, many people 
with endemic goiter, do not react in this manner to iodine, but that it is 
always single special types which develop these symptoms. This proves, 
just as the results of thyroid feeding, that, even if we assume that the 
gland increases its secretion for which, as must again be emphasized, we 
have only indirect proof, some sort of a second factor must be present if 
exophthalmus or thyroidism is to develop. The supposition of a hyper- 
secretion in view of the facts of experiment, does not suffice to explain the 
disease picture. The assumption was first made, principally through 
clinical observations, that exophthalmic goiter and related disease symp- 
toms, depend on increased secretion of thyroid gland tissue. Mobius (40) 
pointed out that there is a sharp distinction between myxedema and 
Basedow’s disease which can be followed in all details, and it was natural, 
with this contrast in the disease picture, to look for a contrast in the 348 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
etiology. Since it was recognized that myxedema is produced by a failure 
of the thyroid, Modius supposed that Basedow’s disease and related 
symptoms are due to excess of thyroid secretion. His theory seemed to 
be much strengthened by the results of operative removal. But it was not 
overlooked that quite a percentage of these patients were not cured or 
that only some symptoms were relieved even though considerable tissue 
was removed. 
Then it was assumed that the secretion was not merely excessive, but 
it entered the circulation in a changed form. The most varied investi- 
gations have been undertaken to demonstrate such a “ dysthyroidism ” 
(45) (40). The first procedure was to inject animals with the fluid ex- 
pressed from the goiters of Basedow’s disease and although isolated, posi- 
tive results were obtained, none of the workers could produce a typical 
Basedow’s disease, but only a few somewhat characteristic symptoms. 
According to Furth (41) tachycardia is the most constant symptom in 
hyperthyroidized animals. But the majority of the authors using similar 
experimental methods, observed only general symptoms of intoxication (43), 
(46) Klose, reporting experiments with dogs which had been in-bred for a 
long time and thus degenerated (fox-terriers), succeeded in inducing a 
typical Basedow’s disease with exophthalmus and tachycardia, by the 
injection of the pressed juice of extirpated exophthalmic goiter tissue. 
But Baruch (47) was not able to verify these findings. The results of 
Klose’s investigations have been interpreted with due care, but it is really 
very difficult to judge in an animal, whether symptoms are present which 
correspond to Basedow’s disease in man, and if the dogs did develop a 
true Basedow’s the statement of Oswald cannot be ignored, viz., that 
the result was achieved in degenerate dogs, perhaps as in humans, 
who react to iodine and increase of thyroid secretion with exophthalmic 
goiter. They may in some way have been predisposed to the disease. 
Oswald (6) also challenged the investigations of Walther and Hosemann 
(48) who believed that the thyroid gland of exophthalmic goiter contains 
a specific secretion, because nerve regeneration can be stimulated in thy- 
roidectomized animals with the juice of the ordinary thyroid gland, but 
not with that of exophthalmic goiter. In such examinations it must first 
be proved that a similar quantity of iodothyreoglobulin [(thyroxin)] 
is present in both glands. Even granted that the thyroid while in the 
body has supplied more secretion, it does not follow that it contains more 
within its substance, since it may have been excreted more rapidly. 
At present, therefore, it must be agreed with Magnus Levy (49) that the 
“question of ‘dysthyreosis’ has not been answered at all satisfactorily 
from a chemico-physiological viewpoint.” All statements made in this 
direction are purely speculative.” THE THYROID GLAND 
349 
If we accept that there is an increased thyroid secretion in exophthal- 
mic goiter, and such an assumption has much probability, there remains 
quite a number of symptoms such as exophthalmus and Grafe’s sign which 
cannot be explained as “functions” of the thyroid gland (50). 
To sum up: from all these statements, it can be concluded that in the 
disease complex of exophthalmic goiter the thyroid gland plays an import- 
ant part. Indeed it can be said that it is always enlarged. But it is not 
the only organ whose altered function determines the symptoms. Other 
organ systems such as the nervous system, and the endocrine glands are 
involved, and disease of the thyroid itself may depend on a primary 
disease of the central nervous system. 
The question of the way in which the nervous system is involved has not 
been cleared up, but certain starting points can be found in the mass of 
observations which we will presently discuss. The oldest theories con- 
sidered exophthalmic goiter an actual nervous disease, believing that a 
change in the sympathetic nerve occurred first, through pressure by the 
goiter. But the symptoms cannot be fully explained as either paral- 
ysis, or as pure overstimulation, or by a combination of stimulation and 
inhibition, although Claude Bernard did succeed in producing exophthal- 
mus in animals by stimulation of the sympathetic nerve. The same is true 
of the vagus nerve. Certainly in some of the symptoms such as vascular 
distention, the sympathetic must be involved; and in others, such as 
tachycardia, the vagus. But this does not justify the assumption that a 
lesion of these nerves is the principal factor in the disease complex. 
With its fluctuating, often unequally developed symptoms, exophthalmic 
goiter appears to be anything else but a circumscribed organic nervous 
lesion, quite apart from the fact that anatomical changes have never been 
discovered in nerve areas. Recently, quite a large number of authors 
distinguish a vagotonic and a sympatheticotonic exophthalmic goiter 
(51). The first shows less tachycardia with less exophthalmus, but sub- 
jectively, considerable cardiac disturbance, diarrhea, and sweating. In 
the sympatheticotonic type, marked tachycardia and exophthalmus are 
present with minor subjective cardiac trouble, but no diarrhea and sweat- 
ing. But this division unquestionably does not do justice to the clinical 
picture. It must be said with Hildebrand (52) “ that the types named are 
rarely seen in pure form, and that generally the symptoms are mixed.” 
The same objections may be brought against the investigations which 
aim to interpret exophthalmic goiter as an organic disease of the central 
nervous system (lit. Sattler (40)). Occasionally, it is possible to elicit such 
isolated Basedow symptoms as exophthalmus (53), tachycardia and similar 
signs, by injury of the medulla oblongata, but the typical disease has not 
been created. On the other hand, actual focal diseases of the medulla 350 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
develop quite different clinical symptoms. On the whole, neurology has 
practically abandoned the theory that it is a nervous disease of organic 
origin, with a circumscribed special location, but rather believes that there 
is a certain general inferiority of the nervous system. Neuroses, constitu- 
tional weakness, predisposition, are the terms with which these viewpoints, 
essentially similar, although differing in details, are characterized. With 
this assumption in mind it is then conceivable that this inferior nervous 
system is especially sensitive to excess thyroid secretion. It is true that 
in the acute variety (“ war-Basedow’s” (54)), which occasionally results 
from excitement or terror in individuals with previously healthy nervous 
systems, it is tempting to think of central stimulation of the secretory 
nerves of the thyroid, somewhat, in the manner as the experiments of 
Asher and Flack have shown. 
The theory, that other endocrine glands are also diseased, seemed to be 
more reasonable from experimental grounds. First the adrenals were 
suspected because part of the so-called Basedow phenomena such as 
tachycardia, exophthalmus, glycosuria a.o. are “adrenalin” symptoms 
(n). They point to stimulation of sympathetic fibres, and it was believed 
for some time, that an increase of adrenalin could be demonstrated in the 
blood (45), (55). But O. Connor (56) has shown that technical errors were 
made. Gottlieb (n) and Frohlich on the basis of these different consider- 
ations, came to the conclusion that because of increased thyroid secretion, 
the organs supplied by the sympathetics become especially sensitive to 
adrenalin. A similar action is known of cocain. According to investiga- 
tions of Kepinow (see Gottlieb), the hypophysis may also be involved in 
this sensitization of the sympathetic system. Furthermore, the experi- 
ments of Capelle and Bayer (57) have shown that adrenalin is not well 
tolerated by patients with Basedow’s disease. In those obscure cases of 
sudden death after operation for exophthalmic goiter (52) such adrenalin 
action may be suspected. In local anesthesia, patients almost always 
receive adrenalin, the action of which is increased if combined with cocain, 
as stated above. It is still an open question whether the number of deaths 
following operation is diminished if general anesthesia is used. Frank 
(58) showed that the tremors of exophthalmic goiter are probably similar 
to those seen normally after adrenalin injections. He speaks of a “sym- 
patheticogenic” tremor (see also “extremities”). But when all is said, 
this excessive adrenalin secretion theory cannot be reconciled very well 
with the observation of actual cases of combination of Basedow’s and 
Addison’s diseases in which the adrenals were absolutely destroyed by 
tuberculosis or atrophy (59). 
In a recent work of Hofstadter (60) our knowledge of the part played 
by the hypophysis, is collected. Three especial symptoms of this disease THE THYROID GLAND 
351 
are possibly related to the hypophysis, viz., polyuria, instability of body 
temperature, and the occasionally observed increased growth in height 
(61). But in this point also attempts are made at an explanation of only 
single symptoms and that on the basis of our other knowledge of the 
hypophysis and not with the direct proof that this gland secretes less or 
more than normal. 
Pettavel (62) describes a case of Basedow’s disease in which the patient 
had shown glycosuria, and changes in the islands of Langerhans could be 
demonstrated at autopsy. 
THE THYMUS GLAND 
The thymus, of all internal secretory glands, has gained much more 
practical importance in the exophthalmic goiter problem than the adrenals 
or hypophysis, since Garre (63) reported his case in which thyroidectomy 
produced no result, and cure was only effected by removal of an hyper- 
plastic thymus. On the basis of Garre’s information, other surgeons have 
removed the thymus in Basedow’s disease, and a number have reported 
cases in which, similar to Garre’s case, thymus removal alone brought 
about a cure or considerable improvement (64). But before we discuss 
this relation of the thymus more fully, we must consider what we know of 
the functions of this gland. 
Hammar’s (65) work tells of its morphology and development. From 
the anatomical standpoint, the fact that the thymus cannot be compared 
to a lymph node, on account of its epithelial ground substance, justifies 
the assumption that it is a secretory organ. Our knowledge of its physio- 
logical importance is based chiefly on extirpation experiments of which 
many have been done. (Full compilation and a critical review of the 
literature can be found in the collective references of Hart, Matti, Klose, 
Biedl, etc. (10), (66)). These experiments apparently give very irregular 
results, but this depends as a whole on technical errors, and after his 
review of the literature, Matti may be justified in concluding, “that 
of all works which report absolutely negative findings after thymus 
extirpation in mammalia, not one can withstand expert criticism.” 
Successful experiments depend above all on a complete and early removal, 
this means in quite young animals, for the function of this gland is exerted 
chiefly during earliest youth, and it is soon relieved or supported by other 
endocrine glands. Anatomically, this importance in metabolism, which 
decreases with advancing age, is shown by its relative greatest weight 
and measurements in earliest youth. In normal adults there is some 
tissue, mainly fat, in the place of the thymus. If then, the thymus has 
been completely removed from a dog or any other mammal during the first 
weeks of its life, the most remarkable symptom that will be observed is a 352 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
decrease of body weight as compared to that of others in the same litter. 
Certain fluctuations are present. The animals become bloated in appear- 
ance, and in the first two to three months, show more fur, so that they 
appear better nourished than the control animals (adipose stage). But 
this is misleading, because the total weight of the operated animal is 
always less than that of the controls. In spite of a good appetite, this 
difference becomes more and more marked during the following months. 
Soon it is noticed that the thymectomized animals, which have a rough 
coat, show retardation of growth, and this developmental check seems to 
affect the legs especially. They remain short, and the bones become 
crooked, with swollen, turgid epiphyses; the other skeletal bones also show 
arrested growth; the body remains small, and the skull appears broad and 
clumsy. If the bones are examined at this stage, they are found to be 
softer than those of a normal animal of similar age; and microscopically 
they show a picture similar to that of rickets. In fact, in all their details, the 
disturbances of endochondral ossification, the macroscopical swelling of 
the epiphyses of the bones of the legs, and the rosary, resemble rickets very 
markedly. These changes affect all the bones and in all parts of the 
skeleton lime free (osteoid) bone tissue can be demonstrated. 
The actual habitus of these thymectomized animals, in addition 
to the position forced by these “rachitic” bone changes, depends on 
a peculiar muscular atrophy or muscle degeneration which is especially 
pronounced in the muscles of the hind quarters. This makes the gait 
more insecure than if it were due only to the bone changes. In later 
stages, this muscle disease progresses to such an extent that the animals 
can hardly stand. The general nutrition becomes steadily worse, until 
death occurs from a most severe cachexia. Thus, it is chiefly a metabolic 
disturbance especially in regard to the calcium balance, which leads to the 
arrested development observed in thymectomized animals. In fowl, this 
disturbance of calcium metabolism is shown in that they often lay eggs 
with a shell deficient in lime, or without shell at all (66). At autopsy 
anatomical changes are found in the other endocrines, especially in the 
thyroid, adrenals and the generative glands. 
These findings again show that some correlation exists between the 
endocrine glands, but at present the relations are very obscure mainly 
because the findings are not uniform. The relations of the generative 
glands to the thymus are brought out even better by castration since after 
this procedure in young animals, normal thymus involution is delayed 
(see above). 
Experiments, to study the functions of this gland, more in detail, were 
made by the injection of thymus extract, or its juice, and by implantations 
(67), (66). The symptoms which appear can, of course, be considered THE THYROID GLAND 
353 
specific only if they give uniform results. The accidental findings recorded 
in such cases are practically valueless in respect to thymus function, for 
they are due to the action of toxins which are found, non-specifically, 
in many tissues. To these belong the disturbed general state of health, 
diminished appetite, loss of weight, pulse acceleration, etc. It is inter- 
esting that after extirpation of the thymus it is impossible to improve or 
eliminate the symptoms, by the injection of its juice intravenously or 
subcutaneously. Quite the contrary, the animals always show such severe 
toxic symptoms, that Klose and Vogt believe the treatment of thymectom- 
ized animals with thymus preparations accentuates the symptoms caused 
by the loss of the gland. This negative result is of great importance in 
our conception of the functions of the thymus. Without doubt, conditions 
are even more complicated than in the other endocrine glands from which 
it is possible to prepare a more or less pure substance, which, when admin- 
istered to other animals, deprived of the corresponding glands, replaces 
either completely or in part, the functions of the particular gland removed. 
To sum up: it is unknown whether the active substance of the thymus is 
in a form of pre-stage, or whether it is an especially sensitive ferment or 
pre-ferment, or finally, whether the function of this gland is perhaps quite 
different from that which we believe it to be. Investigations of the 
ferments have led to only very general results. 
Since we know so little of its normal function, it is clear that its 
function in disease is still more difficult to understand. This applies 
especially to its place in the disease complex of exophthalmic goiter (68). 
In the cases of sudden and unexpected death after thyroidectomy, an 
enlarged thymus is found not rarely at autopsy (Capelle, Klose). With 
such findings, it was first thought that the patient was asphyxiated. But 
since Garre reported the first cure of exophthalmic goiter by extirpation of 
the thymus, and a number of other authors achieved good results from 
this procedure, when thyroidectomy alone proved a failure, it was natural 
to assume that the thymus played a “chemical” part in the disease similar 
to that of the thyroid itself (thymogenous Basedow’s (69)). “The 
conditions for a future Basedow’s disease are laid down in the branchio- 
genic organs while the inciting mechanism starts in the nervous system.” 
Consequently, Hart differentiates between a thyrogenous, thymogenous 
and a thymo-thyrogenous exophthalmic goiter. But we must use great 
circumspection in evaluating the experiments in which investigators 
injected or implanted into animals thymus gland removed from patients 
with enlarged thymus or with exophthalmic goiters and who died with 
apoplectiform convulsions. All that was said above in regard to injection 
experiments holds good for these; it is always necessary to distinguish 
between the toxic action inherent in every tissue, from any specific action 354 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
which may possibly be present. The experiments of Bircher (67) are 
doubtless the most interesting, since he obtained a complete picture of 
Basedow’s disease in five dogs by means of Basedow-thymus. The 
animals, one of which is pictorially reproduced, developed in four days not 
only exophthalmus with other eye symptoms which disappeared com- 
pletely only after five months, but also tachycardia, tremors, and what is of 
exceptional interest, in four weeks they had developed soft goiters which 
persisted. Undoubtedly, these findings are very remarkable, and do not 
lose any value because other authors did not obtain similar results with 
similar experimental procedures. 
What these different results, these accidental findings, show is that 
the question of exophthalmic goiter is not simply a chemico-physiological 
one which can be disposed of by such terms as “ dysthyroidism ” or “dys- 
thymisation,” but that* the conditions are very complex indeed, and at 
present, by no means clear. It is most remarkable how the statements of 
different authors contradict each other in reference to success or failure 
from thymus extirpation in exophthalmic goiter. The last reports from 
even Garre’s clinic show that the failures from this operative method are 
many (70). Other surgeons refuse altogether to have faith in this pro- 
cedure. Indeed Melchior believes that the statement made above that 
death following exophthalmic goiter operation is due to the thymus, has 
been disproved for a long time by the facts (71). 
According to the reports of v. Haberer, there seems to be a regional 
difference in the involvement of thyroid and thymus in exophthalmic 
goiter. The microscopical investigations of Klose have demonstrated 
certain typical recurring changes in the thymus in Basedow's disease. 
Timte'will show whether the conception “Basedow’s disease” can be 
sustained as a distinctive disease, or whether there is included merely a 
number of disease symptoms under this name, which, quite analogous to 
the term icterus, will be separated in time into quite different anatomically 
separate entities. 
Regarding the cardiac disturbances in Basedow’s disease and goiter 
see Krehl’s “The Basis of Symptoms.” From the viewpoint of the sur- 
geon, it can be stated that the cardiac disturbances considered partly a 
result of respiratory difficulty, are not relieved by removal of the respira- 
tory impediment (72). 
The thymus gland is concerned as cause of death not only in cases of 
exophthalmic goiter, but there are numerous reports of sudden deaths, 
generally in youthful individuals, who had no exophthalmic goiter, in 
which, at autopsy, no diseased condition was found except a thymus, 
remarkably large for the age of the patient (73). To the same group of 
“ thymus deaths ” belongs the sudden death in the newborn. In these cases, THE THYROID GLAND 
355 
it was suspected at first that a mechanical compression of the trachea by 
the thymus took place. It is true in children that the diameter of the 
upper thoracic aperture may be too small, and a rather large thymus may 
obstruct the lumen of the trachea, but it does not always depend on the 
weight of the thymus but rather in which direction its development takes 
place, i.e., whether it extends more in length than in breadth (Hotz). 
Many anatomists are quite skeptical of the possibility that the thymus 
may mechanically occlude the trachea, since at autopsy, pressure marks 
are found only rarely on the trachea, and the thymus usually has plenty 
of space in the anterior mediastinum. Undoubtedly, this question is still 
in abeyance (74). But from the clinical viewpoint, it must be admitted 
that in goiter as well, e.g., in the well known small type which dips transi- 
torily into the thorax—sudden severe dyspnea and attacks of asphyxia 
are often observed when astonishingly few findings on the trachea can be 
found at operation. Swellings of the mucosa, perhaps reflexly elicited, 
may possibly come into play, at least, it must be taken into consideration. 
Patients in whom chronic disturbances from tracheal narrowness are 
* 
observed often show an occasional disproportion, for some reason, in the 
space of the anterior mediastinum and in the size of the thymus. These 
disturbances are difficulty in swallowing, emphysema, and cardiac dis- 
turbances (75). If for any reason, a swelling of the thymus occurs, it is 
thought that a sudden acute obstruction of the trachea with asphyxia 
develops. In new born infants, such acute swelling of the thymus is 
observed chiefly from hemorrhage; in older children, it is more probably 
lymph stasis, or inflammatory changes during infectious diseases or 
coughing or, what is of special interest to the surgeon, during anesthesia. 
The compilation made by Klose, who collected 58 such cases up until 
1914, shows that such attacks of asphyxia or respiratory difficulty during 
operation are by no means rare. Without doubt, the number of cases 
which die without operation, must be much larger. 
As stated, the belief that death is due to mechanical factors alone, if 
the only post-mortem finding is a large thymus, is often received very 
sceptically, and it prompts the observer to think more of a physiological- 
chemical eleprent, disturbances in the equilibrium of the endocrine glands, 
sudden toxemias affecting the heart, etc. Paltauf (76) first pointed this 
out. According to his opinion there is found in such cases a combination 
of enlarged thymus, and enlarged lymph nodes, and he believes that a 
special constitutional anomaly exists (status thymolymphaticus) which 
perverts the function of other organs, especially that of the heart. Thus 
the death in individuals with status thymolymphaticus would have to be 
considered a heart death, and not asphyxia (77). This doctrine has its 
special justification in explaining sudden death in adults, in whom the 356 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
space in the upper chest aperture is such that it is improbable that the 
thymus can produce a mechanical closure of the respiratory channels, even 
if the gland had not undergone normal involution. Of course, it must be 
pointed out that Paltauf’s teaching of the coexistence of enlarged thymus 
and enlarged lymph nodes is incorrect (Hart, Matti a.o.); on the contrary 
this combination is observed very rarely. But it does not invalidate the 
reasoning in Paltauf’s teaching, i.e., that some physiological chemical 
factor is at fault if an enlarged thymus is found at autopsy. We do not 
know, however, to what this fault is due. 
The investigations of Barbarossa (78), who showed that animals 
without a thymus, are especially resistant to chloroform, and conversely, 
that after thymus injections the resistance is lowered, leads to the thought 
of a flooding of the organism with thymus secretion in such sudden deaths. 
But on the other hand, other experiments with thymus extirpation and 
thymus juice injection have shown so few positive results, that the 
answer to this question must be reserved. Because patients with enlarged 
thymus often have a hypoplastic chromafline system, with fatty degenera- 
tion, and decrease of the chromaffine cells of the adrenal medulla, other 
writers assume that there is a sudden failure of adrenalin in such cases. 
Since Wiesel, Schmorl and Ingier (79) proved that the adrenalin content 
of the blood is decreased by the anesthetic, it is thought that in people 
with enlarged thymus, i.e., with a hypoplastic adrenal medulla, the 
decrease of adrenalin content finally leads to a catastrophe. To avoid 
this, Delbet (80), who carried out extensive investigations on this point, 
gives his patients adrenalin subcutaneously, before operation, with 
supposedly good results. But bearing in mind the statements made on a 
preceding page regarding adrenalin action in Basedow’s disease, this 
injection must be made with due precautions. 
If it is desired to consider these questions on the basis of clinical 
evidence, it must first be emphasized that the deaths occurring with 
enlarged thymus or enlarged lymphatic apparatus are not always similar. 
But no differences that are consistent can be demonstrated in the cases 
with enlarged thymus as contrasted with those with enlarged lymph- 
nodes. 
The type of death in status thymolymphaticus during anesthesia 
is sudden, often occurring after a few inhalations of chloroform. It is 
often observed in excited individuals, corresponding to observations in 
ordinary life in which people suddenly drop dead after powerful psychic 
disturbances, excitement, etc. (81). Patients, who die in this manner, 
suddenly, at the commencement of anesthesia, succumb from heart 
conditions of the type Hering (82) has described and named as “seconds- 
heart-death.” THE THYROID GLAND 
357 
In another group of cases, death does not occur immediately after or 
during anesthesia, but hours, even days, later. I observed such a case 
in a child after an ordinary uncomplicated operation for hernia. The 
child, a sturdy, perhaps somewhat fat boy, of about four years, did not 
recover after the operation which had not lasted very long. He 
remained in a comatose condition, the pulse was poor from the time 
of operation, and after increasing coma, death took place within 48 hours. 
At autopsy, in addition to a marked status thymolymphaticus, with 
exceptionally large lymph nodes in the abdominal cavity, central necrosis 
and fatty degeneration of the liver were seen. The clinical picture 
recalled the Eck’s fistula dogs reported by Fischler (83). 
The deaths after operation in Basedow’s disease may be similarly 
delayed. It is unusual for patients to die immediately after operation, 
but most often in the evening following, or on the next day. In this 
case also the chief symptom is heart failure, the pulse is very rapid and 
not every beat reaches the periphery; finally there is only fibrillation. 
The hum over the heart, described by Hering as characteristic of “seconds- 
heart-death,” can occasionally be demonstrated in such individuals when 
in extremis (84). The high temperature may in part be explained by the 
restlessness, in part, like all temperature increases after thyroidectomy, 
as absorption fever, bronchitis, or slight wound infection, but whether 
they fully explain these high temperatures is, of course, undecided. Adler 
(85) has discovered interesting relations of the thyroid gland to tempera- 
ture regulation. There are certain changes in the thyroid in hibernating 
animals and he obtained a rise in temperature from 7 to 8°C. to 34 to 
38° in them by the injection of thyroid extract and an increase of 
respiratory rate with awakening. According to Boldgreff (86) dogs whose 
thyroids and parathyroids are removed, lose the faculty of temperature 
regulation. 
Goiters which dip into the chest cavity, swellings, and tumors of the 
thymus, lead to compression symptoms in the mediastinum. The most 
essential function of the mediastinum is to “keep the track clear” (87) 
and allow a number of organs, essential to life, i.e., esophagus, trachea, 
large vessels, nerves, etc. to pass through. But the elasticity of the 
mediastinum is very slight, and, therefore, severe disturbances in these 
organs occur very quickly in space restricting processes. 
. The veins offer the least resistance to pressure, and the blood attempts 
to flow from the root of the superior vena cava by lateral channels into 
the inferior# vena cava. If the lumen of the azygos vein, situated in the 
posterior mediastinum, is free, which is often the case for a long time, this 
channel is used. If it is obstructed the blood flows through the subcu- 
taneous veins which then appear as thick bluish red cords. For unknown 358 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
reasons, this distention does not occur in mediastinal tumors, and a 
uniform edema of the neck and upper chest results with bluish red dis- 
coloration of the skin (Stock’s collar). 
In addition to tumors, air collections in the mediastinum {mediastinal 
emphysema) may lead to such life-endangering conditions. Such a 
mediastinal emphysema may result from trauma, e.g., gun shot wounds, in 
whooping cough (88) and in operations, for instance, from incomplete 
closure of a bronchus after extirpation of a lobe of a lung (89). 
Compression of the vagus nerve leads either to tachycardia (inhibition) 
or to bradycardia (stimulation). Paralysis of the recurrent nerve is a 
diagnostic sign of practical importance in a space decreasing mediastinal 
process. 
The difficulty in breathing in mediastinal tumors is explained by the 
obstruction of the trachea or bronchi and is perhaps increased by an 
edema of the affected portion of the mucous membrane, and by lymph 
stasis. The effects of this difficulty in breathing on the lungs and the 
body generally, will be discussed later. 
The abundant lymph channels and the large lymph spaces of the medi- 
astinum are probably also involved in the compression, but the free anasto- 
moses prevent excessive stasis. But wide dilatation of the lymph channels 
becomes dangerous when infection appears, which may arise when a 
phlegmon in the neck or other neighboring situations spreads to the 
mediastinum. These are usually fatal, since the septic process is able to 
spread rapidly and unhindered. In chronic inflammatory processes, 
extensive connective tissue increase occurs which may clinically simulate 
tumor formation (90). 
The second function of the mediastinum, that of partition between 
the two halves of the thorax, is from a practical surgical standpoint, of 
great importance in the operative procedures which disturb the equi- 
librium of the thoracic organs to the right or left (pneumothorax, thoraco- 
plasty). If the mediastinum becomes too freely movable, mediastinal 
flutter occurs (91). The structural arrangement varies in different species 
of animals. The dog’s mediastinum is very movable, while that of the 
rabbit on account of its greater breadth, is more rigid. When pneumo- 
thorax is produced in a dog, every inspiration pulls the mediastinum and 
the heart toward the closed side. During expiration, it bulges sharply 
toward the pneumothorax. 
The lung oscillates to and fro but carries on no respiratory movements. 
In this way, the gas exchange is completely absent in the lung, even though 
the pneumothorax has not produced cessation of movement. The animal, 
therefore, becomes deeply cyanosed and suffocates in a few moments. 
In rabbits, goats, and other animals, in which the mediastinum is not as THE THYROID GLAND 
359 
movable as in the dog, it is not pulled completely over and against the 
breathing lung during each inspiration so that the breathing of these 
animals is interfered with very little. The rigidity of the human mediasti- 
num lies between that of the dog and rabbit. There are, of course, indi- 
vidual differences which depend on previous inflammatory processes in 
the adjacent pleura, which may increase the rigidity. In cases of exten- 
sive thoracoplasty, this mediastinal flutter can be observed directly in the 
so-called “paradox respiration” (92). The chest wall, from which the 
bones have been removed, is pulled in during inspiration and expanded 
during expiration. 
THE PARATHYROID GLANDS 
The parathyroid glands, which were discovered by Sandstroem in 
1880, are in close anatomical relationship to the thyroid (93). Experi- 
ments have shown beyond doubt, that the extirpation of all the para- 
thyroid tissue leads to grave and fatal tetany (94) (21). The rat lends 
itself very favorably to these experiments, because its parathyroids are 
separate from the thyroid gland and they may be injured or extirpated 
without disturbing the latter structure. This is important, for up until 
about 20 years ago, tetany, particularly that occurring after goiter opera- 
tions, was believed to be due to removal of thyroid tissue. Today it 
can be stated, not only on the basis of these experimental results, but also 
from the anatomical investigations of Erdheim who showed by serial 
sections, that the parathyroids were injured or absent in human tetany, 
that tetany in every case is a result of the failure of function or the absence 
of the parathyroids. Obviously, the degree of tetany depends on the 
relative amount of parathyroid tissue which is destroyed. 
After operation, the most severe symptoms are seen in the acute 
variety, in which the patient a short time after thyroidectomy—perhaps 
in a few hours—develops strong, convulsive spasms with more or less 
asphyxia, diaphragmatic spasm, great increase in muscle irritability 
(Chvostek’s phenomenon), greatly accelerated heart action, high temper- 
ature, etc. This acute tetany generally ends in death in a few hours, but 
fortunately such cases are extremely rare, and doubt may arise from the 
clinical picture that it is a true tetany. The diagnosis is usually made 
because the symptoms followed an operation for goiter and so it is possible 
that many of the published cases are something entirely different. 
The type more frequently encountered, runs a more chronic course and 
usually begins several days after operation. The symptoms, in general, 
are milder; the spasms are not clonic, but tonic; certain muscles are espe- 
cially involved, so that, e.g., the hand assumes the so-called obstetrical 
position. These patients usually recover, and for this reason the assump- 360 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
tion is made either that not all of the parathyroid tissue had been removed, 
or that it had been only injured. Another possibility has been discovered 
by the investigations of Erdheim, who frequently found accessory para- 
thyroids capable of function in the anterior mediastinum, embedded in 
thymus substance, or along the ascending arch of the aorta. V. Eiselberg 
(95) describes such a case with a very interesting Mstory. The patient, 
a woman, had had mild attacks of tetany for years following total extir- 
pation of the thyroid gland. These attacks disappeared after some time. 
Years later, she developed a tumor behind the upper part of the sternum 
which v. Eiselberg removed with great difficulty. Severe tetany promptly 
developed. The tumor proved to be an alveolar carcinoma, but it could 
not be determined whether its origin was a parathyroid gland or some other 
structure, and whether in growing it destroyed accessory parathyroid 
tissue in the anterior mediastinum. 
In addition to the spasms, certain trophic disturbances have been 
observed in the more chronic forms which find expression in such changes in 
the teeth as increased growth in length, increased grinding down, and 
changes in their position, which in animals may interfere sufficiently to 
cause starvation. Alterations in bones closely resembling rickets have 
been described (96); fractures heal more slowly; the callous is exceptionally 
poor in lime salts. In man, the development of cataract has occasionally 
been observed. 
If the patient recover from the acute symptoms, particularly from the 
spasms, there remains for a long time or permanently, a “latent tetany.” 
That is, these individuals are predisposed to spasms which may arise from 
causes which in normal persons would produce no effects. These spasms 
need not be generalized, but may affect particular muscle groups (laryngo- 
spasm, etc.; latent symptoms according to Trousseau, Chvostick, Meinert, 
and others (97)). Since the same phenomena are observed in animals 
when only a part of the parathyroid apparatus is removed, this experi- 
mental “latent tetany” was regarded with great interest because it seemed 
that more knowledge could be gained of those diseases in which spontane- 
ous spasms arise (98). Among them are the tetany of pregnancy (Frankl- 
Hochwart), perhaps eclampsia; the tetany of infectious diseases and 
toxemias; the so-called gastric tetany, and the tetany in children, 
i.e., spasmophilia. 
That pregnant animals, after partial removal of the parathyroids, 
develop tetany very readily is shown in the experiments of Adler and 
Thaler (94). The investigations of Iselin (96) come under this heading. 
He could show that the offspring of parathyroidectomized pregnant rats 
are very sensitive to injuries of the parathyroids and that they quickly 
die with the symptoms of the most acute form of tetany. Haberfeld (99) THE THYROID GLAND 
361 
could demonstrate changes such as sclerosis, round cell infiltration, cyst 
formation or atrophy in all four parathyroids in a case of tetany in preg- 
nancy. Meinert (97) among others, describes a human case of tetany in 
pregnancy. In confirmation of the experimental findings of Iselin, 
just mentioned, the child of this woman developed spasms and died 
early. 
There are a number of isolated observations of tetany occurring in 
infectious diseases, such as those of Moller (10), who found miliary tuber- 
cles in the parathyroid glands. 
Another form which is probably related to poisoning with ergot is the 
so-called occupation tetany which occurs periodically among workers in 
various trades who have their own small shops (cobbler spasm and so on, 
Frankl-Hochwart). In Vienna, this is observed particularly in the 
months from January to March when the Russian rye from the last 
harvest is being used. After March the toxicity of the ergot seems to 
become diminished. The possibility, however, that an “endemic poison” 
such as occurs in cretinism, plays a role cannot be entirely excluded (77). 
Thus far, it has not been possible to examine this view experimentally. 
The tetany which is occasionally seen in peritonitis probably belongs 
to the same group as that in infectious diseases, or in toxemias (100). 
It has been observed, as Bircher points out, only in diffuse peritonitis, 
as, for example, in perforating appendicitis. Anatomical changes in the 
parathyroid glands have not been found up until now so that it is always 
questionable whether there is an injury to the parathyroid glands through 
the absorption of poisons or bacteria from the peritoneum, or whether 
there is a reflexly produced hypofunction, or whether, perhaps, it is some- 
thing entirely different. The similarity of the disease picture, at any 
rate, points to the conclusion that the parathyroid glands are concerned 
in some manner. 
The same may be said of the tetany in diseases of the stomach asso- 
ciated with obstruction (tetania gastrica) (101), (100), but in this case as 
well, it is only the similarity of symptoms which points to participation 
by the parathyroid glands, for even if Haberfeld (99) did find anatomical 
changes in them in one case, there are the negative findings of Erdheim 
and others in contradiction. Stasis and decomposition of stomach con- 
tents are certainly important, but in spite of all efforts, a cramp producing 
toxin could not be recovered from the contents. When the stasis is 
relieved by gastroenterostomy, the tetany disappears. An increased 
viscosity of the blood is said to be important (101). Just what part is 
played by the desiccation which results from inflammatory changes in the 
absorptive powers of the intestinal mucosa is not known with certainty, 
but the theory of desiccation as cause of the tetany has now been aban- 362 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
doned (102). A collective cause of stomach diseases and tetany has been 
ascribed to the vagus nerve. 
The tetany of children, which is now usually given the name of spasmo- 
philia or the spasmophilic diathesis, cannot be distinguished by clinical 
symptoms (103) from parathyroid tetany, even if anatomical lesions 
(hemorrhages, etc.) have been found in only a very few cases (104), (64). 
The increase of tetany in children in the spring of the year is interesting. 
According to Moro (105) all internal secretory glands are more active 
during this season, but this statement does not explain the fact. How 
much the development of spasms is influenced by inexpert artificial feeding 
is also unexplained at present, although it is of course easy to build up 
theories (106). The experiments of Iselin related above, show very 
prettily how the development of such a tendency to spasms in children 
may be visualized. 
Very little is known of the relations of the parathyroids to true epilepsy. 
The convulsions in the latter disease are entirely different from those in 
tetany. But new observations, time and again, seem to point to relation- 
ships between them, as for example, the changes in the dental enamel 
in epileptics (Redlich). Experimentally, epileptic attacks in addition 
to tetany, have been observed after removal of the parathyroids and 
certain parts of the brain (107). Clinical observations are also recorded 
in considerable numbers, in which coincident with and after tetany, 
epilepsy has developed, or in which a childhood spasmophilia was 
transformed into an epilepsy (lit. see Bauer (77), (108)). 
Further, myotonia has been brought into relation with the para- 
thyroids (109); myasthenia is regarded as due to a hyperactivity of the 
parathyroids (no) without, however, it having been possible to demon- 
strate myasthenic muscle reactions in animals with hyperfunctioning 
parathyroids (96); chorea minor, paralysis agitans, spatrachitis (108) 
(Curschmann), osteomalacia and ostitis deformans are other conditions 
which have been placed in the same category, the last two of which interest 
the surgeon particularly. But until now, at any rate, the anatomical findings 
have not been sufficient to justify the assumption of a definite relation 
between them and the parathyroids (hi). But what sort of a causal 
relationship could there be, especially between the parathyroids and 
tetany? The latter seems undoubtedly due to a toxemia, which can only 
be of endogenous origin, i.e., the toxins must be engendered within the 
organism itself. From this it must be assumed that the toxin, which can 
best be regarded as an intermediary product of metabolism, is detoxified 
by intact parathyroid glands. Search for this hypothetical substance 
has been made by numerous workers and by many methods. Biedl in 
his critical summary states that nothing certain is known of its composi- THE THYROID GLAND 
363 
tion, although he himself is inclined to think it is of the nature of amine 
bases. Under these conditions, it is important for the practitioner only 
to form an idea of the manner in which the parathyroids are able to bring 
about a detoxification. Two ways are possible. Either the toxic meta- 
bolic products are collected by the parathyroids and through conjugation 
or other means are rendered harmless (112), or the parathyroids secrete 
a substance—possibly a ferment—into the blood which detoxifies (113) or 
protects the organs attacked (nervous system) (108). 
The decision as to which is the correct one of these two theories, can 
be made by examining the results following the therapeutic transplanta- 
tion and feeding of parathyroid glands (114). There are a large number of 
such observations on record, which indicate that severe cases of tetany 
have been improved by such means. Experimentally, it has also been 
demonstrated that parathyroid transplants grow and function. After 
a certain time, they are destroyed but it is just this destruction which 
proves that their function consists in elaborating some sort of a secretion, 
and not in detoxifying by absorption and conjugation, the hypothetical 
poisonous metabolic products (115). That the transplantation can be 
done conveniently under local anesthesia has been demonstrated in the 
experiments of Passow (116). 
The subject, simple though it may seem from what has been said, is 
not as uncomplicated as it looks. Difficulties of explanation are offered 
especially by the fact that relief of symptoms of tetany has been brought 
about by the administration of preparations of the thyroid gland and of 
iodothyreoglobulin (Kocher). This again emphasizes the close relation- 
ship between the parathyroids and the thyroid as well as between other 
internal secretory glands (117). The latter proposition has been brought 
out by experiments such as those of Guleke, w'ho extirpated the thyroid 
and parathyroids in rabbits, with tetany as one of the results. When the 
adrenals were removed at the same time, no tetany developed, but when 
the thyroid was left intact, and the parathyroids and adrenals were both 
removed, tetany again occurred. This, what might be called antagonism 
demonstrable in the different glands of internal secretion, has been inter- 
preted by Guleke in this way: the adrenals and thyroid stimulate, while 
the parathyroids inhibit the sympathetic (see also Rudinger (98)). These 
reciprocal relations between the thyroid and parathyroids are shown 
further by the hypertrophy of the latter when the former is removed, and 
vice versa (Vassale and others). According to this, the functions of the 
thyroid and parathyroids would seem to be similar, and not antagonistic. 
The relation of tetany to the adrenals is further illustrated in an observa- 
tion of Th. Kocher, who saw tetany with bronzing of the skin after 
complete removal of the thyroid. In the present modest state of our knowl- 364 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
edge on this subject, however, it is probably better to adhere to the facts 
gained experimentally, than to draw too far-reaching conclusions from 
them. 
Many experiments such as extirpation of peripheral nerves, or of the 
spinal cord, have been performed to discover the parts of the body which 
are affected by this hypothetical poison (118). The interpretation of the 
results varies with the different authors; this much, however, seems certain, 
that the tetany toxin does not act on the muscles, but on separate parts 
of the higher nerve centers. The varying pictures in tetany can be best 
explained by such an hypothesis (108). That the sympathetic system 
has its own share in the process seems probable from the work of Falta 
and Kohn (117). 
A discussion of the relation of the parathyroids to calcium metabolism 
—a subject of interest to surgeons because of the bone changes following 
parathyroidectomy—may be found in Biedl (10). 
CAROTID GLAND 
Experimental investigations of the functional importance of the caro- 
tid gland have been stimulated by the occasional occurrence of tumors 
(119). Their results are not uniform. Schmidt obtained no consistent 
findings, either by'bilateral extirpation, or by implantation, so that, with 
Marchand, he is of the opinion, that the carotid gland is a rudimentary 
organ. On the other hand, Betke, who extirpated the carotid gland in 
cats after bilateral ligation of the common carotid artery, found not only 
bone changes reminding him of rickets, but changes in the marrowr and 
in the spleen. What changes were present in the thyroid, parathyroids 
and adrenals was not decided at the time of publishing this work. But 
possibly the bone changes mentioned depend on injuries to these organs. 
THE HEART 
The surgery of the heart is essentially the surgery of injuries. The 
widely accepted belief among the laity that an injury, such as a stab 
wound, is instantly fatal has been recognized as incorrect for a long time. 
Hyrtl has described, to mention an example, how a stag shot through the 
heart, swam across a large body of water. George Fischer published the 
first larger statistical work on this question, and showed that death 
occurred instantly in only 26 per cent, of the cases of heart injury, while 
perfect healing occurred in about n per cent, of the cases (122). Among 
these latter, a needle or a thorn were the instruments in seven instances; 
in five cases, a bullet remained lodged in the heart for years without giving 
rise to any trouble. THE THYROID GLAND 
365 
It had been shown in the early nineteenth century by Bretonneau, 
Larrey, and others (123) that piercing the heart of an animal with a needle 
produced no recognizable disturbance. According to the experiments 
of Kronecker and Schmey (124) it is only when the injury involves a 
certain region, viz., the bundle of Hiss, that sudden death occurs. How 
far this applies to man is not established as yet, but cases occur in which a 
lightning like death occurs in man after punctures (G. Fischer). 
The cause of death in cardiac injuries is quite involved. If there is 
no large wound to the exterior, the question of hemorrhage does not enter, 
because the heart is embarrassed and hindered in its movements by the 
blood poured into the pericardium long before the loss of blood makes 
itself felt. This is called “heart tamponade,” a pathological process 
known already to Morgagni (125). Experimental study of the effects 
of such an effusion into the pericardium has been made by many investiga- 
tors. After injecting oil into the exposed pericardial sac of dogs, the 
arterial pressure falls, and the venous pressure rises in proportion to the 
rise of pressure in the sac (126). According to Molitoris (127) the patho- 
logical processes are quite complicated even though they seem simple 
enough. Following slight injury, the blood pressure falls because of the 
pulling action of the blood in the pericardium and the increased pressure 
against the cardiac walls. At first, the fall in blood pressure is purely 
reflex, and is brought about by dilatation of peripheral vessels. The vagus 
is stimulated, and the heart rate becomes slower with the result that the 
outflow of blood from the wound in the heart is diminished and filling of 
the pericardium is slowed. Moreover, the rate of outflow of blood from 
the opening in the heart is influenced also by changes in the degree of 
expansion of the lungs, according to Sauerbruch (128), but this idea is not 
quite correct as has already been detailed. Can there not be a vagus 
irritation in this connection? 
That a wound in an animal’s heart can be closed by suture was shown 
quite early by Del Vecchio (cited by Barth). Many others have repeated 
these experiments and demonstrated that cardiac action is not disturbed 
by such a procedure (129). As is known, Rehn (130) was the first to 
successfully suture the heart in man. 
Injuries to the coronary arteries lead to heart tamponade just as 
wounds of the heart itself. The demonstration that they are not end 
arteries as Cohnheim believed, is very important in the question of their 
ligation. But'even if anastomoses between the two coronary arteries 
have been demonstrated by Hirsch, Spalteholtz and many others, the 
sudden ligation of one or the other is certainly not an entirely safe 
procedure. 
The numerous experiments have shown that ligation is borne differ- 366 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
ently by different animals; that certain points of ligation are more dan- 
gerous than others, and that in thrombotic occlusion of the coronaries, 
a great difference in results occurs if the occlusion is gradual or rapid 
(131). Unfortunately, a surgeon will not be able to practice the teachings 
of these experiments, but will be compelled to transfix and ligate the 
bleeding point under all circumstances. 
In serous pericarditis—one of the few affections of the heart which 
occasionally needs surgical interference—the danger of heart tamponade 
is not particularly great, in spite of large effusions because the fluid collects 
slowly and the pericardium can adapt itself to it. If paracentesis fails 
in such cases, a window may be cut in the pericardium, as Laewen (132) 
and others have described, to allow egress into the pleural cavity. 
Dry pericarditis is also occasionally adapted to operative interference, 
as was pointed out principally by Brauer (133). Among pericardial 
adhesions, the so-called massive internal ones between parietal and 
visceral pericardium often lead to complete obliteration of the pericardial 
sac. These require no operative procedures. But when the inflammatory 
process extends to the neighborhood and involves mediastinum, lungs, 
diaphragm, and sternum, so as to produce adhesions to the heart, it is 
often necessary to restore movability to these structures in order that the 
heart, which can scarcely beat, may be better able to contract (e.g., by 
extensively removing the ribs). 
The experiments of Goringstein (134) detail the manner and the paths 
by which foreign particles such as bacteria or dyes are absorbed from the 
pericardium. 
Blunt force may also produce varied wounds and injuries as can 
be determined from the experiments of Fischer (122), Schuster, Heiden- 
hain (135) and others. Autopsy investigations of this subject have been 
made by Barie (136). The facts are of occasional interest in the judgment 
of certain accident cases. Such trauma is also felt by the heart when 
attempts are made by massage, to bring the standing heart into activity. 
The anatomical changes found in this connection have been described by 
Bohm (137). There are more or less fine or coarse injuries to the muscle 
fibres. 
Leporski (138) has investigated the effects of light pressure and slight 
injury to the surface of the heart. He found that even a slight injury 
was followed by a fall in the blood pressure and later by fibrillation. 
LITERATURE TO THYROID 
1. Kocher: Arch. fr. klin. Chir., 1883, V. 29, p. 254. 
2. Vincent: Thyroid function summary, Ergebn. d. Physiol., 1911, V. 11. 
3. Horsley: Festschrift, f Virchow, Berlin, 1891; August Hirschwald, V. 1, p. 369. THE THYROID GLAND 
367 
4. Luthi: Mitteil. a. d. Grenzgebieten, V. 15. 
5. Baumann: Zeitschft. f. physiol. Chemie, 1896, V. 21 u. 22. 
6. Oswald: Die Schilddruse Leipzig, 1916, (Veit and Co.) (lit.). 
7. Gottlieb: Deutsche med. Wochenschft., 1896, p. 235. 
8. Kendall, E. C.: Collected papers of the Mayo Clinic, 1915, 7, 393; 1916, 8, 513; 
J. Biol. Chem., 1919, 39, 125. 
9 Notkin: Wiener med. Wochenschrift, 1896; Blum: Berlin, klin. Wochenschrft., 
1898. 
10. cit. by Biedl: lnnere. Sekretion 2 edit., 1913, Urban and Schwarzenberg. 
xi. Gottlieb: Deutsche med. Wochenschft., 1911, p. 2161. 
12. Reid Hunt: J. A. M. A. 1907. 
13. Trendelenburg: Biochem. Zeitschrft., 19x0, 29. 
14. Quervain: Mitteil. a.d. Grenzgebieten, Suppl., Vol. 1904. 
15. Asher and Flack: Zentralbl. f. Physiol., 1910, V. 24 u. Ziegl. Beitrage, 1910, 55. 
16. Andreson: Arch. f. Anat. u. Entwickelungs, 1894. Sarbach: Mitteil. a.d. 
Grenzgebieten, V. 15. 
17. Eppinger: Zur Pathologie u. Therapie d. menschl. Odems, Springers Verlag., 
1917. 
18. v. Bergmann: Zeitschrift. f. experim. Pathol., 1909, V. 5. 
19. Rogowitsch: Zieglers Beitrage, 1889, V. 4. 
20. Zietzschmann: Mitteil. a.d. Grenzgebieten, V. 19, p. 353. Lanz: Volkmanns 
Sammlung klin. Vortr., 1894. Rogowitsch: Arch. f. Physiol., 1888. Hof- 
meister: Bruns Beitrage, 1894, V. 11. v. Eiselsberg: Arch. f. klin. Chir., 1895, 
V. 49- . 
21. Hagenbach: Mitt. a.d. Grenzgebieten, 1907, V. 18. 
22. Falta: Handbuch d. inneren Medicin, 1912, V. 4, p. 445. Kottmann: Zeitschrift. 
f. klin. Med., 1910. 
23. Hanau: Arch. f. klin. Chir., V. 60, p. 247. Steinlein: Arch. f. klin. Chir., 1896, 60. 
Bayon: Verh. d. physik.-med. Ges. Wurzburg, 34-35. 
24. F. K. Walther: Deutsche Zeitschrift. f. Nervenheilkunde, 1909, 38. Marinesco 
and Minea: Compt. rend. Soc. Biol., 1910, 68. 
25. Eppinger: Mitteil. a. d. Grenzgebieten, 1918, Festschrift, f. v. Eiselsberg. 
26. Rudinger: Zeitschrift. f. klin. Med., 1908, 66. 
27. Magnus-Levy: Berliner, klin. Wochenschrift, 1903 u. Zeitschrift. f. klin. Med., 
1904, V. 52. v. Eiselsberg: Naturforschervers, 1913; Wiener med. Woch- 
enschrift, 1902. Kocher: Deutsche Zeitschrift. f. Chir., 1892, V. 34. Bircher: 
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Wochenschrift, 1909-1910, p. 771. Christiani and Kummer: Munchener med. 
Wochenschrift, 1906, p. 2377. 
28. Enderlen: Mitteil. a.d. Grenzgebieten, 1898, V. 3. 
29. Klose: Ergebn. d. Chir., 1914, V. 8, p. 274. 
30. Summary cf. Bircher: Ergebn. d. Chir., 1913, V. 5 u. Ergebn. d. Patholog., 1911, 
V. 13, Kutchera: Wien. klin. Wochenschft., 1909 u. 1910. Biedl: l.c. 
Dieterle, Jahrb. f. Kinderheilkunde, V. 64, p. 576. H. Bircher: v. Volkmanns 
Sammlung klin. Vort., 1890, No. 357. E. Bircher: Brun’s Beitrage, V. 89, 
p. 1. v. Eiselberg: Die Chirurgie d. Schilddruse in Deutsche Chirurgie, 38, 
V. 1. Ewald: in Nothnagels Handbuch, 1909. Hart: Berliner, klin. Wochen- 
schrift, 1917. Schlagenhaufer u. Wagner: v. Jauregg. Beitrage zur etiologie u. 
Patho logie d. endemischen. Kretinismus, Leipszig u. Wien., 1910. Isen- 
schmid: Med. Klink., 1917. Hirsch: Handbuch f.d. hist.-geographischen 
Pathologie, Stuttgart, 1883. 368 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
31. Breitner: Mitt. a.d. Grenzgebieten, 1912, V. 24 u. Wiener klin. Wochenschrift, 
1912. Blauel and Reich: Bruns Beitrage, V. 83. Schlagenhauer and Wagner: 
v. Jauregg Beitrage z. Aetiologie u. Pathol, d. endem. Kretinismus Leipzig and 
Wien, 1910. Wilms: Zentralbl. f. Chir., 1910 u. Deutsche med. Wochenschrft., 
1910. Bircher: Deutsche Zeitschft. f. Chir., 1910, V. 103; Zeitschft. f. exp. 
Path, and Ther., 1911; Med. Klinik., 1910; Zeitschr. f. Chir., V. 112. Hirsch- 
feld and Klinger: Munchener med. Wochenschrift, 13. 
32. H. Bircher: Der endemische Kropf. usw. Basel, 1883. 
33. Kocher: Vorkommen u. Verbreitung d. Kropfes inn. Kanton Bern., 1889. 
34. Lobenhofer: Mitteil. a.d. Grenzgebieten, 1912, V. 24. 
35. Hesse: Arch. f. klin. Med., 1911, V. 102, p. 217. 
36. Schittenhelm and Weichardt: Der endemische Kropf. Berlin., 1912. 
37. Dieterle, Hirschfeld and Klinger: Arch. f. Hyg., 1913, V. 81, p. 128. 
38. Mansfeld and Fr. Muller: Pflugers Arch., V. 143, p. 157. 
39. Reich and Blauel: Bruns Beitrage, V. 82. 
40. Summary c.f. Lattler: in Graefe-Samischs Handbuch d. Augenheilkunde, 1909, 
4. Mobius: in Nothnagels Handbuch, 1896, 22. Chvostek: in Enzyklopadie 
d. klin. Med. Julius Springer, 1917. Enlenburg: in Ziemssens Handbuch, 
1875, V. 12. Fr. Kraus: in Ebsteins Handbuch, 1899, V. 2. Magnus-Levy: 
in v. Noordens Handbuch, 1907, V. 2. Melchior: Ergebn. d. Chir., 1910, V. 1. 
41. Wendelstadt: Deutsche med. Wochenschrift, 1894. Lanz: Mittheil. a. d. Grenz- 
gebieten, 1901, V. 8 u. Deutsche med. Wochenschrift, 1895. Buschan: Deut- 
sche med. Wochenschrift, 1895. Furth: Ergebn. d. Physiol., 1909, V. 8 (lit.). 
42. v. Salis and Vogel: Mitteil. a.d. Grenzgebieten, V. 27, p. 275. 
43. Kocher: Arch. f. klin. Chir., 1910, V. 92. 
44. Marine, D., Kimball, O. P. and Rogoff, J. M.: “Prevention of simple goiter in 
man,” J. Lab. and Clin. Med., 1917, 3, 40; Arch. Int. Med., 1918, 22, 41; Arch. 
Int. Med., 1920, 25, 661; J. A. M. A., 1919, 73, 1873. 
45. Kraus and Friedenthal: Berlin. Klin. Wochenschrift, 1908, p. 1709. 
46. Passler: Mitt. a.d. Grenzgebieten, 1905, V. 14. Klose: Arch. f. Klin. Chir., 
V. 93, p. 649 u. Beitr. z. klin. Chir., 1912, V. 77, p. 601. Pfeiffer: Munchener 
med. Wochenschft., 1907, p. 1173. Schonborn: Arch. f. exp. Pathol, u. Pharmk., 
1909, V. 60. Schulze: Mitt. a.d. Grenzgebieten, 1907, V. 17. Gley: Journ. 
de physiol, et. de pathol. gen., 1911, p. 955. 
47. Baruch: Zentralbl. f. Chir., 1911 u. 1912. 
48. Walther and Hosemann: Zeitschrft. f. d. ges. Neurologie, 1914, V. 23, p. 98. 
49. Magnus Levy: Handbuch d. Path. d. Stoffwechsels (herausg. v. Noorden), V. 2, 
p. 1902. 
50. Fr. Kraus: Handbuch d. prakt. med. von W. Ebstein, 1899, V. 2, Morbus Basedow. 
51. Eppinger and Hess: Die Vagotonie in V. Noordens Sammulung klin. Abhandl., 
Berlin, 1910. 
52. Hildebrand: Arch. f. klin. Chir., 1918, in, p. 1. 
53. Filehne: Sitzungsbericht d. physik. med. Societat in Erlangen, 1877. 
54. Klose: Med. Klin., 1918, p. 1199. 
55. Fraenkel: Arch. f. exper. Pathol, and Pharmak., 1909, V. 60. 
56. O. Connor: Munchener Med. Wochenschrift, 1911. 
57. Capulle and Bayer: Bruns Beitrage d. klin. Chir., V. 72, u. 86. 
58. Frank: Berlin, klin. Wochenschrft., 1919, p. 1090. 
59. Roessle: Verhandl. d. Deutsch. Path., Ges., 1914. 
60. Hofstadter: Mitteil. a.d. Grenzgebieten, 1918, 31, p. 102. THE THYROID GLAND 
369 
61. Holmgren: Nord. med. Arch., 1909, u. 1910. 
62. Pettavel: Deutsche Zeitschrift. f. Chir., 1912, V. 116. 
63. Garre: Chirurgenkongress, 1911. 
64. Sauerbruch: cited by Hart. Med. Klinik., 1915, 1. Rehn: Arch. f. Klin. Chir., 
1906, V. 80. Capelle: Bruns Beitr., 1908, V. 58 u. 1911, V. 72; Munch, med. 
Wochenschrift, 1908, 2. v. Haberer: Arch. f. Klin. Chir., V. 109; Mitteil. 
a.d. Grenzgebieten, Volume 27. Klose: Neue deutsche Chir., 1912, 3 and 
Ergebn. d. Chir., 1914, V. 8. 
65. Hammar: Ergebn. d. Anat. u. Entwickelungsgeschichte, 1909, V. 19. 
66. Hart: Zentralbl. f.d. Grenzgebiete, 1909, V. 12. Ramzi and Tandler: Wiener. 
klin. Wochenschrift, 1909. Klose and Vogt: Arch. f. Klin. Chir., 1910, V. 92 
and Brun’s Beitr., 1910, V. 79. Nordmann: Berliner klin. Wochenschrift., 
1910. U. Soli: cit. by Matti. Matti: Mitteil. a.d. Grenzgebieten, 1912, V. 
24. Matti: Ergebn. d. inneren. Med., 19x3, V. 10. Basch: Jahrbuch f. 
Kinderheilkunde, 1906, V. 64 u. 1908, V. 68. 
67. Capelle and Bayer: Bruns Beitrage, 1911, V. 72. Popper: Akad. d. Wissen- 
schaften, Wien, 1905, 114. Svehla: Arch. f. exp. Path. u. Pharm., 1900, V. 43. 
Gebele: Bruns Beitrage, 1911, V. 76. Bircher: Zentralbl. f. Chir., 1912, No. 5. 
68. Morbus Basedow: collected ref. Glaserfeld. Mitteil. a. d. Grenzgebieten, V. 28. 
69. Hart: Arch. f. Klin. Chir., V. 104, p. 347 u. Virch. Arch., 1913, Vol. 214, Med. 
Klinik., 1915. 
70. Naegeli: Bruns Beitrage, V. 115. 
71. Melchior: Zentralbl. f.d. Grenzgebiete, 1912, Berliner klin. Wochenschrift, 1917 
u. 1919. 
72. Blauel, Muller and Schlager: Bruns Beitrage, 1909, V. 62. 
73. Wiesel: Ergebn. d. Pathologie, 1911, 2 part. Lit. see Friedjung: in Pfaundlers 
Schlossmanns Handbuch d. Kinderheilkunde, V. 3, 2 edit., 1910. 
74. Nissen: Brun’s Beitrage, V. 91, p. 694. 
75. Deneke: Deutsche Zeitschrift. f. Chir., 1909, 98. Ritter: Bruns Beitrage, V. 91, 
p. 689. Zesas: Deutsche Zeitschrift. f. Chir., V. 105 (lit.). Cohn: Mun- 
chener med. Wochenschrift, 1900 u. Deutsche Wochenschrift, 1901. Lange: 
Naturforscherversammlung, 1902. 
76. Paltauf: Wiener klin. Wochenschrift., 1889, 2; u. 1890, 3. 
77. Cf. also Bauer: Konstitutionelle Disposition zu inneren Krankheiten-Springers 
Verlag, 1917, also Wiesel im Handbuch der Neurologie, V. 4. 
78. Barbarossa: cit. by Matti, 66. 
79. Schmorl and Ingier: Deutsch. Arch. f. Klin. Med., 1911, V. 104. Wiesel: Hand- 
buch d. Neurologie, V. 4. 
80. Delbet: Rev. de chir., 1912, V. 32. 
81. Walz: Wurttenb. Korrespondenzbl., 1903, V. 15. 
82. Hering: Der Sekunden herz Tod. Springers Verlag, 1917. 
83. Fischler: Physiologie der Leber. Springers Verlag, 1916. 
84. Rost: Ueber agonale Blutgerinnung Zentralbl. f. Path., 1913, V. 24. 
85. Adler: Munchener med. Wochenschrift, 1919, p. 1039 and Pflugers Arch., 1916. 
86. Boldgreff: cited in Chirurgen kongress-Zentralbl. 4, p. 435. 
87. v. Bergmannt Handbuch d. inneren. Med., 1914, V. 2, Springers Verlag., Die 
Erkrankung d. Mediastinum. 
88. Fr. Muller: Berliner klin. Wochenschrift, 1881. 
- 89. Friedrich: Chirurgenkongress, 1907 u. 1908. 
90. Krall: Naturhist. med. Verein. Sekt. Heidelberg, 1913, Munchener. med. Wochen- 
schrift, 1913. 370 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
gi. Bruns: Beitrage z. Klinik. d. Tuberculose, V. 12. 
92. Sauerbruch-Elving: Die extrapleurale Thorakoplastik in Ergeb. d. inner. Med., 
1913, V. 10. 
93. Summary. Wirth: Zentralbl. f.d. Grenzgebiete, 1910, V. 13. Biedl: Innere 
Sekretion; Falta Die Erkrankung der Blutdrusen Springer, 1913. Phelps: 
“Tetanie,” in Levandowskys Handbuch d. Neurologie, 1913, V. 4. Rudinger: 
Ergebn. d. inn. Med., 1909, V. 2. v. Frankl: Hochwart in Nothnagels Handbuch, 
2, V. 11. Laudois: Die Epithelkorperchen in Ergebn. d. Chir., 1910, V. 1. 
Guelke: die Epithelkorperchen. Neue deutsche Chir., Lief., 9. Me Callum 
Ergebn. d. inneren Med., 1913, V. n. 
94. Vassale and Generali: Arch. ital. de Biol., 1896-1906, V. 25, 26, 33. Rouxeau: 
Compt. rend. Soc. de Biol., 1895, 1896, 1897. Erdheim: Wiener klin. Wochen- 
schrift., 1906, u. Frankfurter Zeitschrift. f. Path., 1911, V. 7. Gley: Arch, de 
Physiol., 1897 u. s Physiologenkongress Turin, 1901. 
95. Eiselsberg: Wiener klin. Wochenschrift, 1906 discussion of Erdheim’s paper. 
96. Iselin: Zentralbl. f. Chir., 1908 u. Neurolog Zentralbl., 1911. 
97. Meinert: Deutsche Zeitschrift. f. Chir., 1908, V. 93. 
98. Vassale: Arch. ital. de Biol., 1897, V. 30. Rudinger: Ergebn. d. inn. Med., 1909, 2. 
99. Haberfeld: Virch. Arch., 1911, V. 203. 
100. Holterhof: Deutsche med. Wochenschrft., 1913. Wirth: Zentralbl. f.d. Grenz- 
gebiete, V. 13. Bircher: Zentralbl. f. Chir., 1913. 
101. Wirth: Zentralbl. f.d. Grenzgebiete, 1910, V. 13. Kussmal: Arch. f. klin. Med., 
V. 6. Fleiner: Deutsche Zeitschrift f. Nervenheilkunde, 1900, V. 5; Arch. f. 
Verdauungskrankheiten, 1901, V. 5; Munchener Med. Wochenschrift., 1903. 
102. Jonas and Rudinger: WTiener Klin.-therap. Wochenschrft., 1904. Falta and Kahn: 
Ztschrft. f. klin. Med., 1911, 74. 
103. Finkelstein: Lehrbuch d. Sauglingskrankheiten, Berlin, 1911. Escherich: Mun- 
chener Med. Wochenschft., 1907. 
104. Erdheim: Ztschrft. f. Heilkunde, 1904, 25. Yanase: Wiener klin. Wchenschrft., 
1907. 
105. Moro: Munchener med. Wchenschrft., 1919. 
106. Wickmann: Handbuch d. Neurologie heraus. v. Lewandowsky, 1914, 5. 
107. Kreidl: Wiener klin. Wchenschrft., 1909, 869. 
108. Gratz: Neurol. Zentralblatt, 1913, p. 1366. Peritz: Ergebn. d. inneren Med., 
1911, 7. Curschmann: Deutsche Ztschrft. f. Nervenheilkunde, 1910, 39. 
109. Orzechowski: Jahrb. f. Psychiatrie, 1904, V. 29. 
no. Chvostek: Wiener klin. Wochenschrft., 1908, p. 37. 
in. Erdheim: Sitzungsbericht der Akademie, Wien, Math, naturw. Klasse, 1907. 
112. Wiener: Pflugers Arch. f. Physiol., 1909, 61. 
113. Medwedew: Ztschrft. f. physiol. Chemie, 1911, V. 72. 
114. Wiebrecht: Bruns Beitrage, V. 92. Schneider: Deutsche Ztschrft. f. Chir., V. 54. 
Krabbel: Bruns Beitrage, V. 72. Danielsen: Bruns Beitrage, V. 66. Eisels- 
berg: Beitrage z. physiol, u. Pathol. Festschrft. f. Hermann, 1908. Bircher: 
Med. Klinik., 1910. 
115. Eiselsberg: Wiener klin. Wochenschrft., 1892. 
116. Passow: Bruns Beitrage, V. 104, p. 343. 
117. Guleke: Arch. f. Klin. Chir., V. 94. Falta and Kahn: Ztschrft. f. Klin. Med., 
1911,V. 74. 
118. Lanz: v. Volkmann’s Sammulung, 1894. McCallum: Zentralblatt f. Pathol., 
1905, V. 76. Falta and Rudinger: Verh. d. 26 Kongr. f. inn. Med., 1909, 
Zentralbl. f. inn. Med., 1909, p. 548. THE THYROID GLAND 
371 
ng. Schmidt: Bruns Beitrage, V. 88. J. E. Schmidt, Betke: Bruns Beitrage, 1914, 95. 
Marchand: Festschrft. f. Virchow, 1891, V. 1. Monckeberg: Zieglers Beitrage, 
V. 38. Neuber: Arch. f. klin. Chir., V. 102. Kauffman and Ruppanner: 
Deutsche Ztschrft. f. Chir., V. 80. Paltauf: Zieglers Beitrage, V. n. CHAPTER X 
CHEST CAVITY 
The pathological physiology of the thoracic viscera is of constantly 
increasing importance to the surgeon for two reasons, first, because 
greater possibilities of operative interference in this cavity are at hand since 
the introduction of methods to control varying pressures; secondly, because 
the complications arising from diseases of the thoracic viscera, especially 
pneumonia, and cardiac weakness, often bring to naught the results of our 
best planned operative procedures. It can safely be said that since the 
spectre of post-operative suppuration has been vanquished by the intro- 
duction of asepsis, the chief danger to surgical patients arises in the tho- 
racic viscera. To control these complications is a most important task for 
operative surgery. 
The lungs are concerned in gaseous exchange (i). Inspired air, rich 
in oxygen, is changed by the diffusion of gases in the alveoli to an air rich 
in carbon dioxide. Bohr (2) opposing the purely physical theory of gas 
exchange, has suggested that the lungs absorb oxygen on the one hand and 
secrete carbonic acid on the other. But this theory, which has an analogue 
in the oxygen secretion in the swimming bladder of fishes, has not been 
accepted as normal for the respiration of warm blooded animals (3). But 
perhaps “secretion” does play some part when there is oxygen deficiency 
in the tissues (4). 
In the processes of inspiration and expiration, forces act on two places; 
on the lungs, and on the thoracic cage. The lungs themselves have a 
tendency to collapse and return to the condition as in the newborn, so 
that if the opposing forces acting on the thorax are removed in the living, 
as for example in pneumothorax, they collapse completely from the 
activity of their abundant elastic fibres (5). The force with which this 
collapse occurs can be appreciated from the pressure which must be 
applied, by high and low pressure apparatus in pneumothorax, to bring 
the lungs in contact again with the pleural parietes. According to Sauer- 
bruch (6) and Friedrich (6) it amounts to minus 7 mm. of mercury. 
This tendency to assume the position of maximum expiration is the 
chief force opposing those acting on the thorax. These latter are divided 
into elastic forces and muscle action. After the chest wall is opened at 
autopsy, not only do the lungs collapse, but the ribs immediately spring 
outward (Paul Bert cited by Minkowski), and give the impression that 
372 CHEST CAVITY 
373 
these elastic forces are important in the enlargement of the thorax (7). 
But this is unlikely, because the tonus of the respiratory musculature is 
the deciding factor in the living (Minkowski (n)). It can be seen 
during operations such as resections of the first rib for tuberculosis 
(Freund’s operation), or in extrapleural thoracoplasty, that the ribs 
spring apart as soon as they are severed from their attachments to the 
sternum, which shows that there is this elastic tension in the thorax, in 
the living as well. Nevertheless, in inspiration, the muscle power, i.e., the 
activity of the various costal elevators and the diaphragm is of greater 
importance. In man, the latter muscle is the most prominent of all in 
respiration. The so-called auxiliary inspiratory muscles operate either 
similarly to the costal elevators, or they increase the longitudinal diameter 
of the chest (the long muscles of the back). The diaphragm and the costal 
elevators usually work synergistically, but in some forms of poisoning 
(chloroform), disturbances in this synchronous action may occasionally 
occur, so that the diaphragm moves as in expiration while the thorax 
carries out an inspiratory movement (8). The chest muscles and the 
diaphragm are also interchangeable in their relative power, thus we find 
increased diaphragmatic respiration in fractures of the upper ribs, or 
after operations on the pleural wall, and conversely, in diaphragmatic 
paralysis as it occurs after operative section (9) or in “crutch” paralysis 
of the phrenic nerve (10) we find augmented thoracic respiration. Fur- 
thermore, a greater thoracic respiration is seen with the diminished diaph- 
ragmatic movement in pulmonary emphysema, pleuritis or pneumothorax, 
as well as in enteroptosis (n). 
The expiratory muscles need not be as powerful for two reasons, first, 
because the extended chest collapses on account of its weight after the 
muscle pull is released, and secondly, the ribs, extended upward and outward 
from the preceding inspiration, tend to assume the expiratory position 
again, principally because of the elasticity of the lungs. As expiratory 
muscles, the internal intercostals and the diaphragm come into play. The 
latter is forced toward the chest cavity more because of the intraabdominal 
pressure than because of active contraction. The extent of its movements 
depends, therefore, not only on muscular contraction, but on the elasticity 
of the lungs acting on the upper surface and the pressure of the abdominal 
organs on its lower surface. 
The importance of the abdominal muscles in the respiratory act must 
not be underestimated, for even though they are used but little in the 
superficial respiration, with which man usually contents himself, their 
non-use in bedfast patients because of the pain from a recent abdominal 
incision, leads to insufficient aeration, and favors hypostatic congestion 
and post-operative pneumonia. 374 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASE 
The transfer of the movements of the thoracic and diaphragmatic 
musculature to the lungs constitutes quite a remarkable mechanism. 
It results only because of the difference in pressure at the border of lungs 
and thoracic wall, which equals “ the sum of the stretching values which 
keep the lungs expanded beyond their elastic equilibrium” (12). In the 
cadaver this “tension difference” is apparent at once, for when the chest 
cavity is opened, the lungs collapse, and the thorax springs outward. 
But in the living, this tension difference is added to by the tissue tonus, 
i.e., the tonus of the lungs and the thoracic wall. For this reason, it is 
different at various places in the thorax, and is expressed in the so-called 
negative pressure of the pleural cavity (Donders), which can be measured 
by introducing a hollow needle. It must be remembered, however, that 
a pleural cavity with a negative pressure does not actually exist in life, 
but on all sides the lung is applied closely to the parietal pleural wall, 
leaving only a capillary space between (13). Burkhardt (14) points out 
that the conception of “negative pressure” has caused considerable con- 
fusion. “ The air flowing into the bronchi forces the lungs against the chest 
wall, and the chest wall presses against the lungs.” This is physically 
incontrovertible. The real difficulty of the question is to demonstrate 
what forces sustain the lung in its tension; especially what forces re-dis- 
tend a lung once collapsed. If we start by considering conditions as they 
exist in the newborn, we know that before respiration begins, the lungs 
lie collapsed in the posterior thoracic space, lateral to the spinal column. 
The negative pressure is absent, a fact of importance in medico-legal 
questions. The lung distends and becomes air containing with the first 
strong inspiration. It might be supposed that it would collapse with the 
next expiration, but the air remains in them. Why? According to Keller 
(15) the bronchioles collapse where they join the infundibula, and thus 
prevent the escape of air. But even if this statement is correct, it would 
explain only a minute part of the distention. At least, it would not 
explain the condition in adults. According to Hermann (16) the chest 
grows more rapidly than the thoracic organs, and a space is formed with 
decreased pressure within, viz., the pleural cavity. The necessary result 
of this decreased pressure would be distention of the lungs by air flowing 
inwards through the bronchi until they lie against the thoracic wall, and 
this notwithstanding the elastic forces present within. But what sus- 
tains the tension in the lungs before this difference in growth is developed 
has not been clearly answered. For the present, the pressure of the 
atmosphere on the bronchial tree must be held chiefly responsible, but 
the expiratory pressure is probably great enough under normal conditions 
to overcome the elasticity of the lungs (see Reineboth (17)). According to 
others, the capillary adhesion between lungs and chest wall, or more CHEST CAVITY 
375 
correctly, between the two surfaces of the pleura, is important also. We 
shall meet this factor again in discussing the re-expansion of a collapsed 
lung. Stovesand (18) believes this adhesive force is really not very great, 
although doubtless present, because when he opened the pleura in rabbits, 
even most carefully, the lungs collapsed at once. But Rosenbach (19) 
contradicts this statement, claiming that it is not easy to obtain a rapid 
and complete pneumothorax in animals by simply opening the pleura. 
This corresponds to observations on man. These capillary adhesions 
doubtless form gradually, and not with the first respiratory movement 
because the air filled lungs of a newborn child may collapse completely 
(20). Rosenbach (19) believes further that a vital tonus is responsible 
for this pulmonary tension, Sauerbruch (9) says it probably depends on 
the vagus. But this question cannot be disposed of by regarding it simply 
as a result of tissue tonus, and more work is needed. 
The respiratory movements aerating the lungs differ according to 
whether the individual is at rest or in motion. At work, not only are the 
respiratory movements increased, but the mean position which the lungs 
occupy is altered, i.e., in the final analysis, the tonus of the respiratory 
musculature is changed. To obtain a clear perception of these conditions, 
the residual air, or the air remaining constantly in the lungs is distinguished 
from the reserve air which can be expelled by the greatest expiratory effort. 
By the greatest inspiratory effort the complementary air is taken in. The 
mean capacity lies between these three values and is the difference between 
inspiration and expiration. It is influenced markedly by various patho- 
logical conditions (21). 
The respiratory movements are controlled by the respiratory centre 
situated in the medulla, which in its turn is stimulated by the carbonic 
acid content of the blood (see Minkowski (1) and Staehelin). When the 
vagus is cut, slow deep breathing results; normally, the respiratory center 
is controlled reflexly by this nerve (22). Each expansion of the lung dur- 
ing inspiration leads to expiration, each passive expiration to inspiration. 
According to Einthoven (23), the right vagus is of greater importance to 
respiration than the left, which is of more importance to the heart. But 
all other centripetal nerves, the facial, trifacial, olfactory, optic, and the 
sensory peripheral nerves, can participate in this regulation, and for this 
reason, fright, offensive odors, pain, etc. all affect respiration. 
It is far more difficult to understand why respiration should occur at 
such regular intervals than that the regulation of the respiratory center 
should occur through nerve tracts. The first factor to be considered is 
direct stimulation by the carbonic acid content of the venous blood. Ro- 
senthal (1) in 1862, found that a pause in respiration occurred—apnea— 
after increased ventilation, whether that was accomplished by bellows, 376 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
or by a few deep inspirations. This he accounted for by improved oxygen- 
ation of the blood from the deep breathing. But since it was shown that 
apnea also occurs when the same air is blown in over and over and thus 
increased in its carbon dioxide content, and that animals actually may 
perish from suffocation in these tests (Verworn), it cannot be the improved 
oxygenation which produced the apnea in Rosenthal’s experimental 
procedure. 
That conditions may occur in which oxygenation is the cause of apnea 
is shown in the fetus which, of course, does not breathe as long as its blood 
obtains sufficient oxygen through the placental circulation; and further- 
more, this was proved by Fredericq’s (24) experiment in which he con- 
ducted the blood of a dog, the lungs of which were ventilated to their 
maximum as in Rosenthal’s experiments, through the head of another dog. 
The second dog also became apneic. According to Hasselbach (25) 
a.o., it is not the carbon dioxide content, but the hydrogen ion concentra- 
tion of the blood which regulates the respiratory mechanism in this 
manner. But it is still an unsettled question whether these stimuli carried 
by the blood to the brain suffice to account for the rhythmicity of respira- 
tion. Sauerbruch (9) is of the opinion that the changing volume of the 
lungs is a stimulus through the vagus. This is conceivable, but does not 
explain the rhythmic respiration after vagus section, which, however, 
Minowski attempts to explain by a metabolic process occurring in the 
central nerve cell itself—“nutrition stimulus.” At any rate this “apnea” 
and its explanation is of great interest not only to the theorist, but even 
more so to the surgeon who encounters it often enough during anesthesia. 
[American and English physiologists have contributed a large share of 
the work on respiration. There is no doubt that the process is under the 
control both of the nervous system and of chemicals in the blood. The 
two gases, oxygen and carbon dioxide, seemed the logical stimulants, and 
so careful attention has been paid to their behavior under various con- 
ditions, and to separate their effects under standard conditions. If an 
animal is made to breathe carbon dioxide in increasing amounts, the 
oxygen concentration being maintained, respirations increase both in 
rate and amplitude in a very precise way. When the carbon dioxide 
content of the air has reached 5 or 6 per cent, the rate increases four or 
five times the normal. Since this increase in rate is proportional also to 
the concentration of free carbon dioxide in the blood, it seems that the 
effect is due directly to the action of the gas on the respiratory center and 
not reflexly from irritation, etc. of the respiratory passages. But increas- 
ing the carbon dioxide concentration in the blood also increases its acidity, 
i.e., the H ion concentration, and it may be this latter factor which pro- 
duces the effect. Scott alkalinized animals by injecting suitable doses of CHEST CAVITY 
377 
sodium bicarbonate intravenously, and then found in spite of a normal or 
decreased H ion concentration, that the breathing of carbon dioxide 
was followed by an increase in respiration. These experiments were done 
on decerebrate cats to avoid the errors induced by anesthetics. Further- 
more,, when acids other than carbonic acid, as for example, hydrochloric 
acid, are given intravenously, the same increase in respiration cannot be 
obtained, for death invariably occurs when a sufficient amount is given to 
increase the respirations equal to inspiring about 5 per cent, carbon dioxide. 
Carbon dioxide, therefore, has a specific stimulating effect on the respira- 
tory center in addition to its acid properties. The reason for this specific 
effect has been given by Jacobs who found it is related to the extra- 
ordinary ease with which it penetrates cell membranes and makes its 
presence felt within. After it has entered the cell, it may be that it acts 
by changing the H ion concentration; at any rate, it is enabled to exert 
its acidic powers much more quickly and readily than other acids, because 
of this penetrating ability. 
Considering the effect of oxygen, it is easily demonstrated that a 
decrease of its percentage in the inspired air will lead to rapid, shallow 
breathing. Deficiency in the blood may be brought about by two other 
means, viz., diminishing the amount of available hemoglobin to carry it, 
as in carbon monoxide poisoning, or diminishing the rate of blood flow 
through the lungs as occurs in decompensated heart disease. Barcroft 
has suggested that the terms anoxic, anemic and stagnant, respectively, 
be used to designate these three forms of anoxemia. 
As stated, when an anoxemia is begun, it leads to rapid, shallow breath- 
ing, which in its turn prevents adequate ventilation, so that, for example, 
an anemic anoxemia will have an anoxic anoxemia added to it, and so on 
in a veritable vicious circle. 
Finally, this rapid breathing will “wash out” carbon dioxide until the 
concentration of this substance in the blood becomes much lowered. 
This tends to “alkalosis,” which is compensated by the excretion of alkali 
in the urine, the conversion of more ammonia into urea, etc. Hyperpnea 
from any cause such as voluntarily, pain, or perhaps incomplete anesthesia, 
will also tend to this alkalosis, the condition being termed “acapnia” 
by Y. Henderson. When this alkalosis is established, or tends to be, the 
administration of carbon dioxide by inhalation would seem to be the 
logical procedure, but its use must be attended with caution (26) (see 
remarks and references on acid-base regulatory mechanism in section on 
kidney, page 290).! 
Furthermore, respiration has considerable influence on the blood 
distribution. It is generally understood that the negative pressure which 
occurs during inspiration leads to a sucking of the blood into the large 378 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
intrathoracic vessels, including the heart itself, without considering 
the pulmonary circulation. But from the very nature of the problem it 
has been possible thus far to bring only indirect proofs of this view. The 
#-ray observations of Hofbauer (27), as well as the anatomical investi- 
gations of Hasse (27), must be classed with these. The net result is, that 
various authors interpret the influence of respiration on peripheral circu- 
lation in quite different ways (28). Ledderhose (29) has discussed in 
detail the interesting inspiratory oscillations in the superficial veins which 
are of interest to surgeons, especially in varices. There is a contrast in the 
filling of the arm and leg veins, which is doubtlessly related to intra- 
abdominal conditions, i.e., diaphragmatic movements. At any rate, 
Eppinger and Hoffbauer (30) proved with plethysmographic measure- 
ments that the upward movement of the diaphragm decreased the volume 
of the leg and increased that of the arm. Be that as it may, that respir- 
ation has an influence on the circulation in the peripheral veins is undeni- 
able, since it can be observed at any time that the veins in the neck 
subside with deep inspiration and swell on compression. Minkowski (1) 
emphasizes that the increasing negative pressure when the heart is entering 
diastole and is easilv distensible, is also important. 
Our knowledge of the influence of respiration on the volume and rate 
of flow in the pulmonary vessels is even less definite. It must be stated in 
advance that Lichtheim (31) could demonstrate no change in the blood 
pressure when the pulmonary artery to one lung was ligated, a finding 
verified by Tigerstedt (32) and Gerhardt (32). But the latter succeeded 
in obtaining considerable increase of pressure in the right ventricle after 
experimental pulmonary fat embolism. According to this, the assump- 
tion entertained for some time, that the capillary network of the lungs 
was so extensive that resistances within them could hardly be capable of 
affecting the total lesser circulation—cannot be entirely true. But at the 
same time, it must be realized that the resistance in the pulmonary capil- 
laries is always exceptionally low, from which it follows that increase of 
blood pressure in the lesser circulation leads directly to an increase of the 
blood capacity of the lungs. Therefore, the lungs, in this relation, occupy 
a special position among the organs, because in a limb, or in any other 
organ, the result of increase of blood pressure is increased rate of blood 
flow, without increase in the actual quantity present at any one time 
(14). 
But in addition, the blood content of the lungs depends not only 
on the blood pressure maintained by the heart, but also on the pressure in 
the pulmonary blood vessels themselves, and then not only on that within 
the blood vessels, but also on the pressure in those outside of the lungs. 
This has been beautifully illustrated in the experiments of Jager (cited by CHEST CAVITY 
379 
Burkhardt). He placed lungs removed from the body, into an airtight 
glass container and regulated the pressures within the trachea, pulmonary 
vessels, and the space of the container, the latter representing the pleura. 
This procedure demonstrated that incorrect figures are obtained if the 
pressure in the pulmonary arteries and veins is not equalized with the 
pleural pressure. This factor has often been neglected. 
In the third place, the blood content of the lungs depends on the 
pressure within the alveoli. 
The values of these different factors necessarily change during inspira- 
tion and expiration, in pneumonic processes, in pleural exudates, or in 
pneumothorax. There is a difference of opinion, not completely recon- 
ciled, on whether a collapsed lung contains more blood than one distended 
with air. Ebert (33) calls attention to the necessity of differentiating 
between inspiration and expiration and the position in the inspiratory or 
the expiratory phase. Sackur (34) found less oxygen in the blood in the 
carotid arteries after complete collapse of a lung, from which he concluded 
that the collapsed lung in pneumothorax took up practically all of the 
blood in the lesser circulation, and it could not be oxygenated. There- 
fore, the animal asphyxiated. Sauerbruch (6) supported this idea, which 
has been given the name of “short circuit theory.” Unfortunately it 
has been proved incorrect. Brauer (35) very tellingly says the blood 
content is not proportional to the degree of distension of the lung, but to 
the pressure difference between pleura and bronchial tree. It is self 
evident in pneumothorax, that this difference is always less than normal, 
and the result must be greater compression of the capillaries with a dimin- 
ished amount of blood in the collapsed lung. Even the experiments of 
Cloetta (36) and Rohde (14) cannot alter this logic. As Burkhardt (14) 
points out, the pressure changes did not involve the large vessels in these 
experiments; therefore, the results, interesting though they are in detail, 
cannot be applied to pneumothorax (see previous page) and Bruns (37) 
showed in his experiments, that the blood content of the collapsed lung 
is demonstrably decreased after even a few seconds. Propping (38) 
reinvestigated this work and proved its correctness. Lohmann and Muller 
(39) arrived at similar results; by one experimental procedure they found 
no difference in the blood content of the collapsed and the aerated lung, 
while in another the blood content of the aerated lung was increased as 
compared to that of the collapsed lung. Gerhardt (32) investigated the 
effect of artificial exudates, and found that when small in amount, they 
did not impede the capillary circulation; it was only after exudates large 
enough to produce respiratory disturbances were formed, that resistance 
in the capillaries from increase of pressure in the lesser circulation was 
obtained. 380 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
During inspiration and expiration the conditions in the pulmonary 
circulation are exceedingly complex. Tendeloo (12) constructed a model 
of tubes intended to represent these blood vascular conditions. He 
concluded that the vessels are longer and less tortuous when the lungs are 
slightly expanded and this increases their capacity. With further dis- 
tention the vessels flatten out, which possibly lessens their total capacity. 
But in the complicated circulation in the pleural cavity, it would lead to 
wrong conclusions, if excess value were placed on any one factor, in this 
case, the capillary network of the lungs. Ebert (33) in his investigations, 
has avoided this one-sided viewpoint, and found that the pulmonary 
circulation is improved during inspiration, and impeded during expira- 
tion. Neither the air content of the lungs per se, nor the density or rarity 
of the air inspired, has an appreciable influence on the pulmonary circula- 
tion. These experimental results correspond very well with the prevailing 
opinion supported by Bohr, that the lungs are supplied with more blood 
during inspiration than during expiration. 
Regarding the changes in the circulation of the chest by increase in 
the intraalveolar pressure, i.e., with the third factor mentioned above, 
it was shown and can easily be recognized by anyone, that during cough- 
ing, or any act increasing abdominal pressure, as defecation, a swelling 
of the neck region occurs. This denotes an impeded venous return flow. 
Gerhardt and his pupil Romanoff (40) demonstrated in animals, that an 
increase of pressure of even 8 mm. mercury in the bronchial tree leads to 
such a severe impediment of the pulmonary circulation that not merely 
is the pressure in the pulmonary artery and in the jugular vein increased, 
but the pressure in the carotid artery falls. Pathological processes in 
which expiratory dyspnea occurs, as in chronic coughs, lead, therefore, to 
manifestations of congestion in the right ventricle (hypertrophy and 
dilatation (6), (41)). 
If the chest wall is suddenly opened without taking due precautions, 
the patient may collapse rapidly with urgent dyspnea. This may be 
designated as “ pleura-reflex.” Many workers have recently experimented 
exhaustively with this question (42). Accordingly, a large number of 
cases described as “pleural reflexes” may be considered as suffering from 
arterial air emboli (Brauer, see later). On the other hand, there is a 
possibility that reflexes can be incited from the pleura which possesses 
abundant modified Paccini bodies (43), but this reflex depends not only 
on the sensitivity of the pleural cavity, but also on that of the different 
parts of the lungs. Knowledge of these conditions has been considerably 
increased by operations under local anesthesia, in which it was found that 
the parietal and diaphragmatic pleurae are sensitive to pain everywhere 
while the visceral pleura possesses only a few sensitive areas (44). Tem- CHEST CAVITY 
381 
perature and tactile sense are entirely absent. Pain sensations of the 
parietal pleura can be differentiated from those of the skin (Hoffmann). 
The costal pleura seems to be the most sensitive part, for a mere touch 
quickly leads to blood pressure changes resulting from the pain which 
ensues. The lung parenchyma itself is insensitive to pain, the same is 
true of the branches of the pulmonary artery, and the distal ends of the 
bronchi, but cutting through the larger bronchi in man induces collapse. 
The pleura is also said to be able to induce cough reflexly (45). In fact, 
a sudden spasmodic, irrepressible cough is seen frequently in paracentesis 
or rib resection for empyema. Kohts (cited by Staehelin 46) has been 
able to induce cough from the pleura experimentally, and according 
to Frankel, a coughing spell can be produced in patients with pleuritis 
by light pressure on the intercostal spaces. 
According to experiments performed by Langendorff and Zander, 
and also by Cordier (cited by Zesas), the pleural reflex is supposed to 
depend on the vagus, and does not occur after it is cut. V. Saar could 
demonstrate that it is caused chiefly by stimulation of the pleural parietes 
(with exception of the diaphragm). According to prevalent opinion it 
is due to a mild, but long lasting form of pleural reflex in pleuritis, that 
contraction of the intercostal muscles takes place, which leads to the 
pulling in of the side of the chest. The rigidity of the abdominal walls 
in this disease is also considered a result of reflex action. 
How this supposed pleural reflex causes the sudden death in open pneu- 
mothorax must remain undecided for the present. A similar death occurs 
if one of the main bronchi is suddenly occluded. Lichtheim (5) in his 
verification of the experiments of Traube, observed that the lung becomes 
markedly distended and hyperemic when the main bronchus is obstructed. 
This might also obstruct the healthy lung, in which case these sudden 
deaths could be considered due to insufficient respiration. 
Dyspnea with open pneumothorax probably has no connection with 
the pleural reflex; at least it occurs in a similar manner when the vagus 
has been previously cut (Sackur). The elimination of one lung does not 
suffice to explain the condition, since it is known that in a resting individual 
with one-tenth of the respiratory surface active, no dyspnea occurs (Hof- 
bauer). There must be insufficient oxygenation of the venous pulmonary 
blood, for the oxygen content of the carotid blood falls considerably early 
in pneumothorax (Sackur, Bruns). In long continued cases, this dimin- 
ished oxygen content of the carotid blood is not so marked; it may even 
become normal after strenuous respiration, although it must be recognized 
that the blood flow through the collapsed lung is probably diminished. 
Sauerbruch, on the other hand, takes the stand, as stated above, that the 
collapsed lung is better supplied with blood than the distended lung; and 382 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
since the blood cannot be oxygenated in the former but must take up all 
its supply from the latter, it follows that the total arterial blood leaving 
the lungs is a mixture of oxygenated and non-oxygenated blood. We 
have already discussed this conception critically, and can only add that, 
according to general clinical experience, a closed unilateral pneumothorax 
does not cause the severe discomfort produced by an open one. Quite 
the contrary, tuberculous patients with their operative pneumothorax, are 
comparatively comfortable. 
The dyspnea with open pneumothorax, cannot then be explained 
by the elimination of the function of one collapsed lung, but resides in the 
fact that the healthy lung cannot perform its function perfectly with its 
partner in this condition. It is hindered first by a mediastinal flutter, 
and then by the “pendulum-air” (Brauer). This means that with every 
expiration, air is forced into the collapsed lung and with every inspiration 
is rebreathed into the healthy lung. Naturally, this air is soon used up 
and prevents sufficient fresh air from entering the normal lung. 
These respiratory disturbances here described are the chief symptoms 
in the disease picture of pneumothorax. In open pneumothorax they 
assume such an importance that the occurrence of this condition must be 
absolutely avoided. Fortunately not every small opening produces an 
instant complete pneumothorax as in the cadaver; but that from a moder- 
ately large opening becomes complete only after several inspirations 
(see p. 442) (47). 
The disturbances in the greater circulation are due chiefly to the fact 
that the increased pressure in the right ventricle and in the large veins 
disturbs the sucking up of the venous blood (Sauerbruch). 
At the time of its occurrence, there may be a passing pressure increase 
in the greater circulation, but as the experiments of Friedrich have shown, 
this pressure depends on the pressure within the pulmonary arteries 
(44). 
Experiments made in low pressure chambers showed that with the increase 
of the extrapulmonic pressure, the pressure in the pulmonary artery 
is also increased, and vice versa. 
Consequent to the decrease in the pressure differences between the 
bronchial tree and the pleura, the resistance in the lesser circulation is 
increased, which in turn produces an hypertrophy of the right ventricle, 
which can be demonstrated experimentally as well as clinically (37), (48). 
The flow of venous blood into the right heart may likewise be impeded, 
and this explains the cyanosis of such patients. Then, must be added, 
that through kinking of the mediastinum, the large vessels are mechanic- 
ally displaced, and the low position of the diaphragm impedes the outflow 
of the inferior vena cava. CHEST CAVITY 
383 
Nevertheless, clinical experience has shown that these circulatory 
disturbances assume dangerous proportions only with a pre-existing 
weakened myocardium. Hartl (99) has placed the body under higher 
pressure, and the head under normal pressure, and then studied these 
influences on the blood distribution. By this experimental procedure, 
the blood is forced into the lesser circulation, and blood pressure rises, a 
finding which might eventually be utilized in hemorrhage. 
If it is the removal of the pressure differences between the bronchial 
tree and the lung surface which leads to these severe disturbances, read- 
justing this pressure difference, either by increasing the pressure in the 
bronchial tree (increased pressure) or diminishing the pressure over the 
lung surface should remove these dangers (decreased pressure) (50). 
Frequent controversy resulted over the question of whether increased 
and decreased pressure were physiologically similar (51). According to 
the critical work of Burckhardt (14), this must be admitted absolutely 
for the stationary condition of the pressure difference, but by the intro- 
duction of the differentiation process, they are not similar. Schlesinger 
(52) in lung extirpations, has repeatedly obtained pneumothorax in the 
unoperated side. The cause is not quite clear, but he believes it is due 
to the higher pressure, because Sauerbruch and Robinson (53) saw nothing 
similar with decreased pressure. Robinson frequently observed a pleuritis 
in lung extirpation under increased pressure, which he interprets by saying 
that the cavity produced under high pressure conditions possesses normal 
air pressure, and that, therefore, the organ of the other side does not push 
over as quickly as it does with the decreased pressure procedure. 
How far such a distended lung participates in gas exchange, i.e., in the 
actual respiratory process, is not as yet clear (Friedrich (44)). Of course, 
it does not perform respiratory movements. 
A closed pneumothorax is frequently produced operatively in the 
treatment of pulmonary tuberculosis. The disturbances caused by this 
condition are, according to the above statement, slight. It promotes 
healing of the tuberculosis, first, by collapsing cavities which gives them a 
better chance to cicatrize. Furthermore, it is hoped that a functional 
rest of the lung can be obtained and thereby influence the inflammatory 
process favorably. Actually, complete rest is not possible, because, as 
stated above, the lungs as a whole are moved constantly to and fro by the 
pendulum air and the oscillations of the mediastinum. These movements 
are even more pronounced after extrapleural thoracoplasty, at least if the 
radical operation has been performed, and in the beginning, conditions are 
similar to those of open pneumothorax. Pendulum air and mediastinal 
flutter are so pronounced that the operated lung is bulged forward with 
each inspiration, and pulled back with each expiration (“paradox respi- 384 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
ration”) (53). But even if a pneumothorax or thoracoplasty does not 
place the lungs completely at rest, they lead to functional rest at least, 
since actual respiratory movements decrease or cease almost entirely. 
Furthermore, in pneumothorax and thoracoplasty, connective tissue 
grows rapidly and by encapsulating tuberculous foci, is an able curative 
factor (54). The cause of the connective tissue growth is not entirely 
understood, but Sauerbruch is of the opinion that functional rest leads to 
the formation of connective tissue, just as we know it in other tissues, 
e.g., muscle. Furthermore, the lymph stasis which occurs in these col- 
lapsed lungs is a supposed factor, for Shingu (55) showed that soot collects 
in the connective tissue and the lymph nodes of collapsed lungs, but in 
the alveoli and bronchi of the breathing lung. In pathological anatomical 
investigations, the lymph channels were found dilated (Kostler). 
Nor is it clear how much the circulatory changes favor connective 
tissue formation, especially since authors, as stated above, are by 
no means of united opinion in regard to the blood supply of the col- 
lapsed lung (56). We only know at present that connective tissue for- 
mation has been observed following ligation of both the pulmonary arteries 
and the pulmonary veins (57). But it is difficult to say which is the 
primary factor, functional elimination of the lung or the circulatory changes. 
To add to the confusion, Bruns (37) found such connective tissue growth 
experimentally not only in a collapsed diseased lung, but also in a collapsed 
healthy organ. 
The process by which the cavity of a pneumothorax is obliterated 
differs from that in the expansion of the fetal lung. Roser (58) disproved 
the oldest view, viz., that the cavity was filled by granulation tissue just 
as in other deep wounds, in that the lung expands after operation for 
empyema and fills the pleural cavity. As investigations of others have 
shown, a distention of the bronchus occurs before distention of the lung, 
but even if the increased pressure in the bronchial tree is not sufficient to 
explain the expansion, it does become great enough during coughing and 
abdominal compression to overcome the elastic forces of the lung (19,) 
(17), (59), (45). It is the custom to favor this distention by allowing the 
patient to blow up air cushions, into bottles, etc. as soon as possible. 
But the air continuously flowing in through the opening in the chest 
opposes these efforts. 
Reineboth investigated the advisability of changing the size of this 
opening in order to influence distention but he found it made no difference. 
The advice of Schede and Thiessch to prevent inflow of air as far as possible 
by an airtight bandage, or by attaching a valve to the drainage tube is of 
more practical importance. Perthes’s suction apparatus works on the 
same principle. CHEST CAVITY 
385 
As x-ray pictures have shown, redistention of a lung always begins at 
the hilus (60). Roser and Bouvertt point out that this redistention is also 
favored, i.e., recollapse is prevented, by the presence of adhesions between 
both pleural surfaces, and this idea seems reasonable. Finally, the cavity 
decreases also because the mediastinum is pulled over from the other side, 
the diaphragm becomes elevated, and the ribs sink inward. 
After complete removal of a lung, the resulting cavity is obliterated, 
not only by the organs in the vicinity, including the heart, the other lung, 
the mediastinum and the diaphragm, but also by the bony thoracic wall 
which adapts itself to this dead space in a very short time. In experi- 
mental animals, the ribs flattened themselves from the angle towards the 
sternum, so that in a few weeks the whole cavity created by the removal of 
the lung, was completely filled up (61). 
In exudative pleuritis, the conditions are somewhat different, in spite 
of the similarity to closed pneumothorax it otherwise has. First, it must 
be recognized that the exudate is under peculiar physical conditions. The 
fluid occupies a horizontal position only when air is present in the pleural 
cavity, usually it is driven very high on the lateral pleural wall because of 
the irregular negative pressure in the pleural space. Thus it does not 
collect at the lowest point simply by gravity. If the pressure is measured 
in puncturing pleuritic exudates, as is often done, it is always found to be 
negative, provided that the height of the level of the fluid is taken into 
consideration (62). The negative pressure is explainable by the compen- 
satory enlargement of the thorax. This enlargement is not passive, but 
active; it involves not only the diseased, but also the healthy side of the 
chest. If the power of the inspiratory muscles fail, severe compression 
symptoms with circulatory disturbances may suddenly occur (62). These 
latter are, as a whole, similar to those of closed pneumothorax, but are 
more severe for two reasons, the fluid cannot be compressed, and its 
weight is greater than that of air. Consequently the changes in the 
activities of the mediastinum and the diaphragm are much more pro- 
nounced in exudates, and the danger of a kinking of the vessels is greater. 
The characteristic death seen in large pleuritic exudates has been related 
to this kinking of the lower vena cava (63). This death is very sudden 
and errors in prognosis are easily made. The removal of the exudate 
should, therefore, not be delayed too long. 
Notwithstanding the compensatory enlargement of the chest cavity, the 
exudate exerts pressure on the lung surface, as evidenced by the develop- 
ment of circumscribed atelectatic areas. In larger exudates, the weight 
of the fluid column is sufficient to explain the atelectasis even if the pres- 
sure at the upper margin of the fluid is negative, as explained above; but 
in smaller exudates, the explanation is more difficult. O. Rosenbach 386 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
(19) speaks of a change in the pulmonary tonus, which might mean that 
the capillary attraction between the two pleural surfaces is suspended in 
localized areas, and at these places the elasticity of the lung would be the 
predominant force. 
These circumscribed atelectases hinder oxygenation because the blood 
flows through portions of the lung which are not aerated, but in pleuritis 
the alteration in breathing with its diaphragmatic and circulatory dis- 
turbances probably depends primarily on the pain during inspiration. 
The work of Siebeck, Bittorf and Forschbach (64) gives information on 
this subject. 
These various disturbances may be entirely absent when the exudate 
is encapsulated (see Clairmont a.o. (65)). 
A special type of operative lung compression is the diaphragmatic 
paralysis produced by cutting of the phrenic nerve (66). Apart from its 
elevated position on the paralyzed side, a “paradox” movement of the 
muscle occurs, since it does not descend, but is pulled upwards like a 
collapsed sail during each inspiration. In bilateral paralysis, the impedi- 
ment to respiration may be severe enough to cause dyspnea on slightest 
exertion. After phrenic nerve section no change which might be inter- 
preted as due to compression, can be demonstrated in a normal lung 
(Schepelmann). 
The type of dyspnea seen in ascites, large ovarian tumors, pregnancy, 
etc., is also due to the pathological position and function of the diaphragm, 
which is forced upward and impeded in its movements. The ribs are 
occasionally elevated on account of the abdominal distention, and this 
adds to the trouble by bringing them into the inspiratory position. 
Quite different in many ways to lung compressing processes, is a condi- 
tion included under the name of emphysema in which both the chest and 
the lungs are enlarged. It is an open question whether “chronic intersti- 
tial pulmonary emphysema” is etiologically a distinct disease. Pro- 
nounced cases of dyspnea show at autopsy enlargement of the alveoli and 
atrophy of the interalveolar tissue. The cause of dyspnea is the decreased 
vital capacity of the lungs (see Siebeck). In a certain sense, the thorax 
assumes the inspiratory position permanently, but the movements are 
handicapped in both directions. The thoracic enlargement also flattens 
the diaphragm (67). Bronchial catarrh is a complication which makes 
it difficult in a given case to decide how much of the dyspnea is due to 
the emphysema, and how much to the bronchitis. The hypertrophy of 
the right heart is usually interpreted, without further question, as an 
expression of the increased resistance in the lesser circulation. This 
latter is perhaps partly due to the diminished calibre of the vessels from 
the marked inspiratory position (see above), but the experiments of Licht- CHEST CAVITY 
387 
heim (31) cited above, oppose this view. He showed that the blood pres- 
sure remains entirely unchanged in both the greater and lesser circulation 
when the pulmonary artery is ligated, so that narrowing of the blood 
channels alone cannot explain the hypertrophy of the right heart. These 
experiments have been confirmed by Gerhardt, but the results were quali- 
fied by showing that they apply only when the body is at rest, while during 
activity, even a slight narrowing 6f blood channels in the lungs offers 
resistance to the heart. 
Furthermore, the chronic cough of these patients also occasions a pres- 
sure increase in the lesser circulation. Up to the moment when the glottis 
opens, the air in the bronchi is strongly compressed while the thorax 
struggles to assume the inspiratory position. The increased pressure in 
the bronchial tree, and the pressure exerted by the ribs clash during the 
coughing spell. This leads to such marked compression of the vessels 
within the lungs, as Gerhardt could demonstrate, that the pressure falls 
even in the carotids. The .r-rays show that the heart becomes smaller 
during the pressure test of Valsalva, which points to the fact that it 
receives less blood from the lungs. Then to this must be added that 
numerous capillaries are destroyed along with the pressure atrophy of 
lung tissue. Furthermore, in emphysema the normal pump action of the 
respiratory excursions is absent. This must be chiefly responsible for 
the venous stasis in emphysematous patients, to which must again be 
added, in relation to the lower extremities, that the low position of the 
diaphragm compresses the inferior vena cava (30). Numerous differences 
in detail occur in the individual cases of this common disease. Even if 
an emphysematous patient can be recognized from the barrel-chest, short 
neck with distended veins, impeded respiration with physical exertion, 
and cyanosis of face and neck, there are still individuals with overdisten- 
tion of the lungs who do not belong to this class. 
Two factors are observed so regularly in emphysema, viz., over- 
distention of the lungs, and altered excursions of the thorax, that it seems 
reasonable to see in either one of these changes the cause for the other, 
inasmuch as overdistention of the lungs would bring the thorax into the 
inspiratory position, and conversely, the inspiratory position of the 
thorax overdistends the lungs. W. A. Freund (68), as is well known, 
has shown in his anatomical investigations that the rib cartilages display 
a “yellow degeneration;” they increase in length, but lose their elasticity. 
Calcification of the cartilages appears. This lengthening of the ribs, which 
may amount to 1.2 cm., lifts the chest, and forces the ribs into the inspira- 
tory position. These cases would represent those in which primary 
changes in the chest wall have produced an over distention of the lungs 
as a secondary consequence. Puncture of the ribs, palpation, and rr-ray 388 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
pictures have all shown that these changes in the cartilage occur quite 
frequently, so that the recognition of a separate disease picture is prob- 
ably justified. 
The findings of W. A. Freund have been verified by v. Hansemann, 
but are disputed by Sumita (69). 
If, notwithstanding the findings in the costal cartilages, there is still 
doubt that this is actually the primary change, the improvement which 
appears immediately after operation, according to the uniform statements 
of all authors, proves that the least the rigidity of the thorax does is to 
render the suffering much more intense (70). Of other changes in the 
thoracic wall leading to fixation in the inspiratory position, must be 
mentioned the arthritic changes in the costo-vertebral articulations (71), 
and the kyphosis in senile spondylarthritis, described by Loeschke (71). 
In this kyphosis, the ribs above the hump are in the inspiratory position, 
and those below in the expiratory position. Similar malpositions of the 
ribs are also found in tuberculous spondylitis. Finally, Wilms (51) 
(Schenker) claims that this inspiratory position in emphysema is caused 
by spasm of the respiratory musculature, because they are under increased 
nerve tonus, and he believes he has demonstrated an hypertrophy of 
these muscles. 
The second group of authors hold that the primary factor in emphy- 
sema is the overdistention of the lungs. Of course, the secondary thoracic 
enlargement cannot be due to “a mechanical pressure,” exerted by the 
lungs on the thoracic wall, for their strength is not sufficient. 
The primary enlargement of the lungs may be due to “dynamic 
causes,” as they are called, i.e., the lung loses its elasticity (Virchow), or 
to “mechanical” disturbances, such as chronic bronchitis with cough or 
asthma (72). Numerous examples may be found in support of both 
possibilities, and in the majority of cases it is probably impossible to take 
a decided stand. Eppinger and Hess (73) bring the emphysema of 
youthful individuals in relation to vagotony. They believe that an 
increased tonus of the bronchial musculature is present in such patients, 
and it makes expiration more difficult. For information concerning the 
bronchial musculature itself, see Lohmann and Muller (74). 
It would lead too far astray to discuss single cases, like the vicarious 
emphysema which results when larger portions of the lungs are rendered 
useless, or that due to unusual exertions (for instance, unaccustomed 
mountain climbing, etc.), since they have less interest for the surgeon, 
but the emphysema due to narrowing of the respiratory passages must be 
considered. It may follow goiters, mediastinal tumors, even obstruction 
of the nasal passages. Cervells (70) saw lung distention in dogs, whose 
nostrils had been completely closed. Kuhn (46) who caused a dog to CHEST CAVITY 
389 
breathe for a long period of time through his suction mask, also found 
emphysema; likewise Ludsucki who operatively narrowed the trachea in 
rabbits. Hirtz, Koehler and Schall performed similar experiments 
(75)- 
The cause of this distention is to be found in the deeper inspiration 
than expiration which follows stenosis. Inspiratory dyspnea is produced, 
and thus the mean capacity is increased. This occurs in acute stenosis 
(i.e., we find marginal emphysema in the drowned, or in the asphyxia 
deaths from blood aspiration), as well as in chronic stenosis (see later). 
Strenuous expiration alone does not lead to emphysema (76). 
It is easily understood how lung distention is exceptionally favored 
during coughing or compression, and therefore, chronic bronchitis is 
almost universally considered one of the chief causes of pulmonary emphy- 
sema. Occupational factors, such as blowing wind instruments, lead to 
emphysema, or, probably more accurately, to an increase of the residual 
air, since it is undecided whether this is true emphysema or not. 
Undoubtedly, not all persons subjected to similar causes will develop the 
disease (76) and it seems necessary to assume that there is a certain pre- 
disposition in some patients. 
Ribbert (77) points out, that the enlarged bronchioles themselves, by 
compressing the larger bronchi, are a purely mechanical obstruction to the 
emptying of the air. 
The changes in respiration caused by chronic narrowing of the respira- 
tory passages (e.g., by goitre, etc.), were first studied experimentally by 
Koehler (78). It was shown that slight narrowing leads to deeper 
inspiration, so that no deficiency in oxygenation occurs, on the contrary, the 
alveolar air often contains less carbon dioxide than normally, and the 
carotid blood does not contain more. Since expiration is not increased 
proportionally, the mean capacity of the lungs must be increased when the 
air channels are narrowed, and thus there is a tendency to emphysema. 
This greater inspiration often does not compensate during more strenuous 
muscular exertion, and then goiter patients complain of dyspnea. They 
are also in great danger when the breathing surface is diminished by 
pneumonia; during which disease compensation may fail. In high grade 
stenoses, the equilibrium is not maintained even during rest, and the 
patient finally dies of asphyxia, if not from previous failure of the damaged 
heart. 
In acute asphyxia, accumulated carbon dioxide is the first substance 
to make itself felt, anesthetizing the patient after a preliminary stage of 
excitement; then the results of oxygen deficiency dominate the picture 
with convulsions, dilatation of the pupils, and respiratory failure. The 
heart stops later. But as long as it beats, recovery is possible, and there- 390 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
fore artificial respiration must be used persistently. In this condition, 
the chest is fixed in a deep inspiratory position and the patient endeavors 
to increase inspiration still more. The pressure of the air in the pleural 
cavity is constantly diminished and the skin of the flanks is pulled in. 
The explanation of the cyanosis still offers great difficulty in such respira- 
tory obstructions, but it seems quite reasonable to suppose that blood 
changes occur. It is known that discoloration of the blood is caused, not 
by accumulation of carbon dioxide, but by decrease of oxygen, yet decrease 
of oxygen is not present during the cyanotic stage of asphyxia. During 
anaesthesia, as every surgeon knows, it is not uncommon to see the blood 
suddenly become darker as soon as a slight excess of anesthetic is adminis- 
tered, or respiratory hindrance occurs. In this form of cyanosis, dis- 
coloration of the blood doubtless occurs, but the oxygen and carbon 
dioxide content during the asphyxia are not known. 
The club fingers often seen in chronic chest conditions offer a problem of 
either congestion or some form of nerve alteration. There is a certain 
analogy to acromegaly, but changes in the hypophysis are by no means 
always present. The report of Klauser (79), who observed marked club 
fingers with a shoulder luxation of long standing, without a sign of con- 
gestion in the arm, but with a paralysis of the hand, shows that injuries 
to the peripheral nerves may lead to these peculiar changes. 
We have discussed the blood distribution and its changes during 
breathing and after operative pneumothorax and we may now briefly 
review other conditions which also effect it. Changes in the position of 
the body, as for instance the elevation of the pelvis, during operation have 
a decided influence on the blood supply. When the pelvis is elevated, 
a much heavier blood column rests on the heart and may readily cause 
acute dilatation, as Trendelenburg (80) among others, could show with 
the arrays. For this reason, and also because of changes in the cerebral 
circulation, this position should not be maintained for much longer than 
10 minutes, unless very necessary. We must also bear in mind the severe 
acute change in the blood distribution after such operative interferences 
as the temporary compression of the aorta and the pulmonary artery 
necessary in the Trendelenburg (81) operation for removal of pulmonary 
emboli. Lawen and Sievers (82) carried out such experiments on animals, 
in which they made accurate observations of the heart action, blood pres- 
sure and pulse. They found that the heart can withstand a compression 
of the aorta and the pulmonary arteries for six minutes and still recover. 
Compression of the superior vena cava was much more dangerous; after 
three minutes cerebral symptoms made their appearance. That the 
conditions in man are similar has been shown in operative cases in which 
by Trendelenburg’s method, removal of pulmonary emboli was attempted CHEST CAVITY 
391 
(83). The conditions following compression of the abdominal aorta as 
required in Momburg’s belt, are far less damaging to the heart. 
Of all embolic processes, i.e., the carrying of blood clots or foreign 
substances through the blood channels to different organs of the body, 
pulmonary emboli with their frequent fatal results, hold the chief interest 
for the surgeon. Therefore, the whole question of embolism is best 
discussed here. 
The pathological physiological consequences are greatly dependent 
on the sort of material deposited, i.e., fat, air or blood clot. 
Emboli of blood clot presuppose thrombus formation in some part of 
the body, knowledge we owe to the first work of Virchow (84) which still 
remains the classic. The great majority of all thrombi carried to the 
lungs originate in the veins of the leg; their cause, and the experi- 
ments concerning them will be discussed later. Why a thrombus, which, 
of course, often develops without previous embolism should become 
suddenly detached, is not known. A diminution of heart action, which is 
of great importance in the further transport of emboli, probably does not 
cause detachment of a clot, neither is there anything known of the fer- 
mentative processes which cause softening of a thrombus with some 
degree of regularity. 
Such an embolus of blood clot reaches the lung through the right heart 
and the pulmonary artery. If small, it leads to an atelectatic area, which 
can become the seat of secondary inflammation. If it is large, it quickly 
leads to heart failure and asphyxia with compression of the pulmonary 
artery, as in the experiments of Lawen and Sievers (82) mentioned above. 
It is not necessary to describe in detail the interesting pathological 
anatomical findings which occur in lung infarction since they are of no 
surgical interest. 
Another very essential question, for the comprehension of embolism, 
has been carefully studied; and this is the retrograde transport of solid 
particles through the blood channels (85). Such a backflow occurs when 
two currents of unequal size mix. The force of one of the currents may 
be strong enough to fill the mutual stem only temporarily, but it will at 
once produce a retrograde movement in the weaker current (86). Such 
pressure fluctuations in the veins are in close relation to respiration, and 
especially to sudden changes in the intrathoracic pressure, as, e.g., in 
coughing (87), asphyxia, etc. Ernst (88) thus describes a retrograde 
embolism which was possibly the result of artificial respiration, and he 
points to similar possibilities in chloroform anaesthesia. Experimentally, 
it was found that foreign bodies of low specific gravity are often driven far 
into the veins of the extremities (89). According to the observations 
of Ribbert in vivo, and the experiments with models (90), these foreign 392 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
bodies are carried chiefly in the marginal current of the veins. Retro- 
grade transport of large emboli, however, cannot be due to a gradual 
backflow as Ernst believes, but must be from a sudden strong power revers- 
ing the current. 
With open foramen ovale, thrombi may pass from the right to the 
left heart, and then into the arterial circulation, where they may produce 
embolic occlusion of vessels, especially in the brain (paradox-embolism). 
But it has been proven absolutely by the experiments of Teutschlander 
that the old idea of O. Weber (91) is correct, viz., that very small clots 
can pass through the pulmonary circulation. Teutschlander traced 
particles of India ink from the leg veins of an animal into its cerebral 
arteries. But it must be a very minute particle, such as India ink granules, 
or isolated bacteria, or it will not pass through the pulmonary circulation. 
If larger emboli are found in the greater circulation it must be supposed 
that either there is an open foramen ovale, or an endocarditis, or a vessel 
with thrombi on its wall. Such clots circulating in the greater circulation 
may, of course, reach any organ and produce infarction. At present these 
arterial emboli are of interest to the surgeon, only if occurring in the 
extremities, since, in this case, their operative removal is often successful, 
and a limb otherwise lost can be saved (92). 
Fat globules (93) are undoubtedly the most frequent emboli. Ever 
since Zenker described the first case, this very satisfactory experimental 
subject has been thoroughly examined, especially from the surgical 
viewpoint. The fat enters the veins chiefly from the bone marrow when 
it is loosened by any kind of injury, and it is then carried by the venous 
blood to the heart and from there to the lungs. The injury may be very 
slight; according to Ribbert tapping the tibia with a hammer suffices; 
indeed Fritsche could find fat in the lungs of perfectly healthy rabbits. 
Possibly in this case, the agitation of the bones from chasing the animals 
and their occasional impact against the cage was sufficient. Fat emboli 
in eclampsia can be attributed to a similar slight trauma (Virchow), but 
such small quantities of fat are of no clinical importance (94). Large 
masses are, however, very much so. They appear frequently after frac- 
tures in older people, and especially if considerable concussion was 
caused by the accident, for instance, in a fall from a great height. The 
reason why old persons show this tendency is that their bone marrow 
is more fatty and richer in oleic acid, i.e., more fluid as age advances. 
The fat gains entrance first into the veins of the bone marrow, and 
from there into the lesser circulation, but there is also absorption through 
the lymph channels, by which it is carried through the thoracic duct into 
the greater circulation. In the investigations of Fritsche who produced 
fractures after ligating all the veins in the legs of rqbbits, it seems in CHEST CAVITY 
393 
severe bloody fractures the fat was taken up by the blood vessels, while in 
milder breaks the lymph channels were favored. According to Reiner 
(95) its transport by the blood can be observed directly before the Esmark 
bandage is removed, if a cannula is tied into the saphenous vein after 
orthopedic operations in a bloodless field. Fat globules are mixed with 
the blood, but Lexer could not verify this statement. We have often 
found fat in the venous blood of the traumatized limb immediately after a 
severe injury. 
Riedel obtained fat emboli through the lymphatics by injecting oil 
into the abdominal cavity. Fat emboli from other organs, for instance, 
the subcutaneous tissue, are of far less importance than those from the 
bone marrow (Grondahl), although in the first case described (Zenker), 
the fat came from the liver. Fat embolism also occurs from inflammatory 
processes in fat containing organs, especially from osteomyelitis, while 
there is little danger from burns, toxemias and general metabolic distur- 
bances. It is thought that fat absorption in osteomyelitis is favored by 
the liquefaction incident to the inflammatory process. 
In a broader clinical sense, fat embolism of the lesser circulation must 
be differentiated from that of the greater circulation (96). Since, as 
stated, the fat reaches the right heart through the veins, the question arises 
of how it can enter the greater circulation at all. An open foramen ovale 
is not always present, and the fat must necessarily pass through the lungs 
(97). It is possible that this is favored by the forced respiration which 
occurs when the fat first occludes the pulmonary artery. At any rate, as 
Virchow pointed out, the passage of fat from the lesser into the greater 
circulation is a complex process. Groendahl performed an experiment 
with a rabbit in which he injected oil, then removed a kidney, then made a 
pneumothorax, and finally extirpated the other kidney, after which he 
found that the second kidney contained very much more fat than the 
first. He concludes that an essential factor for the passage of fat is the 
extent of the pulmonary vascular area, but this experiment permits of 
another interpretation. According to the same author, the diameter of 
the pulmonary vessels is not important, but we may assume that the 
quantity of the fat circulating in the blood cannot be ignored. 
A large number of cases in which fat emboli are found in the lungs 
at autopsy show no clinical symptoms, and respiratory disturbances 
occur only when a larger number of pulmonary capillaries are occluded. 
Pathologically anatomically, edema and capillary hemorrhages are 
found, both of which probably increase the respiratory difficulties. The 
marginal emphysema, usually observed, must be considered due to this 
impeded respiration, but the reason for the irritative cough which often 
develops immediately after the embolism is not clear (98). It is also 394 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
unknown whether a preceding fat embolism favors inflammatory processes 
in the lungs (pneumonia after fractures in the aged). 
In th6 pulmonary vessels, a part of the fat is saponified by the alkaline 
blood serum and thus prepared for absorption (Beneke (99)); another part 
is taken up as fat droplets by the vessel endothelium. The remainder 
passes through the lungs, as stated above, and appears in the greater 
circulation. 
Theoretically, it may be distributed among all the organs, but practi- 
cally, the brain is the only one of serious importance. According to 
Grondahl, the fat remains in this organ because there is an exceptionally 
large blood supply flowing through small capillaries which are presumably 
less capable of dilatation. But slight nutritional disturbances in the brain 
are also quickly detectable clinically. It is characteristic of cerebral fat 
embolism that it does not occur immediately after injury probably 
because the fat is retained at first in the lungs. For this reason, pul- 
monary symptoms often precede brain symptoms. The latter consist 
of lessened threshold to pain (Czerny), restlessness, anxiety, increased 
temperature, numbness and paralyses, and must be considered as true 
localized symptoms. Increased brain pressure has not as yet been 
observed, probably because cerebral reactions (lymphstasis, etc.) develop 
slowly. 
The fat may pass the capillaries of the greater circulation as well, and 
be eliminated in the urine. 
Air embolism (100) occurs through the sucking in of air into an open 
vein. This presupposes that the venous pressure is low, or actually 
negative, which is especially true of the veins close to the heart. This 
low pressure is still further decreased by a previous loss of blood (101). 
By using excess or negative pressure anesthesia, this danger of the entrance 
of air can be greatly reduced (102). On the other hand, an excess pressure 
in the thorax is obtained by abdominal compression during anesthesia, by 
which a retrograde transport of air through the veins is possible (88). We 
observed a case in which an area of softening in the brain occurred from 
this accident following a goiter operation. A similar case was described 
by Van de Kamp (103). 
Furthermore, the veins must gap in order to permit the entrance of 
air, and, therefore, veins passing out through spaces in the fascia are espe- 
cially endangered, as well as those which are superimposed on a tumor 
(e.g., goiter) and thus pressed flat. 
Air embolism is more dangerous than fat embolism, because an air 
bubble acts like a valve in blood vessels and interrupts the blood stream. 
It is only necessary to recall what occurs when an air bubble is enclosed 
in an irrigator tube to appreciate the conditions. It is not quite clearly CHEST CAVITY 
395 
understood where this interruption of the circulation, in other words, the 
cause of death, takes place. The only fact known is that in experimental 
air embolism a measurable quantity of air is found in the right heart, and 
it is possible to keep the animal alive in a certain percentage of cases by 
sucking out this air (104). Whether death occurs because the right heart 
is unable to press the contained air bubbles out (105), i.e., cannot contract 
sufficiently, thus interrupting the blood supply to the lungs, or whether 
the air occludes the pulmonary capillaries has not been definitely settled 
at present. Perhaps both causes operate, and the form of death depends 
on the rapidity of the entrance of the air. Passage of air from the lesser 
into the greater circulation occurs only in occasional instances. Air 
bubbles are rarely found in the brain and the old theory of Bichat of 
“brain death” from air embolism is abandoned. 
The case is different when air is injected into the arteries, or enters 
the portal circulation, in which latter case it must pass through the liver 
(see Wolf). Here the bubbles are broken into minute globules which pass 
without obstructing capillaries. Wolf always found air not only in the 
femoral vein after its injection into the femoral artery, but also scat- 
tered throughout the whole circulation. The death resulting is then 
probably a “brain death.” Clairmont (65) describes a clinical case of 
arterial air embolism in a patient with opened interlobar empyema. 
Embolism occurred during a change of dressings. 
As stated, much depends on the rapidity with which air enters; Wolf 
could inject 100 to 200 c.c. slowly without causing death. It may be 
assumed that a large part of the air is quickly liberated through the lungs, 
and it is of interest, conversely, that experimental air embolism may be 
produced by blowing air into the trachea (106). It is not known whether 
most things similar has been observed during the use of the excess pressure 
method, unless the observation of Schlesinger (cited on p. 383) is inter- 
preted in this way. The various animals used in these experiments are 
by no means equally sensitive to this procedure (104). 
A special form is seen in divers who are released too quickly into the 
air from a high-pressure diving bell. During the rapid decrease of pres- 
sure, gas is liberated from the blood cells (107) and there are minute air 
globules scattered everywhere in the vessels. Of course, puncture of the 
heart to liberate the air does not help in these cases. 
As already stated, postoperative lung complications are the causes of 
the greatest number of deaths after operation (108). Investigations have 
shown that they may be due to many factors, and have a most varying 
pathological basis; First, there are postoperative pneumonias which are 
due entirely to the anesthesia, and for a while ether was considered very 
dangerous for the lungs (109), (108). This question was approached 396 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
experimentally, and the difference in results depends chiefly on the con- 
centration of ether or chloroform which comes in contact with the lungs. 
Poppert, who worked with a rather concentrated ether and chloroform 
vapor, came to the conclusion that the injury, especially from ether, is 
quite considerable. But Holscher obtained no changes in the lungs, 
except a slight hypersecretion of the bronchial mucous glands. Lichten- 
berg found scattered atelectasis and emphysema of the edges after 
thesia of long duration. If the animals were killed 24 to 48 hours after 
the anesthesia was concluded, pneumonic infiltration and true broncho- 
pneumonia could be demonstrated. Offergeld (no) arrived at similar 
results. 
It can well be realized that a lung injured by anesthesia is especially 
liable to infection, but how do infective organisms reach the lungs? 
Durck’s (iii) investigations have shown) in the first place, that the nor- 
mal lung is not free of bacteria. During anesthesia, they may enter the 
smaller bronchi from the mouth by aspiration, as was showm by Holscher 
in animals. He placed solutions of dyes in the mouths of anesthetized 
animals, and after longer anesthesia could find the dye, together with 
mucus, in the deeper bronchi, but this flow did not take place if the animal 
had been anesthetized with the head hanging downward. Aspiration of 
the contents of the mouth could also be avoided by turning the head side- 
ways, cleaning the mouth of mucus, etc., precautions which should, there- 
fore, be considered as very essential. The experiments of Holscher, to 
discover if anesthesia injured the ciliated epithelium, resulted in negative 
findings. 
[After their experimental experience with war gases, Winternitz and 
his collaborators were led to investigate the lymphatics of the trachea and 
larger bronchi. It was found that the submucosa of the trachea contains 
a very rich plexus of lymphatics which anastomose with similar channels in 
the bronchi at the bifurcation, and these in turn communicate with lym- 
phatics of the smaller bronchi, and so on. Infection (pneumococci), intro- 
duced into the lumen of the trachea by needle puncture or by insufflation, 
spread via these lymphatics to the lung, provided the epithelium of the 
trachea was damaged. But these lymphatics are also protective, in that 
most of the drainage from the trachea and bronchi flows into the regional 
lymph nodes. The possibility of a direct pathway is present, however, and 
this may well be utilized in certain postoperative lung infections (112).] 
Anesthesia furthermore reduces the immunity of the organism as 
a whole to bacteria. Snel (113) injected anthrax bacilli into the lungs of 
anesthetized frogs. While normal frogs are immune and do not react to 
this injection, anesthetized animals developed anthrax pneumonia and 
died. CHEST CAVITY 
397 
As stated above, after anesthesia, small hemorrhages can frequently 
be demonstrated in the lungs, a proof of circulatory disturbance. But the 
latter may result after operation quite independent of anesthesia, i.e., 
from insufficient aeration, from painful abdominal incisions, or from a high 
position of the diaphragm, as for instance, in peritonitis. Heart distur- 
bances, which often depend on anesthesia, may also lead to such circulatory 
changes. The net result is hypostasis, or a local pulmonary edema, and 
this especially favors the development of pneumonia. 
A further injury, to which patients are exposed during all operations, 
is chilling; and its influence on the lungs has been investigated by Henle 
and Heile (114) who poured ether over anesthetized rabbits, and noted 
a marked fall in the temperature of the body. The lungs showed hyper- 
emia, hemorrhages, and injury to the alveolar epithelium. In all these 
cases the anesthesia was of very short duration. 
Embolism constitutes one of the most severe circulatory disturbances 
of the lungs, as stated above. Pneumonia, caused by fat emboli, is occa- 
sionally seen after fractures; postoperatively it is more likely to be due 
to small embolic blood clots. Gebele (115), in 40 animals, obtained 12 
cases of pulmonary embolism by means of varied operative procedures (i.e., 
ligation of the larger abdominal vessels, handling of bowel, etc.). In 
the presence of emboli, naturally, pathogenic organisms may reach the 
lungs and a pneumonia is the certain result. 
But pathogenic organisms enter the lungs by the lymph channels far 
more frequently than in blood clots. Goebel (116) investigated this 
question by injecting the intestinal wall with bacteria and India ink, after 
which he found these particles in the pulmonary lymph vessels. Lymph 
channel connections between the lungs and the abdominal cavity have 
often been demonstrated anatomically (117). Tillmann (118) and v. 
Lichtenberg point out that this, perhaps, explains the comparatively large 
number of cases of pneumonia following ulcerative processes in the stomach 
and intestines. Nevertheless, great care must be exercised in drawing too 
far reaching deductions of the clinical picture of post-operative pneumonia 
from the fact that isolated bacteria are experimentally carried through 
the lymph channels. The chest and the abdominal cavity, notwithstand- 
ing the numerous lymph tracts between them, are in fact two distinctly 
separate regions, as is proved over and over again by rarely finding an 
empyema with peritonitis, and vice versa. At the same time the anatomi- 
cal relations are especially favorable for infection of the pleura from the 
peritoneum. The pleura, indeed, just as the peritoneum, has a certain 
immunity to pathogenic organisms. According to the investigations of 
Notzel, it is necessary to inject three to four times the quantity of bacteria 398 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
into the pleura to kill an animal as compared to the quantity required in 
subcutaneous or intravenous injection (119). 
It can be seen from the extensive literature regarding pneumonia after 
contusion of the lungs, that trauma itself may cause post-operative pneu- 
monia or bronchitis (120). It is supposed the injuries produce small 
hemorrhages in the lung tissue, or at least, that the vitality of the lung 
tissue is diminished. Finally, as Chiari (121) points out, nervous distur- 
bances of the bronchi similar to. those in asthma, i.e., changes in the secretion 
of the mucous membranes, incited by the trauma, must be added as 
causative factors. 
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399 
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39. Lohmann and Muller: Sitzungsber. d. Ges. z. Bef. d. Ges. Naturwissenschaften zu 
Marburg, 1913. 
40. Romanoff: Arch. f. exp. Path. u. Pharm., 1911, V. 64. 
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43. Dogiel: Arch. f. mikrosk. Anat., 1903, V. 62. 
44. Hoffman: Naturhist. Med. Verein. Heidelberg, 1919. Friedrich: Arch. f. Klin. 
Chir., V. 82, p. 1160. 
45. Gerhard: Deutsche Chir., 1892, Lief. 43. 
46. Staehelin: Jahreskurse f. arztl. Fortbildung Februar heft, 1914. 
47. Reineboth: Deutsches Arch. f. Klin. Med., V. 58. 
48. Hirsch: Deutsches Arch. f. klin. Med., V. 64 and 68. 
49. Hartl: Beitr. z. Klinik. d. Tuberkulose, V. 12. 
50. Sauerbruch: Bruns Beitrage, V. 76 and 79. Brauer: Mitteil. a. d. Grenzgebieten, 
V. 13. 
51. Sauerbruch: Ergeb. d. Chir., 1911, V. 2. Tiegel: Mitteil. a. d. Grenz. 3 Suppl. 
Seidel: Grenzgebiete, V. 17. Garre-Quincke Lungechirurgie, Fischers Verlag, 
2 edition. 
52. Sclesinger: Arch. f. Klin. Chir., V. 95. 
53. Robinson: Deutsche Ztschrft. f. Chir., V. 102. Sauerbruch: Ergebn. d. inn. Med. 
1913, V. 10. 400 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
54- Muralt: Munchener Med. Wochenschrft., 1909, V. 50. Kistler: Beitr. z. Klinik. 
d. Tuberkulose, V. 19. Gratz: Beitr. z. Klinik. d. Tuberkulose, 1908, V. 14. 
55. Shingu: Beitr. z. Klinik. d. Tuberkulose, 1908, V. 11. 
56. Bruns-Sauerbruch: Mitteil. a. d. Grenzgebieten, V. 23. 
57. Tiegel: Arch. f. klin. Chir., V. 95. 
58. Roser: Berliner klin. Wochenschrft., 1878. 
59. Schede: Deutsche med. Wochenschrft., 1885. Weissgerber: Berliner klin. 
Wochenschrft., 1879. 
59. Bouveret: cited by Reineboth. 
60. Jochmannr Ztschrft. f. Elektrotherapie, 1906. H. Curschmann: Physik. u. Med. 
Monatshefte, 1904. 
61. Friedrich: Arch. f. Klin. Chir., V. 87, part 3. 
62. Gerhardt: Deutsches Arch. f. Klin. Med., V. 92. Weitz: Arch. f. exp. Path, and 
Pharm. Festschrft, for Schmiedeberg. 
63. Eppinger: Allgem. u. spez. Pathol, d. Zwerchfells Wien, 1911. 
64. Bittorf and Forschbach: Ztschrft. f. Klin. Med., V. 70. Sieback: Deutsches 
Arch. f. Klin. Med., V. 100. 
65. Clairmont: Arch. f. klin. Chir., 19x9, V. 111. 
66. Schepelmann: Arch. f. klin. Chir., 1913, V. 100, p. 985. Sturtz: Deutsche med. 
Wochenschrft, 1911-1912. Sauerbruch: Munchener med. Wchenschrft., 1913, V. 
12. 
67. Hofbauer: Erg. d. inn. Med., 1909, V. 4. 
68. W. A. Freund: Beitr. z. Histologie d. Rippenknorpel, Berlin, 1898. Der Zusam- 
menhang gewisser Lungenkrankheiten mit primaren Rippenknorpelanomalien 
Erlangen, 1859. Arch. f. klin. Chir., V. 92. Chirurgenkongress, 1910. 
69. v. Hansemann: Arch. f. klin. Chir., V. 92. Sumita: Deutsche Ztschrft. f. Chir., 
V. X13. 
70. Seidel: Bruns Beitrage, 1908, V. 58. Hoffman: Zentralbl. f. Chir., 1909. 
Friedrich: 39 Chirurgenkongress. 
71. v. Salis: Frankf. Ztschrft. f. Pathol., 1910, V. 4. Loeschke: Deutsche med. 
Wchenschrft., 1911. 
72. F. A. Hoffman: “Emphysem. u. Atelektase” in Notnagel’s Handbuch, V. 14. 
73. Eppenger and Hess: “Die Vagotonie,” by Noorden Samml. klin. Abh., 1910. 
74. Lohmann and Muller: Sitzungsbericht. d. Gez. z. Bef. d. ges. Naturwissensch. z. 
Marburg, 1912. 
75. Schall: Beitr. z. Klinik. d. Tuberkulose, V. 14. 
75. Hirtz: These de Paris, 1878. Kohler: Arch. f. exp. Pathol, u. Pharm., V. 7. 
76. Prettin andLeibkind: Munchener med. Wchnschrft., 1904. 
77. Ribbert: Virch. Arch., 1916, V. 221. 
78: Morawitz and Siebeck: Deutsches Arch. f. klin. Med., V. 97. 
79. Klauser: Munch, med. Wochenschr., 1912, p. 929. 
80. Trendelenberg: Prakt. Ergebnisse d. Geburtshilfe u. Gynakol, 1912. 
81. Trendelenberg: Arch. f. Klin. Chir., 1908. 
82. Lawen and Sievers: Deutsche Ztschrft. f. Chir., V. 94. 
83. Sievers: Deutsche Ztschft. f. Chir., V. 93. Trendelenberg: Deutsche med. 
Wchschrft., 1908 and Arch. f. klin. Chir., 1908. 
84. Virchow: Frorieps Notizen, 1846. 
85. v. Recklinghausen: Virch. Arch., v. 100. 
86. Beneke: Marchand-Krehl, “Handbuch d. allg. Pathol.,” V. 2, 2. 
87. Heller: Deutsche Arch. f. Klin. Med., V. 7. CHEST CAVITY 
401 
88. Ernst: Virch. Arch., V. 151. 
89. Ribberts: Zentralbl. f. Pathol., 1897. Arnold: Virch. Arch., V. 124. Risel: Virch. 
Arch., V. 182. Frerichs: Klinik. d. Leberkrankheiten, 1858, V. 2. 
90. Bouma: Virch. Arch., V. 151. 
91. O. Weber: Pitha Billroth Handbuch d. Allg. Chir., V. 1, p. 87. Teutschlander: 
Naturhist. med. Verein. Heidelberg, 1916. 
92. Matti: Konespondenzblatt. f. Schweizer Arzte, 1913. 
93. Busch (lit.): Virch. Arch., V. 35, Riedel, Deutsch. Zeitschrft. f. Chir. v. 8, Virchow 
in Virch. Arch., V. 5. Tromberg Grenzgeb., 26; Fritsche, Deutsche Ztschrft. f. 
Chir., V. 107, Grondahl; Deutsche Ztschrft. f. Chir., V. in. Busse Korrespon- 
denzblatt. f. Schweizer Arzte, 1913, Reiner, Munchener, med. Wchschrft. 1907- 
1, Ribbert, Deutsche med. Wchschrft., 1900, Beneke, Ziegler’s Beitr., 22 
Werzejewki, 10 Kong, Deutsch. Gess. f. 4, 465 Orthopadie (discussion here,). 
94. Schmorl: Uber Puerperaleklampsie, Leipzig, 1893. 
95. Reiner: 10 Orthopadenkongress. 
96. Payr: Ztschrft. f. Orthopad Chir., V. 26. 
97. Busse: Korrespondenzblatt. f. Schweizer, Arzte, 1913. Tromberg: Mitt. a. d. 
Grenzgebieten, V. 26. 
98. Fibiger: Compare Grohndahl, 1. c. 
99. Beneke: Ziegler’s Beitr., V. 22. 
100. Wolf (Luftembolie): Virch. Arch., 1903, V. 174 further Beneke, in Marchand- 
Krebl, “Allg. Path.” 2, 2. 
101. Becker: Ztschrft. f. Medizinalbeamte, 1911. 
102. Tiegel: Chirurgenkongress, 1912. 
103. Van de Kamp: Dissert. Munchen, 1913. 
104. Kleinschmidt: Chirurgenkongress, 1912. Jehn and Naegeli: Ztschrft. f. d. Ges. 
exp. Med., 1918, V. 6. 
105. Cohnheim: Allg. Pathol., 1877, V. 1. 
106. Beneke: Arch. f. Entw.-Mech., 1910, V. 33. Marchand: Vierteljahrsschrft. f. 
prakt. Heilkunde, 1876, V. 33. 
107. Hoppe-Seyler: Muller’s Arch. f. Physiol., 1852. 
108. W. Lich ten berg: Zentralbl. f.d. Grenzgebiete, 1908, V. n; Bruns Beitrage, V. 57; 
Munchener Med. Wchschrft., 1909. 
109. Lowit: Ziegl. Beitrage, V. 14. Stursberg: Mitteil. a.d. Grenzgebieten, V. 22, 
p. 11. Poppert: Deutsche med. Wchschrft., 1894 and 1897, Deutsche Ztschrft. 
f. Chir., V. 67. Lengemann: Bruns Beitrage, 1900, V. 27. Lindemann: Zen- 
tralbl. f. path. Anat., V. 11. Holscher: Arch. f. Klin. Chir., V. 57, p. 175. 
no. Offergeld: Arch. f. Klin. Chir., V. 75. 
in. Durck: Munchener med. Wochenschrft., 1904. 
112. Winternitz, M. C., Smith, G. H., Robinson, E. S.: “Pathway for bacterial inva- 
sion of resp. tract,” Bull. J. Hopkin’s Hosp., 1920, 31, 163. 
113. Snel: Ztschrft. f. Hyg. u. Infectionskrankheiten, V. 40. 
114. Henle and Heile: Arch. f. klin. Chir., V. 64; Chirurgenkongress, 1901. 
115. Gebele: Bruns Beitrage, V. 43. 
116. Goebel: Mitt. a.d. Grenz., V. 18. 
117. Kelling: Chirurgenkongress, 1905. Kuttner: Bruns Beitrage, V. 14. Franke: 
Deutsche Ztschrft. f. Chir., V. 119. 
118. Tillman: 15 Internat. Med. Kongr. Lissabon, 1906. 
119. Notzels: Bruns Beitrage, V. 46. 
120. Stern: for lit. Traumat. Enst. inneren Krankheiten, Jena, 1910. Venus: Zentral- 
blatt. f. d. Grenzgebiete, 1909.' 402 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
121. Chiari: Brims Beitrage, V. Si. 
122. Georg Fischer: Arch. f. klin. Chir., V. 9, p. 571. 
123. Barth: Schriften «L Natmrforscher-Gess. in Danzig, 1902, V. 10. 
124. Kronecker and Schmey: Deutsche med. Wehenschrft., 1884, p. 364. 
125. Rose: Deutsche Ztschrft. I. Chir., V. 20, p. 319. 
126. Cohnheim: Allg. Pathologic, 2 edition, 1882, p. 21. Riegel: Deutsches Arch. f. 
klin. Med., 1882, V. 31, p. 471. Placzek: Vierteljahrsschrift f. ger. Med., 1902. 
Lewis: Jonm. ol Phys., 1908, p. 233. 
127. Molitoris: Wiener klin. Woehenschrft., 1919, p. 868. 
128. Samerbrach: Arch. f. klin. Chir., V. 83. 
129. Elsberg: Brans Beitrage z. klin. Chir., V. 25, p. 426. Bode: Brans Beitrage z. 
klin. Chir., V. 19, p. 167. 
130. Rehn: Arch. f. klin. Chir., 1897, V. 55. 
131. Michaelis: Ztschrft. f. klin. Med., V. 24, p. 270. Frey: 10 Kongr. f. innere Med., 
1891. Porter: Jonra. Physiol., V. 15. Panum: Virch. Arch., V. 25, p. 308. 
132. Laewen: Mnnchener med. Wehenschrft., 1919, p. 5. # 
133. Kolb: for lit. Berlin Klin. Wehenschrft., 1913. Brauer: Arch. f. Klin. Chir., V. 
71. 
134. Goringstein: Brains Beitr. z. klin. Chir., V. 86, p. 229. 
135. Heidenhain: Deutsche Ztschrft. f. Chir., V. 41. Schuster: Ztschrft. f. Heil- 
kunde, 1880, p. 417. 
136. Barie: Revue de medicine, 1881, p. 132. 
137. Bohm: Mitt. a.d. Grenzgebieten, 1914, V. 27, p. 567. 
138. Leporski: cited in Chirargenkongress-Zentralblatt, V. 4, p. 151. CHAPTER XI 
BRAIN AND SPINAL CORD 
In the great majority of surgical diseases of the brain and its mem- 
branes, the symptom complex, known as “increased pressure” plays the 
foremost role (i). To this belong headaches, slowing of the pulse, 
choked disc, unconsciousness, convulsions, respiratory paralysis and 
similar symptoms. They are incited when there is a disproportion in the 
contents of the skull and its capacity, whether it be that the vault of the 
skull is driven into the brain, as in a depressed fracture, and the space is 
decreased, or whether it be a swelling of the brain against the resistance 
of the unyielding walls of the skull. In both cases there results a pressure 
on nerve cells, and this mechanical irritation in the form of injury of the 
nerve cells leads to the above mentioned symptoms. Recently, Reichardt 
(2) measured the relation between the capacity of the skull and the volume 
of the brain, and secured figures which show that an increase of brain vol- 
ume plays a large role in the establishment of “increased brain pressure” 
and, for example, in brain tumors without hydrocephalus, the brain 
volume is still increased even after removal of the tumor. 
Since the various parts of the brain differ in their functions, it is 
obvious that pressure on the motor area of the cortex must give different 
manifestations than pressure on the medulla oblongata. But these local 
effects are not as difficult to understand as the general symptoms, 
which appear in greater or less degree in all cases, but do not seem to 
follow pressure on any special part. The older theories (1), (3) sought an 
explanation in a factor which would affect the whole brain equally, that is, 
in disturbances of circulation. These theories, principally, through the 
influence of v. Bergmann and Kocher, have so dominated the literature, 
that disturbances of the brain cells on which symptoms of brain pressure 
must depend in the final analysis, have been relegated to the background, 
even though attention was called quite early to the onesidedness of such 
theories (4). But not only the experimental results, but also the experi- 
ence gained at operations have emphasized the consideration of brain 
pressure as “a mechanical injury to nerve tissue” (1), (5). The circulatory 
disturbances are supposed not to alter nutrition but merely to afford a 
possibility for a compression of the nervous elements (Hauptmann). 
This appears to be the other extreme; for circulatory disturbances may 
not be entirely guiltless in the production of brain pressure symptoms. 
403 404 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
The peculiarity of the circulation of the brain lies in the fact that this 
organ is enclosed in a non-yielding capsule. It cannot, therefore, become 
enlarged like other organs, and an increase in fluid content from passive 
congestion or from increased arterial flow, leads to brain pressure symp- 
toms. It is not the blood vascular system alone which plays a part in 
its circulatory phenomena, but the cerebral circulation is still further 
complicated by the presence of cerebrospinal fluid. According to newer 
opinions, the physiological purpose of this fluid is “ to provide a mechanical 
safeguard for the centers and a regulatory mechanism for the blood 
supply of the brain” (6). The brain literally swims in this fluid. It is 
not to be compared casually to lymph, for it lacks the nutritive sub- 
stances which the lymph carries. According to Mestrezat (7) there 
is no noteworthy mixing of lymph and fluid, even in the perivascular 
spaces. 
Its origin is by no means understood (8). That it is no simple transu- 
date from the blood is certain from its chemical composition, for it con- 
tains more crystalloids than blood serum. On the other hand, secretory 
stimulants, such as pilocarpin, increase its pressure. Whether it is secreted 
from the choroid plexus only or from the “vessels and substance of the 
nervous system” also (9) is still uncertain, although newer investigations 
seem to show that the cells of the brain and spinal cord are also concerned. 
Bungart (10) resected and ligated the subarachnoid space of the spinal 
cord of animals in two places and allowed the isolated space to empty 
itself. After 12 hours it was again filled with fluid. Clinical observations 
in the sacculated meningitis of fractures of the vertebrae have indicated 
that the fluid is formed in all parts of the central nervous system. This 
question is of surgical importance, because in hydrocephalus, attempts 
have been made to destroy the source of the abnormal formation of fluid 
by removal of the choroid plexus (n). This procedure is rational only, 
of course, if the choroid plexus is principally at fault. 
Its chemical composition is also of surgical interest, because the large 
number of lumbar punctures for spinal anesthesia in patients with healthy 
central nervous systems have supplied normal fluids for analysis. The 
statement that 1 per cent, of albumen is normal (Riecken and others) 
has been found incorrect (Bungart). Ordinarily, only the very faintest 
trace is present, but even a slight stimulus leads to an increase. Thus 
Bungart, in patients who had trouble after spinal anesthesia, found 
albumen in a second puncture fluid when none had been present in the first. 
The irritation in this case was chemical. Larger amounts with leucocytes, 
occur in bacterial inflammations (infections), but in addition, slowly pro- 
gressing chronic conditions, particularly late syphilitic inflammations, such 
as tabes and paresis, lead to pathological albuminous bodies in the fluid BRAIN AND SPINAL CORD 
405 
which can in general be recognized only after precipitation with ammonium 
sulphate (12). 
The quantity which can be produced, especially in gunshot wounds 
when the ventricles are opened, is well known to surgeons; although in 
this case, it is doubtful if the conditions are normal. Nau and Hermann 
(13) showed that the fluid in the lumbar region would return to its original 
pressure in 20 minutes, when a large quantity had previously been 
removed. 
The fluid flows into the cerebral veins, partly by way of the Pacchion- 
ian bodies and partly through the perivascular lymph spaces. Some, 
however, flows toward the lymph vessels of the neck, as Hill and Ziegler 
(14) have determined by the injection of dyes. Furthermore, the sub- 
arachnoid space is in communication with the sheaths of peripheral nerves, 
as Bungart (10) has shown by strychnin injections, and this latter fact is 
of extreme importance in the spread of tetanus. 
Increase of pressure leads to increased absorption (3) and this mechan- 
ism functions so smoothly that there need be no fear of increased brain 
pressure during the induction of spinal anesthesia. The procedure of 
allowing a considerable amount of fluid to flow out before injection of the 
anesthetic is superfluous. 
The fluid is present both in the subarachnoid space and in the ventri- 
cles, but it has lately been questioned whether this system of canals is 
really one unit, i.e., if the fluid in the ventricles communicates with the 
fluid in the subarachnoid space through the foramen of Magendie and 
other openings. Schmorl (15) showed that in icterus, the subarachnoid 
fluid, but not that in the ventricles, was discolored. Conversely, other 
substances do not pass from the fluid in the ventricles to the cerebrospinal 
fluid. The question of whether there really is a foramen of Magendie in 
humans, is of therapeutic interest. For, until now, we have thought that 
a lumbar puncture in hydrocephalus also empties the ventricles and that 
their fluid escaped through the foramen of Magendie into the subarach- 
noid. There have even been extensive operations on the spinal column 
designed to allow a lengthy drainage of fluid from the ventricles in hydro- 
cephalus. Furthermore, it was thought that acute hydrocephalus often 
arose as a result of the closure of the foramen of Magendie through 
inflammatory products. The findings of Schmorl are so consistent, how- 
ever, that it seems better to consider our opinions of hydrocephalus and 
its therapy by lumbar puncture incorrect. This necessitates the view 
that the flow of fluid in general is so small, that it is reabsorbed in practi- 
cally the same place it was formed. But this is refuted by Schmorl him- 
self, who observed an icteric color in the subarachnoid fluid as soon as the 
ependym of the choroid plexus was injured. 406 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
In practical surgery, this conclusion may be drawn from Schmorl’s 
findings. In all cases of dilatation of the ventricles, and in the different 
varieties of hydrocephalus, it is a more physiological proceeding to practice 
methods of direct drainage of the ventricular fluid, such as puncture of the 
ventricles, the Anton-v. Bramann puncture of the corpus callosum, 
ventricular drainage, etc. 
The subarachnoid space is so completely separated from the subdural 
space that even easily diffusible poisons do not pass the boundaries, as 
Bungart (io) has shown. 
The question of whether there is a flow of liquid in the cerebrospinal 
fluid itself, ignoring the debatable communication with the ventricles, 
has been the subject of repeated investigations. The current plays a 
definite part in spinal anesthesia, and it is thus accepted on experimental 
and observational grounds, but the results of injecting dye particles (16) 
must not be applied to humans without furtherknowledge, both on account 
of the different posture of the body and anatomical differences. The 
observation of Propping (17) that there were symptoms of paralysis of the 
region of the medulla oblongata in a half hour after a spinal anesthesia 
with tropakolain is in the last analysis an infrequent event, from which 
we can draw conclusions regarding the normal flow of fluid only with the 
greatest caution. According to Reichmann we have at present no definite 
proof that a flow really occurs and yet the findings of Graf Haller, that 
nodding movements of the head increase the pressure by 10 cm. of water 
or more, seem to show a sort of pumping of the fluid which is carried 
backward into a cistern at the end of the fourth ventricle, and indicates 
the presence of a current (18). 
The pressure factors in the subarachnoid space have been studied not 
only on the living and on cadavers, but also on models (19). The latter 
are not all alike, since Grashey conceives the vertebral canal as a container 
with rigid walls and Propping, more correctly, considers it somewhat 
elastic by reason of the fat and veins in the epidural space. In a sitting 
posture, the fluid pressure is not zero at the foramen magnum occipitale, 
but at about the upper thoracic vertebrae (20), so that, as Propping 
showed, puncture between the atlas and occipital bone allows air to be 
sucked into the vertebral canal. These models do not accurately imitate 
the relations in the living subject, for in the latter, while reclining, there 
is a pressure of from i to 12 cm. of water, while it is zero in a cadaver. 
This may be related to the tension of the tissues, particularly the dura 
mater. 
Not only are pulse beats and respiratory movements transmitted to 
the fluid, but congestion in the large veins of the neck is registered on the 
manometer. BRAIN AND SPINAL CORD 
407 
If we now return to a consideration of circulatory factors in the produc- 
tion of brain pressure, we can expect, theoretically, an increase through 
conditions in the arterial, venous and cerebrospinal fluids (21). But these 
three factors are so adjustable that increase of one leads to a diminution 
of the other. Since Burrow’s (22) time, therefore, we speak of a constant 
content of the skull, rather than the constant quantity of blood, as in the 
older description of Monroe who disregarded the fluid entirely. Leyden 
(23) increased the cerebrospinal fluid by the injection of egg albumen into 
the subarachnoid space and all the symptoms of acute brain pressure 
resulted. If the blood pressure was lowered simultaneously the symptoms 
were manifested so much the earlier. 
He argued that the entrance of the symptoms depends on anemia of 
the brain. This same thought lies at the basis of the work of others 
(3), (24) who, in general, produced brain pressure, not by increasing the 
quantity of fluid, but by pressure over the cerebral cortex. They found, 
uniformly, that these manifestations appear only when the pressure 
exerted on the brain is increased above the blood pressure, and further 
that experimental cerebral anemia through ligation, or embolic occlusion 
leads to exactly the same signs (3). Finally, Cushing demonstrated that 
these phenomena appear when the pressure and the coincident anemia 
are slowly increased, and persist until the anemia becomes sufficient to 
stimulate the vasomotor center and cause more blood to be brought to the 
brain through a general rise of blood pressure. This has great practical 
significance, because through Breslauer (5) we find in acute brain pressure 
(e.g., in fracture of the skull), an increased blood pressure, even before 
the typical symptoms such as slowing of the pulse, etc., are distinct. 
The presence of this increased blood pressure is explainable by these 
experiments of Cushing. 
The correctness of these observations is beyond doubt, but their inter- 
pretation is not quite clear. Sauerbruch and Hauptmann, by producing 
pressure on the brain and simultaneously recording the blood pressure, 
have shown that the behavior of the pulse and respiration does not 
change even when the circulatory factors of the brain have again become 
normal. By this it can be deduced that the symptoms are not entirely 
dependent on circulatory disturbances, but are also influenced by injury 
to the nerve cells, either through pressure per se, or secondarily, through 
the intimately connected circulatory disorders. We must think as Geigel, 
that these latter cannot be judged simply by autopsy findings, since they 
depend not so much on the quantity of collected blood, but on how much 
oxygenated blood was flowing through the capillaries, and how it was 
distributed. Brain pressure symptoms may also be present, therefore, 
without anemia (5). 408 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
If pressure is exerted on the brain, venous obstruction occurs first, 
i.e., passive congestion; tighter compression will involve the arteries 
with subsequent anemia. Through passage of fluid toward the vertebral 
canal the effects are diminished at first; soon, however, the cerebellum 
closes the foramen magnum and its full influence is exerted on the brain 
itself. 
Following such a circumscribed pressure are found the umbilications, 
whose presence has not been explained, despite numerous investigations 
(6), (25). Forcing out of the tissue fluids certainly plays a part, for von 
Albert and Schnitzler observed an increased flow of brain fluid from a 
cannula tied in the sheath of the optic nerve, when they increased the 
brain pressure. Besides this, the pressure on the vessels and cells may 
cause this umbilication. However, the question does not seem to merit 
the significance that has been attached to it. 
At all events, it follows from this discussion that a correlation between 
fluid pressure and brain pressure is not to be expected without further 
evidence. No certain conclusions can be drawn from the pressure of the 
fluid obtained by lumbar puncture. But not infrequently in diseases 
or injuries which are partners to brain pressure, there is an increase of 
fluid in the vertebral canal and in the ventricles, which on puncture flows 
out under increased pressure. A congestion in the venous circulation 
seems to be the best explanation for this “hydrocephalus,” for congestion 
would offer obstruction to the absorption of fluid (26). On the contrary, 
however, Breslauer, in researches on this subject, never produced an 
hydrocephalus in animals by ligation of the vena magna Galeni or of the 
veins of the neck, nor had he better success by mechanical compression 
of the aqueduct of Sylvius. 
For a conception that an acute hydrocephalus follows interruption of 
the communications of the foramen Magendi, see above in the text, the 
places of formation and the means of egress of the fluid. 
Passive congestion alone, therefore, cannot lead to increase of fluid. 
The circumstances are as complicated as in ascites, in which it is often 
necessary to assume the presence of an inflammatory factor. According 
to the investigations of Finkelburg (27), an increased formation of fluid 
follows alcohol poisoning, and this author believes the headache after a 
revel with Bacchus is due to an acute hydrocephalus. Tumors may act 
on the brain similarly through unknown chemical substances, or by 
mechanical injuries (see Reichardt (2)). 
It is not unlikely that these secondary changes determine the differences 
between experimental and clinical brain pressure, particularly the chronic 
variety which we see in our patients. All these researches on animals BRAIN AND SPINAL CORD 
409 
give us knowledge only of what is happening during a short time interval 
as we allow a pressure of measured intensity to act. 
In our patients, however, conditions are different, insofar as certain 
lasting injuries have been instantly inflicted by the pressure on the delicate 
nerve cells; if the pressure continues for a longer time, as in brain tumors 
or in unreduced depressed fractures, a whole series of later disturbances 
cloud the picture. 
It is unessential whether we ascribe these secondary complications to 
toxins or inflammation, or something else, it is essential that we regard them 
as an indication of an increase in the combined contents of the skull (2). 
The pathology itself is brought about by these complications in a reduced 
space, and it is toward this space reduction that we must direct our therapy. 
Since, therefore, this secondary swelling of the brain (Breslauer) involves 
the entire organ, it follows that these same symptoms will be called forth 
secondarily by pressure on, or disease of any or all parts of the brain. We 
have mentioned, as an example, their occurrence after ligation of the 
arteries (Hill). Further, even when the cerebrospinal fluid has a free 
means of egress, local decreases of space in the skull may bring about a 
generalized brain pressure (28). The latter, as has been emphasized before, 
is independent of pressure conditions in the cerebrospinal fluid. 
Therefore, it is always damage to brain cells with especial emphasis on 
those in the medulla oblongata, which makes so many etiologically differ- 
ent diseases so similar; and the reason for the rapid involvement of the 
brain as a whole, lies in the anatomical fact of its enclosure in the unyield- 
ing cranium, irrespective of the great delicacy and high functional capacity 
of its cells. In the most widely different diseases of the brain, in tumors, 
injuries, concussions, inflammations, hydrocephalus, the so-called pseudo- 
tumor cerebri, etc. (29), there are always the same general symptoms, such 
as slowing of pulse, vomiting, faintness, headaches, changes in respiration, 
increased blood pressure, convulsions and disturbances of consciousness, 
and pupillary changes (30). The similarity of symptoms does not neces- 
sarily point to a similarity of etiology. 
Other phenomena to which Breslauer calls attention, arise in large part 
from pressure on the medulla oblongata. To these belong the distur- 
bances of circulation and respiration, but the cause and location of still other 
disorders have not yet been found. 
It is thought that the seat of consciousness is situated in the cerebral 
cortex and that disturbances of this sphere (fainting and the like) are due 
to anemia of this part. Breslauer (31), however, showed in animals that 
pressure at anyplace picked out at random on the cortex cerebri, never led 
to loss of consciousness, but that it did occur with considerable regularity 
when pressure was increased in the posterior fossa, particularly around the 410 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
medulla oblongata. That an injury to the human cerebral cortex does 
not cause unconsciousness, is well known from war experiences. It 
is always possible, even if not probable, that these mechanical irritations 
are not adequate to produce an effect on the cerebral cortex, granting that 
it is the seat of consciousness. It could be pictured that injuries to the 
vasomotor center in the medulla oblongata would disturb the function of 
the cerebral cortex, and with it, consciousness would be abolished. 
But it seems to be fairly well established through the investigations of 
Roy and Sherington (32), Breslauer, and others, that the cerebral vessels 
are not under the influence of the vasomotor center, and that pressure on 
the medulla oblongata does not lead to anemia. In pharmacological 
poisonings also, we now assume that there is direct action on nerve cells 
(33) rather than through circulatory changes. Thus excitement or sleep 
can both be accompanied by either hyperemia or anemia. Even if it can 
be said with certainty from the investigations of Breslauer that unconscious- 
ness results from injury to the medulla oblongata, it does not follow that 
all disturbances of consciousness are controlled from this site alone, for 
hemorrhage in the internal capsule will produce this effect. A definite 
localization of the seat of consciousness is not possible at present. 
A symptom not readily correlated with brain pressure but present in 
this condition, is choked disc (34). Authors are not in agreement regarding 
its origin, and its investigation has been pursued chiefly by ophthal- 
mologists. The various theories may be grouped as follows: the mechan- 
ical theory, that is, congestion and increased flow of fluid; the inflammation 
theory, inflammatory products reach the papilla through the fluid; and 
the neurotropic theory, vasomotor nerve filaments to the papilla are 
injured by the increased pressure. All of these ideas recognize somewhere 
the relation of choked disc to brain pressure, and for surgeons, it is neces- 
sary only to remember that the relief of the pressure through trephining, 
will check the progress of the choked disc and improve it. We have 
learned from the gunshot wounds of the war, that it requires 14 days or 
longer for a choked disc to develop. 
Still another symptom must be mentioned here, viz., dilatation of the 
pupils. According to the clinical observations and experiments of Hoessly 
(30) this arises in generalized brain pressure from a centrally originating 
stimulation of the sympathetic and a decrease of tonus of the oculomotor 
nerve. There occurs, therefore, not only a paralysis of the basal centers, 
but also an irritation of the antagonist, namely, the sympathetic. In 
localized pressure, as for example, hemorrhage from the middle meningeal 
artery, we frequently see a unilateral dilatation on the side subjected to 
the pressure (Hoessly), a fact of practical significance. 
Concussion of the brain (35) follows pressure exerted for a short period BRAIN AND SPINAL CORD 
411 
of time, usually from a blow transmitted through the skull. The brain 
is driven to the opposite side, and wave-like motions scatter themselves 
throughout the cerebral substance. 
The elasticity of the brain should not be undervalued in the application 
of such force (35), (36). The factors involved have been analyzed both 
on models and skulls, and it has been found that the skull has an elasticity 
coefficient between that of a hollow sphere of brass and one of wood. 
Just as with a sphere, its surface is flattened by the application of a force, 
and its diameter enlarges longitudinally, vertical to the place struck; for 
example, a blow across the temples elongates its long diameter and 
increases its height. If the force is sufficient, a bursting fracture (3 7) occurs 
at the instant when it has reached the apex of its described alteration in 
shape. As a consequence the line of break gapes widely at the time. 
Since the skull retains its elasticity, even when fractured (v. Bruns), it 
springs back to its normal form, and during the recoil, it pinches all sorts 
of tissue, hair, fat, etc., in the line of fracture. If a scalp wound is pro- 
duced at the same time, foreign bodies such as bits of cloth and portions 
of the hat or cap may also be included. Needless to say, there is great 
danger of infection of the brain and its membranes. On account of the 
vaulted form of the surface of the skull, the pulling forces which are 
involved in depressing the inner table, are greater than the pressure forces 
acting on the outer table. The result is that the inner table is usually 
broken over a wider radius and this increases the danger of compression 
of the brain. On the other hand, the division into an outer and an inner 
table acts as an added protection, inasmuch as the external table can be 
pressed against the inner table without injuring the latter (Tillmann). 
There is definite damping of the strength of the force. ' By the same line 
of reasoning, forces, acting from within outward (gunshot wounds), cause 
greater injury to the external table (verified by the investigations of 
Tee van (38)). 
The changes undergone in the form of the skull explain the course of 
the lines of fracture to a certain degree (see also Korber, Bohl and others), 
but because of its physiological make up, the brain also has a decisive 
influence which was first recognized in gunshot wounds. If a shot from 
a modern army rifle at a short distance (about 50 meters) strikes the head, 
the skull and its contents are completely shattered. By piecing together 
the splinters it can be seen that both a point of entrance and exit are 
present; from this it surely follows that the shot passed through one side 
of the skull before the so-called explosion effect occurred (Tillmann (39)). 
We are not dealing with hydraulic pressure in this case, that is, the ordi- 
nary pressure on the brain, since the explosion must occur when the bullet 
enters tfie inner surface of the skull, and it must be assumed that active 412 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
forces are transmitted.from the bullet to the brain, and that movements 
of the particles of the brain cause the bursting. This force which the 
projectile transmits to the brain, and this in turn to the skull, is called a 
hydrodynamic pressure (40). Experimentally, the same conditions were 
obtained by shooting through a lead box filled with either water or starch 
paste, but whether the active forces are transmitted to the human brain, 
which is, of course, no fluid mass, or only to the fluid and the blood, is 
difficult to say. The so-called Kronlein (41) shot which causes the brain 
as a whole to fly out of the shattered skull, seems to indicate that the fluid 
is the only carrier of the force. According to Mertens (42) a rotary move- 
ment of the bullet, imparted by the rifling of the barrel, is necessary for 
this peculiar explosive act. But the correctness of this view is questioned 
by Franz (43) who after investigations on bullock brains and human skulls, 
believes that the results of the Kronlein skull shots are in harmony with 
the hydrodynamic theory. 
That injuries by blows or falls on the head may be increased through 
the brain is shown by Tillmann’s researches on models (36). He struck a 
glass bulb filled with gelatine and found that the hydraulic pressure 
broke the globe. The so-called indirect fractures, for example, those of 
the roof of the orbit, can be explained only through such a transmission 
of forces (44). These fractures are true contrecoup breaks. Most of 
those which had formerly been described as contrecoup are produced 
otherwise according to the investigations of v. Wahl (45), and Messerer 
(36), i.e., by extension of the other lines of fracture. 
The spread of the lines of force in the brain has also been studied on 
models (36). It was desired to determine how much the brain was 
mechanically moved by a blow or fall. The researches of Ferrari are par- 
ticularly instructive. After placing small bits of colored glass in the brain 
and striking the skull, he found a widespread splintering of the glass bits, 
even without fracture of the skull itself, provided that the glass was placed 
no deeper than 5 mm. below the surface of the brain. Felizet, in using 
paraffin filled skulls, observed an indentation of the paraffin at the place 
where the blow was struck, and a bulging outward of the opposite side, 
which is a good illustration of the way the so-called “contrecoup” arises, 
that is, damage to the cerebral cortex exactly opposite the point on the 
skull where the blow impinged.' The brain, through its change of form 
and on account of its soft texture, is moved toward the opposite side and 
may be seriously crushed from the resistance of the bones. 
Many attempts have been made to imitate brain concussion; but 
there resulted either a very severe change which was more than a “con- 
cussion of the brain,” or no symptoms at all (46). These researches 
are not entirely meaningless, however, since the fact that the human brain BRAIN AND SPINAL CORD 
413 
reacts to even slight concussion with unconsciousness, etc., contrary to the 
brain of an animal, may be on account of anatomical peculiarities, and 
because of the higher development of functions in the brain of man. It can 
be said definitely that all of these acute injuries, concussion, contusion, gun- 
shot wounds, etc., show the same general clinical symptom complex, and 
differ only in the degree of severity. They probably are alike in their main 
pathological physiological fundamentals. 
This conception was not always the generally accepted one. Since 
Kocher’s time, the phenomena of commotio-cerebri have often been looked 
upon as due to the rapidly occurring anemia. This conception is founded 
particularly on the investigations of Cushing who allowed saline solution 
to flow rapidly into the subarachnoid space, after which he found a com- 
pression of the veins and then of the arteries. This view was soon disputed 
by Koch and Filehne. Breslauer also was unable to demonstrate an 
anemia of the cerebral cortex after all sorts of acute injuries to the brain, 
so that the foundation of the teaching that pressure anemia of the brain 
is the cause of the clinical manifestations in concussion, rests on very 
insecure ground. 
According to the work of Koch and Filehne, it is questionable whether 
the blood supply and its changes are of any importance at all. These 
authors found in frogs, whose blood vessels had been emptied of blood and 
filled with saline solution, that hammering of the skull produced changes 
in the pulse and respiration, analogous to those in commotio cerebri. 
The same commotio cerebri with much increased blood pressure, was also 
obtained in dogs and rabbits by the same procedure. The objection that 
they are “ reflex] disturbances ” is not valid, even if the conclusions of 
Massland, Saltikoff (Kocher (35)), and Sauerbruch (47) are not to be 
doubted, that by blows on the chest and abdomen, such disturbances of 
respiration and pulse are also obtained. 
Quite apart from the purely mechanical changes in the calibre of the 
vessels in concussion, the blood supply of the brain is, at times, still further 
compromised by the fact that the vasomotor center itself is involved in the 
injury. This may lead to very long standing changes in the blood supply 
of the brain, especially hyperemia, and clinical symptoms, often resembling 
those of brain tumor, may appear (48). 
The symptoms of concussion have often been described as reflex (36), 
(48), but the length of time that these manifestations continue does not 
justify this view. However, there is nothing against the view that they 
are due to direct injury of the ganglion cells especially those in the medulla 
oblongata. As mentioned above, Breslauer could even relate the presence 
of the most unexplainable of all the symptoms, unconsciousness, with 
pressure on the medulla oblongata. Koch and Filehne insist that a blow 414 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
on the medulla of animals gives signs which have a marked resemblance to 
those of brain concussion. 
As the pathological anatomical foundation of these injuries to brain 
cells, descriptions have been given of diffusely scattered blood extravasa- 
tions (Bright, 1813), and degenerations in the ganglion cells. The fact 
that the capillary hemorrhages are greater in the gray matter than 
in the white, is evidence of the correctness of Tillmann’s view that 
the white and gray matter separate because of their different specific 
gravities (49). 
Of great practical interest are the alterations in the vessels which lead 
to “traumatic secondary apoplexies,” (50). Obviously there must be an 
incomplete tear or injury in a vessel wall, which, after a few days to a few 
weeks, softens and leads to hemorrhage. A similar event can occur in the 
very important middle meningeal artery (51). With this possibility in 
mind, such patients will not be allowed to pass from observation too early, 
and if secondary hemorrhage occurs—fortunately, it is easily diagnosed— 
an early operation can be performed. 
The acute inflammations of the brain and its membranes comprise 
another group of diseases which may finally lead to brain pressure. Inflam- 
mations of the brain substance run a course peculiarly their own. The 
organ reacts very slowly, and apparently passively to entering irritants, 
so that it is not customary to see a brain abscess before about the beginning 
of the second week after injury (52). Fever is often absent; the abscess 
grows but slowly, and often in periodic advances. A so-called membrane 
is formed around the abscess, but according to Cassirer (53), this is not in 
the nature of an actual encapsulation. Hand in hand with this poor 
resistance, there is a high susceptibility to infection, and in puncturing 
brain abscesses, great care must be taken to avoid infecting other parts with 
the needle. 
Just as suppuration and inflammation in other tissues are known as 
abscesses and phlegmons, so in the brain, abscesses are differentiated from 
encephalitis (54). The limited reactive ability mentioned above, makes 
the spread of abscesses to encephalitis less common than the spread of 
abscesses in soft parts to phlegmons. In fact, a brain abscess may be pre- 
sent for years without leading to a progressive encephalitis, and in this 
respect, the brain resembles bone tissue. There are, however, certain 
similarities between encephalitis and a phlegmon, for example, in war 
experiences, brain abscesses frequently were followed by an encephalitis 
after operative interference. Just as in phlegmons elsewhere, an acute 
progressive encephalitis may arise a few days after a penetrating wound of 
the skull without previous abscess formation (52). We observed a fatal 
diffuse encephalitis following exertion, in an individual who had a small BRAIN AND SPINAL CORD 
415 
scar in the brain, from a gunshot wound inflicted a year previously. In 
other cases, the immediate predisposing cause is not so apparent. 
A circumscribed encephalitis may also develop, especially in prolapse 
of the brain. In animals, Schifone and later Blegvad (55) studied the 
causes of brain prolapse. Anatomical investigations of human cases, date 
from Schrottenbach (56). With him, we must distinguish the primary 
prolapse which arises from increased pressure as soon as the bones and 
dura are separated, from the secondary prolapse which develops a longer 
or shorter time after trephining, without a heightened brain pressure. 
Finally, there is a local encephalitis, and in animals, this is observed only 
when the brain has been injured in some way after the skull is opened. In 
humans, the study of war wounds has shown that such prolapses disappear, 
of ttimes very rapidly, with the cessation of inflammation. The impression 
is gained that this rapidity is not due to organization with connective 
tissue, and subsequent shrinking, as Schrottenbach believes, but is chiefly 
due to the removal of inflammatory products, constriction of the dilated 
vessels, etc. 
The danger of meningitis consists in the absorption of toxic substances 
through the extensive surface of the meninges, until it is no longer com- 
patible with the life of the individual. The patient then dies of the 
infection. Meningitis leads, also, to an increase of brain pressure, in 
certain cases from the accumulation of meningeal fluid alone, particularly 
in the type called meningitis serosa first described by Quincke (57). 
Its peculiarity lies in an aseptic increase in the fluid or in circumscribed 
or general edema of the meninges. In certain cases, this is a collateral 
edema, e.g., in inflammations of the skull, head injuries, etc., but there are 
no grounds for believing that there is any fundamental difference from 
collateral edema in other parts of the body. It is only because of the 
paucity of space in the skull that it leads to early brain pressure, and thus 
to severe general manifestations. This meningitis serosa has also been 
observed in infectious diseases, in which case a chemical irritant may have 
interfered with the exchange of fluids. A case of Doenitz (cited by 
Axhausen (58), illustrates this possibility. A severe purulent aseptic men- 
ingitis followed the use of a rubber tube in the connection for spinal anes- 
thesia. In purulent infectious meningitis, the brain pressure symptoms 
are increased because of changes in the cerebral blood supply, but no 
detailed investigations of this question seem to have been made. 
Epilepsy was the first disease of the brain which was subjected to 
operative interference, at least, skulls from the stone age have been found, 
which plainly show the smooth opening produced by a trephine, depres- 
sion fractures in other situations denoting that epilepsy was probably 
present. In later years (59), even until the last decade, operation for 416 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
epilepsy was attempted only after trauma, and thus it came about that a 
sharp distinction was made between traumatic epilepsy (symptomatic) 
and one not traumatic (true). 
This is not a happy differentiation and epilepsy has lately been con- 
sidered as a symptom complex (60). Just as in abdominal surgery, the 
group of symptoms known as ileus arises from all sorts of diseases, so 
does this symptom complex of epilepsy arise from all sorts of brain diseases 
and injuries. Unquestionably, this theory has the great advantage of 
throwing the least number of obstacles in the path of scientific investiga- 
tion, and when the necessary fundamentals are established through 
clinical observation and experiments, a suitable classification can be made. 
Redlich and Binswanger (61) have already devised a grouping into chronic 
and acute, depending on the number of attacks. This conception seems 
useful from the therapeutic standpoint. 
For the production of an attack of epilepsy, an altered irritability of 
specialized brain cells is necessary (Binswanger (61)). This is often heredi- 
tary and statistics have agreed that about 30 to 40 per cent. (Binswanger), 
of epileptics have a neuropathic family history. Animals also show differ- 
ing dispositions. It is much easier to produce an epileptic seizure in 
guinea-pigs than in dogs; moreover, different animals of the same species 
differ in their susceptibility. Whether the inherited tendency shows the 
same and specific changes in all cases, has not been determined, but prob- 
ably not; at least the anatomical changes which we are accustomed to 
regard as signs of this disposition differ in individual cases. We often 
find outspoken signs of degeneracy: webbed fingers, polydactylism, etc. 
while in other cases there is only an increased irritability of the vegetative 
system (62). Microscopically, all sorts of changes are found in the brain, 
sclerosis of the hippocampus major, and so on, i.e., signs of degeneration 
of the brain itself (63). 
In epilepsy, following gunshot wounds of the brain, the Barany test 
is said to give indications of a general injury of the cerebrum (64). Of 
special interest, but not as yet answered, is the question of how great a 
part the secretions of the endocrine glands play in the reactive power of 
the brain cells, and if then the tendency to epilepsy is in reality an altera- 
tion in the internal secretions (Bauer (62)). 
As stated, in addition to this predisposition, there is another external 
factor, so to speak, which arises from trauma, spacfe reducing processes, 
poisoning, psychical insults, etc. This factor is easier to study experi- 
mentally, and a larger number of investigations have been made. 
Attempts were also made to discover whether the onset of epileptic 
attacks was determined by injury to a particular part of the brain; in 
other words, whether there is a site, or center of epilepsy. The move- BRAIN AND SPINAL CORD 
417 
ments during the attacks seem to point to involvement of the motor area 
in the ascending frontal convolution. 
This particular view is supported by the classic studies of Fritsch and 
Hitzig (65), who discovered that electrical stimulation of this region leads 
to movements of the opposite extremities and that typical epileptic 
seizures could be brought about by such stimuli. Studies of the effect of 
injuries, or electrical or cold stimuli, or the implantation of foreign bodies 
under the dura have been of times repeated (66). These animal studies 
in combination with the clinical, anatomical and operative findings of 
Jackson on humans, have shown that a certain percentage of cases can be 
cured by the removal of either the stimulated area of the brain cortex, or 
the cause of irritation. It is not necessary to say that the results of these 
studies have not shown any special “epileptic center” in the cerebral 
cortex. Indeed Brown Sequard (66) has shown that in a guinea-pig, 
injury of different parts of the brain stem, and even of the spinal cord and 
peripheral nerves was sufficient to incite epileptic seizures when he had 
removed the combined cerebrum and cerebellum. At the suggestion of 
Westphal (67), he struck the head of a guinea-pig with a percussion ham- 
mer and the decerebrated animal showed immediate convulsive attacks. 
It is well known, however, that guinea-pigs are easily made epileptic. 
Brown Sequard reached the conclusion at which Westphal Van Der Kolk 
arrived, that an epileptic seizure could be compared to the discharge of an 
electric current, and that it is brought about by a disturbance of the 
medulla oblongata (68). It might be mentioned that one of the famous 
decerebrated dogs of Goltz died during a spontaneous epileptic attack. 
Nothnagel believed that the “convulsion center” is located in the 
pons, and was inclined to think with Kussmaul and Tenner, that it is in 
the floor of the fourth ventricle in relation to the vasomotor center (69). 
Ziehen (70) found a place in the pons of rabbits which gives rise to tonic 
convulsions after electrical and mechanical stimulation, and in humans, 
we know of the tetanic spasms that follow hemorrhage into the ventricle, 
supposedly from pressure on the brain stem. 
On the other hand, Munck showed that a dog which had been made 
epileptic by long continued irritation of its cortex, still had convulsions 
after division of the spinal cord. So it must be acknowledged that stimuli 
for epileptiform seizures can be incited from the cerebral cortex alone. 
On the basis of all these investigations, the cortico-medullary theory 
must be considered the most rational; that is, there is no special part of 
the brain diseased, but the “discharge” of impulses is related not only 
to the cerebral cortex, but there is also irritability of the central, “subcor- 
tical motor apparatus of the pons and medulla oblongata” (Binswanger). 
Such a “discharge” apparently may be liberated from any part of the 418 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
brain. Knowledge of the organic disease has, therefore, reached this status, 
and operative procedures, in a certain percentage of cases, have been suc- 
cessful in removing those changes which produce convulsions. 
Another aim of the investigative work was to determine what sort of 
injury would bring forth the attacks. It was stated above, that they 
may be caused by cerebral injury, especially from pressure following a 
depressed fracture. It is not difficult to understand this type of long 
standing mechanical irritation. Doubtless, it will be found that a trau- 
matic etiology occurs more often than is ordinarily supposed. This has 
been corroborated at autopsy, for in patients with a seemingly genuine 
epilepsy, definite signs of skull injury have been found consistently. 
But statistics of peace times, show that the disease had a traumatic origin 
in only 3 to 15 per cent, of cases. 
Other factors have, therefore, been suspected particularly the relation 
of poisons and toxins to the disease (60). Of the most practical applica- 
tion are the studies on the effects of alcohol, especially absinthe. It 
is not necessary here to go into the debated question of whether it is the 
alcohol or the ethereal oil in experimental absinthe epilepsy, which pro- 
duces the convulsions, but the fact that epileptics are made worse by 
alcohol is well known (71). The traumatic epilepsy of the war provided 
a large amount of material for study, especially because it occurred 
frequently in individuals who were previously healthy and not predisposed 
to it. It is often surprising to see the attacks resist every form of treat- 
ment and then disappear after total abstinence. Like alcohol, lead, also, 
is harmful. These toxic epilepsies are often differentiated from “true” 
epilepsy (72) and yet considering our meagre knowledge of the entire 
subject, it seems that such a division is arbitrary. 
From clinical observations (61) and animal experiments also (73), it 
seems probable that bacterial toxins may cause an epilepsy. Cases of 
stubborn epileptic attacks in syphilis have beeh known to disappear after 
inunctions. Tilmann (74) is inclined to return to the idea of the previous 
infectious changes in the arachnoid which he saw so often at operation, in 
cases of genuine epilepsy. These chronic inflammatory changes in the 
arachnoid may act as irritants to the cerebral cortex, and thus to seizures. 
Tillmann believes these changes are much more potent irritants than a 
splinter of bone pressing on the brain, and, therefore, the conclusion follows 
that the causative mechanisms of traumatic and true epilepsy have much 
in common and there is no fundamental difference between the two. 
The extent and distribution of the changes in the arachnoid vary, however, 
in individual cases, and operative procedures in cases of true epilepsy are 
more difficult than in traumatic. Further investigations are necessary 
to show whether these explanations are correct, or whether they are not BRAIN AND SPINAL CORD 
419 
just a trifle too simple. Tillmann’s statement that these changes in the 
arachnoid are observable only in the living during operation, and not at 
autopsy, seems worthy of further observation. 
Search has been made for familiar chemical substances which would 
produce convulsions, but less violent than those of strychnine, or tetanus 
toxin. Landois (75) was successful in applying creatin to the brain surface 
of animals. This, and other metabolic substances were chosen because 
epilepsy has been, and still is, regarded by many as a poisoning of the 
central nervous system, through toxic products of metabolism. This 
opinion is especially emphasized in French literature (76). 
Recently, Sauerbruch (77) produced typical clonic and tonic convul- 
sions in monkeys by the injection of cocain into the blood stream after 
their cerebral cortex had been injured. The dose necessary was only one- 
fifth of that which produced convulsions in normal monkeys. This 
hypersusceptibility increased steadily following the operation until finally 
twitching of the jaws occurred without the drug. This could also he 
brought about by means other than operative damage to the brain, as, for 
example, by producing fatigue of the central nervous system by passive 
movements of the extremities. By this method, the same phenomenon is 
obtained as in electrical stimulation of the cerebral cortex, i.e., an ever- 
increasing irritability of brain cells. 
Another group of investigations was designed to discover the part 
played by changes in the blood supply of the brain. It is well known 
that exsanguinated animals show spasm-like twitchings somewhat similar 
to epileptic seizures (78). This occurs not only when fowl are butchered, 
but also in mammals. Similar spasms develop after ligation of the caro- 
tids, in which case the poor blood supply, or better, the insufficient oxygen 
supply, is held responsible. For this reason, convulsions occur when all the 
cerebral veins are ligated, and the gaseous interchange hindered in this 
way (79). Sauerbruch (77) studied this subject by varying the pressure 
applied to the brain and producing alternate anemia and hyperemia in 
dogs made epileptic with cocain. He was also successful in obtaining 
repeated epileptic seizures by this method. Care is always necessary in 
applying the results of these animal experiments to humans, since Bier 
(80) was never able to bring about an attack in an epileptic by tying a 
tight band around the neck or by suddenly removing it, and yet Momburg 
and Eastmann (81) have cured, or at least greatly improved cases of 
chronic epilepsy by diminishing the calibre of the carotids. The effect 
of such a slight decrease in circulation is naturally quite different physio- 
logically from the effects of anemia, but it is conceivable that such 
diminution of blood supply will diminish the irritability of the cells. 
The relation of brain pressure to epilepsy has been repeatedly investi- 420 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
gated from the surgical standpoint, especially during the attacks, because 
of the hope of the therapeutic influence of reducing the pressure. Kocher 
(82) was of the opinion that attacks were brought about by a sudden 
increase of pressure, and as a matter of fact, Ito found this increase in 
guinea-pigs. He attributed it to functional hyperemia. But the results 
of measurements obtained through trephine openings in the skulls of epilep- 
tics and non-epileptics, showed such small differences that no conclusions 
can be drawn from them. Tillmann and Bungart (74) found in a patient 
who had an epileptic attack following puncture of the ventricle, that the 
pressure of the ventricular fluid did not rise until the seizure was well 
established. They concluded from this, that Kocher’s idea is incorrect. 
It must not be forgotten, however, that this case of tumor of the cerebello- 
pontine angle with secondary hydrocephalus was entirely different, and 
these seizures must not be compared to true epilepsy without further 
qualifications. On the other hand, Nowatzki and Arndt (83) found that 
the brain pressure was normal before, increased only during the first tonic 
stage, and decreased during the clonic twitchings. After what has been 
said, it is obvious that the value of this work will not be known until it is 
settled whether the fluid pressure per se gives information of brain pressure. 
The operative brain findings in true epilepsy give no certain answer to this 
point. In individual cases, the dura is tightly stretched, the brain is not 
pulsating or bulging; in other cases, there is nothing indicative of height- 
ened pressure (84). A number are cured or improved by trephining for 
tension—Mockel reports 25 per cent, cures and 25 per cent, improvement 
and as many in true as in traumatic epilepsy, but his statistics cover 
only small series of cases. We do not know if the brain pressure was pre- 
viously high in these cures, so that the different types of epilepsy differ 
in this respect, nor do we know what other factors might be concerned in 
the cure. Wilms (see Mockel) considers the possibility of the escape of 
some sort of toxic substances through the trephine opening; but this is 
all conjecture. In animal work, Ito and Mockel thought they could 
show that trephined animals would not have an epileptic attack as 
easily as an untrephined one, and that the attacks could be more easily 
controlled. 
Operative surgery of the central nervous system seeks not only to 
remove the symptoms of general brain pressure, but also to improve local 
injuries which make their presence known by paralyses. Brain surgery 
is, therefore, also a “surgery of the motor area” (v. Bergmann). These 
paralyses originating from local pressure, will entirely or partly disappear 
if they arise from an extradural hematoma from rupture of the middle 
meningeal artery. According to v. Bergmann (1), a localized reduction of 
blood supply is sufficient to abolish the function of the motor area of the BRAIN AND SPINAL CORD 
421 
cortex. Pressure continued for a longer time brings about swelling 
changes in the nerve cells and fibres. Other diseases, such as tumors or 
cysts following injuries, cause paralyses not only through pressure on the 
nerve cells, but also by a sort of inflammatory process (see choked disc). 
The extent and region of paralysis depends on the localization of the disease 
processes. Animal experiments and operative findings on man have each 
contributed their share, and our knowledge of the topography of the brain 
has'been much enriched in the last decades (85). 
In the nature of things, operative procedures, per se, produce a local 
injury. It should be remembered that in operations in which the corpus 
striatum is injured locally, there is marked post operative rise of tempera- 
ture at times (86). Unimportant brain tumors have occasionally pro- 
duced psychical disturbances of a general type Avhich have disappeared 
after removal of the tumor (87). 
Since there are intracranial sympathetic branches, for example, the 
ganglion ciliare, or the plexus woven around the cavernous sinus, injuries 
to these may give rise to hyperalgesic zones in the neck through radiation 
to the cervical segments. Wilms (88) was the first to draw attention to 
this symptom. 
In surgical diseases of the spinal cord, the general symptoms of 
increased pressure are far less important than those of local origin which 
give rise to paraplegia. The histological changes which the cord suffers 
from pressure have been well studied in animals by placing aseptic foreign 
bodies, laminaria tents, bird shot, etc. extra- and intradurally in the 
spinal canal (89). Swelling and vacuolization of the cells usually fol- 
lowed, due mostly to lymph congestion. Inflammatory changes were 
occasionally observed (see Enderlen). It is an open question whether the 
lymph congestion acts mechanically on the nerve tissue or whether it 
interferes with nutrition (90). 
The effects of concussion of the spinal cord are similar to those of the 
brain so the reader is referred to that paragraph (36), (82). Experimental 
investigations have been undertaken by Schmaus and Newton (91). The 
most important pressure producing conditions in man are tuberculosis of 
the vertebrae (92) and gun shot wounds. In both cases, inflammatory 
changes are added to aseptic pressure. This has been investigated 
experimentally by Israi and Babes, among others, using mustard oil in 
the spinal canals of dogs. Particularly in caries of the vertebra, the 
question is often debated of whether the myelitis follows the pressure, 
or whether it is from the spread of inflammatory processes (93). Such 
an accentuation of one pathological process should always be avoided 
in a complicated disease. That both may cause the paralysis in question 
is shown by our experiences in laminectomy for vertebral caries. 422 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
In gun shot wounds also, the mere mechanical influence of a foreign 
body embedded in the spinal cord should not be considered without 
recognizing the danger of an infection spreading from it. This question 
is, of course, important in the decision of removal or non-removal of the 
bullet in any given case. Braun (94) has carried out experiments to 
clear these points. He embedded small shot in the spinal cords of dogs 
and then examined the changes histologically, coming to the conclusion 
that “the gravity of the lesions depends on the amount of injury done to 
the cord while the shot is being embedded, and on the amount of space 
encroached upon by the shot.” The histological changes (89), (95) which 
follow injuries are manifested in two hours by swelling of the axis cylinders 
which rapidly spreads and increases in amount. Later, proliferative 
changes begin. This swelling and cell edema gradually diminish, and 
thus is explained the early spread and later improvement of the paralyses. 
An experiment by Braun shows, however, that these injuries which bring 
about paralyses are caused in part by the presence of the foreign body 
per se. In one of his dogs, in which he had produced severe paralyses 
by placing a shot in the spinal cord, he brought about an improvement by 
its removal. This agrees in general with war experiences, and early 
removal of the bullet seems best, because the danger of secondary infection 
is always present (96). 
The effects of section of the cord on the general metabolism have been 
reported by Hari (97). Section at the neck is followed by diminished 
oxygen consumption and blood pressure, while section through the dorsal 
and lumbar regions has no observable influence. The diminution of gas 
exchange and the blood pressure run parallel, so that both are probably 
related to a certain degree to each other. The decreased gas exchange 
may follow the slowing of the circulation. 
The clinical result of such compression or injury is spastic paralysis. 
Normally, the sensory stimuli coming from the periphery are weakened 
by inhibitory impulses flowing in the pyramidal tracts from the brain. 
If these latter fibres are injured or destroyed by pressure, “the ‘tension’ 
of the gray matter of the spinal cord, by receiving the unweakened sensory 
stimuli is increased, and there is a lowered threshold of response” (98). 
These processes are, of course, not understood in their entirety, but of this 
much, we are certain, that spasms do not arise in an extremity when all 
its sensory fibres are cut, or they are diminished in degree if their irrita- 
bility is lowered. This has been shown in the results of the Forster opera- 
tion, that is, resection of posterior sensory roots of the cord in spastic 
paralyses. Such paralyses appear, of course, not only after pressure on the 
spinal cord, but also in all sorts of brain affections, provided that the 
inhibitory fibres in the pyramidal tracts are involved. S toff el (99), in BRAIN AND SPINAL CORD 
423 
his operation, attacks the other side of the reflex arc, namely the motor 
parts, by cutting twigs of the motor nerves close to their insertion in the 
muscle. In this way, the nervous control is also weakened. 
Diseases of the vertebral column itself are no different in principal 
from diseases of the extremities. The influences on the organism of the 
much used therapeutic measure of suspension by the head may be briefly 
mentioned. Experiments covering this question were done by Anders 
and Joachimsthal (100), etc. Anders attempted to discover how the 
increase in length of the spinal column is brought about, while Motschut- 
kowsky (cited by Joachimsthal) studied its influence on the spinal cord. 
Certain changes in the position and tension of the roots and meninges were 
recorded, but they do not seem to have any particular meaning. The 
same may be said of its influence on circulation, as brought out by 
Joachimsthal. 
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1. Lit. see Bergmann: Kronlein, Kuttner in Handbuch d. prakt. Chirurgie, 4th edit,. 
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der Blutversorgung des Gehirns,” Stuttgart, 1890. Hill: Phys. and Path, of 
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4. Adamkiewicz: Wiener med. Wchscrft., 1888; Sitzungsber d. akad.; Wien, 1883 
and 1890; Wiener klin. Wchscrft., 1897. 
5. Sauerbruch: Grenzgebiet, 1907, 3 Suppl. Breslauer: Grenzgebiet, V. 30. 
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7. Mestrezet: Liq. cephale rachidien. normal and path. Paris, 1912. 
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10. Bungart: Festschrift d. Kolner Akad., 1915, p. 707. 
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Deutsche Klink. am. Anfang des 20 Jahrhunderts. 
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18. Reichmann: Ztschrft. f. d. ges. Psychol, and Neurol, 1912. Haller: Grenzgebiet, 424 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
19. Grashey: Exp. beitrag. z. Blutzirkulation i.d. Schadel-Ruckgradshohle; 
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32. Ray and Sherrington: Journ. of Physiol., 1890. 
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34. Wilbrand and Sanger: “Neurologie des Auges,” V. 14. 
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37. Bohl: Deutsch. Ztschrft. f. Chir., V. 43, lit. 
38. Teevan: Handbuch d. prakt. Chir., 4th edit., V. 1, p. 65. 
39. Tillmann: In Wilms-Wullstein, Lehrbuch d. Chir., 6th Edit., V. 1, p. 69. 
40. Coller and v. Schjerning: Ueber. d. Wirkung u. Bedeutung d. neuen Handfeuer- 
waffens Medizinalabt. d. preuss. Kriegsminist., 1894. 
41. Krohnlein: Chirurgenkongress, 1899; Brun’s Beit., 1900, 29. 
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46. Pirogoff: Grundzuge d. Kriegschirug., p. 74-75. Stromeyer: Handbuch d. Chir. 
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50. Bollinger: Festschrft. f. Virchow, 1891, V. 2. 
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Vienna, 1909, Der Hirnabscess. BRAIN AND SPINAL CORD 
425 
54- see Boschard, Neue Deutsche. Chir., 18, 3. 
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Boenninghaus: “Die Meningitis serosa,” Wiesbaden, 1897. 
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63. Alzheimer: Ver. deutscher Nervenarzte, 1913, 7. 
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71. Magnan: Arch, de physiol., 1873, V. 5. 
72. Heilbronner: Handbuch d. inneren. Med., V. 5, p. 837. 
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75. Landois: Deutsch. med. Wchschrft., 1887. 
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78. Kussmaul and Tenner: Moleschott’s-Untersuchungen zur Naturlehre, 1857, 
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79. Herman and Esches: Pfluger’s Arch., 1870, 3. 
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85. Brodmann: Neue Deutsche Chir., 18. 
86. Cited by Thale: Mitt. a. d. Grenzgebiet, V. 3. 
87. Friedrich: Deutsche Ztschrft. f. Chir., V. 67, p. 656. 
88. Wilms: Mitt. a. d. Grenzgebiet, 1903, V. 2. Also Clairmont, ibid, V. 19. 
89. Enderlen: Deutsche Ztschft. f. Chir., V. 40. Kahler: Prager. Ztschrft. f. Heil- 
kunde, 1882. Rosenbach and Schschterbak: Virch. Arch., V. 122. 426 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
90. Rumpf: Pfluger’s Archiv., V. 26. 
91. Newton: Brit. med. J., 1913, p. 1101. Schmaus: Munch, med. Wchschrft., 
1899, 1. 
92. Babes: Vierteljahrschrift f. Dermat. u. Syphilis, 1882, V. 9. Schmaus: “Die 
Kompressionsmyelitis bie Karies,” d. Wirbelsaule Habilitationschrift, 1890. 
93. Michaud: These de Paris, 1871. 
94. Braun: Deutsche Ztschrft. f. Chir., V. 94. 
95. Schifferdecker: Virch. Arch., 1876, V. 67. 
96. Heineke: Lehrbuch d. Kriegschr. Borchard Schmieden. Marburg and Ranzi: 
Arch. f. Kb'n. Chir., V. hi and Wiener klin. Wchschrft., 1915. Perthes: 
Bruns Beitrage, V. 97. 
97. Hari: Biochem. Ztschr., 1918, V. 89. 
98. Forster: Ergebn. d. Chir., V. 2, p. 176. 
99. Stoffel: Vulpius-Stoppel Orthopad-Operationslehre Stuttgart Enke. 
100. Anders: Arch. f. Klin. Chir., V. 38, p. 58. Joachimsthal: Arch. f. Klin. Chir., V. 
49, p. 460. CHAPTER XII 
EXTREMITIES 
The framework of the body, particularly of the extremities, is made up 
of the bones, in conjunction with the joints, tendons and muscles. 
The shapes of the bones are closely related to their functions, and since 
these in their turn depend on the action of the muscles, it follows that 
muscles and bones are mutually interdependent. In all therapeutic 
measures, therefore, particularly in fractures, we must bear in mind this 
close relationship. We cannot attain ideal healing of a fractured bone 
without considering the functions of the muscles involved, and vice versa. 
The task of bone tissue is to offer resistance to push or pull (i), and the 
long bones are also subjected to bending stresses. The performance of 
these functions is the stimulus which preserves their form and structure, 
and if it is removed or diminished as in paralyses, atrophy follows from 
the activities of osteoclasts. In addition, a so-called flat or smooth 
atrophy has been described by certain authors (Roux (i), p. 228), but we 
will speak of this disuse atrophy in greater detail a little later. 
The finished bone is not built homogeneously, but as is well known, 
consists of an outer compact layer, and an inner spongy layer. The 
marrow cavity occupies the center. The hardness, density and elasticity 
depend in the main on the superficial layer of the compacta, but these 
three parts vary under physiological and pathological conditions. Young 
bones are more elastic, in that they contain relatively less inorganic matter 
(2); the bones of adults, on account of their greater calcium content, are 
harder and denser, and, therefore, break less easily than those of children, 
but since the periosteum is stronger in the latter, the so-called green stick 
fracture is more common, that is, a fracture in which the bone is bent, but 
the periosteum remains unbroken and prevents displacement of the 
fragments. 
The form taken by a fracture, ignoring the influence of the force, is 
determined by the shape of the bone. Bending breaks are more common 
in long bones, compression fractures in short bones. The direction taken 
by the lines are in accordance with the physical laws of pull, push and 
pressure, and it is possible, as shown in every surgical course, to reproduce 
a given fracture experimentally on a cadaver, after the action of the forces 
producing the break have been studied in the patient. In general, longi- 
427 428 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
tudinally running lines indicate compression, transverse lines, bending or 
shearing. 
The displacement of the fragments is closely dependent on the muscu- 
lature, for every muscle in the body is stretched somewhat beyond its 
natural length and has a definite tension with each position assumed by 
the joint. For this reason the central end of a tendon quickly retracts 
after severing, and, in a break of the bony scaffolding, which determines 
the tension of the muscle, the fragments are pulled toward and over each 
other, and the displacement occurs in the longitudinal axis. The tension 
is retained after death, for the muscle retracts when it is severed (3). 
This passive stretching allows of a quick approach of its points of 
attachment at the very beginning of contraction. If the muscle were 
thoroughly relaxed at the beginning of a movement, a part of its strength 
“would be lost without producing a mechanical effect” (Luciani). But 
the traction is not entirely passive, but is influenced by what we call 
“tonus,” that is by a tension which is an expression of the livingenergj-of 
the muscle (Luciani), and which depends on its nervous innervation. 
Accurate measurements of the tension imposed on the bones normally 
and when weight is applied, are given by Grunewald (4). 
Muscle tonus is the most important force which holds the bones against 
each other and keeps the joint surfaces in contact. The latter, of course, 
are held in their definite positions by the capsule and ligaments, but 
these means of support are not sufficient to keep them safely in position. 
In certain situations, shoulders, hips, and fingers, atmospheric pressure, 
as shown as early as 1836 by E. Weber (6), helps to press the head into the 
socket and keep it there. Experiments and measurements recording the 
effect of this factor on the various joints have been made by Aeby (7). 
But it is certain that muscles play the largest part in the approximation of 
the surfaces, for if they relax or become paralyzed, a very insecure joint is 
the result. Abnormal mobility as seen in contortionists, or in rachitic 
children, depends on a pathological relaxation of the musculature (8), or 
perhaps on the ability of the particular person to allow the antagonists to 
become more relaxed during certain movements than is possible in a 
normal individual. Bing (9) found certain histological changes in the 
musculature of rachitic children, which he believes is responsible for the 
abnormal laxness; furthermore, he found a diminution of their electrical 
irritability. 
In functioning, muscles alternately exert pressure and pull and these 
forces are functional stimulants to the bones and may lead to changes in 
their structure. This internal remodeling shows itself particularly in the 
spongy trabeculae, and is one of the best and earliest known functional 
adaptations in the body (10). If the bone is used vigorously, it hypertro- EXTREMITIES 
429 
phies, and a change in its internal structure occurs “trajectorially.” 
It may also increase in size locally, under increased demand for function 
as, for example, the thickening of the cortex on the concave side in bowing 
of the legs (Roux, p. 226). These changes in the form, etc., do not occur 
as R. Fick (11) believed, from “plasticity,” as in a piece of clay, but accord- 
ing to “a regulated reaction of the bone and cartilage in response to differ- 
ent mechanical stimuli,” which Roux (1) calls “the functional adaptation.” 
There is no necessity of discussing the question which has played such a 
large role in surgical literature, of whether the largest number of cases of 
pathological bowing can be better explained by pressure, or by a response 
to functional demand. The impression is gained from reading the 
different works, that the arguments were really far fetched (12). In their 
more general relations, all these deformities follow the ordinary laws of 
statics and mechanics just as the normal movements of the joints. Details 
of this may be found particularly in the assembled work of R. Fick and 
Strasser (13). 
The above remarks (14), that readjustment of the skeleton may occur 
in adults through action of muscles, brings up the question of whether the 
growth of the skeleton is related to the muscle anlagen in embryonal 
life also. This does not seem to be the case in a certain lower animal 
according to the investigations of Braus (15), who found rather a wide 
independence in the development of the skeleton and the musculature 
(“ self-differentiation ”). 
That the form of muscle also depends on the skeleton has been shown 
experimentally by a number of workers who started with the known 
observation, that negroes, even when very muscular, usually have a small 
calf in comparison with Europeans (16). The development of the calf 
muscles is closely associated with the length of the tuberosity of the os 
calcis; if this is long, the tendon of Achilles is short, and the calf muscles 
are more prominent (as in Europeans). If the tuberosity is short, the 
Achilles tendon is very long and the muscles of the calf are confined to a 
small localized prominence a short distance below the popliteal space, 
while the remainder of the calf shows no bulging (as in negroes). Marey 
and Joachimsthal produced a definite change in the calf musculature of 
animals by shortening the tuberosity of the os calcis; an alteration in 
length of muscle and tendon which is obviously an adjustment to changed 
function. It follows from this, that a smaller circumference of a joint does 
not necessarily point to a less important function. 
Now a muscle which grossly seems of uniform structure does not have a 
uniform function throughout. Modern physiology, (seeLuciani), takes the 
standpoint that in every striated muscle there run two kinds of fibres, the 
red, rich in sarkoplasm and the white, rich in fibrils. The red fibres are 430 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
said to contract more slowly, and, as Grutzner, puts it, are an “internal 
brake,” that is, they prevent a rapid relaxation after contraction. In lower 
animals, this differentiation of function often lies in different muscles (17). 
Thus, according to v. Uxkull (18) the spine of the Echinoidea (Sea Urchin) 
has an outer movement muscle and an inner “brake” muscle. The latter 
functions so that “with every change of body weight, either in the direc- 
tion of increase or decrease, changes in the tension are equalized.” To 
preserve the proper degree of tension, this function is regulated by impulses 
from the centers. In mechanics, there is nothing to compare with this 
exquisitely regulated mechanism. The muscles are not as a rubber band 
which stretches a certain amount with a small weight, and correspondingly 
more with a heavier weight, but there is a definite threshold and nothing 
occurs until this is passed, after which there is maximum contraction. 
These remarks, of v. Uxkull, apply in a general way to the muscles of the 
human, even if there is no actual separation of the two muscle 
groups. 
In man, the knowledge of this double function was first gleaned from 
the anatomical studies of Boekes (19), who found in each fiber both medul- 
lated and non-medullated nerves, which ended among the fibres in different 
ways. By careful dissection, he separated quite clearly these two kinds 
of nerve filaments. Physiological and clinical investigations (20) based 
on these studies, differentiated the rapid muscle twitchings from the more 
leisurely muscle tonus, as Mosso (21) had already done, but contraction 
and tonus are so intimately connected in all muscular movements as well 
as in their function of support, that it seems unprofitable to differentiate 
them for clinical surgical purposes, except in certain particular questions. 
Thus, for example, the muscle cushions of amputated arms robbed of their 
natural insertion, lose more or less of their tonus. 
For practical purposes still another division has been established (22). 
If a peripheral stimulus such as an injury reaches a muscle it reacts in 
different ways, according to whether it carries a load or not. If it carries 
a load, as for example, the biceps with a fixed elbow joint, it becomes 
hard (tonus function) without changing its length. If it is unloaded when 
the stimulus is applied (biceps with a movable elbow joint), it shortens 
without becoming hard. This point of view has considerable significance 
in the management of fractures. The injury which occurs to the muscle 
at the time of fracture, and the damage after the injury, such as compres- 
sion between the broken ends is very irritating to it. The ends of the 
fragments are pulled over each other with greater force than if only the 
normal tonus were operating, and the muscle stubbornly resists every 
effort at separation by contracting and remaining in a state of board-like 
rigidity. Efforts to overcome this resistance with sudden force lead to EXTREMITIES 
431 
severe damage. In the first few hours after injury, the muscle is said to 
be in a state of shock, according to Zuppinger-Christen (23), so that it does 
not react to these different injuries, but this idea is not generally accepted 
(Matti (2)). 
We have, until now, spoken only of the function of muscles in connec- 
tion with their likeness to an elastic band, and their activities in holding 
the skeleton firmly together. They have a second function, viz., the serv- 
ice of locomotion by shortening and elongating. In every such compli- 
cated movement, and these are seemingly the least complicated in our 
body, a whole group of muscles and not a single one acts, so that, as Du 
Bois-Reymond (24), points out, the morphological grouping of muscles, 
as taught in anatomy, gives an entirely false picture of their functional 
performance. Even the more recent classification into certain systems 
regards an action occurring in a limited time as a “special case,” for, if 
the movement occurs toward one or another direction, entirely different 
groups are called into action in each case. Thus, there is a continuous 
change in the grouping, and there are “antagonists” and “synergists” 
only at the time of movement, and not in the permanent sense taught by 
anatomy. This is further complicated by the fact that a number of 
muscles pass over two joints, and contribute to the movements of both. 
The influence of a muscle, however, reaches still further. As pointed 
out particularly by Otto Fischer (25), it does not, in the main, seek to 
move only one joint, but to bring a whole part of the body into motion, 
and it follows that the muscle finally acts not only on those joints and 
bones over which it plays, but also on joints which are apparently entirely 
out of its sphere of action. This has important practical bearing. We 
will see in discussing muscle and bone atrophy, how this distant influence 
makes itself felt. The same holds true in deformities. 
This influence is exerted not only when they actually contract, but also 
when they enter a state of tonus, and like a transmission belt, bring about 
movements. This coordinated movement of muscles may be illustrated 
when the knee is forced to bend and the heel to rise by the flexing of the 
hip joint (26). 
The variety of movements which muscles covering several joints are 
able to bring about, makes it necessary that they slide over the bones 
underlying them, but only when the joints involved are moved in a 
particular way. During the opposite movement, the muscle remains 
quiescent. This fact is used in therapeutic measures, as for example, the 
fragments of a fractured patella are brought as closely together as possible 
by strong flexion of the hip with the leg extended at the knee. Further- 
more, it explains why the adherence of a muscle to a fracture leads to such 
disturbances of motion. 432 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Since the amount to which a muscle can shorten is limited, and since 
according to Schwann’s law this power diminishes rapidly as its length 
decreases, it follows when a muscle covers several joints, that the movement 
of one joint is incomplete when the other joint is also moved, because the 
strength of the more than one jointed muscle fails. For this reason, we 
cannot easily extend the knee in a sitting posture, or close the hand freely 
with the wrist maximally flexed, nor open the hand with the wrist fully 
extended. This is spoken of as the “relative insufficient length of muscles 
crossing two joints” (27). 
In every joint, or rather in each of the extremities as a whole, there is a 
position in which all the muscles are in equilibrium, i.e., no muscle is 
particularly stretched or particularly relaxed, and there is definite rest for 
the limb. In the leg, this is when the knee and hip are bent and the ankle 
in such a position that the foot points slightly downward. These rest 
positions have secured full recognition in the modern treatment of frac- 
tures. If we apply a stretching bandage to a leg in this rest position, we 
need much fewer weights to correct the shortening than if the knee and 
hip are extended and the foot is in a right angled position, that is, all the 
muscles are evenly relaxed and the pull which is necessary to compensate 
for a longitudinal displacement, according to the above remarks, meets 
the least resistance. This lighter weight, of course, produces a smaller 
injury to the muscles. As a consequence, the functional results in frac- 
tures treated in a semi-flexed position are considerably better than those 
treated in full extension. That the much used position of extended knee, 
almost extended hip, foot in a right angled position, is unphysiological, can 
be demonstrated at any time on one’s own body by the feeling of stretching 
and fatigue. No person without compulsion would assume this position 
asleep in bed. 
These rest positions are equally important in the arm, as in a typical 
fracture of the radius or humerus. If an arm broken into the diaphysis is 
bound in a triangular splint, there will result a dislocation to the periph- 
ery, and after healing, the patient holds the hand so that the back of the 
hand instead of the thumb, is anterior. Therefore, when the humerus is 
directed away from the body at an angle of 450, it is necessary to bring 
the forearm parallel to the ground. 
The injury which occurs even with passive stretching, is effective also 
in a paralyzed muscle. The muscle loses its elasticity and tonus (28). 
Therefore, the rule in paralysis of the radial nerve, not to allow the hand to 
hang, but to keep it on a splint in a mid position, otherwise the extensors 
will be so damaged that their function will not return completely, even 
when innervation is reestablished. 
By muscle sense, we understand with Sherrington, the total sensory EXTREMITIES 
433 
impulses which originate in the motor apparatus, namely, muscles, tendons 
and ligaments. That muscles are sensitive to pain is seen in goiter opera- 
tions during which the muscles are divided and sutured. Probably the 
pain sense is related to the nerves which accompany blood vessels, at least, 
the sensitivity of the muscles is still preserved, even increased when the 
plexus supplying the arm is completely paralyzed (29). In stretching, 
the muscle is also sensitive to pain. 
Furthermore, a muscle has a pronounced sense of position, although it is 
questionable whether we are aware of the position occupied by a certain 
joint by means of this “deep sensitivity,” or through sensory paths from 
tendons, joint capsules, and ligaments. Modern physiology and neuro- 
pathology have taken a stand on this question (lit. seeLuciani (3)). It 
may be said that there is a relation between skin sensitivity and deep sen- 
sation, but in spite of disturbances in the former, there is a definite appre- 
ciation of the position of the parts of our body from deep sensations (30). 
Particularly instructive and consistent are the experiences of surgeons, not 
only with local anesthesia, but also in injuries to single nerves. We know 
that a finger that has been made insensible by a local anesthetic injected 
at its attachment to the hand, does not know its position in space, even 
though the muscles and higher located tendons are undisturbed in their 
innervation. Similar observations have been made in injuries of single 
nerves in the arm or leg. More exact experiments have been made by 
Lehmann (31). He could find changes in position sense and movement 
disturbances only through injury of the tibial, ulnar and median nerves. 
In his experiments, for instance, it was easy to separate skin sensitivity 
from position sensitivity of the thumb, by paralysis of the median nerve. 
The skin of the thumb is, of course, partly supplied by the radial nerve. 
In lower animals, the independence of skin sensation and deep sensation 
is shown best by Claude Bernard’s experiments, in which he removed 
the skin of a frog and found no changes in its ability to move. 
In regard to the second question of whether deep sensation is trans- 
mitted from muscles, or from joints and ligaments, physiologists believe in 
general, that the sensitivity of ligaments is more important than that of 
muscles, particularly because of the consideration that the latter, especially 
when they cover several joints, have such varied functions. It is, therefore, 
not very probable that the sensations of definite position in a joint are 
transmitted from the muscles alone, although from the standpoint of the 
surgeon, the position sense of a muscle must not be underestimated. At 
least, in amputations and disarticulations, there is a greater surety of 
movement and better knowledge of the momentary position of the oper- 
ated member, if the muscle parts or tendons are sutured over the stump. 
Furthermore, the experiences with artificial joint mobilizations have shown 434 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
that the patient with closed eyes, can tell exactly what position his joint 
occupies, even if all the capsule and ligaments have been removed (32). 
The whole subject of position sense is made still more difficult by the 
fact that central sensations arise, which precede an actual movement. A 
number of the most prominent physiologists and psychologists such as 
Johannes Muller, Helmholtz, Wundt (33) and others are of the opinion 
that we not only feel the movements which are carried out, but also 
intended movements. But this theory of central innervation which can 
only be mentioned here, does not receive general recognition (see Luciani 
(3)). How the final regulation, and switching about, or shunting of muscle 
function and its sensation are controlled in the centers, is shown among 
other ways by the surgical observations in the learning of a new function 
in muscle transplantations. This “learning anew” occurs consciously 
at first. When, for example, as in one of E. Schmidt’s published cases, 
the latissimus dorsi was transplanted on the biceps, the patient at first 
could bend his arm only if he consciously prepared himself to teach back- 
ward. Later the bending was done without such a preparation. The 
same occurs in the building of muscle channels according to the method of 
Vanghetti-Sauerbruch (34). Of course, the conditions are not so compli- 
cated in this case, since, whenever possible, flexing muscles are employed 
to flex, and vice versa. If this is not done, but flexors are united to 
extensors, the weakness of the extensors in comparison to the flexors is at 
once apparent, since, by this artificial arrangement, they must learn this 
function gradually (34). 
A similar lesson must be learned in paralyses when a movement is 
taken over by other muscles. It may happen that a small part of a 
muscle will attempt to perform a new function, while the larger part 
goes on quietly with its old function. Thus Kron (35) could so teach the 
pectoralis major that its clavicular portion replaced the paralyzed deltoid. 
Finally, it must be recalled in this connection that certain individuals 
who have had a limb amputated, still have the sensation as though the 
member were present, and think they can move the toes of the amputated 
foot. 
If a limb is partly paralyzed or if its movements are hindered by stiff- 
ness or partial ankylosis, every movement demands an increase of innerva- 
tion force, and patients are exhausted after small efforts, even if the work 
performed is trifling compared with that needed to tire a normal muscle. 
All this leads to the conclusion that the theory of central innervation 
has much in its favor. 
If a muscle loses its point of insertion it not only fails to keep pace with 
the general body growth, but also atrophies. This is the reason stumps of 
amputations done during childhood become conical in shape (36). EXTREMITIES 
435 
That such a highly differentiated structure and one whose function is so 
nicely adjusted to the place in which it lies, should withstand transplanta- 
tion poorly in spite of ability to learn new tasks is quite obvious. The 
possibilities of transplantation have been studied in both animals and 
man (37). Eden, who has recently reviewed the literature, reaches the 
conclusion “ that, as yet, there has been no proved successful case of free 
muscle transplantation.” The transplanted muscle heals, but in a short 
time it is replaced by connective tissue. The difficulty of all these pro- 
cedures is that muscles, blood vessels and nerves, are all an inseparable 
unity, and an interruption of the blood supply for even a short duration 
is tolerated very poorly, and, as we will see, without its nerve supply, the 
function is entirely lost. 
The question of whether wounds and defects are filled in by connective 
tissue, or whether there is a power of regeneration, is answered in a dif- 
ferent way by the clinician than by those who base their conclusions on 
animal experiments. Zenker (38) had pointed out that a widespread 
regeneration must take place following the necrosis of muscle during 
typhoid fever, since at later autopsy no fibrous scars are found, but, on 
the contrary, muscle tissue capable of functioning. Kuttner and Landois 
(39) also take the viewpoint, that, in time, human striated muscle regen- 
erates much more widely than seems to be indicated by animal experi- 
ments. They also point out that a complete regeneration of striped 
muscle tissue may be observed in old completely healed fractures which 
may be studied at a later autopsy. Finally, Bier (40) insists that, in 
man, even large muscle defects may be filled in by functioning muscle 
tissue, and almost the whole of the pectoralis major may be rebuilt after 
amputation of the breast. In contradistinction to these experiences 
in man, there are found in animals only slight beginnings of regeneration, 
with single muscle buds, when an injury with loss of substance is pro- 
duced (41). The difference may be explained by the probability that 
muscle regeneration requires a much longer time for completion than has 
been allowed in animals, but if, and how, functional muscle tissue arises 
in muscle scars cannot be found in the cited works. 
Healing of a fractured bone occurs by the growth of the so-called callous, 
the details of which can be found in text books of pathological anatomy. 
A point of argument which is not completely settled, concerns the part 
played by the bone marrow in the formation of callous. From the patho- 
logical anatomical viewpoint, the significance of marrow callous was held 
to be small, but surgeons were always of the opinion that the marrow takes 
a prominent part in the healing of a fracture, particularly after their 
experiences with operations for pseudo-joints (42). To make a pseudo- 
arthrosis heal, it is necessary to freshen up the ends of the bones until heal thy 436 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
marrow appears. Many procedures which are followed by particularly 
successful healing of pseudarthroses have carried out this exposure of 
healthy marrow unintentionally. Recently, Martin has shown experi- 
mentally, that the formation of new bone depends on the work of marrow, 
cortex and periosteum. Transplantation of periosteum is successful only 
if some of the superficial layer of bone is carried along (43). This agrees 
very well with the experience in resection of ribs, where the bone is 
incompletely rebuilt after subperiosteal removal. Bier also emphasizes 
this statement on evidence from his experimental investigations. When 
the circulation is disturbed in a bone, fractures will heal poorly (44), but 
division of the nerves is without influence, as experiments and numerous 
clinical experiences, especially during the war, have shown (45). 
The pain sensations of bone have been studied by many, and the experi- 
ments of Nystrom are especially valuable because they were done very 
carefully on himself (46). As is well known, he found the periosteum 
so richly supplied with sensory nerves that exceptionally severe pain wras 
felt even on simply touching the part or slightly stroking it. The pain 
was different from that experienced when the skin was cut; it was 
more diffuse and “blunt,” as Nystrom calls it. The cortex sepa- 
rated from its periosteum is completely insensitive; the compacta is 
similarly so to a depth of several millimeters. The marrow cavity is not 
insensitive throughout, as Nystrom in contradiction to earlier investiga- 
tions, has shown beyond criticism. He speaks of a diffuse dull ache. 
Probably the nerves are present only sparsely, since needle pricks elicited 
pain only here and there, and Nystrom believes they lie on the inner side 
of the corticalis. The spongiosa is also supplied by pain nerves, but 
equally as sparsely. That the bone marrow in rabbits is very sensitive 
has been shown in studies on osteomyelitis. But the nerves are not dis- 
tributed uniformly in the skeleton, at least the statement is made (47) 
that short and flat bones are less sensitive than long bones. Joint and 
epiphyseal cartilages are insensitive, and the pain in dislocations of joint 
cartilages is to be explained by pressure on the bones (joint mice) 
(48). 
If an extremity is placed at rest, or spared for any reason, not only do 
the muscles atrophy, but as the investigations of Sudeck (49) have shown, 
the bones also (39). In the leg, the quadriceps is especially affected, while 
the flexors remain intact for a longer period, and in resections of the knee 
joint, for example, there is a later contracture of the flexors. A muscle, 
the seat of such a simple atrophy, shows a diminution of its electrical 
irritability without reactions of degeneration. Such cases are generally 
spoken of as disuse atrophy implying that the muscle deteriorates through 
nonuse. Atrophy may, however, occur so rapidly in acute inflammations EXTREMITIES 
437 
or after injury to joints, that one is inclined to think of some special 
pathological physiological process to account for it. There are also 
many other considerations against regarding this process as arising merely 
from disuse. 
It will help in an understanding of the question if we first consider 
our knowledge regarding increase in muscle mass under normal conditions. 
The widely held belief that the laborer has a stronger arm than the man 
who works with his brain is entirely erroneous. The mass of muscle is 
influenced much more by the original muscle anlagen, as Grunewald (50) 
among others has stated, and increase in size through exercise occurs 
only when the muscle performs particularly hard work by lifting a heavy 
weight in a given time. An increase in musculature presupposes an 
increased load over short time intervals. If a muscle works against an 
ordinary load over a longer time, for example, in long distance swimming, 
running, etc., no increase in size takes place (51); and furthermore, a 
musculature made especially massive by manipulation or exercise becomes 
weaker when the individual ceases these exercises even if he performs 
ordinary physical labor the whole day. We see this very often in those 
unfortunate patients whose muscles, enlarged by orthopedic procedures, 
decrease again, when the patient resumes his regular work, even if it is 
rather heavy. Strength muscle is, therefore, to be differentiated from 
endurance muscle. The effect on the musculature of more work in a time 
unit, must not be confused with the results of more work in endurance, 
as was done, among others, by Horvart (52), and Grunewald (50). 
Work hypertrophy of muscles in adults does not follow simply because 
of better blood supply or nutrition, but is always an adaptation to greater 
loads. Simple laws of mechanics are basic for hypertrophy, and the only 
difference in the work capacity of a muscle and a steam engine lies in the 
inability of the latter to enlarge independently, and to compensate for 
increased demand by proportionate enlargement of its piston diameters, 
an ability which the muscle has by virtue of increase in its mass. 
The statement that at times a muscle will atrophy following too great 
a demand for work, as for example, the muscles of the thumb in a file 
cutter, must be accepted with caution (54). Furnohr could show in his 
cases, that the seeming overwork atrophy was really a progressive muscu- 
lar dystrophy, and the work was a secondary factor (55). In general, 
we know that an overstretched muscle also atrophies (56). 
The question now arises if a healthy man can bring a muscle to atrophy 
through sparing it. As far as it concerns a muscle hypertrophied by 
previous exercise, the question has been answered above in the affirmative. 
Endurance muscles retain their circumference stubbornly, so that a general 
muscular atrophy is said to be a certain indication of some pathological 438 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
process in the affected limb. But this is to be taken with a grain of salt, 
because experiments have shown that atrophy of the musculature and bone 
will take place in healthy animals after a limb is kept in complete rest; a 
finding which certainly agrees entirely with clinical experience (57). 
Particularly enlightening are the anatomical investigations of Sulzer. 
Partial rest also will lead to atrophy of muscles and bones in animals. 
Schifif and Zack, Brandes, and Krauss (58) and many others, observed, 
after severing the tendon of Achilles in rabbits, that an atrophy occurred, 
involving not only the gastrocnemius, but also the other muscles of the leg 
and the os calcis. This fits in with the previous remarks regarding the 
influence of several jointed muscles on distant parts of a limb (O. Fischer). 
Further, Grossmann obtained an atrophy of those muscles of the larynx 
supplied by the inferior laryngeal nerve after section of the superior laryn- 
geal; but these experiments are certainly much confused, and it seems 
deceptive to speak of a partial rest position in this case. For, as must be 
repeatedly emphasized, the work which must be done by a muscle to 
retain the equilibrium, and thus keep an extremity in its normal position 
(internal work), is considerably greater on the whole than that required to 
casually change the rest position (for example, flexing the arm), (external 
work) (59). When the internal work of a muscle is taken from it by 
removal of the activity of its antagonists, it is injured in its function (in 
case it has no other antagonists), to an amount corresponding to not only 
partial but complete immobilization. On such a complete abolition 
of even the smaller movements is founded the superiority of all really 
fixative bandages in the treatment of inflammations, which Heidenhain 
(60) has recently brought again to attention from some observations on 
himself. 
A seeming separate type among the causes of muscle atrophy is disease 
of joints. In this case, atrophy is said to occur in an exceptionally short 
time, in fact, without a previous complete inactivity of the muscles (61). 
A number of authors therefore assign the reason to direct extension of the 
pathological process from joint to muscle or to nerve endings, a conception 
which was not borne out pathologically anatomically, entirely apart from 
the fact that the atrophy of muscle groups distant from the diseased 
joint would not be sufficiently explained by this reasoning (62). 
The widest acceptance has been won by the reflex theory as proposed 
by Brown-Sequard (63). Raymond, Deroche, and Hoffa sectioned the 
posterior roots of one side of the lower dorsal and upper sacral cord in 
animals, and produced an inflammation of both knee joints by injections 
of irritant chemical substances such as turpentine or silver nitrate. 
Muscle atrophy occurred only on the side in which the nerve roots were 
intact. Therefore, a break in the sensory reflex arc protects from atrophy EXTREMITIES 
439 
and this demonstration seems to prove Vulpian’s reflex theory that stimuli 
from inflammatory joints pass from the sensory arc to the motor cells of 
the anterior columns and damage the trophic centres of the muscles 
belonging to them. At the autopsy of a patient with muscle atrophy of 
one leg, Klippel (64) found a diminution in the number of ganglion cells 
in the spinal cord on the diseased side, but Duplay and Vazin (65) in 
experimental joint inflammations found no such change. 
This reflex theory was immediately combated, and Sulzer (57), for 
instance, insisted that in the experiments of Reymond-Deroche, the atrophy 
following section of the roots in the sensationless leg was not so outspoken 
because the leg in question was not spared as the other one, on account of 
lack of pain. Schiff and Zack (57) carried out experiments in opposition 
to the reflex theory in the following way. They sectioned the dorsal 
spinal cord transversely, which left the reflex arc intact. Following this, 
they observed a rapidly progressing disuse atrophy of both legs. When 
they injected turpentine into the knee joints of animals so prepared, they 
found the musculature remained stronger in the injected leg than in the 
other,while according to the reflex theory, the reverse should have occurred. 
Schiff and Zack explain this curious finding by assuming that there is a 
constant irritation from the arthritis acting reflexly on the musculature. 
The conditions are said to be exactly opposite to those expected according 
to the Vulpian theory. 
At any rate, these experimental results show once more that in the last 
analysis a muscle remains normal because of continuous nervous impulses, 
which produce what we call tonus; and in truth, it seems from clinical 
experience that these impulses are enabled to produce their optimum 
effect when the musculature is in a mid-state, i.e., when there is equal 
muscular tension between flexors and extensors, adductors and abductors, 
etc. 
Further, von Tilmann (56) and Kremer (56) have called attention to 
the possibility that atrophy in all sorts of diseases of the extremities can 
be produced by overstretching. Each muscle, of course, has a certain 
elasticity which has been measured fairly accurately by physiologists (66). 
It is known from the work of Mosso (67) and others, that a muscle which 
has been stretched from its resting position retracts somewhat after the 
weight is removed, but it never returns to its original length. This Til- 
mann could confirm, and it is very easy to believe that a muscle can be 
damaged by prevention of its return to a normal resting position over a 
certain length of time. Thus an atrophy of individual leg muscles can be 
due to overstretching from partial or complete flat foot. Such an 
unphysiological overstretching takes place when the leg is placed on a 
Volkmann’s splint with the hip and knee extended, and the foot flexed 440 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
at a right angle; a position in which we must keep the limb in joint inflam- 
mations for other reasons which need not be discussed here. 
Roux (i) showed that an atrophy following disuse occurs only in those 
dimensions which “functioned more weakly.” If we, therefore, prevent 
extension and flexion of a joint, atrophy occurs only in the length of the 
muscles belonging to it. The same considerations apply to bone atrophy 
in which the degree and rapidity can be followed by x-ray studies (68). 
It also progresses with extraordinary rapidity, and in animal work, 
clear cut changes can be noticed in two to three weeks after placing a limb 
in a plaster cast. The histological changes in bone atrophy have been 
recorded by Roux (i). 
In children—less clearly in adults—a well marked disturbance of 
growth of the affected limb also occurs (69). This is not because of injury 
to the epiphysis as Konig (70) believed, since bones in which the epiphysis 
is not affected at all are also retarded in their growth. Wolff showed 
by accurate measurements, that it is only the foot which is backward in 
its growth, no matter what the disease of the leg (infection of knee joint, 
etc.), and he is, therefore, of the opinion, as is Sudeck also (68), that the 
nervous system is involved. 
The above mentioned remarks against the Vulpian reflex theory in 
its original form apply, of course, to bone atrophy. But the fact must also 
be explained that not only do those bones and muscles atrophy which 
are themselves placed at rest, but others also which seemingly are not at 
rest. It was stated above that the muscles are not to be regarded as 
single objects but as groups, and in truth, modern descriptive anatomy 
teaches that many, even distant muscles, belong to such “kinetic chains.” 
It seems comprehensible that when one link of the chain is injured the 
others will suffer in more or less degree, since their stimuli are then sent 
through different paths. That bone atrophy is related to muscle atrophy 
and is dependent on it, cannot be shown in all cases, but it is not improb- 
able that the relation is there nevertheless. 
Disturbances in the normal stimulation lead, therefore, to atrophy, 
and, to repeat, the impulses which are followed by “external” work of the 
muscle (for example, flexing the arm) are not the only ones of importance, 
but the continuous ones which determine the “internal” work (the posi- 
tion of the joint) are of equal if not greater significance. The true value 
of these little movements in surgical treatment, particularly in the manage- 
ment of fractures, was first recognized by Bardenheuner (71) who placed 
particular emphasis on the necessity of patients innervating their own 
muscles to avoid atrophy while on an extension apparatus, while the 
opposite was practiced by Lucas Champoniere who treated fractures 
in utmost extension from the beginning, that is, he valued the “external” EXTREMITIES 
441 
work of the muscles and passive movements of the joints more highly. 
But the superiority of active innervation to all passive manipulations for 
the health of the muscles, is now fairly well established. 
The theory of Grunewald (50) that the atrophy depends on a lack of 
hormones as in the process of involution of the uterus, lacks sufficient 
evidence. 
The atrophy of muscles following section of the nerves supplying them 
has been studied particularly by neurologists (72). Jamin’s work on 
animals showed that there is a diminution of the primitive striae with 
disappearance of the cross striations in a short time, and finally, gradual 
complete disintegration of the muscle fibres (73). In general, it is said 
that this progressive degeneration causes the muscles to lose their faradic 
irritability in 12 days; a statement which must be modified by the findings 
of Vulpian and Perthes (74). The latter showed in operations on gun- 
shot wounds of the nerves, that the naked muscle retains its faradic irri- 
tability for considerably over a year, but the nerve loses it in 72 hours 
after section. The microscopical findings of Heidenhain show that all 
the fibres in such muscles are not destroyed, but that many are only 
diminished in size and still show cross striations, a finding which Vulpian 
and Stier (75) had previously obtained in the calf muscles of rabbits. 
According to the studies of Nasse, bone atrophy also occurs after nerve 
section (76), but it is said to be less extreme and to occur less quickly than 
that in joint diseases or enforced rest (see Sudeck). This is probably 
referable to the longer preservation of the musculature following nerve 
section. 
Further results of a lengthy enforced rest are stiffening and contracture 
of the joints. Pathologically anatomically, such joints develop callous 
and thickenings of the tissue, which show roentgenologically as dense 
shadows; calcification and new bone formation also occur. Briefly, the 
change in the connective tissue is a consequence of failing functional stimu- 
lation (Roux (1)), and less differentiated tissue takes the place of more 
highly differentiated structures. The stiffness which develops even after 
a short enforced rest, depends on changes in the muscles. According to 
Marey’s law, the length of the red fibres of a striated muscle is proportional 
to the extent of the movements which the joint to which it belongs carries 
out, and inactive atrophied muscles are said to show a shortening of these 
fibres (77). In the days before bacteriology, it was debated whether these 
stiffenings of the joint were caused by an inflammation or a “bed-sore of 
the cartilage.” Doubts were based on the experimental investigations 
of Mentzel (78). Now the question has been shelved, since it makes no 
difference in practice if we call the described pathological anatomical 
changes an inflammation or not. The main point is that they are not due 442 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
to bacteria, nor are the cases of pure immobilization, even if special investi- 
gations of the latter are lacking. The changes in joints following immobiliza- 
tion in plaster casts have been accurately studied in animals, and shrinkage 
of the capsule and ligaments was found, which, as Reyher points out, occurs 
later than the atrophy of muscles (see above Regnier (79)). Changes 
in the cartilage are to be found only when they have not been in contact 
during the period of rest. This again shows the significance of functional 
stimulation which continually wears down the cartilages. It explains why 
extension does not protect against joint changes, but on the contrary, 
separation of joint surfaces1 injures the cartilage. 
The synovial cells are so closely related to the cartilage cells that, 
according to Braun, they change to cartilage in the places where they 
experience an abnormal stimulation. Vice versa, the joint surfaces often 
become covered with a non-vascular connective tissue layer which accord- 
ing to Reyher arises from the joint cartilage (80). 
An accumulation of fluid in the joint after function is resumed is found 
in patients who have been placed at rest for a long time. Von Volkmann 
(81) assumed that this effusion followed tears and pulls of the shrunken 
synovial membrane, a view which Reyher and Moll could confirm in ani- 
mals. Pathologically anatomically, the picture is that of a synovitis with 
swelling of the villi and synovial prolongations which resist movements. 
All of these changes did not disappear in the animals even months after 
removal of the fixing bandages, nor did the function return to normal; an 
object lesson showing the gravity of placing a joint in enforced rest. The 
degree of stiffness in humans depends not only on the length of time of rest, 
but also on individual idiosyncrasies. We know that the joints of so-called 
rheumatics become stiff in a much shorter time than those of other individ- 
uals, and the tendency to stiffening increases with age, perhaps because 
the nutrition of the connective tissue is poorer and the threshold leading to 
shrinking of connective tissue is more easily and quickly passed than in 
younger individuals. In “ rheumatics,” we conceive of “ a general retarda- 
tion of assimilative and breaking down processes ” (82), but exact knowledge 
in this field is still very meager. Further investigations are necessary to 
determine the status of joint stiffenings and the absorption of the new 
tissue in relation to Grawitz’s views concerning the transformation of 
fibrillar tissue into cells (83). A beginning is found in the work of 
Bussmann (84). 
The stiffened positions which joints assume when they do not perform 
their function on account of inflammation, or enforced rest for a time, 
are called contractures (85). The contracture position of the knee-joint 
is flexion; that of the hip is flexion, abduction or adduction. An explana- 
tion of these well known typical position anomalies was proposed by EXTREMITIES 
443 
Bonnet (Paris 1845) (86). He injected fluid into the joints of cadavers 
after removing all the muscles and found that when the amount of fluid 
reached a certain degree the joint assumed a position characteristic of its 
contracture position. He concluded that the capacity of the joint was 
greatest in this position, and that, therefore, in effusions, the contracture 
occurred purely mechanically by the increase of fluid. This idea is in- 
correct, as A. Fick (87) and others have shown, for the total capacity of a 
joint remains the same no matter in which position the bones happen to be, 
but the tension of the capsule, ligaments and muscles is changed with each 
change of position. The significance of the tension of these soft parts is 
shown by the experiments of Bonnet, however, inasmuch as he obtained 
these changes by injecting fluids only when all the muscles, etc. had been 
previously removed (88). Clinical experience also contradicts Bonnet’s 
theory, for in marked hydrops, a joint is not always in its contracture 
position (89). 
When a joint changes its position, some of its ligaments, and parts of 
the capsule and muscles are stretched and others are relaxed. There is a 
position for every joint in which the sum of the stretch of all the soft parts 
belonging to it is at a minimum. This is the rest position mentioned 
above, which can easily be found by discovering the most comfortable 
position. The sensation of comfort depends on the fact that the tension 
of the soft parts, particularly of the muscles, is less than in any other 
position, and in an effusion, the patient assumes the position in bed in 
which tension is felt least. In contractures, there is not simply an over- 
balance of single muscle groups, as Lucke (90) has asserted, but the joints 
become ankylosed following enforced rest or inflammation, as has been 
detailed above. 
These reasons, correctly known to Weber (91), do not necessarily 
mean that a joint cannot ankylose in another position; in such a case we 
must look for another explanation. This applies particularly to the 
position of abduction of the hip in the first stage of coxitis. Konig (88) 
has pointed out that in an early stage such patients continue walking, 
but spare the leg by holding it in the position of abduction. In special 
contracture positions, particularly of the arm, the element of gravity is 
added, which brings the affected part in a position other than that of rest. 
Obviously a pathological luxation will affect the contracture position. 
It is not difficult to understand the deviations in paralyses, destruction 
of certain muscle groups, contractions of certain muscles the site of inflam- 
mations or suppuration, or in skin cicatrices (92). 
The contractures in flat foot are classified among the inflammatory 
group (93). In this case there are peripheral muscle contractions, but 
what sort of stimulus brings the muscle to such spastic positions is 444 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
unknown. A bacterial infection is, of course, excluded. Probably they are 
irritating processes such as arise in injuries of sensory nerves in which 
reflex contractures are also observed. Furthermore, such reflex con- 
tractures are often very noticeable in fractures, e.g., of metatarsals 
(foot swelling) (94). 
They disappear after rest, wet dressings and baking, usually in a few 
days even when the foot is so firmly fixed that there is no difference from 
an “organic” contracture. 
It seems superfluous to use, as Herz (95) does, the comparative greater 
strength of the flexors as an explanation of the various forms of con- 
tracture, especially since R. Fick (5) has shown that on the contrary the 
extensors are definitely stronger, for example, in the knee joint, even when 
the flexors of the leg (gastrocnemius, etc.) are included (96). 
Contractures in flexion which cannot arise from a rest position also 
occur, as, for example, after the patient has recovered from a resection 
of the knee. We also see in bed-fast patients that the contractures in 
later stages are in positions beyond the rest position (strongly flexed), and 
in such cases there is more extensive atrophy of the quadriceps than of the 
flexors, in other words, the flexors predominate. It is not known why the 
quadriceps and the gluteals and deltoids as well, should atrophy so much 
more rapidly than other muscles, but just as in disuse atrophy, a reflex 
cause has been assigned (97). Fischer (98) believes the greater 
atrophy of extensors is due to the stronger construction of their fascia and 
thus circulatory changes will occur more readily. Jansen (99) correlates 
it with the different lengths of the bundles and fibres by assuming that in 
increased tonus the weaker flexors, adductors, and inward rotators pre- 
dominate, and vice versa, in diminished tonus. It is interesting to know 
that the extensors are said to have a different electrical irritability than 
flexors (100). Grunewald (101) offers as the reason that the extensors of 
the leg in humans are phylogenetically much younger and, therefore, are 
particularly sensitive. In monkeys, the lower extremity is as yet more a 
grasping than a supporting organ. But why this should be coupled with 
increased sensitiveness is, of course, not explained. 
Practical surgery classifies all of these possible contractures into 
arthritic, myogenic, tendonogenic, neurogenic and dermatogenic, a 
classification which seems of therapeutic usefulness. 
Furthermore, these contractures influence the shape of the bones. 
We have already spoken of the effects of the musculature on their form. 
The changed push and pull to which the bones in the neighborhood of a 
contractured joint are subjected bend them in accordance with the 
principles of statics and dynamics. That the spinal column and trunk are 
also involved is easily understood from the discussion of the effect of the EXTREMITIES 
445 
musculature on distant parts. Those conditions which we call deformities 
are produced in all probability by the continuation of muscle contractures 
and stretching (102). That such bendings can furthermore be brought 
about by general diseases such as rickets, osteomalacia and similar con- 
ditions, shall only be mentioned here, since, at least in their acute stage, 
they fall in the domain of internal medicine. 
The relation of these joint changes following immobilization, to arthri- 
tis deformans is still debatable. At present we look upon arthritis 
deformans in about the same way in which tuberculosis was regarded before 
the discovery of the tubercle bacillus; that is, we are compelled by patho- 
logical, anatomical and clinical findings to group and identify disease 
pictures. Just as before the discovery of the tubercle bacillus, much was 
considered tuberculous which has subsequently been proved otherwise, 
for example, the necroses following subcutaneous serum injections in 
rabbits—so it is with the various chronic joint diseases. 
As an introduction we must pause at the pathological anatomical 
findings in early cases, but it is to be expected that authors do not agree 
in their interpretations (103). This much is known, particularly from 
the extensive work of Pommer, that in arthritis deformans the regressive 
changes are primarily in the cartilage (p. 185 and 229) while the subchon- 
dral changes, “the extension to the marrow cavity and vessel canals” 
and the other changes in the bones themselves, are secondary. Axhausen 
describes this process very minutely. According to him, the first mani- 
festation is necrosis of cartilage, and this is the cause of all the further 
changes in the joint. These aseptic necroses are not to be confused with 
sequestra. Pommer disagrees with Axhausen in the explanation of the 
necroses and considers them “consequences of the injuries done to the 
cells in the most superficial layer by the grinding of the cartilage and 
abraded areas of bones.” But Axhausen bases the interpretation of his 
findings on very interesting animal experiments. He produced localized 
necroses of the joint cartilage with an electric needle, and later found all 
the changes characteristic of human arthritis deformans, including the 
spread of the localized reaction to the whole joint, in which respect it is 
still more comparable to the arthritis deformans of man. It cannot be 
denied that these experiments are convincing. Pathological anatomical 
findings parallel the changes for us, by experiment we can follow them 
as they occur, and it is certainly shown by his experiments that an injury 
leading to necrosis of the cartilage may initiate all the pathological ana- 
tomical changes which we consider characteristic of arthritis deformans. 
That distinct forms of arthritis deformans may develop in this way was 
shown by Axhausen (103) in three cases in which, following injury of the 
knee joint, there was found a localized necrosis of the cartilage at the site 446 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
of injury and around it, hyperplasia of subcartilage marrow, rim osteo- 
phytes, tags of synovia, etc. These experimental studies place a new 
aspect on the long known fact that arthritis deformans can develop after 
injuries. The injury causes the necrosis of cartilage, but the fact that the 
arthritis develops much more frequently after luxations than after other 
types of injury (103), is not completely explained. Thus far it has never 
been demonstrated, although it seems reasonable that damage to cartilage 
is particularly likely to occur in dislocations (Axhausen). In opposition, 
the experiments of Magnus (104) and the pathological anatomical studies 
of Tashiro (104) show that in suppurative inflammation of joints and 
similarly in gonorrheal arthritis, many cartilage necroses arise, and while 
a true arthritis deformans is rare, these often lead to an ankylosing arth- 
ritis. The relationship of arthritis deformans to these necroses is not 
altogether clear, but it cannot be concluded that it will develop whenever 
necrosis occurs. The studies of Gies (105) give general information on 
the healing of injuries to cartilage. 
To approach the investigation of the etiology from the clinical stand- 
point, it is necessary to clearly define what chronic joint diseases shall be 
considered arthritis deformans. Pommer on the basis of his anatomical 
studies does not include ankylosing joint inflammation (103, p. 232), but 
considers senile hip arthritis, as arthritis deformans. Therefore, when 
Stempel (106) describes senile hip arthritis as an ankylosing hip joint 
inflammation, he departs from the customary nomenclature and this leads 
to misunderstanding. It seems necessary to adopt Pommer’s strict 
anatomical classification before progress can be made in this difficult 
subject. 
It is hard to explain the so-called spontaneous arthritis deformans; in 
the case of “secondary” arthritis deformans, we always have the time of 
injury, trauma or suppuration, from which to date the reactive processes. 
Even if we take the views of Axhausen as a basis, we cannot evade the 
question of how necrosis of the cartilage can occur without trauma. 
In the arthritis of youth, there is, of course, infection, but the discussion 
of the exciting causes is not necessarily exhausted with this. 
There are two other theories, both proposed in the last few years, 
the one of Wollenberg (103), which regards it as a consequence of nutri- 
tional disturbances of the cartilage with particular reference to arterio- 
sclerotic changes, and that of Preiser (107), which places the responsibility 
on changes in the statics of the joints. Wollenberg believes that chronic 
local disproportions between arterial supply and venous return initiate 
the various regressive and progressive manifestations, and that the under- 
nourished bone reverts back to cartilage which needs less nutrition. The 
blood supply, too small for bone, is now too abundant for cartilage, and EXTREMITIES 
447 
the latter becomes hyperplastic. This theory might have been fruitful, 
but it was developed to too minute detail, and thus was laid open to 
opposition. The principal reason which may be brought against it, is 
that in arthritis deformans the arteriosclerosis is not confined to the 
diseased joint, but is general and it seems inexplicable that the changes 
should be localized to one joint. Pommer believes that the changes in the 
vessels are secondary. To support his views, Wollenberg also had recourse 
to animal studies; he shut off the circulation of the patella of a dog by 
circular punctures around the bone. After a time, he found changes 
which he considered indicative of arthritis deformans, a conclusion which 
was immediately questioned (108). By control experiments it was demon- 
strated that the changes found in the patella were only the reaction to a 
coincident injury to the bone, or to necrosis of the cartilage, or simply to 
pure inflammatory processes. At any rate, these experiments gave no 
evidence for the arteriosclerosis theory, and Wollenberg’s views have little 
in their favor. 
From his investigations on the changing position of the acetabulum, 
Preiser (109) reached the conclusion that pressure of the head of the femur 
on an unusual place or unevenness of the joint surfaces would lead to the 
disease (improper static relation). In later work (107) he leaves the 
question open of whether these static anomalies injure the joint directly 
or through the blood vessels. 
Kroh (no) investigated the theory by changing the static conditions 
of the joints of animals by all sorts of intra-articular manipulations. He 
actually obtained marked deformities, which not only remained localized, 
but spread to the whole joint and showed a tendency to progress. But 
it is questionable, if such severe intra-articular manipulations may be 
taken as confirmatory evidence of Preiser’s “static” theory. 
In humans, also, it has been observed that an arthritis deformans often 
develops in such falsely weighted joints (e.g., genu valgum); on the other 
hand, as Konig (in) particularly pointed out, arthritic alterations occur 
in joints which show no static displacements. 
If the conditions of pressure within joints are of such significance, it is 
pertinent to ask if an increased pressure of long duration could not initiate 
these changes. We know a few of the mechanisms which ease the bumps 
and shocks of movement in a joint (112); in addition to the cartilage and 
the rims of cartilage, they are the synovial membranes, the fat, tendons 
and ligaments, and last, but not least, muscle tonus. On these as a whole, 
depends the “elasticity” of the movements. Whether it is diminished 
in those individuals, perhaps with a constitutional peculiarity, who show a 
tendency to arthritis deformans, is not known at present. But the possi- 
bility cannot be disregarded, and a search has been conducted for tend- 448 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
encies toward gout or changes in calcium metabolism, etc. (see Wollenberg 
(103), p. 413). Lane (113) speaks of a “ scrofulous ” or “ strumous ” disposi- 
tion. There is an inheritable bodily condition which favors the develop- 
ment of gout, obesity, diabetes, calculi, arteriosclerosis, rheumatism, etc. 
(Bauer (82)), but in spite of many attempts, arthritis deformans has 
never been shown to be related to gout (114). 
The senile chronic deforming joint processes are usually distinguished 
from true arthritis deformans (see Weichselbaum (115), Axhausen (108)). 
We can, therefore, sum up the present state of our knowledge by saying 
that those cases which arise after injury are well explained by the experi- 
ments of Axhausen; that there are cases, however, in which an injury 
cannot be demonstrated; further, that the severity of the joint changes is 
not simply proportional to the severity of the injury. This means that 
some, as yet unknown factor, other than cartilage necrosis, is concerned. 
The development of a joint mouse bears a certain relationship to arth- 
ritis deformans. Since Monro (116) in 1726, first found a body in the 
knee joint of a woman, who had a defect in the external condyle of the 
femur, injury as a cause of free bodies in the joint has again and 
again played a role in the literature, although it was much combated 
by Laennec and his students. There are several reasons which may 
be enlisted in opposition to this theory of the traumatic origin of 
loose joint bodies. In the first place, a history of trauma is usually absent, 
or it is at most only insignificant, and such as might occur almost daily. 
In the second place, the trouble does not begin, as a general rule, in imme- 
diate association to an injury but months and years afterward. The shape 
of most joint mice is incompatible with the theory of their traumatic 
origin. As Konig remarks (117), pieces of cartilage may be torn loose 
and remain hanging to joint tendons, but they would not appear as 
“flat pieces from the outer surface of articulating bone ends.” Careful 
pathological anatomical studies have shown that this view is correct. 
“Up until the present, there has been no case recorded which showed that 
a flat arthophyte arose by primary detachment following a single trauma” 
(118). On the other hand, the studies of Budinger have shown that 
partial detachment of cartilage is not uncommon, and it is at least conceiv- 
able that such partially loose bodies may become completely detached 
by movements of the joints. At any rate, the material Budinger used for 
study was derived from such severe traumatism that he doubts the value 
of his own cases. Poncet and Kragelund (119) were able to cause small 
pieces of cartilage to fly off, by directing tangential blows on the knee 
joints of cadavers. Others succeeded in producing joint mice by injury 
to animals, but found that such detached pieces almost always became 
attached to the wall of the joint (120). The bony part dies, and accord- EXTREMITIES 
449 
ing to Bier (121) is absorbed by the synovia; the cartilaginous part remains 
living, a finding which is also true of the joint mice of humans. Still it is 
incorrect to conclude just because of the agreement in the histological 
findings in man and animals, that the loose joint bodies in man are 
detachments. Cartilaginous tissue has great tenacity of life and resis- 
tance, as shown, for example, in the transplantation experiments of Seggel 
(122). Bier (121) calls attention to the fact that loose joint bodies are 
generally covered all around with cartilage which is supposed to protect 
it from the solvent action of the synovial fluid. 
In the joint mice of humans, the first thing to explain is the time 
element, why a piece of cartilage becomes loose years after an insignificant 
injury. Is there an actual causal relation between injury and joint 
mouse? The work of Marten (123) illustrates the clinical course on this 
point. Cases coming to autopsy showed that there were occasional 
localized necroses of joint cartilage which led to the demarcation of a 
fragment of cartilage and bone (124), and as the preparations of Klein 
(125) showed, to the formation of a loose joint body. But the question 
still remains of whether this form of cartilage necrosis and the subsequent 
appearance of joint bodies are the usual course of events and whether 
there is a relationship of injury to later demarcation of the cartilage. 
Konig, who has given the name osteochondritis dissecans to this patho- 
logical process, believes that a mild injury may damage a localized place 
severely enough to lead to necrosis; a later “dissecting” inflammation 
loosens and separates the part. At the same time he believes that there 
is a spontaneous osteochondritis dissecans, the causes of which are still 
obscure, but which arises without previous injury and runs the same 
pathological anatomical course. Ludloff (126) supports the opinion 
that such an osteochondritis might arise from injury to blood vessels. 
It occurred to him that in the cases involving the knee joint, the osteo- 
chondritis always developed at one circumscribed spot, namely, on the 
internal condyle of the femur near the insertion of the posterior crucial 
ligament, and he tried to discover by #-ray and anatomical studies a 
special peculiarity of the blood vessel distribution of this place (127). 
These considerations have, however, been contradicted (Kirschner (128) 
and others), even if the clinical observations were correct. 
These ideas of a cartilage necrosis leading to a dissecting osteochondri- 
tis were supported and elaborated by Axhausen on the basis of his above 
mentioned animal experiments, and pathological anatomical studies (103). 
By pricking the surface of the joint with an electric needle, he could 
obtain necrosis of cartilage and the same demarcation process in the 
bone as is found in human osteochondritis dissecans and its sequel—changes 
in the entire joint—as was mentioned above. He believes accordingly 450 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
that the production of joint mice and arthritis deformans may be regarded 
from a similar point of view; the primary process is always a necrosis of 
the cartilage which may be caused by a mild trauma. As a consequence, 
there is separation by a process of granulation, and a formation of joint 
mice or arthritis deformans. Whether primary necrosis of the cartilage 
may be caused by something other than trauma remains an open question 
(vide supra). 
It is quite logical to believe that a joint mouse may break off in a well 
marked arthritis deformans (129) and that by continuous irritation of 
the joint, new necroses may occur and new fragments be freed. Further- 
more, such loose bodies may arise from cartilaginous tags or parts of the 
capsule (Fischer (129)). 
These loose bodies may grow even if they are free in the joint. The 
histological processes which may finally lead to three fold increase in size 
were found to depend on “periosteal apposition” and on “cartilage pro- 
liferation” (130). According to Schmieden, the connective tissue of the 
dissolved bony part seems to play an important part, and regressive proc- 
esses, especially necrosis of the cartilage, are demonstrable in its vicinity. 
The necessary nutrition must be procured from the surrounding synovial 
fluid, possibly as in plasma cultures of tissue. There is a certain similarity 
in the growth of a joint mouse and the growth of the head of the radius 
when the latter is dislocated and not replaced. It might also be called an 
example of how cell growth is held in check and regulated by function. 
If the articulating end of a bone escapes from its ligaments, the restriction 
to growth is removed and that part of the bone may grow disproportion- 
ately. In the case of the head of the radius the nutrition comes, of course, 
wholly through its blood vessels. 
That muscles should undergo necrosis, that there should occur what 
we know as gangrene when all the vessels are ligated, is not difficult to 
understand. Pathologically physiologically of far more interest are the 
consequences of diminished nutrition which leads to connective tissue 
replacement and to the so-called ischemic contracture (131). Insufficient 
arterial supply with venous stasis has long been accepted as the cause of 
these changes in the muscles. Many lay particular stress on the venous 
stasis and its consequent carbon dioxide poisoning (132). If this view is 
correct, it should be very easy to produce an ischemic muscle contracture 
in animals. And yet this is not the case. Shutting off the arterial flow, 
as for example, in the so-called Stenson’s experiment (ligation of the aorta) 
(133), or the application of a tourniquet to the thigh, indeed leads to a 
breaking down of muscle fibres and nuclei, and functionally, to the beginning 
of a stiffening, as the description of Heidelberg has shown. But if the 
animals are later allowed to run around, the muscles quickly recover and EXTREMITIES 
451 
regenerate. The same result is obtained after ligation of veins (Kroh), 
and clinical experience has shown that ligation of the femoral vein which 
is often done for pyemia (134), does not lead to ischemic contracture. 
Circulatory disturbance alone, therefore, is not sufficient to bring this about. 
Unless the affected limb is placed at rest, and indeed it need not be 
bandaged, the inactivity alone suffices to produce the described changes. 
Clinically, the cause of circulatory alterations in particular cases may be 
varied. Ischemic muscle contractures are mainly seen following supra- 
condylar fractures of the humerus and in fractures of the middle of the 
forearm (135). In the first case, a tearing of the intima of the cubital 
artery often occurs or a mechanical compression of this vessel by the 
displaced fragments. In fractures of the forearm, as Kroh has shown in a 
case of crushing, a hemorrhage may force the musculature into a typical 
contracture position and lead to the circulatory disturbance. • 
The venous stasis and the edema increase not only the circulatory 
difficulties, but also the inactivity of the muscles. Bardenheuer calls 
attention to the venous “suction cups” lying in the bend of the elbow, 
therefore the flexors particularly are damaged. 
Venous stasis is of practical surgical interest from other viewpoints 
than simply that of circumscribed ischemic musculature. We see, for 
example, how the flap in plastic operations becomes swollen and blue when 
turned on its pedicle. The thin walled veins are more or less kinked, 
the venous blood cannot flow out freely, carbon dioxide accumulates in the 
free edges of the flap, and the capillaries are compressed by the swelling. 
If no further therapeutic measures are undertaken, the edges become 
necrotic, but simple puncture allows egress to the venous blood and the 
vitality of the cells is preserved. Similar conditions are met elsewhere in 
surgery, e.g., in fractures. Here also we may improve the disturbed 
local circulation and prevent gangrene by allowing the obstructed blood 
to escape. 
Such edema in the muscles is a hindrance to normal movements, and 
attempts are made to relieve it by massage. The justification is shown 
by the observation of Kroh, but its importance must not be overestimated. 
For example, Kroh terms the conditions in stiffness of a muscle after 
exertion as “greater blood stasis and transudation;” as proof, he calls 
attention to an increase in its volume, but this explanation seems too 
mechanical. How insignificant is the functional diminution of the muscu- 
lature in the edema of nephritis. Edema is often the expression of a 
diseased condition in the vicinity of musculature, and not the primary 
cause, although, of course, it may further damage its function. 
Under the influence of v. Volkmann’s wrork on ischemic muscle con- 
tracture, participation by peripheral nerves was disputed for a long time, 452 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
and a sharp distinction was made between damage to muscles by nerve 
injuries, and by interference with circulation. It was supposed to be 
characteristic of ischemic muscle contracture that the muscle could still 
be electrically stimulated through its nerve, while the direct electrical 
irritability had long disappeared. In spite of this, a participation and 
injury of the nerve cannot be denied, in fact, in many cases, it must be 
considered of causal importance in the development of this disease picture, 
since by its involvement, the damaging inactivity ife increased. That 
tight bandaging, per se, reduces the sensation in an extremity is an observa- 
tion which can be made daily in operative cases, and which has been 
examined experimentally by Neugebauer, Kroh and others. To eliminate 
the effects on the nerve trunk of the pressure of a bandage, Kroh com- 
pressed his own brachial artery and obtained a distinct sensory distur- 
bance in his hand in 12 to 14 minutes. More interesting is an observation 
of the same author, who, after isolated compression of the femoral artery, 
noticed a distinct disturbance of sensation in the area supplied by the 
sciatic nerve. This shows how closely nerve conduction is related to cir- 
culatory disturbances. In animals, he of ten observed a complete motor and 
sensory paralysis in the distribution of single nerves of the leg after liga- 
tion of vessels. In ischemic muscle contractures in humans, Barden- 
heuer, Hildebrand, Kroh, and many others often demonstrated sensory 
disturbances quite conclusively. 
The damage, therefore, comes from two sources, blood supply and 
nerve supply. In the well developed case, the nerves can be pinched by 
the connective tissue and further hindered in their activities. To remedy 
this condition, Hildebrand transplanted the nerves and obtained good 
results. 
Ischemic muscle contracture in its details, is, therefore, considerably 
complicated, but the basal causes arise from circulatory changes and 
inactivity. The importance of plaster casts in the production of this 
condition must, therefore, be judged from this viewpoint and it should be 
particularly remembered that it is not necessarily the result of a bandage 
which is too tight or binding, but that it favors contractures because it 
keeps the muscles at rest. The circulatory element, e.g., rupture of the 
intima of an artery, may add to the trouble if it is applied too tightly or if 
the limb subsequently swells. 
A congenital disease which must be considered from the micro- 
scopical appearance of the muscle as an ischemic contracture is torticollis 
or muscular wry-neck (136). This idea has been generally recognized 
only since the work of Voelcker (137), who observed a number of changes 
in patients with wry-necks, such as a deformity of the ear muscles, which 
indicate that the child’s head had already assumed an oblique position EXTREMITIES 
453 
in utero. This position of the fetus leads to pressure on the artery of the 
sternocleidomastoid muscle and thus the fundamentals for the production 
of an ischemic muscle contracture are fulfilled. Schloessmann (138) 
confirmed the views of Voelcker. The other theories of traumatic or 
inflammatory origin are contradicted by the pathological anatomical 
findings which indicate an ischemic origin. 
Another disease of muscles which reduces their freedom of movement 
is concerned with bone formation; myositis ossificans. We know from 
normal histology that bone may arise not only from periosteum but also 
from connective tissue. In myositis ossificans, the question of the histo- 
genesis of the bone has played the leading role. 
In general, a division is made between a progressive and circumscribed 
myositis ossificans. The former has been of only casual interest until 
recently. It is thought that there is a constitutional anomaly; the tissues 
have less ability to become more highly differentiated and arrive at full 
development, but the nature of the process is not known in detail. It is 
not hereditary, but such patients often show other degenerative processes. 
Up until now, there have been from 70 to 80 cases published, mostly in 
surgical literature (139). Symptoms may be improved by removing 
irritant bone particles, etc., but the course of the disease is not influenced 
in the least. 
Localized myositis ossificans is of far more interest and practical impor- 
tance. The question arises, however, whether all the conditions included 
under this term are really pathologically similar to it or to each other. 
The fact that bone tissue appears in lungs, testes, lymph nodes and muscles, 
does not necessarily justify the belief that these pathological processes 
are alike. 
The cases of myositis ossificans circumscripta which are heing subjected 
to much discussion at present are those which develop after injury of the 
supporting apparatus, i.e., when there are pieces of bone in the muscle in 
the close vicinity of the site of an injury (140). 
Still other types of cases, intermediate one might say, are those in 
which an injury has occurred to tissue with no recognizable relation to the 
skeletal system. These are, for example, the bone formations in lapar- 
otomy scars, such as have been described by Ropke (141). Here we can 
only conclude from the rarity of its occurrence, that there are individuals 
whose tissues are peculiarly prone to bone formation, but we have at 
present no idea of the nature of such a disposition. We very often meet 
with such differences in wound healing in our patients. Some have tight 
scars, others soft, some develop a large callous, some a pseudo-arthrosis, 
some are predisposed to keloid formation, and so on. 
At present, it is not possible to correlate these different healing tenden- 454 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
cies with the “types” elaborated by the studies of constitutions. It has 
been frequently asserted, of course (Wilms and others), that people with 
the “arthritic” or “rheumatic” diathesis are more liable to connective 
tissue growth and cicatricial contractures, but it is easy to discover oppos- 
ing observations. Judgment in all these things is so difficult because of 
the many uncontrollable outside factors which interact in the firmness of a 
scar, such as slight deviations in the method of injury, etc. The healing of 
the aseptic operative incision is, after all, a remarkably similar one in 
the many patients who are daily operated. Deviations in the healing 
process occur only in those suffering from some general disease (142). 
In infected or crushed wounds, the conditions are different. Old axioms 
of the laity which speak of a “good or bad healing skin,” have much justifi- 
cation, but we can hardly investigate this scientifically, because of the 
difficulties in evaluating outside factors such as virulence of infection, 
tissue destruction, etc. That these outer factors do play a role was made 
evident in large numbers of cases during the war (see among others, 
Voelcker (143)). 
There are a few special situations which the process seems to elect. 
Following luxations of the elbow, the bone formation is often quite typical 
in places at which the periosteum has been torn off with pieces of joint 
capsule (144). The so-called horseback rider’s, infantryman’s, or bayonet- 
tier’s bones owe their origin to coarse tears of the muscle with possibly a 
partial pulling off of the muscle from the bone. There is a difference of 
opinion as to whether this bony foundation in the muscle arises from 
detached threads of periosteum or from connective tissue (145). That 
periosteum detached from bone is capable of producing new bone is a well 
established fact, shown by taking fragments or suspensions of finely divided 
periosteum and introducing them into the muscles or soft parts (146) 
when cartilage or bone formation results. The conditions applying to 
traumatic myositis ossificans were imitated quite accurately in animals by 
Berthier, but it has never been possible to produce a progressive growth of 
bone. It may be due to a difference in the tissues of animals and man; 
indeed dogs are far less useful than rabbits in such bone formation investi- 
gations. It cannot be concluded that the subject is exhausted by 
accepting detachments of periosteum as the cause of the disease. Sudeck 
and Pochhammer are of the opinion that the method of growth, par- 
ticularly the duration, points to a periosteal origin of the bone, since hetero- 
plastic bone transplants develop differently. This opinion is contradicted 
by Gruber, and is really not entirely satisfactory. 
The two views are again and again expressed as various workers 
enter this field; the one, that the bone fragments are entirely separate 
from the main bone of the extremity and develop in the substance of the EXTREMITIES 
455 
muscle, a point for its connective tissue origin; the other lays stress on an 
injury to the bone, and accepts the experimental result even if it is not 
entirely established, that there is growth from detached fragments of 
periosteum, which are supposed to be scattered far into the muscles (147). 
Why could not the circumstances be similar to those in the formation of 
callous? In this process, there is first an hyperplasia of connective tissue, 
which is not penetrated by a growth of periosteum, but, according to the 
prevailing opinion, by “direct metaplasia turns into reticulated bone” (2). 
That this metamorphosis does not result independently, but is influenced 
by periosteum and bone marrow is naturally understood. The latter, 
however, do not rebuild the bone themselves, but by a sort of indirect 
influence bring this end about through the medium of connective tissue. 
How much of this influence is owed to the blood supply, which according 
to Lexer and Delkeskamp (148), arises from the vessels of the periosteum, 
that is, from the tissue chiefly concerned in the formation of bone, is 
not known. But we do know that fractures heal badly when the cir- 
culation is disturbed (44). Probably we are justified in considering that 
such an indirect influence acts in myositis ossificans traumatica, a belief 
which will allow the opposing views on the histogenesis of the disease to be 
better correlated. 
Bone formation may perhaps be favored by the hemorrhage because of 
nutritional disturbances in the injured tissue (Bier (149), in opposition to 
Hildebrand (149)). At least, Liek (150) showed that bone formation 
took place in the kidney after ligation of its vessels. 
When all is said, however, it still remains inexplicable why this bone 
formation should occur so rarely. Many people ride, yet few develop 
myositis. Is it because there are small differences in the manner of 
injury, or does it reside in differences in individuals, that is, to a special 
“predisposition” (Kuttner)? That there are variations in the ability to 
form new bone is shown in any active surgical practice. The examples 
given by Kuttner seem to make it probable that these different predis- 
positions have definite significance in myositis ossificans. 
This method of discussion now leads to a consideration of the bony 
overgrowths following nerve affections. Wilms (151) called attention 
to the bone formation in the muscles of tabetics which occur in addition 
to the arthritic changes. He declares that these changes are found 
primarily in those muscles which are attached to joints held in contracture 
positions; and thus it may be an injury which causes the bone formation. 
Later observers concur that these changes are found quite commonly in 
many other nervous diseases (152). Some could indeed find them in 
bedfast patients in whom every possibility of trauma was excluded, but 456 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
whether the condition is inflammatory or is a growth disturbance due to 
nerve paralysis, has not been determined (153). 
NERVES 
The surgery of peripheral nerves has gained in interest and importance 
through the problems of the war. Many theoretical questions have 
arisen, especially in connection with the healing of nerve wounds, and the 
subsequent restoration of function. 
We may accept from the embryological studies of Hiss and the experi- 
mental work of Harrison (154), that all nerve fibres grow from ganglion 
cells and that following injury, the peripheral part of the nerve degenerates 
and a new nerve arises by the outgrowth of the central portion and 
subsequent union with the peripheral portion. 
This growth of the central end begins immediately after the injury, 
but necrotic tissue, blood, granulation tissue, or lateral displacement of 
the stump, prevent the outgrowing fibres from finding the peripheral 
ends. The fibres grow into the tissues, obstacles change their course, 
and so they lose their direction. In this way a neuroma and a thickened 
scar around the wounded nerve develop. Neuromas may be prevented 
in amputations, by Crushing the nerve and closing its sheath so that the 
separate axis cylinders cannot grow (155). As soon as the fibrils 
from the central and peripheral ends touch or when their union is accom- 
plished by suture, there again ensues a functioning nerve fibre. 
The previously accepted view was that the central end grew into the 
peripheral end, under the direction of the ganglion cell. But according 
to Bethe (156), this is untrue, for the central stump enlongates only a few 
centimeters and particularly in younger individuals, the peripheral part 
can regenerate completely before it joins the central stump. Such “auto- 
genous regeneration” does not lead to a permanent nerve, because this 
newly grown peripheral part degenerates, but there is justification in the 
assumption that in permanent regeneration the central end does not 
simply grow into the peripheral piece, but that the latter takes an active 
part through a “stimulatory action” of the former. 
Such a severed nerve can grow not only into its peripheral portion, 
but the surgical experience of the last few years has shown that 
it can grow directly into a muscle into which it has been transplanted 
(157). New endings develop and the muscle is re-innervated (neurotisa- 
tion). (The work of Erlacher (158) gives anatomical data regarding the 
nerve endings in muscles.) 
This fact is of great biological interest, reminding us of the ingrowth of 
nerve fibres in embryonal life which has been studied particularly well by EXTREMITIES 
457 
Braus (159). He transplanted the buds of extremities to either the head 
or tail end of the embryo of amphibians shortly after their appearance and 
before nervous elements had appeared. By this means the bud came under 
the influence of “strange” nerves. A completed limb arose and what is 
more remarkable, the motor nerves wandered in, and innervated the 
muscles. In like manner, the sensory nerves developed independently of 
the motor nerves. Furthermore, the branches of the nerves were exactly 
similar to those in a normal extremity. The forces which bring about such 
a phenomenon are unknown, but there are analogies in other tissues, e.g., 
the metamorphosis of ordinary ectodermic cells to true lenses (eyes) 
when the ectodermic cells are brought into contact with the optic vesicle 
(Spemann, cited by Braus). The contact of tissues is sufficient, therefore, 
to stimulate such growth. Similar forces are probably concerned in 
causing the nerves of adults to wander into and supply an otherwise 
entirely strange muscle. 
It is also possible to unite two different motor nerves in adults, as for 
example, to transplant the accessorius or hypoglossal to the facial, in facial 
paralysis (160); in fact, the motor hypoglossal may be united to the 
sensory lingual; after which an outgrowth of hypoglossal fibres occurs, with 
partial, if not complete, innervation of the tongue (161). The first of 
these experiments was done by Flourens (cited by Bethe), who severed 
both branches of the brachial nerve of a fowl and sewed them together 
crosswise. Elaborate experiments of this kind were carried out by 
Spitzy (162) who hoped that his results could be used in infantile paralysis. 
There are many possibilities in nerve grafting, and although the practical 
results have been none of the best, their theoretical foundation is, of 
course, not disturbed. These operative and experimental results show the 
extensive ability of the human locomotor apparatus to learn new functions. 
The facial or motor trigeminus in the experiments of Braus, were used 
for the nerve of an extremity, and the nerve of the tongue, when grafted, 
can learn to move the muscles of expression of the face. This learning of a 
new function as in a transplanted muscle occurs in the centers. 
The separate strands of the peripheral nerves are not isolated in their 
course to a ganglion but anastomose freely with one another. Neverthe- 
less, it is possible to trace a degenerated strand in cross sections of the 
nerve, high up in the plexus, e.g., after extirpation of a muscle (163). 
These individual strands do not always occupy the same place in a 
nerve, as Stoffel (164) states, but change their positions in individual 
preparations (165). 
The motor nerves can be stretched to a certain extent without showing 
changes in function, but the amount as stated by various writers differs. 
Six centimeters may be taken as the upper limit (166), corresponding to 458 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
from 24 to 38 per cent, of their length. It must be remembered that 
stretching also loosens the nerves, and probably most of the stretching 
is spent on surrounding tissues and hardly any on the nerve substance 
itself. But obviously there must be some room for play, when, for 
example, we flex the knee joint, the sciatic is much less stretched than 
when it is extended. During flexion the nerve has also a slightly tortu- 
ous course, which Stoffel (167) demonstrated in monkeys by fixing the 
tissues in situ. 
With the exception of severing of nerves, the most important conditions 
requiring surgical interference are neuralgias (168) and neuritis. Curi- 
ously enough, nerve injuries on the whole cause little pain as the accumu- 
lated reports of the war testify. Patients seldom complain of troublesome 
sensations in a paralyzed limb, as in amputations. Why they are present 
following amputations and usually absent in gunshot wounds of the nerves, 
is unknown. But there are individual cases of the latter in which excep- 
tionally severe pain is felt (169). According to Popper, it usually 
follows penetrating wounds of the plexus or high up on the sciatic, that is, 
in injuries near the spinal cord. He assumes that a concussion reaches 
the centers, as evidenced by vasomotor phenomena, and that inflammatory 
irritation is superadded. According to Schlossmann, a neuritis actually 
arises at the site of the wound. Perthes (170) could show that freezing 
of the nerve above the site of injury was sufficient to block the conduction 
and allay the pain. 
Following such pain, contractures in neighboring muscles result with 
rapidly increasing stiffening of the joints, the contractures being due 
probably to reflex disturbances (171). The part played by such “reflexes” 
in joint stiffening has already been discussed. 
True neuralgia has also been the object of operative procedures. 
The methods designed to destroy or remove a diseased nerve do not interest 
us here. The open method for nerve stretching has given opportunity to 
study many changes which have been regarded as immediate causative 
factors. Thus varices have been described (Quenu), narrowing of their 
paths, e.g., through foramina (Bardenheuer), inflammatory growths (Ren- 
ton), pressure from enlarged lymph nodes (Partsch (172)), etc. But all 
of these anatomical changes have been the exception, the majority do not 
show such gross mechanical causes. Edinger states that the primary 
cause is a functional change in the vasomotor nerves of the vessels which 
supply the nerve and the pain is supposed to be incited by a change in the 
blood supply. 
Elaborate studies of the effects of nerve stretching on neuralgia have 
been made, but we have arrived at no clearer understanding of the problem 
than to say that after stretching, the nerve is loosened from its adjacent EXTREMITIES 
459 
tissue (neurolysis), and certain modifications of the nerve substance have 
occurred similar to tuning a violin string (neurokinese (173)). The state- 
ment is made that the sensory paths are made non-conductive more 
quickly than the motor paths. Whether this actually takes place remains 
to be investigated. The fact cannot be denied that certain nerves 
recover after injury much less readily than others. Thus, e.g., the 
peroneal portion of the sciatic nerve remains paralyzed much longer than 
the tibial part, according to Hoffmann (174), because the former has a 
poorer blood supply. 
Neuropathic bone and joint diseases are closely related to arthritis 
deformans. The principal pathological anatomical difference lies in the 
fact that in the former diseases the soft parts surrounding the joints take 
part in the process (175). As has been mentioned in connection with 
myositis ossificans, the joint changes in nervous diseases are particularly 
grotesque. Von Volkmann (176) believed that the destruction became so 
severe because sensations are diminished and patients walk about with 
slight injuries, and thus traumatize the joints all the more. Charcot 
(177) states, on the other hand, that some sort of a trophic nervous influ- 
ence must be concerned. His general anatomical findings have not been 
confirmed by later observers (178), and muscle atrophies seem to be 
exceptional (152). 
We have touched upon the question of trophic nerves in speaking of 
muscle atrophy in joint diseases. Similar considerations suffice for the 
bone atrophies in paralyses. That a paralyzed limb lags behind in growth 
can be seen in poliomyelitis. It has not been decided whether there is a 
specific trophic influence at work or whether the growth disturbance is only 
a consequence of the enforced rest from paralysis. The animal experi- 
ments in which mixed nerves like the sciatic were severed, throw no light 
on the subject (145). 
Since the diseases in which such trophic changes appear (tabes, syringo- 
myelia, spina bifida, etc.) chiefly affect the sensory nerves, experiments 
were devised to find a relation between the degree of pain sensitivity and 
the reaction of the body to invading injurious substances (inflammation). 
It was soon found that there was a definite relation between the condition 
of the blood vessels and sensation; and these views are supported by 
observations in local anesthesia. 
The influence of cocain was first made use of in ophthalmology (179). 
Later Spiess (180), after observations on the mucous membrane of the 
nose, built up his theory of the influence of pain in causing inflammation, 
but on the whole, his ideas have not been accepted because they are too 
hypothetical. In surgery, it was observed that a spina bifida, etc., did 
not take part in the reactive hyperemia following the removal of an 460 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
Esmarch bandage on the leg, which called attention to the relation between 
sensory nerve paths and vasomotor nerves. In nerve injuries, as Bres- 
lauer (181) points out, the immediate results of section must be differ- 
entiated from the later results. In the first eight days (study of Bier 
(182)), a change in the vasomotor reaction does not take place; later, the 
ability of vessels to actively dilate after peripheral stimulation is lost 
(mustard oil experiments of Bruce (183) and Breslauer), while vasocon- 
striction remains intact. Breslauer concludes from studies on patients 
with gunshot wounds that these defective reactions of the vessels are also 
guilty in the production of trophic disturbances, as, for example, per- 
forating ulcers, etc. Reactive hyperemia is, of course, a protective 
mechanism, and it is absent in an extremity with sensory paralysis 
because the vasodilators are injured, that is, the vasodilators belong to 
the cerebro-spinal system, the vasoconstrictors to the sympathetic 
(Breslauer). The same explanation is given by Trendelenburg (184) for 
the finding that in pigeons after section of the posterior roots, the feathers 
on the operated side grow much more slowly than those on the other. 
OSTEOMYELITIS 
Our knowledge of osteomyelitis as a distinct entity dates from quite 
recent times. The first description is by Chassaignac in 1853, following 
him came the works of Demme, Gosselin, Boeckel, Roser, Waldeyer, 
Volckmann and in the year of 1874, those of Lucke (185). The first 
experimental attempt to discover the nature of osteomyelitis was made 
by Rosenbach (186), in 1878, who allowed all sorts of physical and chem- 
ical irritants to act on the bone marrow, finally arriving at the conclusion 
that bone marrow phlegmon could be produced by no kind of irritant 
except of infectious origin. He was also the first to obtain an osteomye- 
litis of hematogenous origin, without particular interference of the general 
well being, by direct injection of pus into the blood stream, after fracturing 
a bone. On the whole, Kocher (187) confirmed these results by similar 
experimental procedures, only a short time after Rosenbach. But 
Kocher believed that the condition could arise from the absorption of 
decomposition products from the intestinal tract, a view which he tried 
to support by the injection of solutions of caustic potash into the marrow 
of a traumatized bone. After the wound had healed, he added an infected 
and putrid calcium solution to the food. The animal then developed 
a subacute osteomyelitis in this leg. At that time, the nature of the 
irritants causing osteomyelitis was not clear, for easily understood reasons, 
since pure cultures of staphylococcus pyogenes aureus had not been iso- 
lated by Becker until 1883 (188), and shortly after, Rosenbach cultured 461 
EXTREMITIES 
osteomyelitis pus, by the methods of Robert Koch which were just then 
published. With pure cultures of staphylococcus at hand, experimental 
efforts to produce osteomyelitis followed in rapid succession (189), with 
the uniform finding that it was possible, particularly in young rabbits, 
to produce an osteomyelitis very similar to that in man by the injection 
of pure cultures of staphylococcus in the ear veins, and that a mild trauma, 
such as tapping the bone was helpful in the production of the condition. 
We can picture the action of trauma by assuming that the injury 
diminished the bactericidal substances. Either the bacteria settle at 
this “locus minoris resistentiae,” or the trauma strikes a bone in which 
the bacteria are already present, but harmless. 
Later bacteriological examinations of the pus showed that it was not 
only the yellow staphylococcus which causes this disease, but all pyogenic 
organisms have the same ability, that is, staphylococcus albus, or citreus, 
streptococci, colon bacilli, b. typhosis, pneumococci, pneumobacilli, b. 
influenzae, gonococci, etc. These studies have established, then, that 
acute osteomyelitis is an hematogenous infection of the bone marrow 
usually by the staphylococcus. The question immediately arises of why 
the bone marrow, particularly that of children, is so predisposed to 
suppuration, when the cocci are present in the blood and reach all the other 
organs of the body in the same manner. As a reason, the first factor 
suspected was the distribution and size of the blood vessels. Lexer, 
Kuliga and Turk (190) and others have carefully injected the vessels of 
bones and photographed them with the #-rays, by which means a good 
idea of their distribution can be obtained. Lexer assumes that groups 
of staphylococci do not reach the smallest capillaries, but remain clumped 
in the vessels of somewhat greater calibre. These larger vessels are 
found in the middle portion of the bone, while the vessels toward the 
epiphysis become smaller. It so happens that the capillary network in 
the middle part is particularly richly branched. These would all be 
factors favoring the deposit of the staphylococci in this situation. Bac- 
teria which are thought to travel singly and not in clumps, in the blood 
stream, e.g., the tubercle bacillus, reach the epiphysis and are halted in 
the finest branches. This theory seems very illuminating, but certain 
opposing considerations cannot be ignored. In the first place, we know of 
parts in the human body where the slowing of the blood stream can be 
much greater than in the bone marrow, and where, in spite of this, a 
hematogenous suppuration practically never arises, for example, in the 
corpora cavernosa; furthermore the studies of Bier (191) and his students 
have shown that hyperemia tends to inhibit infection. This latter 
point is prettily shown by the studies of Samuel (192) and Roger (192) in 
which after producing hyperemia in the ear of a rabbit by section of the 462 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
sympathetic, they found that it w£s most difficult to infect it, while it 
became infected easily after section of the auriculotemporal nerve. 
The manner of distribution of the blood vessels can influence the 
deposition of bacteria to a certain degree, but it cannot be the only and 
final cause of the development of osteomyelitis. Other factors are con- 
cerned whose details are not known, but perhaps the presence of chemical 
affinities between tissues and bacteria is the key to the riddle of the sus- 
ceptibility of certain tissues to inflammatory changes. Many examples 
may be gathered from surgical pathology. There are patients who always 
suffer from osteomyelitis of special bones, for example, the metatarsal 
or metacarpal bones, and it is also well known that patients with suppura- 
tive arthritis frequently develop metastases in other joints. Experimental 
pathology also offers numerous examples of this process. Thus, Rascinski 
describes a strain of dysentery organisms which he injected subcutaneously 
or intraperitoneally with always the same grave changes in the intestines 
only. 
We know, particularly from the studies of E. Fraenckel (193), that 
bacteria may frequently be present in the bone marrow as well as in other 
organs without demonstrable reaction on the part of the tissues. There 
must be still another factor to initiate the real disease of the bone marrow. 
The bacteria remain quiescent as long as the protective forces of the 
organism and the toxins of the bacteria are in equilibrium. It would, 
however, be erroneous to conclude that osteomyelitis occurs only in a 
weakened individual, for on the contrary, a severe local reaction such as 
an acute osteomyelitis, may be an expression of a particularly high 
immunity of the entire organism against the invading bacterium. This 
much has been established by animal experiments; the subcutaneous 
injection of diphtheria toxin in a guinea-pig with low immunity is followed 
by severe local inflammation and necrosis of the skin, but the final result 
is not fatal, while a control animal shows no local reaction, and yet 
dies. On the whole, our knowledge of antibodies and what we should 
understand by them, why one individual should fall a victim so easily 
to osteomyelitis and another not, is still very incomplete. But the view 
that its development is the result of simple lodgement of bacteria in the 
bone marrow is too one sided and inconclusive. 
The histological changes and the course of an acute osteomyelitis 
depend in largest measure on the type and virulence of the bacteria, by 
which we mean not only the peculiarities of the living bacterium, its 
metabolism, etc., but also peculiarities of the dead bacterium, especially 
of its endotoxins, for it is well known that dead bacteria or their extracts 
may produce pus (194). 
Antibodies are found in large amounts in the serum since the bone EXTREMITIES 
463 
marrow is the chief laboratory for their production. They are named 
agglutinins, bacteriolysins, hemolysins, the latter of which are of practical 
significance in the diagnosis of osteomyelitis (195). 
In the bone marrow itself, the bacteria may bring about pathological 
anatomical changes of the most varied degree from violent suppuration to 
connective tissue overgrowth. It is also possible to imitate these varied 
forms experimentally by the injection of bacteria (196). 
In the further course of osteomyelitis there begins the formation of 
sequestra. This necrosis of a circumscribed part of a bone in a living 
body has kept authors busy for a long time and supplied material for 
extensive experiments. 
As early as 1855, Hartmann (197) produced bone necrosis with seques- 
trum formation by blocking the nutrient foramen with a sponge laid in 
the wound. In 1877 Busch (198) obtained total necrosis of bone in rab- 
bits by passing an electrically charged wire through them. W. Koch 
(199) ligated the nutrient vessels or plugged them with emboli; Barnabo 
(200) removed a portion of periosteum aseptically, or applied £-rays. 
Some of these experiments, especially those of Busch, were planned to 
study both regeneration of the marrow after its destruction and its ability 
to produce bone (Rost (196)), (42), (198), (189). From the results it can 
be stated that marrow has the ability to regenerate completely, and in a 
few weeks after complete destruction, newly formed marrow will be 
present to the original amount and with little histological difference from 
the original. 
By. the injection of certain irritants (particularly paraffin oils) it can 
be shown that the marrow reacts by marked connective tissue production 
(Rost), in imitation of the clinical bone diseases such as ostitis fibrosa and 
others, which are characterized by the replacement of marrow by con- 
nective tissue. In these, it is not certain if there is an irritant chemical 
involved, which varies with the different diseases, but produces a similar 
histological change. In the osteomyelitis of mother-of-pearl workers 
first described by Englisch (201), and later investigated roentgenologic- 
ally, it is not improbable that the disease belongs to this group, and results 
from the action of conchiolin on the bone marrow. The circumstances 
surrounding the osteomyelitis of horn workers are less clear, but the 
writers regard this also as due to chemical irritation. In the latter disease 
there is an acute progressive suppurative osteomyelitis, but not called 
forth without the presence of infection. Experimentally, circumscribed 
abscesses were formed in which infection could be excluded with certainty 
by the injection of turpentine, mercury and certain other chemicals (202). 
If an osteomyelitis develop in the vicinity of a joint, i.e., in an epiphy- 
sis, the infection may spread and lead to a suppurative arthritis. Joints 464 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
have a very low resistance to infection, as found both clinically and experi- 
mentally. Magnus consistently obtained a typical joint infection in 
rabbits with 0.5 c.c. of an attenuated culture of staphylococci. Notzel 
believes that the synovial fluid is a good culture medium (203). 
In man, infectious material may also reach a joint via the blood 
stream, or be introduced through direct injury. 
The clinical picture of suppurative arthritis is usually that of a very 
severe infection with high fever and marked prostration. The danger 
of a generalized infection is by no means light. But it is not only the 
virulence of the organisms which causes the severity of the symptoms, but 
also the anatomical and physiological peculiarities of joints themselves. 
A joint is a fairly homogeneous space, although in some, the knee for 
instance (204), certain subdivisions of practical importance may be made. 
Such a homogeneous space becomes infected rapidly and equally, and when 
pyogenic organisms are introduced, they are brought in contact with a 
large surface in a short time. This is equally true in chronic arthritides, 
something which is not often considered. 
In clinical work, it is often observed that patients suffering from tuber- 
culosis of some other organ, suddenly develop a painful transudation in a 
previously healthy knee joint, and the future course of events proves that 
it was the beginning of a tuberculous inflammation. The widely spread 
belief that the type of infective agent (gonococcus) can be diagnosed, from 
the sudden onset of a markedly painful arthritis, is perhaps true, but with 
modifications. 
This rapid swelling was also obtained in animals by Notzel, Dreyer, 
Magnus, Perez, and others. 
But the rapid spread of bacteria cannot alone explain the severe 
general symptoms. The question is rather, are the bacteria and their 
toxins absorbed from a joint particularly fast and freely? This question 
has not as yet been answered satisfactorily (205). Studies of hemorrhages 
in joints had absorption as only a secondary interest. They have already 
been mentioned in the discussion of the fact that blood remains fluid in 
the abdominal cavity, and we refer to that paragraph. According to 
numerous anatomical investigations, the synovia are not in very intimate 
contact with lymph vessels, but as in all other parts of the body, the tissue 
fluids between the cells flow imperceptibly into the actual lymphatic 
system. Therefore, it is not possible to inject these vessels of the leg 
from within a joint (206), but their anatomical relations to those surround- 
ing can be found in the investigations of Tillmann (207). 
Braun, by injection of watery fluids, demonstrated a diffuse staining 
of the intracellular tissue of the synovia. The soluble part of the dyes was 
found later in the lymph nodes of the groin. The particulate elements EXTREMITIES 
465 
were phagocytosed by leucocytes which were then taken up in the 
circulation. 
Absorption, however, occurs very slowly, according to the investiga- 
tions of Braun. Cecca injected solutions of potassium iodide into joints 
and from the rate of its excretion in the urine, concluded that absorption 
begins in about 50 minutes. By massage, Mosengeil and Kroh hastened 
absorption, but damage to the synovia could not be excluded, as R. V. 
Volkmann pointed out. The latter is of the opinion that in injuries of 
the knee joint, blood is absorbed only at injured places by the tissues under 
the synovia, while the synovia itself hardly absorbs at all. 
Daily clinical experience also shows that absorption from the inper 
surface of a joint is slow. Carbolic acid poisoning very rarely follows 
the injection of this substance into a joint. Effusions into the knee are 
absorbed very slowly, but inflammatory factors may play a role in this case. 
Viewed from the opposite standpoint, it is remarkable that increased 
joint fluid is not observed more often in severe general anasarca (cardiac 
decompensation, Braun), even if it does occur, according to Muller (208), 
more commonly than is supposed. 
Notzel’s experiments contradict these views. He discovered bacteria 
in internal organs in as short a time as five minutes after their injection 
into a joint. On the basis of his studies, he has advanced the rather 
startling view that the lymph nodes are not protective against infection, 
since, in his investigations, the bacteria passed through the lymph system 
so rapidly. His statements and conclusions, as might be expected, met with 
instant opposition (209). The first argument was that in injecting the 
bacteria, he introduced some directly into the blood stream. We know 
nothing definite, however, of the activity of the blood vascular system in 
absorption of joint effusions. In later experiments, Magnus could not 
confirm Notzel’s findings. 
To conclude, slow absorption is the very thing which does not 
explain the grave general symptoms. It is evident that further investiga- 
tions are necessary. 
The destructions of joints, well known in general pathological litera- 
ture, as well as the contracture positions in effusions, have been studied in 
animals by many workers (210). Dreyer paid particular attention to the 
therapeutic measures in suppurative arthritis. In the treatment of joint 
diseases with effusion, therapeutic measures must be varied to suit the 
individual case. Temporarily disregarding the treatment of the infection, 
per se, stretching of the capsule is a danger which must be met by puncture 
because the synovia cannot absorb the fluid very rapidly and a flail joint 
may result. According to Payr, however, a certain amount of fluid is 
beneficial in preventing the excessive growth of connective tissue. 466 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
To prevent refilling, all sorts of irritant substances such as tincture of 
iodine, carbolic acid, etc. have been injected. According to Hildebrand 
(211), this refilling takes place because the nerve endings which surround 
the network of capillaries are stimulated from the inner layers of the syno- 
via. These nerve endings are said to be concerned in the pouring out of 
the effusion, and Hildebrand believes that irritants reduce the abnormal 
sensitivity of the synovia and thus prevent the reaccumulation of fluid. 
This theory is not exhaustive for, of course, we see joint effusions in com- 
pletely paralyzed limbs. 
A further measure to prevent shrinking of the capsule and ligaments, 
consists in applying extension. There have been many investigations of 
the pressure relations during extension and of the force which must be 
exerted to separate joint surfaces (212). To these belong also the investi- 
gations of the tensile strength of the ligaments (213). The occurrence 
of so-called sprain fractures is a voucher for the fact that ligaments are often 
fastened tighter than bones. 
These studies have shown that the application of extension apparatus 
reduces the pressure when the synovial membrane is normal; in a joint 
altered by inflammation or by effusion the opposite occurs, i.e., a height- 
ened pressure. But the results in the separate joints are varied. Why 
extension diminishes the pain is not entirely clear on these grounds, 
but possibly the changes in tension alone, even if the pressure is not 
reduced, are sufficient to modify the nerve endings. 
Tuberculosis of bones like osteomyelitis is a blood borne infection. 
Experiments have established the interesting fact which can be used in the 
judgment of industrial accidents, that contrary to what occurs in osteo- 
myelitis, the lodgement of tubercle bacilli in bone is not particularly 
favored by injury (214). 
The peculiarities in the course of this disease can be explained by the 
type of infective organism and the body reaction to its invasion. In a 
general way, however, the considerations as outlined under osteomyelitis, 
apply to tuberculosis. The fact that tuberculous fistulae heal with great 
difficulty, which leads us not to incise tuberculous abscesses, but puncture 
them, has been explained by Jochmann and Batzner (215) in the following 
way: in tuberculous inflammation, lymphocytes take part, and these con- 
tain no tryptic ferment such as is present in polymorphonuclear leucocytes; 
without this enzyme, the body is not able to dissolve the tuberculous 
tissue. Batzner, therefore, treated such fistulae successfully with trypsin. 
It is doubtful though, if this hypothesis is correct. According to Rost (216), 
substances which stimulate granulation tissue are set free by the death of 
body cells, and it is quite conceivable that the injected trypsin acted 
favorably in this roundabout way. Furthermore, when mixed infection 467 
EXTREMITIES 
is superadded, polymorphonuclear leucocytes containing trypsin are 
present in abundance and still the fistulae do not heal. This question 
has not as yet been answered. 
The mutual relationship between the muscular and skeletal systems 
which has been emphasized in this book becomes particularly clear after 
operative procedures on joints, particularly in their artificial mobilization. 
It is amazing to see how a new and useful joint develops even after complete 
removal of all the ligaments and parts of the capsule, together with a 
complete modification of the ends of the bones. The same laws and the 
same forces which interact at the first appearance of a joint in embryonal 
life, play a similar role in the final architecture of our operatively made 
joints. That the normal shape “ in the strict sense of the word is fashioned 
by the muscles” was quite clearly realized by Ludwig Fick (n) as early 
as the year 1845. 
In general, we seek to make from the ends of the bone a head similar 
to that found in the normal joint. It must be emphasized that this is the 
only correct way; the ball and socket are not developed just arbitrarily. 
In embryonal life, the end of the bone close to the insertion of muscles 
becomes the socket, and the end distant, the ball, as Rudolf Fick (11) 
expressed these laws of development. It is, therefore, the functions of 
muscles, pull, push and polish, which determine the future shape of the 
joint, and by changing the place of insertion of muscles, the shape and kind 
of joint can be modified. 
After the ends of bones have been roughly shaped with chisel, saw and 
file, we place a piece of soft tissue between them to prevent union. This 
procedure was initiated by Helferich (217), who in 1894, implanted a 
piece of muscle while artificially mobilizing a joint, and thus gave this par- 
ticular joint operation a tremendous impetus. It is possible to obtain a 
functioning joint without the interposition of soft parts, but the results of 
utilizing this suggestion of Helferich have been far superior. Numerous 
clinical and experimental studies have sought to discover other materials 
to place between the bone ends. Foderl, Roser, Chlumsky, Hubscher 
(218) used silver and gold foil, tin, celluloid, pig’s bladder, etc. Narath, 
on the basis of the investigations of Foderl, once used a pig’s bladder 
between the bones in a man. A fistula developed, but the final result was 
good. At the present time, because of better healing, tissue from the 
patient himself is used. Fascia, fat and periosteum have all been tried. 
American surgeons (Murphy (219)) usually use a soft part flap with a 
pedicle, while German surgeons prefer a free transplantation. Both 
methods seem to yield the same end results. 
After a certain length of time, a capsular space appears between the 
ends of the bones and eventually contains a viscid, sticky fluid (220). 468 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
The bone ends themselves are covered with a tough connective tissue 
which has the gross appearance of cartilage and in a number of cases, this 
has been confirmed microscopically (221). This covering does not arise 
from the interposed material, indeed, the same lining develops without 
placing soft parts between, as was shown by Kocher and recently by 
Schmerz and Schepelmann (222). 
The formation of the space has been studied experimentally, particu- 
larly by Rehn, and it was found that fatty tissue remains only along the 
edges, while the central part disappears, after undergoing a very typical 
metamorphosis (223). In the zone of degeneration cysts appear, and 
the final joint space is formed by their confluence. But Payr has a differ- 
ent idea. In his opinion, the principal factor is trauma, which acting 
as in the development of bursae, in hallux valgus, finally leads to the 
formation of cysts. Payr relates the formation of the joint space to the 
cyst formation in ganglia, on which subject he had earlier made extended 
histological studies (224). But in this he is opposed by Ledderhose (225) 
who regarded the spaces in ganglia as true cystic tumors. At present, 
we cannot answer the question of how cysts filled with clear fluid develop 
in the tissues. It may be mentioned, however, that such cysts develop 
in parts of the body which have nothing to do with preformed bursae, 
as for example, the hygromata derived from unusual bursae in the popliteal 
space (221), which Langemak (226) believes, on the basis of his extensive 
histological studies of this subject, develop from fatty tissue. He observed 
a smooth transformation of fat to connective tissue, which later became 
a thickening composed only of collagen practically bloodless in the centre. 
Softening now took place and the collagen was changed to fibrinoid and 
albuminoid. The increase of fluid in such hygromata is, therefore, not an 
exudative process, but only a dissolving of collagen fibres. This would 
hold true for the space formation in artificially mobilized joints in which 
Salkowsky found “synovin” (227). 
The normal synovial fluid is said to be a decomposition product and 
not a real secretion, but this view is doubted by Rudolph Fick (n). 
According to Bier (221) the synovial fluid contains ferments, which dis- 
solve certain tissues, particularly bone. Therefore, when a peg of bone 
or ivory has been placed through the joint and the two bone ends in 
an arthrodesis, it is usually dissolved in a short time. Again, according 
to Bier, this property of bone tissue destruction also plays a role in the 
regeneration of joints. 
The composition of synovial fluid varies according to whether the 
joint is quiet or in motion (8o). It contains more water at rest; in motion, 
more solids, which are supposed to arise from decomposition products 
of the joint walls. EXTREMITIES 
469 
As mentioned above, ligaments and capsule develop in an artificially 
mobilized resected joint in almost the same relations as in the normal 
joint. The capsule is rebuilt from periarticular healthy tissue even when 
all fragments of the old capsule are carefully removed (Payr). It must 
be pictured here also that it is the performance of function which causes 
this adaptive change. But in this process there is an analogy to the 
development of capsule and ligaments in embryonal life (see R. Pick (n) 
p. 44), where it is also bound up with the function of the joint. 
The dependency and relationship of the completed capsule to the 
musculature is seen again in the fact that pinching of the capsule during 
movements is prevented by the muscles. Furthermore, in anatomy, 
certain muscles are even called capsule tensors. But it is better perhaps 
to think of this stretching of the capsule as R. Fick does, viz., that it is 
due to the tonus or the elasticity of the muscles and there is no actual 
“tensing” of the capsule. 
That nature is able to rebuild a functioning joint with even much less 
help than is given by interposing soft parts and modelling bone ends, is 
shown in the classical treatise of v. Langenbeck (228) who not only 
observed a rebuilding of finger joints after subperiosteal resection, but also 
saw a whole new head of a humerus appear after resection. His work 
was based on Heine’s animal experiments in subperiosteal resections, a 
work which was repeated by Ollier (229). Rebuilding of an elbow joint 
has been described by Jagetho and one of the hip by Schmieden (230). 
In contrast to these simple resections are the experiments of implanting 
whole joints obtained by amputation or from cadavers (231). In this 
way, a new joint can also be obtained, but as learned from the pathological- 
anatomical investigations of Borst (232) and M. B. Schmidt on both 
human (cases of Enderlen) and animal material, these joints do not take 
on life, and thus are no different than the artificial ivory joints of Konig 
(233). These questions are so thoroughly discussed in general surgery 
that we need go no further into them here. 
VEINS 
The veins of the body are subjected to a pressure, corresponding to the 
mass of blood which is supported vertically above the respective vessels 
(234). On account of the upright position of man, the highest pressure 
is exerted in the veins of the lower extremity. In adults, it amounts to 
15 cm. mercury, it is therefore almost as great as the pressure in the aorta. 
As is well known, the walls of the veins are much weaker and less elastic 
than the walls of the aorta, and this pressure would, of course, stretch 
them to the breaking point if there were no special mechanism to support 470 
THE PATHOLOGICAL PHYSIOLOGY OF SUKGICAL DISEASES 
it. The mechanism consists of the centripetally opening valves, and from 
the investigations of Delbert (235) we know that the pressure on the walls 
of the femoral vein is reduced from 15 to 1 cm. mercury by their presence. 
They are able to withstand considerably more pressure; in the experiments 
of Lowenstein, those in the greater saphenous vein were still competent 
under 50 centimeters of mercury (236). But they are not entirely effi- 
cient, and the healing of wounds of the leg is much delayed by unfavorable 
circulatory conditions if the patient allows the lower extremity to hang, 
while if the patient lies down, the reparative processes are hastened since 
the hydrostatic pressure is reduced to zero. 
The forward movement of the blood occurs according to the laws of 
communicating tubes, and that forced into the arteries by the heart shoves 
the blood column in the veins before it. This passive venous circulation 
is helped considerably by the action of the muscles which first compress 
the veins and then allow them to expand and thus pump the blood forward 
(237). On account of this lack of changing muscle function, occupations 
which require long motionless standing on one place, baking, washing, 
surgery, etc., are said to predispose to varicose veins. This pumping 
action of the muscles has been used therapeutically in the treatment of 
this condition. Thus Katzenstein (238) proposed to transplant the saphe- 
nous vein to a channel prepared in the sartorius muscle. Such veins, 
in which advanced secondary changes are present are not likely to recover 
completely after this operation, but Katzenstein always noted a subjective 
improvement. The patients had a sensation as though the leg had become 
lighter in weight. 
As the chief cause in the development of dilated veins in the lower 
extremity, that is, for the formation of varices, the purely mechanical 
hydrostatic pressure has always been emphasized. Obstruction to the 
blood, flow, from intraabdominal tumors or pregnancy, or collections of 
fat at the foramen ovale, or very many other things are said to be the 
immediate exciting causes. This on the whole, can certainly not be true, 
for these latter troubles occur in many individuals but only a few develop 
varices, and then we have seen above, that the valves in the veins can 
withstand a much greater rise of pressure without becoming incompetent 
if they are normal. 
The fact that varices may be present at birth and may be hereditary 
makes it possible that the primary change is in the walls of the veins. 
Anatomical search for deficiencies has been made (239), but for purposes 
of discussion, the studies of normal veins as brought out in the work of 
Lowenstein (236) and others are more useful. Lowenstein believes that 
in “normal youthful individuals there are two different types of veins, 
those which possess particularly weak musculature at the sinuses, and EXTREMITIES 
471 
those in which the weakest musculature is at a place distal to the valves.” 
The development of the various changes, i.e., so-called sinusectasias and 
true varices, are said to depend on these anomalies. 
Ledderhose (240) has called attention to the fact that the dilatation 
in varicose veins in the majority of cases is not proximal and central from 
the valves, but distal and toward the periphery, which cannot be brought 
into harmony with the opinion that varicose veins result from hydrostatic 
pressure. Hasebrok (241) explains this in a different way. He believes 
that the whole theory of hydrostatic pressure as a cause is incorrect, and 
that the dilatation is brought about by transmission of arterial pulsation. 
He showed in models that arterial waves spread directly not only to those 
veins lying in their immediate neighborhood, but also to those which, as 
the veins of the skin, are relatively distant from the arteries. Indeed, in 
the models there appeared and remained, localized dilatations distal to 
valves which had been introduced into the thin rubber tubes. That these 
observations may be applied to conditions in the human subject is shown 
by a number of facts. The most interesting, is Hasebrok’s conception of 
the so-called Trendelenburg experiment, which (242), as is well known, 
consists in emptying the veins of the skin by stroking the leg and then 
compressing the saphenous vein below the groin. If the leg is lowered 
while the pressure is retained, the vein remains empty or fills very slowly 
from the periphery; but as soon as the pressure is released, the blood flows 
in very rapidly from above downward. This experiment shows the rela- 
tion of incompetent valves to varicose veins. It must, however, be first 
discovered if the valves in the veins communicating between the saphen- 
ous and those lying deeply are competent. The fact that in incompetency 
of the valves of the tributary veins, Trendelenburg’s operation of tying 
the saphenous vein gives poor results is explained by Hasebrok in this 
manner; that the arterial pulsation waves are transmitted particularly 
vigorously to the veins in the skin (superficial veins). Hypertrophy of 
the vessels is also said to result, a finding which previously had been 
thought due to the consequence or response of the veins to the increased 
hydrostatic pressure. These pulse waves act more energetically the more 
the outflow is checked, and in this way Hasebrok explains the develop- 
ment of varices in abdominal tumors, etc. Furthermore, the waves are 
increased when the blood flow is particularly large in amount, and this 
accounts, for example, for the isolated varices occasionally seen in the 
arms of heavy laborers. That an arterial pulse can be frequently seen 
in greatly filled veins and varices, had already been emphasized by 
Ledderhose. 
Undoubtedly this theory is attractive, because so much in the pathol- 
ogy which remains hazy by the hydrostatic theory can be explained by 472 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
this. The mistake should not be made, however, of regarding the matter as 
settled. In outspoken varices, hydrostatic pressure plays a very large role. 
For the explanation of the beginning of varices, the arterial pulsation wave 
theory can be drawn upon to advantage. But we should never disregard 
the conception that weakness of the walls also plays a part, although it 
can only be said that definite dilatation may be present at birth, in the arm 
as well as the leg, and that varicose veins undoubtedly are present in 
certain families. 
But weakness of the walls may furthermore be acquired. To this 
class belong the varices of syphilis, a subject with an extensive literature 
(243). In addition, injury may occur from other infectious diseases and 
toxemias, but our knowledge is much less certain. Some injuries are 
assumed to be due to certain metabolites, as for example, in pellagra, in 
chlorosis, or other general systemic diseases. In pregnancy also, accord- 
ing to the opinion of the majority of the authors, the varices are not due 
to passive congestion alone, but to some sort of toxin which perhaps is 
related to the internal secretory mechanism. Kushimura (244) advances 
the theory that all of these injuries, high blood pressure in addition, do 
not act directly but indirectly through the nervous system and the changes 
in the walls of veins result from alterations of tonus. Very likely the 
idea of a weakness of walls cannot be escaped, even with this theory. 
Lesser (245) considers varices production as a neoplastic growth. 
Thrombosis very frequently occurs in these varicose veins, especially 
when the patients are compelled to lie abed on account of some other cause. 
The fundamentals of the morphology of thrombi are treated in general 
pathology and general surgery (246). For surgeons, the causes of the 
development of thrombosis are of decided importance, for post-operative 
disturbances from this cause, and sudden death from resulting emboli 
mar the results of many operations. It is necessary in considering the 
experimental studies in this subject to emphasize that coagula found in 
dead animals are often very difficult to distinguish with certainty, from 
ante-mortem thrombi. Post-mortem coagula often have the structure 
and surface markings which are regarded as characteristic of thrombi 
(247), in which the markings are the result of the movement of blood 
(Zahn). How much the surface markings of post-mortem clots are influ- 
enced by the agonal processes cannot always be determined at autopsy 
(246), (248). It is possible, perhaps, to produce the morphological 
structure of post-mortem clots experimentally (249), for example, 
when an animal is rapidly injected intravenously with collargol. 
The entire blood clots, but the heart continues to beat. Such agonal 
coagulation must be reckoned with, if false conclusions are to be avoided 
in experiment. EXTREMITIES 
473 
There is considerable similarity between the production of a thrombus 
and the usual coagulation, and a large number of the factors which lead to 
coagulation of blood outside the body are also important for coagulation 
in the living body. The first is a slowing of the rate of blood flow. In 
speaking of the experiments on the thrombus question, we will return to 
the fact that thrombi form only when this occurs. Secondly, the condition 
of the vessel walls plays a large role. We know of numerous physiological 
experiments and observations during blood transfusions, that coagulation 
is diminished if the vessel walls with which the blood comes in contact 
are made smooth with paraffin. Finally, the same enzymic and pre- 
cipitation processes must operate as in coagulation in a test tube, and 
changes in the equilibrium of the composition of the blood favor the 
formation of clots. 
The various experiments were directed toward all of these three 
factors, but the most comprehensive and clearest are those which took 
as their starting point changes in the rate of blood flow and injury to 
vessel walls. The experiments of Brucke (250) are fundamental; he 
found that the blood in ligated vessels remains fluid. If this were not 
true, the surgeon could scarcely sew a vessel and certainly organ trans- 
plantation would be impossible. Damage or destruction to the vessel 
wall initiates coagulation and the blood finds a “crystallization center” 
in the debris (246), (251). Just as good a crystallization center can be 
provided with any dead substance, e.g., a silk string in the lumen of the 
vessel (252). The finer processes of this form of thrombosis were studied 
by microscopical observations on the omentum or web of living frogs, 
where it was found particularly in the experiments with ligation, that the 
blood flow was first slowed. Such delicate structures as the vessels in 
the omentum were damaged severely enough to cause thrombosis by 
even touching with any sort of chemical. The experiments of Huter, 
Schwalbe (253) and others are of great interest in abdominal surgery. 
Huter found that touching with ether led to thrombosis. The human 
omentum seems to be less sensitive, at least, nothing was heard of throm- 
bosis in this structure when peritonitis was being treated by ether. Throm- 
bosis is produced much more readily by the injection of all sorts of chemical 
irritants directly into the vessels. Zahn used Lugol’s solution. To 
produce a shrinking of varices by thrombosis, Linser advises the use of 
bichloride of mercury injections and a method of treating hemorrhoids 
is based on the same viewpoint, i.e., carbolic acid injections. Thermic 
influences act in the same way when they reach the vessel wall from with- 
out. Clinically, extensive thromboses are well known in burns and frost 
bite. Gangrene from cold, which was observed frequently during the 
war with predilection for mild cold, depends on such thromboses; in 474 
THE PATHOLOGICAL PHYSIOLOGY OF SUEGICAL DISEASES 
burns also, thrombosis of the smaller vessels with later involvement of 
the larger vessels is very common. Experimental studies of the effect 
of heat were made in the rabbit’s ear by Klebswelt (254), Eberth-Schim- 
melbusch and others, while Zahn and others studied cold. That the 
relation of vessel wall injury to the development of thrombi should not be 
pictured too mechanically is clear from the findings of Enderlen (255) and 
Borst on transplanted vessels. They found but insignificant scales of 
clot along the suture line in autoplastic transplanted vessels; in homeo- 
plastic transplants, it is true that the wall was destroyed, but there was no 
thrombosis (256). In heteroplastic transplants the walls were completely 
destroyed and obstructed by thrombi. It follows that the protection 
against coagulation offered by a healthy vessel wall is some sort of “vital 
specific one.” 
These experiments were comparatively simple and led to uniform 
results, but the nature of thrombosis is by no means explained by them. 
The majority of post-operative thromboses require for explanation the 
assumption of the additional factor of change in the composition of the 
blood. There are many investigations of this point. A number of chem- 
ical substances such as collargol, ether and chloroform, glycerin, pyro- 
gallate, bichloride of mercury and others lead to coagulation on being 
injected intravenously (246), (249), (257). We know further that 
transfusion, particularly when foreign blood is used, predisposes to clot 
formation and this was the main reason that transfusion was deserted 
for the subcutaneous administration for a time (258). Serum injections 
are often followed by coagulation; the rabbit often reacts with thromboses 
to the injection of ox serum (259). This hypersensitiveness increases 
with successive doses, and in anaphylactic shock, which, as is known, is 
initiated by repeated injections of the same serum, thromboses in the 
lungs are of fairly common occurrence (see discussion of anaphylaxis, 
p. 289). As a cause for this coagulation, changes in the enzymic content 
of the blood have been suspected. Arguing from normal coagulation, 
the first thought is precipitation of fibrin ferment, and substances such 
as fibrin, blood or pressed tissue juice, pus, extracts of tumors, etc., have 
been injected intravenously with coagulation as a result (260). With a 
similar idea in mind, Volcker (261) recently attempted to produce thrombi 
by the intravenous injection of clotted blood from the same species. Ob- 
viously, these various experiments were actuated by clinical aims. Thus 
Volcker believed that broken up blood in an operative field might, by 
direct entrance into veins, lead to thrombosis and embolism. According 
to the investigations of v. Durings (262), an absorption of fibrin ferment 
may take place after crushing a hematoma, by which coagulation is 
favored. The majority of post-operative thrombi do not occur at the EXTREMITIES 
475 
operative site, but in the saphenous vein, especially when it is varicose. 
This is further evidence for the view that circulatory disturbances are 
predisposing factors, as has been mentioned above. The experiments 
of Wright (263), who obtained thrombi by the injection of the pressed 
juice of the testis only when the tissues were rich in carbon dioxide allows 
the significance of circulatory disturbances to appear in still another light. 
Important works in which pus was introduced into the blood stream 
sought to show the influence of bacterial infections in thrombus produc- 
tion (264). It seems that we may expect thrombosis in a certain per- 
centage of cases, after the injection of large numbers of streptococci, B. 
diphtheria and B. typhosus, but B. coli cause no thrombosis. Clots can 
be obtained with much more certainty by the injection of the products 
of bacterial metabolism (toxins), (even with those of B. coli), and it 
may be that the thrombi obtained by introducing bacteria around the 
vessels is brought about by a filtering through of their toxins. This 
latter condition was not found when streptococci were used, which agrees 
very well with clinical data. When the lodgement of bacteria is favored 
by a local slowing of the circulation, the intravenous injection of B. 
coli both living and dead, leads to local thrombosis, and perhaps post- 
operative thrombophlebitis may arise in man under these conditions. 
Investigations have also been made to determine if a “weakened condi- 
tion” predisposes to thrombus formation, a point of importance in clinical 
work, but in animals made anemic by hemorrhage, Vaguez (265) obtained 
no thrombi. 
Comparison of experimental results with clinical experience leads to 
the conclusion that bacteria and their metastatic implantation are of 
great significance in the development of thrombi. The question of 
whether blood coagula or aseptic broken down hematomata are predisposing 
causes will have to be settled by statistical studies. The view that 
pressure on the veins of the leg, e.g., in Trendelenburg’s position, brings 
about thrombosis, rests on insecure grounds. Trendelenburg (266) 
himself gives good evidence that such an origin is improbable. 
Usually, organization tissue grows rapidly from the wall of the vessel 
into the thrombus. Clinically, it is usually considered that organiza- 
tion is complete in 21 days and the danger of loosening of the thrombus 
with embolism has disappeared; microscopically, the organization is 
completed much earlier. Embolism and its results have been discussed 
under diseases of the lungs. 
The development of leg ulcers depends directly on varicose veins and 
their resultant passive congestion (234). After the skin has been damaged 
by thrombotic and lymphangitic processes, mild injuries, or long standing 
pressure, as in tight shoes, etc. are sufficient to lead to ulceration. This 476 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
view has the advantage of being simple, and is the one predominant at 
the present time, but whether it is correct in all cases is doubtful. Exten- 
sive ulcers are often present without corresponding varicose veins, and 
conversely, ulcers are often absent with marked varices. Verneuil calls 
attention to the fact that dilatation of deep veins is often present when 
the superficial ones appear normal. But all ulcers and wounds of the leg, 
even when varicose veins are not present, heal poorly when the patient 
is not at rest, an indication that the stasis which is present when the leg 
is allowed to hang retards the healing of all wounds. But whether this 
poor ability to heal which is present in normal persons as well, is only a 
consequence of the retarded circulation in the legs, or whether it is related 
to a different healing ability in different parts of the skin of the human 
body, cannot be answered at present. It does not seem to depend on a 
peculiarity of the arterial supply of the skin, for Spalteholtz (267) demon- 
strated only small differences in the density of the subpapillary network 
in the sole of the foot and the calf of the leg. It would be interesting to 
know if this same poor healing is found among Japanese and Orientals, 
who, because of their short stature and because they spend many hours 
of the day in a squatting position, suffer much less from varicose veins 
than Europeans. If passive congestion is to be placed in the foreground 
of causes, it is remarkable that in varices, the foot on which the highest 
blood column presses is almost never the seat of an ulcis crurae. It is 
not clear why a leg ulcer should be found almost always from above the 
ankle to the middle of the leg. Of course, the pumping of the veins is 
particularly poor because most of the muscles become tendons in this 
situation. 
From French sources the view has often been expressed that leg ulcers 
must have a nervous cause, and certain anatomical findings are used as 
evidence (268). These may be secondary, but the fact is always con- 
spicuous that legs with ulcers are objectively cold and the subjective 
temperature and touch sensations are lowered. All of these things can, 
of course, be explained by the local findings and disturbed metabolism 
of the part. Therapeutically, nerve stretching has been advised. 
When one of the larger vessels of an extremity is ligated, the blood 
flows rapidly through the so-called collaterals toward the periphery, and 
thus the nourishment is assured. From antiquity, investigations have 
been made concerning the details of the development of this collateral 
circulation (269). The critical time is during the first immediate adjust- 
ment, which Bier (182) describes as the “preliminary” collateral circula- 
tion, which will be discussed in a moment. 
O. Weber (270), Marey, and others believed that the blood is dammed 
up towards the center, causing a rise in blood pressure, which mechanically EXTREMITIES 
477 
drives it into the part made anemic by the ligature. That there is a 
general increase of blood pressure of some duration was recently con- 
firmed by Katzenstein (271), who found it in the collateral vessels also. 
But it is questionable if this increase is significant in the production of 
collateral paths when small vessels are ligated, although it is doubtless 
true that pressure differences are set up (272). V. Recklinghausen and 
Nothnagel (273) lay great stress on its diminution in the anemic area, and 
Bier believes differences of pressure cause the fluids to flow into the net- 
work of blood vessels. But he has an opinion of his own when he believes 
that the anemic area has a “pulling” power, which sucks up the blood, 
as a sponge fills when it is placed in water. He was led to this conception 
principally through observation of the reactive hyperemia following the 
removal of an Esmarch’s bandage. It is doubtful, however, if this latter 
reaction is analogous to the response of the capillaries after ligation. 
Katzenstein (274) justly emphasizes that when an Esmarch bandage is 
removed the conditions are similar to those in a canal when a lock is 
opened; an excess of water streams off and later the normal fall of the 
river bed is resumed. But the remark of Bier, that when vessels of 
medium size are ligated, the collateral circulation appears not merely 
according to the laws of pressure differences, but also according to the 
laws of flow in capillary tubes, is quite correct. He believes it is not only 
physical laws which determine the distribution of blood, but there is also 
a vital activity of the capillaries themselves, chiefly in the prevention of 
venous backflow. Obviously these phenomena are not clearly under- 
stood because we have little knowledge of the active part played by 
capillaries in the total vascular bed. The arteries supplying the intestine 
apparently have many collaterals, yet ligation is poorly tolerated and it 
may be that it is due to their inability to suck up blood. Bier believes 
that this “blood sense” of an organ runs parallel to its general sensitivity, 
and an organ which has no pain sense lacks also this pulling power (275). 
The development of a collateral circulation, furthermore, is inde- 
pendent of the nervous system, at least, as far as it concerns a large nerve 
supplying an extremity. Those lying in the vessel walls were not taken 
into consideration in the experimental methods of these authors (Bier, 
Katzenstein and others). The influence of nerve stimulation on the 
peripheral blood pressure was investigated with the conclusions that 
certain considerations could be held regarding the nerve supply of an 
extremity in the development of collateral paths, but these experiments 
were so complicated that most writers believe they point to nothing 
definite (Bier, Katzenstein and others) (276). 
The same rules are applicable when venous trunks are ligated; viz., the 
development and activity of the collateral circulation is dependent not 478 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
merely on the anatomically demonstrable collateral paths, but also on the 
reaction of the organ to changes in its venous circulation (277). Thus, for 
example, ligation of the vena cava distal to the entrance of the renal vein 
is well borne, while ligation above leads to death even though the veins 
of the kidney have sufficient anastomoses with the vena azygos, etc. In 
the formation of venous collaterals, the primary rise of pressure is impor- 
tant in overcoming resistances. If the nutrition of an extremity is less 
endangered when both large artery and vein are ligated simultaneously 
is answered variously. This question has not been investigated 
sufficiently. 
If, on account of arteriosclerosis, the circulation of an extremity is not 
adequate, the leg may be saved in certain favorable cases by shunting the 
arterial blood into the veins (278), since the valves do not completely 
prevent backflow. In animals, such anastomoses have been attempted, 
but in general the results have been unsuccessful (279), (256). 
If an artery wall is punctured or a small wound communicates with the 
lumen, the blood burrows into the surrounding tissue, which may 
encapsulate it and lead to the formation of an aneurysm. What is known 
as an arteriovenous aneurysm arises when both artery and vein are 
ruptured and a communication develops between them. In either case, 
in addition to the usual subjective symptoms of pain and fatigue, there is 
the objective symptom of bruit, which, in arteriovenous aneurysm, may 
be heard over almost the entire extremity. As the investigations of 
Verth (280) have shown in the latter, quite considerable disturbances of 
the general circulation appear which show themselves in hypertrophy and 
dilatation of the heart, and reflex irritability of the heart and large 
vessels. 
The explanation of this bruit has led to much discussion (281). Franz 
anastomosed arteries and veins and studied the advent and disappearance 
of vessel sounds under experimental conditions which were similar to those 
occurring naturally. He found that there first arose a continual roaring 
sound which became discontinuous and changed its character when the 
vein was ligated toward the heart, while tying the peripheral end had no 
influence. It seems clear, therefore, that the sounds in an arteriovenous 
aneurysm arise in the vein and not in the artery and that they are related 
to the well known venous hum. * Furthermore, it may be said from these 
researches, that the presence of bruit is not due to the clashing together of 
arterial and venous blood, as Billroth, among others, thought. 
The old investigations of Th. Weber (282) which are now used in the 
explanation of the murmurs of endocarditis, apply as well to these bruits. 
If a glass tube is connected to a faucet and water allowed to flow through, 
no sound is audible until the rate of flow has reached a certain degree when EXTREMITIES 
479 
roaring sounds are heard. In aneurysms, we may assume that the 
increased rate of flow in the veins produces the roaring sounds. Other 
factors which probably contribute are vibrations of the wall of the vein 
and the above mentioned whirlpool at the narrow place of the anastomosis 
(von Bramann). According to Israel, such a venous murmur from 
increased rate of blood flow appears during every intravenous saline 
infusion if the fluid passes in under a certain pressure. The newer investi- 
gations of Muck have also shown that the venous murmur is related to this 
increased rate of flow. 
In contrast to these venous noises we are led to consider the arterial 
murmurs. A sound is heard in an artery when a stethoscope is pressed 
against the vessel with sufficient force to narrow the lumen. Every 
surgeon is familiar with the peculiar scraping, intermittent character of the 
arterial murmur named after Wahl, which arises on cutting a larger artery. 
The scraping sound is increased during the arterial diastole (heart systole- 
Brugsch-Schittenhelm (283)). Since this sound arises only when an 
artery is opened, it is due in all probability to the change of flow of the 
blood mass from a narrow tube to a larger space. The bruit over soft 
goiter may be explained in a similar manner, that is, the change from 
narrow to wide in the arterial network. According to Bier (cited by 
Israel), the sound heard momentarily when an Esmarch bandage is 
removed, is due to the same cause. 
The pain and the feeling of fatigue are due, no doubt, to pressure 
on neighboring nerves and to nutritional disturbances. 
Without an external wound being manifest, a tearing of even large 
vessels may occur from all sorts of trauma. This has given occasion 
for the experimental examination of the elasticity of vessels, by which it 
was shown that the elasticity of both arteries and veins is very great, and 
exceptional circumstances are necessary to tear them (284). According 
to Botticher, the greatest danger is from sudden stretching. Even if the 
vessel is not completely severed, the intima may tear, roll up and thus 
partially obstruct the lumen. 
Another very important possibility of vessel destruction must still 
be mentioned. If a foreign body, for instance, a drainage tube, is placed 
in the neighborhood of an artery (285), gradual erosion may occur. 
Corneliani, in 1843, discovered this fact in animals, and later Beyme (286) 
published clinical observations of such cases. 
When small vessels are torn subcutaneously, we obtain what every 
layman knows as a “black and blue mark.” Eschweiler (287) subjected 
this phenomenon to experiment and found that the “ black and blue mark ” 
arises only when the blood is present not deeper than 1 to 1.5 mm. under 
the skin. The color is derived from blood pigments, and it makes little 480 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
difference whether the blood is arterial or venous, but it is dependent to a 
considerable degree on the thickness of the hemorrhagic infiltration. 
The diseases of the lymphatics are closely related to disturbances of the 
blood circulatory system. Both serve to convey to the cells the nutrition 
on which depends all those functions which we identify with life 
(206). 
According to the present day viewpoint, the lymph in its vessels comes 
from the tissue fluids which bathe the individual cells, and is a product of 
both the substances in the blood capillaries and those produced by cell 
metabolism. How this fluid reaches the lymphatic channels is a question 
much discussed, but one which interests the surgeon but slightly. The 
flow of lymph is very slow, intrathoracic changes of pressure during respi- 
ration, contractions of muscles in the extremities, and of muscle fibres 
in the lymph vessels themselves, combine to force it onward. To this 
is added the pressure exerted by the newly formed tissue fluid and lymph 
(vis a tergo). This slow rate of flow is very effective in allowing the 
interchange of fluids between cells and lymph, and the lymph apparatus 
may be looked upon as our immediate organ of nutrition. Since this 
fluid reaches the individual cells, it is obvious that an endless number of 
injurious substances may reach them through this medium. They may 
be metabolic products, toxins of all sorts, and particularly bacteria. 
Our knowledge of the part played by the lymphatic system in the 
struggle with bacteria, is quite extensive (288). According to Halban, 
the lymph nodes comprise a particularly valuable defense against invading 
organisms, which they hold purely mechanically, as if they were soot or 
pigment granules. They might be called filters in the line of the lymph flow. 
The length of time the organisms are held in the nodes, according to Hal- 
ban, depends on their virulence; non-pathogens pass through very quickly, 
and soon reach the internal organs, wdiile on the other hand, pathogenic 
organisms are held back. There thus occurs a purposeful selection. The 
bacteria are not usually destroyed in these organs which are poor in anti- 
bodies, but their virulence is weakened in ways unknown in detail. If, 
in performing this service, the nodes are broken down by suppuration, 
scar tissue replaces their parenchyma and they are ultimately entirely 
changed in structure. 
It is a very pertinent question if new ones appear at the site of such a 
destroyed node, or of those removed operatively. According to experi- 
ment and observation, it seems fairly certain that they may be regenerated 
by budding from other nodes, or new ones may arise from fat tissue (289). 
That lymph channels also may be built anew has been knowm for a longer 
time. After amputation of the breast such regenerated lymph nodes may 
be felt in the fat as small nodules. EXTREMITIES 
481 
Lymphedema, i.e., insufficient emptying of tissue fluids and lymph 
from subcutaneous tissue, is quite common (290). It is in this condition 
especially, that the close relationship between the blood and lymph vas- 
cular systems is brought out. Edema cannot be explained solely as an 
obstruction of lymph channels, as we will mention more definitely in 
speaking of elephantiasis, for experiments show that even after extensive 
removal of lymph nodes, stasis of lymph does not necessarily occur 
(289), (291). Clinical observations agree with this, provided that a 
complicating wound infection does not set in, or that the main trunk, the 
thoracic duct, is not ligated. In the latter case, marked dilatation of 
lymph channels occurs, especially those of the abdomen, although experi- 
mental results are not always consistent, because of anatomical anomalies, 
and the presence of collateral paths. 
A disease in which lymph stasis is the prominent clinical feature is 
elephantiasis which is at present regarded as caused by obstruction to 
lymph drainage, usually from an inflammatory process. In Arabian 
elephantiasis, an infection of the lymphatic vessels with filaria Bancrofti 
(292) leads to the enormous swellings of the legs and scrotum. Elephan- 
tiasis graecorum is a particular form of lepra infection (293). The patho- 
logical physiological factors in that seen in our latitudes are most evident 
in cases in which the lymph nodes of the groin have been extirpated, or 
where carcinoma has invaded those of the arm, as in carcinoma of the 
breast. It has not been satisfactorily determined if stasis from destruc- 
tion of the lymph nodes will fully explain the production of the colossal 
swellings, or if, as Carle and Jambon (294) believe, there must be added a 
lymphangitis. The fact remains, that we see a fairly uniform dilatation 
of all the lymph channels of the affected limb, with later fibrous thicken- 
ings and increases of connective tissue. It is exceedingly difficult to 
determine how much of this change is secondary (295). Undoubtedly, 
inflammations, especially those of an erysipelatous nature which patho- 
logically anatomically are inflammations of the smallest lymph channels, 
do occasionally lead to an elephantiasis. Edematous swelling of a limb 
in infections, e.g., the hand in phlegmons, is, of course, an every day surgical 
occurrence, but it is of shorter duration, and the secondary changes such 
as take place in elephantiasis do not occur. It is not difficult to under- 
stand that tuberculous and syphilitic inflammations, as well as blunt 
traumata (Rydygier) which destroy lymph channels, should bring about 
an elephantiasis, or that cardiac disease or nephritis may produce this 
condition permanently. The edema in syringomyelia is entirely unex- 
plained (Remak); it may be due in part to the frequent phlegmons which 
arise in this disease (296). 
But it is difficult to understand the elephantiac swelling of the leg in 482 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
those cases in which there is no demonstrable obstruction or destruction 
of lymph vessels. In the congenital type, it may be assumed that the 
amniotic band led to an interruption of lymph channels (297). But there 
still remain the so-called sporadic cases occurring mostly in young indi- 
viduals, in whom, without any known cause, a slowly developing and 
increasing swelling of the leg appears. Whether we must assume here, 
as in varices, an unknown cause of the dilatation, or whether there is an 
obstruction in the groin is as yet not known. It is important in the treat- 
ment to know if the deeper lymph channels, i.e., those in the muscles and 
bones, are also diseased, since attempts to give relief have been made by 
anastomosing the superficial with the deep channels, for example, by 
removing the muscle fascia (298). Unfortunately our knowledge of the 
pathological physiological occurrences in elephantiasis has not been 
enriched by the results of such procedures. Based on the view that the 
production of lymph is dependent on arterial supply, Carnochan (299) 
advised ligation of the femoral or iliac artery. This has been tried fre- 
quently but the results were poor, possibly because the disease had pro- 
gressed too far. The rationale of the operation seems correct, even if the 
actual etiology of the disease is not taken into consideration. The results 
of excision of wedged shaped pieces from the skin are due to the interrup- 
tion of the blood circulation, and in a similar way, the ligation of the 
saphenous vein in varices, to the interruption of the lymph channels 
(300) 
Giantism and clubbed fingers are related superficially to elephantiasis 
(301) It has already been mentioned that clubbed fingers develop 
particularly in chronic suppurative lung diseases, and in cardiac lesions, 
but may be found also in all sorts of other conditions, such as liver dis- 
eases, or unilaterally, in aneurysms of the subclavian artery. How far 
their etiology may be regarded from a single viewpoint is at present not 
clear. Most authors believe clubbed fingers are only a symptom of an 
hypertrophy of various parts of the body, thus, the face especially is said 
to show a thickening (302). 
Clubbed fingers are considered closely related to the hypertrophic 
osteoarthropathy of Pierre Marie (v. Hoffmann (303)). But knowledge 
of the etiology of this latter disease is also very hazy at present. The 
publications of Braun (304) are interesting, inasmuch as he found changes 
in the hypophysis in three cases from which it might be assumed that 
clubbed fingers have something to do with acromegaly. It remains, of 
course, an open question how these changes in the hypophysis were 
produced, and how they are related to the primary condition, i.e., the 
disease in the lungs. Bamberger (305) offers the opinion that certain 
toxic substances are absorbed from the lung abscesses and these lead to EXTREMITIES 
483 
giantism. His experiments however, in which he administered to rabbits 
by rectum, the sputum from bronchiectatic cavities to obtain an increase 
in size of the extremities, similar to clubbed fingers, yielded only negative 
results. 
LITERATURE TO EXTREMITIES 
1. Roux: “Terminologie der Entwicklungsmechanik,” Engelmann, Leipsig, 1912, p. 
227. 
2. Matti: “Die Knochenbruche u. ihre Behandlung,” Springer, 1918, p. 29. 
3. Luciani: Human Physiol., 3rd. Vol., Chapter I, Macmillan Trans., F. Welby. 
4. Grunewald: Ztschrft. f. orthop. Chir., 1919, 39. 
5. Lit. see Fick: Handbuch d. Anat. u. Mechanik d. Gelenke, 2, p. 247 and Handbuch 
der Anat. des Menschen v. Bardeleben. 
6. E. Weber: Mechanik d. menschl. Gewerkzeuge, Gottingen, 1836. 
7. Aeby: Deutsche Ztschr. f. Chir., V. 6. 
8. Hagenbach-Burckhardt: Ztschr. f. Orthop. Chir., 1907, 18, 358. 
9. Bing: Med. Klinik., 1907, No. 1. 
10. v. Meyer, H.: “Die Statik u. Mekanik. d. menschl. Knochengerustes,” Leipsig, 
1873. Wolff, J.: “Die innere Architektur d. Knochen,” Berlin, 1870; “Ueber 
die Wechselbeziehungen,” zwischen d. Form. u. Funktion, Leipsig, 1901; 
Ztschrft. f. Orthop. Chir., V. 2. 
11. Fick, R.: Handbuch d. Anat. des Menschens, 2-1-p. 43. 
12. Ghillini: Arch. f. klin. Chir., V. 52. Hueter: Arch. f. klin. Chir., V. 2 and 9. 
Korteweg: Ztschrft. f. Orthop. Chir., V. 2. Wolff: L. C. Wien. klin. 
Wchschrft., 1893; Ztschrft. f. orthop. Chir., V. 2. Lorenz: Wiener klin. 
Wchschrft., 1893, No. 9, 10, 11. v. Volkmann: Krankheit d. Bewegungsor- 
ganen in Pitha-Billroth’s Handb., V. 2; Virchows Arch., V. 22. 
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14. Fuld: “Experimental proof,” Arch. f. Entwicklungsmechanik, 1901, V. 11. 
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Pathol., 1913, V. 12; Pathologen Kongress, 1913. Klemperer: Zeitschrft. 
f. klin. med., V. 10. Orthmann: Virchow’s Arch., V. 90. Uskoff: Virchow’s 
Arch., V. 86. 
203. Dreyer: Bruns Beitr., V. 75. Notzel: Arch. f. klin. Chir., V. 81. Magnus: 
Arch. f. klin. Chir., V. 102. Perez: Deutsche Ztschrft. fur Chir., V. 63. 
204. Payr: Munchener med. Wchnschrft., 1915, No. 37-39. 
205. Neuhaus-Hildebrand: Arch. f. klin. Chir., V. 81, p. 422. Cecca: La clin. Chir., 
1907. Riedel: Deutsche Ztschrft. f. Chir., V. 12. Notzel: Arch. f. klin. Chir., 
V. 81. Kroh: Deutsche Ztschrft. f. Chir., V. 94, p. 215. Jaffe: Arch. f. 
klin. Chir., V. 54. Braun: Deutsche Ztschrft. f. Chir., V. 39. Mosengeil: 
Arch. f. klin. Chir., V. 19. Pagenstecher: Mitt. a. d. Grenzgebieten, 1912, V. 
25. Tillmann: Arch. f. Mikrosk. Anat., V. 12. 
206. Most: “Chir. d. Lymphgefasse,” Neue Deutsche Chir., V. 24. 
207. Tillman: Zentralbl. f. Chir., 1875 and Arch. f. mikrosk. Anat., 1876, V. 12, p. 679. 
208. Muller: Deutsche Ztschrft. f. Chir., V. 100, p. 385. 
209. Ribbert, Kruse, and B. Fischer: Niederhein. Ges. f. Natur-u. Heilkunde, Bonn, 
1908. 
210. Gies: Deutsche Ztschrft. f. Chir., V. 18, p. 8. Schablowsky: Arch. f. klin. Chir., 
V. 70, p. 762. 
211. Hildebrand: Arch. f. klin. Chir., 81, 412. * 
212. Konig Paschen: Deutsche Ztschrft. f. Chir., V. 3. Schultze: Deutsche Ztschrft. 
f. Chir., 1877, V. 7. Reyber: Deutsche Ztschrft. f. Chir,, V. 4. 
213. Fessler: Deutsche Ztschrft. f. chir., V. 82. 
214. Friedrich: Deutsche Ztschrft. f. Chir., V. 53. Friedrich u. Nosske: Zieglers 
Beitr. z. pathol. Anat., 1899, V. 26. Muller: Deutsche Ztschrft. f. Chir., V. 25. 
215. Jochmann and Batzner: Arch. f. klin. Chir., V. 95, p. 89. 
216. Rost: Deutsche Ztschrft. f. Chir., V. 133. 
217. Helferich: Chirurgenkongress, 1894; Arch. f. klin. Chir., V. 48. THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
490 
218. Chlumsky: Zentralblatt f. Chir., 1900. Foderl: Ztschrft. f. Heilkunde, V. 16. 
Hofmann: Arch. f. klin. Chir., V. 80; Bruns Beitr., V. 59. Hubscher: Korre- 
spondenzbl. f. Schweizer Arzte, 1901. Lexer: Arch. f. klin. Chir., 95; Munche- 
ner med. Wchenschrft., 1913; Deutsche Ztschrft. f. Chir., 135; Zentralbl. f. 
Chir., 1917; Die freien Transplantationen Neue Deutsche Chir., V. 26 a, 1919. 
Roser: Zentralblatt f. chir., 1898. Payr: Munchener. med. Wochenschrft., 
1910; Ztschrft. f. orthopad. Chir., V. 27; Arch. f. klin. Chir., V. 99; Deutsche 
Ztschrft. f. Chir., V. 129. 
2x9. Murphy: J. A. M. A., 1905, p. 1573 and 1912, p. 985. 
220. Homeyer and Magnus: Bruns Bfeitrage z. klin. Chir., V. 94. Segale: Bruns 
Beitr. z. klin. Chir., V. 87. Rehn: Chirurgenkongress, 1910, Arch. f. klin. Chir., 
V. 98. Sumitz: Arch. f. klin. chir., V. 99. Tappeiner: Arch. f. klin. Chir., V. 
107. 
221. Czerny: Arch. f. klin. chir., V. 13. Doutrelpout: Arch. f. klin. Chir., 9. Bier: 
Deutsche med. Wochenschrft., 1919, p. 620. 
222. Schepelmann: Bruns Beitr. z. klin. chir., V. 108. Schmerz: Zentralbl. f. chir., 
1916. Kocher: Chirurgenkongress, 1901. 
223. Eisleb: Bruns Beitr. z. klin. Chir., V. 102. 
224. Payr: Deutsche Zeitschrft. f. chir., V. 49. 
225. Ledderhose: Deutsche Ztschrft. f. chir., V. 37. Franz, Arch. f. klin. Chir., V. 70. 
226. Langemak: Arch. f. klin. Chir., V. 70. 
227. Salkowsky: Compiled by Bier, Deutsche med. Wchenschrft., 1919, p. 620. 
228. v. Langenbecks: Arch. f. Klin. Chir., V. 16. 
Ollier: cited by Jogetho, Deutsche Ztschrft. f. Chir., V. 4. 
230. Schmieden: Chirurgenkongress, 1913. 
231. Kuttner: Arch. f. klin. Chir., V. 102; Zentralbl. f. Chir., 1911. Lexer: Arch. f. 
klin. chir., V. 90 and Med. Klink., 1908. 
232. Borst: Pathologenkongresz, 1912. 
233. Konig: Zentralbl. f. chir., 1912. 
234. Nobl: Der Varikose Symptomenkomplex lit., 2 ed., 1918. 
235. Delbet: Sem. med., 1897. 
236. Lowenstein: Mitt. a. d. Grenzgebieten, 1908, V. 18. 
237. Braune: Festschrft. f. Ludwig, 1874. 
238. Katzenstein: Zentralbl. f. Chir., 1911. 
239. Schambacher: Deutsche Ztschrft. f. Chir., 1899, V. 53. 
240. Ledderhose: Mitteil. a. d. Grenzgeb., 1906, V. 15. 
241. Hasebrock: Deutsche Ztschrft. f. Chir., V. 136. 
242. Trendelenburg: Bruns Beitr., V. 7, “Naturforscherversammlung,” Leipzig, 1907. 
243. Hoffmann: lit. Arch. f. Dermat., 1912, 113. 
244. Kushimura: Virchows Archiv., 1905, 179. 
245. Lesser: Virchows Arch., V. 101. 
246: Zahn: Festschrft. f. Virchow, 2, p. 201. Eberth and Schimmelbusch: “Die 
Thrombose,” Stuttgart, 1888. Ferge: Med. Naturn. Arch., V. 2. Beneke: 
Marchand-Krehl Handbuch. d. allg. Pathol., 22. Aschoff: Virch. Archiv., V. 
130; Med. Klinik., 1909; Naturforscherversammlung, 1911. 
247. Rost: Zieglers Beitr., 1911, V. 52. 
248. Ribbert: Deutsche med. Wchenschrft., 1916, and Zentralbl. f. Pathologie, V. 27. 
Marchand: Zentralbl. f. Pathologie, V. 27, p. 193 and 457. 
249. Rost: Zentralbl. f. Pathol., 1913. 
250. Brucke: Virchows Arch., 1857, V. 12. EXTREMITIES 
491 
251. Zahn: Virch. Arch., 1875, V. 62. 
252. Zurhelle: Ziegler’s Beitrage, 1910, V. 47; Ztschrft. f. Gyn., 1908. Virchow: Ges. 
Abh. Frankfurt, 1856. 
253. Huter: Allg. Chirurgie, 1873. Schwalbe: Ziegler’s Beitr., V. 7. 
254. Klebs-Welt: Zieglers Beitr., V. 4. 
255. Enderlen: Deutsche Ztschrft. f. Chir., 1909, V. 99. 
256. Stich: Bruns. Beitr., V. 53 and 62. 
257. Silbermann: Virchows Archiv., V. 117. Kaufmann: Habilitationsschrift, Bres- 
lau, 1888. Lob: Bioch. Zentralbl., 1907, V. 6. 
258. Ziemssen: Samml. klin. Vortr., 1887. 
259. Landois: “Die Transfusion d. Blutes,” Leipsig, 1875. Coca: Virchows Archiv., 
1909, 196. Biedl-Kraus: Ztschrft. f. Immun. Forsch., 1910, V. 7. 
260. Edelberg: Arch. f. exp. Pathol., 11. Angerer: “Klin. u. exper. Studien uber d. 
Resorpt. v. Blutextravasaten,” Wurzburg, 1879. 
261. Volcker: Chirurgenkongresz, 1914. 
262. v. During: cited by Hofmeister and Schreiber in Handbuch d. prakt. Chirurgie, 
V. 5, p. 7, 4th edition. 
263. Wright: Journ. of physiol., 1891, 12. 
264. Dietrich: Zentralbl. f. Pathol., 1912. Lob: Virchow’s Arch., V. 153. Fromme: 
Naturforscherversamml., 1908. Heller: Bruns Beitr., 1909, V. 65. Jakowski: 
Zentralbl. f. Bakt., 25 and 28; Monatsschrift f. Gyn., V. 14. Bardeleben: 
Arch. f. Gyn., 1907, V. 83. Talke: Bruns Beitr., 1902, V. 36, p. 339. 
265. Vaguez: These de Paris, 1890. 
266. Trendelenburg: Prakt. Ergebnisse der Geburtshilfe u. Gynak., 1913. 
267. Spalteholtz: Arch. f. Anat., 1893, p. 1. 
268. Quenu: Traite de Chirurgie de Duplay et Reclus, 1890, V. 2. 
269. Schultz: Deutsche Ztschrft. f. Chir., V. 9. Greifenberger: Deutsche Ztschrft. 
f. Chir., V. 16. Riedel: lit. Deutsche Ztschrft. f. Chir., 1876, V. 6. 
270. O. Weber: in Pitha-Billroth’s Handbuch der Allg. spez. Chir., 1865. 
271. Katzenstein: Deutsche Ztschrft. f. Chir., 1905, V. 77, p. 189. 
272. Bier: Deutsche Ztschrft. f. Chir., V. 79. 
273. v. Recklinghausen: Deutsche Chir., V. 2 and 3. Nothnagel: Ztschrft. f. klin. 
Med., V. 15 and 17, suppl. 
274. Katzenstein: Deutsche Ztschrft. f. Chir., V. 80. 
275. Krehl: “Pathol. Physiologie,” F. C. W. Vogel, Leipzig, trans. Hewlett. 
276. De Ahna: Pflugers Arch. f. d. ges. Physiol., V. 12. Zuntz: Pflugers Arch. f. d. 
ges. Physiol., V. 17. 
277. Jordan: Bruns Beitr., V. 14, p. 279. Goldmann: Bruns Beitr., 1905, V. 47, p. 162. 
Niebergall: Deutsche Ztschrft. f. Chir., V. 33, p. 540 and V. 37, p. 268. 
278. Wieting: Deutsche med. Wochenschrft., 1908, V. 28. Deutsche Ztschrft. f. Chir., 
V. no. 
279. Exner: Wiener klin. Wchenschrft., 1903. 
280. Verth: Deutsche Ztschrft. f. Chir., V. 151. 
281. Israel: Deutsche Ztschrft. f. Chir., V. 149. Franz: Arch. f. klin. Chir., V. 75. 
Muck: Munchener Med. Wchenschrft., 1916. Vignolo: Policlinico, 1902. 
Bramann: Arch, f., klin. Chir., V. 33, lit. Wahl: Deutsche Ztschrft. f. Chir., 
V. 21. 
282. Th. Weber: Cited by Sahli, Lehrbuch d. klin. Untersuchungsmethoden, 6 edition. 
283. Brugsch-Schittenhelm: Lehrbuch d. klin. Untersuchungsmethoden, 1908, V. rio. 
284. Wertheim: Annales de Chemie and de Phys., 1847. Botticher: Deutsche 
Ztschrft. f. Chir., V. 49. 492 
THE PATHOLOGICAL PHYSIOLOGY OF SURGICAL DISEASES 
285. Heinecke: Deutsche Chir., V. 18, p, 11. 
286. Beyme: Deutsche Ztschrft. f. Chir., V. 140. 
287. Eschweiler: Deutsche Ztschrft. f. Chir., V. 23. 
288. Halban: Arch., f. klin. Chir., V. 55. Wiener klin. Wchshrft., 1898. Manfredi: 
Virchow’s Arch. V. 155. Viola, Ztschrft. f. Hyg., V. 30. Notzel: Arch. f. 
klin. Chir., V. 81. Bruns Beitr., V. 51 and 65. 
289. Zehnder: Virchows Arch., V. 120. Bayer: Arch. f. klin. Chir., V. 49. Ritter: 
Deutsche Ztschrft. f. Chir., V. 79. De Vecchi: Mitt. a. d. Grenzgeb., V. 23. 
De Groot: Deutsche Ztschrft. f. Chir., V. 119 and 122. 
290. Gross: Deutsche Ztschrft. f. Chir., V. 127 and 138. Arch. f. klin. Chir., V. 76 and 
79- 
291. Cohnheim: Virchows Archiv., V. 47. 
292. Gobel: Ergeb. d. Chir., 2. Rost: “Fiber Flariasis,” Klin. Therapeut-Wchn- 
schrft., 25. 
293. Winiwarter: Deutsche Chir., V. 23. Draudt: Ergeb. d. Chir., V. 4. Helfuch: 
Inaug. Dissert. Heidelberg, 1919 for lit. 
294. Carle and Jambon: Gaz. des. Hospiteaux, 1904. 
295. Bockhardt: Monatsschrft f. prakt. Dermat., 1883. 
295. Bramann: Munchener med. Wochenschrft., *1902. Favarger: Wiener klin. 
Wchnshrft., 1901. Kuhn: Wiener klin. Wchenschrft., 1905. Schmidt: Bruns 
Beitr., V. 44. 
296. Rost: Munchener med. Wchenschrft., 1918. 
297. Nonne: Virchows Archiv., 125. Reinsbach: Bruns Beitr., 1898, V. 20. 
298. Lanz: Zentralbl. f. Chir., 1911,1 pt. Kondolean: Munchener med. Wchenschrft., 
1912 and 1915. 
299. Carnochan: Cited by Winiwarten, 1. c. 
300. v. Eiselsberg: Wiener klin. Wochenschrft., 1906. 
301. Freytag: Diss. Bonn., 1891. Sternberg: Nothnagels spez. Path, and Therapie, 
V. 7, 2. 
302. Ebstine: Arch. f. klin. Med., V. 89, p. 67 for complete lit. Mitteil. a. d. Grenz- 
gebielen, V. 22, p. 311. 
303. v. Hoffmann: Arch. f. klin. Med., 1919, V. 130, p. 201. 
304. Braun: Med. Klinik., 1918, pt. 1. 
305. Bamberger: Ztschrft. f. klin. Med., 1891, V. 18. INDEX OF AUTHORS 
Abderhalden, Emil, 41, 57, 67, 112, 127, 
i93 
Abderhalden, E. and London, 112 
Adamkiewicz, 403, 417 
Adamski, Johann, 114 
Adler, 314, 317, 357, 360 
Adrain, 256, 257 
Aeby, 428 
Aksne, 302 
Albarran, 281, 285, 293, 309 
Albarran and Guyon, 301 
Albeck, Ileus, 225 
Albert, 18 
Albert and Schnitzler, 408 
Alberts, G., 71 
Albrecht, P. A., 53, 151 
Albu, 208, 225, 265 
Albu and Kretschmer, 209 
Albu and Lexer, 269 
Aldrich, 233 
Alexander and Reko, 6 
Alexandre, 12 
Allard, 284, 285 
Allen, 322 
Alvarez, 44, 45, 61 
.Alzheimer, 416 
Anders, 423 
Andreson, 340 
Andrews, 231 
Angerer, 474 
Anghel, 257 
Anschutz, W., 205, 222 
Antonini, L., 76 
Aoyama, T., 133 
Aquapendente, Fabricius ab, 177 
Archibald, Edward, 102. 103 
Aristotle, 176 
Arnd, 241 
Arnold, 119, 391 
Asakura 292 
Aschoff and Bacmeister, 113, 132, 133 
Aschoff, L., 124, 134, 256, 260, 263, 472 
Aschoff, Ludwig, 37, 40 
Ascoli, 287 
Ash, 312 
Asher, 148, 153 
Asher and Flack, 340 
Asher and Spiro, 171 
Askanazy, 249 
Auche, 8 
Auerbach, 12 
Aufrecht, 134, 301 
Axhausen, 264, 266, 415, 446, 449 
Axhausen and Pels, 447 
Babera, 125 
Babes, 421 
Babkin, B. P., 41, 49, 81, 123, 190 
Baetzner, 279 
Baggerd, 298 
Bahr, 443 
Bail, 242, 246 
Bainbridge and Dale, 126 
Bajardi, 435 
Bakes, 179. 292 
Balser, 102 
Baltzner, 279 
Bamberger, 482 
Banti, 156 
Baracz, 192, 215 
Barbarossa, 356 
Barbera, 124, 125 
Barcroft, J., 378 
Bardach, 153 
Bardeleben, 330, 475 
Bardenheuer, 440, 450, 458 
Barie, 366 (ref. 402) 
Barker, 267 
Barnabo, 463 
Baron, 120 
Barsony, Theodor, 56 
Bartel, 320 
Bartels, 327 
Barth, 101, 295, 296, 365 (ref. 402), 448 
Baruch, 348 
Basch, 351 
493 494 
INDEX OF AUTHORS 
Bauer, 298, 324, 326, 355, 362, 416, 442, 
448 
Bauer, Julius, 53, 77, 78, 130, 248, 267 
Bauereisen, 305 
Bauhin, 176 
Baum, 239, 293 
Baumann, 338 
Baumgarten, 309, 310, 311 
Bayer, R., 149, 152, 153, 155, 157, 222, 
431, 480 
Bayliss, W. M. and Starling, E. H., 43, 44, 
57, 194, i97, 198 
Bayon, 341 
Beattie, 179 
Beaumont, Wm., 81 
Beaussenat, 257 
Beck, 25, 320, 412 
Becker, 294, 318, 394, 433, 460, 461 
Begrer, 410 
Beirn, O., 200, 217 
Bell and Hirschberg, 267 
Beloussow, 130 
Beneke, R., 76, 165, 190, 391, 392, 394, 
395, 445, 472 
Benker, 180 
Berard and Petel, 277 
Beresnegowsky, 267, 268 
Berg, 138 
Berg, A. A. H. and Snapper, I., 129 
Berger, 157 
Bergmann and Bastgen, 407 
Bergmann, G., 76, 78, 176, 277, 341, 357, 
403, 411, 420 
Bergmann and Guleke, 114 
Bergmann and Lenz, 200 
Bernard, A., 24 
Bernard, Claude, 1, 5, 6, 68, 69, in, 117, 
119, 127, 282, 349, 433 
Bernard and Salomon, 309 
Berndt, 320 
Bert, Paul, 372 
Bertelle, G. and Falta, W. and’Schweeger, 
O., 149 
Bertelsmann and Man, 307 
Berth, n 
Berthier, 454 
Berthold, 329 
Bertog, J., 138 
Besancon and Griffon, 74 
Best, 70 
Best, F. and Cohenheim, O., 36 
Bethe, 456, 457 
Bethe and Parnas, 430 
Beyme, 479 
Bial, 184 
Biberfeld, 292 
Bibergeil, 162 
Bickel, A., 42, 58, 63 
Bidder, 435 
Biedl, 7, 98, 99, 289, 323, 324, 326, 327, 
339, 34°, 341, 342, 351, 359, 362, 364 
Biedl and Kraus, 304, 307, 474 
Bier, 52, 234, 419, 435, 449, 455, 460,468, 
477, 479 
Biernacki, E., 5, 42 
Biers, 461 
Billard and Cavillie, 135 
Billroth, 9 
Bing, 428 
Binswanger, 416, 417 
Bircher, H., 14, 342, 344, 345, 352, 354, 
361, 363, 415 
Birkenbach, 287 
Bittorf, 254, 372 
Bittorf and Forschbach, 386 
Blad, 139 
Blauel, 199 
Blauel and Reich, 344 
Blaul, Muller and Schlager, 354 
Blayney, 265, 266 
Blenkle, 453 
Blessing, 458 
Blevgad, 415 
Bloch, 198, 436 
Blum, 339 
Blumenfeldt, 157 
Boas, I., 60, 209 
Bockhardt, 481 
Bode, 365 (ref. 402) 
Boeckel, 460 
Boehm, 198, 209 
Boeke, 430, 457 
Boenninghaus, 415 
Boetzel, 303 
Bogen, H., 42 
Bogoljuboff, 330 
Bohl, 411 
Bohm, P., 125, 366 (ref 402) 
Bohn, 140 
Bohr, 372, 380 
Boldgreff, 357 
Bollinger, 414 INDEX OF AUTHORS 
495 
Bolton, 78 
Bonchardal and Sandras, 97 
Bonin, 74 
Bonneken, 241 
Bonnet, 443 
Borbjarg and Fischer, 184 
Borchard, 414, 455 
Borchardt and Wjasmenski, 457 
Borchers and Klatsch, 194 
Bordenheuer, 253 
Bordet, 244, 246 
Borggreve and Hessel, 217 
Borgzecky, 300 
Borst, 170, 469 
Borst and Enderlen, 293 
Borszeky and Genersich, 225 
Borzeky, 56, 63, 225 
Bose and Heyrovsky, 196 
Botticher, 479 
Bouchard, 225, 287 
Bouisson, 238 
Bouma, 391 
Bourdenko, 117 
Bouveret, 384, 385 
Boyer, 201 
Boysen, I., 133 
Braatz, 295 
Bradford, 286 
Bramann, 478, 479, 481 
Bramann and Rammstedt, 324 
Brand, 125, 320 
Brandes, 438 
Brandi, 320 
Brauer, 366, 374, 378, 379, 380, 382, 383 
Brauer and Roth, 378 
Braun and Boruttau, 225, 226, 227, 248, 
249, 250 
Braun and Heinrich, 63, 71, 416, 422, 464, 
482 
Braun and Honckgeest, 44 
Braun, Tuffier and Payer, A., 51 
Braun, W. and Seidel, H., 51, 52 
Braune, 470 
Brauning, H., 38 
Braunschweig, 152 
Braus, 429, 457 
Breitner, 344 
Bremer, F., 96 
Brenner, A., 79, 264, 266 
Breslauer, 403, 407,408, 409,410, 413, 460 
Breton, M., 97 
Bretonneau, 365 
Breus, 75 
Bright, 414 
Broca, 449 
Broca and Tridon, 462 
Brodmann, 421 
Brogsitter, 151 
Brohmann, 176, 177 
Bronadel, 14 
Brosch, 29 
Brown, 229 
Brown and Sequard, 289, 318, 417, 438 
Bruce, 460 
Brucke, 163, 165, 473 
Brugsch, 267 
Brugsch and Klemperer, 313 
Brugsch and Schittenhelm, 479 
Brun, H., 80 
Brun, Max, 46 
Brunacci, 2 
Brunn, 256, 259, 306, 321, 411 
Brunner, 241, 454 
Bruns, 60, 358, 378, 382, 384 
Bruns and Saurbruch, 384 
Buch, 172, 174 
Buchanan, 253 
Buchbinder, 242 
Buchner, 246, 462 
Buchwald and Litten, 293 
Budinger, 448 
Bumm, 318, 438 
Bungart, 404, 406 
Bunge, 104, 122, 231, 298 
Burchardt, 242 
Burci, 161 
Burger and Fischer, 130 
Burkhardt, 162, 183, 374, 378 
Burn, 179, 438 
Burrow, 407 
Buru, 438 
Busch, 217, 315, 392, 463 
Busch and Biebergeil, 162 
Buschan, 346 
Busse, W., 72, 74, 236, 392, 393 
Bussman, 442 
Buttermann, ix 
Buxton, A. St. C., 6 
Cahn, 17 
Cammerer, 75 
Camus, L. and Gley, E., 97 496 
INDEX OF AUTHORS 
Cannon, W. B., 37, 39, 40, 44, 47, 50, 194 
Cannon, W. B. and Blake, J. B., 56 
Cannon and Moser, 21 
Cannon and Murphy, 52 
Canon, 244 
Capelle and Bayer, 350, 351, 352, 353 
Carle and Jambon, 481 
Carlson, 47, 48, 66 
Carlson and Luckhardt, 25, 40 
Carlsson, 180 
Carnochan, 482 
Carnot, 104 
Carriere, G., 4 
Casagli, F., 58 
Cassirer, 414, 459 
Cathelin, 309 
Cecca, 464 
Cervells, 388 
Chalatoff, 133 
Championiere, Lucas, 440 
Chantemesse and Widal, 74 
Chaput, 233 
Charcot, 438, 459 
Charrin, 74, 257, 418 
Chassaignac, 460 
Chauffard, 132 
Chiari, 103, 1x8, 398 
Chittenden and Richards, 3 
Chlumsky, V., 54, 58, 60, 467 
Christiani and Kummer, 342 
Chrobak, 251, 253 
Chvostek, 346, 359, 362 
Clairmont and Haberer, 131, 139, 167, 
169, 245 
Clairmont, P., 3, 4, 7L 80, 386, 395, 421 
Clairmont and Ranzi, 229, 249 
Claisse, P. and Dupre, E., 8, 13 
Clark, 253 
Clerk, A. and Loeper, 97 
Cloett, 379 
Cobbet and Valte, 230 
Coca, 474 
Coenen, 297, 298, 444, 463 
Cohn, M., 29, 66, 81, 293, 305, 355 
Cohnheim, 190, 192, 201, 285, 288, 365 
(ref. 402, 481), 395 
Cohnheim, Julius, Fredrich, 59, 76 
Cohnheim and Litten, 118 
Cohnheim and Marchand, 41, 137 
Cohnheim, Otto, 37, 38, 40, 41, 96, 98 
Cohnheim, O. and Klee, P., 57, 96, 126 
Cohnheim and Roy, 283 
Colasanti, 124 
Coller and v. Schjerning, 4x1 
Condray, 312 
Connor, O., 350 
Conrad, 459 
Conradi, H., 134, 305 
Contejean, 70 
Copemann and Winston, 126 
Cordier, 381 
Cordua, 163 
Corneliani, 479 
Corner, 255 
Cornil and Carnot, 179 
Cornil and Condray, 448 
Corning, 14 
Cosenthino, 120 
Councilmann, 463 
Courmont and Gabonlay, 461 
Courtade, D. and Guyon, J. F., 43, 126 
Courvoisier, 128 
Couvelaire, 16 
Cozzolino, 303 
Crede, 152 
Crile, 229 
Curschmann, 362, 364, 385 
Curtis, 149 
Cushing, 403, 407, 413 
Cushing and Livinggood, 241 
Cushny, A. R., 279, 280 
Cuvier, 177 
Czermak, 17 
Czerny, 151, 155, 394, 468 
Dagaew, W. F., 57, 64, 66, 68 
Dal Fabbro, 12 
Dalla Vedova, R., 76 
Damascelli, 436 
Danielsen, 167, 168, 186, 363 
Danilewsky, 68 
Danilewsky and Selensky, 150 
Dastre, 58, 126, 127 
Dauriac, 199 
David, 196 
Davis, N. C., Hall, C. C. and Whipple, 
G. H., ns 
Dax, 436, 455 
De Ahna, 477 
Deaver, J. B. and Sweet, J. E., 102 
Debaisieux, 3x4 
Decastello, H., 157 INDEX OF AUTHORS 
497 
Decker, J., 74 
De Dominici, 98 
de Filippi, F., 66 
De Groot, 480 
Delbert, 478 
Delbet, 356 
Delezenne, C., 97, 127 
Delkeskamp, 455 
Del Vecchio, 365, 480 
Demarquai, 318 
Demme, 460 
De Meyer, 98 
Deneke, 355 
Denk, 264, 265, 266, 267 
De Quervain, 323 
Deroche, 438 
Dette Santi, 312 
Deucher, 409 
De Vecchi, 481 
De Voogt, 136 
De Witt, 20 
Dieterle, Hirschfeld and Klinger, 342, 344 
Dietl, 300 
Dietlen, 199 
Dietler, 23 
Dietrich, 475 
Dieulafoy, 258 
Diliberti and Herbin, 265 
Disse, 71, 282, 283 
Dittel, 320 
Dittrich, P., 8 
Doberauer, 105 
Doenitz, 415 
Doepfner, 412 
Dogiel, 126, 380 
Doll, 298 
Donati, Mario, 76 
Donders, 374 
Doutrelpout, 468 
Doyen, 60 
Doyon, 115, 126 
Doyon and Dufort, 125 
Draudt, 481 
Dreike, 190 
Dreyer, 223, 464, 465 
Dreyfuss, 413 
Droge, 148, 155 
Drumond, 122, 179 
Dubar and Remy, 167 
Du Bois and Reymond, 372, 431 
Ducchesi, Virgilio, 39, 44 
Dudgeon and Roos, 179 
Dunin, 301 
Duplay, 439 
Durck, 396 
During, 474 
Eastman, 419 
Eastmann, 210 
Eberle, 97 
Ebert, 379, 380 
Eberth and Schimmelbusch, 472 
Ebstein, 482 
Ebstein and Nicolaier, 314 
Ebstein, Wilhelm, 76, 208, 313, 349 
Eckhard, 282, 285 
Edelberg, 474 
Edebohl, 292 
Eden, 435 
Edinger, 3, 68, 456 
Edkins, J. S., 41 
Egau, E., 39 
Ehret and Stolz, 134 
Ehrhard, 140 
Ehrhardt, 116, 117 
Ehrlich, 148, 149, 150 
Ehrmann, 14, 17, 101 
Eichel, 230 
Einhorn, 203 
Einthoven, 375 
Eiselsberg, 326, 342, 360, 363, 482 
Eiselsberg, Freiherr, 72, 177 
Eisenmenger, 119 
Eisleb, 468 
Eliasberg, 155 
Ellenberger, 38, 42 
Elliot, 152, 314 
Elliot, T. R. and Smith, E. B., 43,194,198 
Elmendorf, 289 
Elsberg, 365 (ref. 402) 
Elze, 37 
Emelianoff, 152 
Enderlen, 22, 179, 190, 296, 301, 302, 321, 
328, 342, 421, 422, 461, 469, 474 
Enderlen and Hess, 196 
Enderlen, Hotz, and Magnus Alsleben, 
118, 121, 123, 192, 213, 214, 221, 226, 
249,250 
Enderlen and Justi, 140 
Enderlen and Zumstein, 138 
Engelhardt, G. and Neck, K., 72 
Engelhorn, 173 498 
INDEX OF AUTHORS 
Engelmann, 302 
Englisch, 463 
Engstrom, 241 
Eppinger, 128, 129, 340, 341, 385 
Eppinger and Hess, 78, 349, 388 
Eppinger and Hofbauer, 378, 387 
Eppinger and Ranzi, E., 156 
Erdheim, 359, 362 
Erhard, 119, 140 
Erkes, 242 
Erlacher, 435, 456 
Erlanger, 456 
Erlanger and Hewlett, 266 
Ernst, 391, 394 
Esau, 190, 255 
Escherich, 99, 362 
Eschweiler, 479 
Esmarch, 267 
Eulenberg, 346, 463 
Evans and Brenizer, 267 
Ewald, 123, 264, 342, 343 
Exalto, 63 
Exner, 491 
Exner, Alfred, 43, 49, 478 
Exner, A. and Heyrowsky, H., 132 
Exner, A. and Jaeger, 44, 172 
Exner, A. and Schwarzmann, 49 
Eykmann, 16, 18 
Falloise, 225, 226 
Falta, 341, 359 
Falta and Kahn, 362, 363, 364 
Falta and Rudinger, 363, 364 
Faltin, R., 151 
Faulhaber, 37 
Faulhaber, M. and Redwitz, E. F., 65 
Favarger, 481 
Felizet, 411, 412 
Feltz and Ritter, 287 
Fenwick, 71 
Ferge, 472, 473 
Ferrarin, 292 
Ferrier and Adam, 230 
Fessler, 466 
Fibich, R., 71, 79 
Fibiger, 393 
Fick, A., 373, 428, 429, 436, 443 
Fick and Gabler, 429 
Fick, R. and Strasser, 429, 444, 467, 468 
469 
Filehne, 349 
Filehne and Ruschhaupt, 285 
Finger, 316 
Finkelnburg, 408 
Finkelstein, 362 
Finsterer, 140, 181 
Fiori, 295 
Fischer, 444 
Fischer, Georg, 364, (ref. 402, 366 
Fischer, O., 431, 438 
Fischer and Benzon, 299 
Fischl, 264, 298 
Fischler, F., 105, no, hi, 1x2, 113, 118, 
119, 121, 124, 128, 211, 357 
Fisher, 411, 450 
Flechtenmacher, 66 
Fleckseder, R., 3, 4, 5, 6, 99, 100 
Fleig, 96 
Fleiner, W., 23, 37, 38, 184, 209, 361 
Fleischl, 128 
Flint, 267 
Florain, L., 3 
Florchen, 136, 292 
Florken, 136 
Flourens, 457 
Flugge, 463 
Foderl, 467 
Forderreuther, 175 
Forssel, Gosta, 37 
Forster, I., 134, 422, 444, 458 
Forster, O. and Kuttner, H., 46, 49 
Foulerton and Hillier, 308 
Fraenkel, E., 353, 462 
Francke, 306 
Frank, 308, 328, 350, 430 
Franke, 123, 173, 239, 254, 261, 303, 304, 
397, 436 
Franke and Rabe, 119 
Frankel, 28, 139 
Frankel, J., 139 
Frankel and Krause, 134 
Frankfurter, 359 
Frankl and Hochwart, L. and Fohlich, A., 
43, 201, 314, 316, 326, 359; 361 
Fransen, 176 
Franz, 412, 478 
Fratlin, 453 
Fredericq, 376 
Freiberg, 155 
Frerichs, 130, 286, 391 
Freudenberg, 319 
Freund, W. A., 165, 387, 388 INDEX OF AUTHORS 
499 
Frey, 193, 433, 434, 439 
Frey and Harley, 130 
Frey and Lury, 157 
Freyer, 322 
Freytag, 482 
Friedemann, U., 97 
Friedjung, 354 
Friedlander, 248, 414 
Friedmann, 97, 413 
Friedrich, 177, 241, 253, 256, 358, 372, 
380, 382, 383, 385, 414, 420, 421, 466 
Friedrich and Nosske, 466 
Frisch, 322 
Fritsch, 49 
Fritsch and Hitzig, 417 
P’ritsche, 392 
Frohlich, 327, 350 
Frohlich and Meyer, 175, 314, 316 
Fromme, 303, 475 
Fuchs, 459 
Fuld, 429 
Funke, 255 
Furbringer, 323 
Furnohr, 437 
Fursterer, H., 79 
Furth, 346, 348 
Futterer, 77 
Gaetani, 282 
Galen, 176 
Galeni, 408 
Galippe, 12 
Gama and Alquie and Felizet, 411 
Gant, 206, 207 
Gamier, 226 
Garre, C., 100, 351 
Garre and Eckhardt, 300 
Garre and Quincke, 372, 383 
Gaultier, 2, 10 
Gawrilow, 292 
Gayett and Bonnet, 441 
Gebele, 352, 397 
Gegenbauer, 171 
Geigel, 403, 407 
Gelle, 99 
Gelpke, 293 
Genersich, 199, 225, 227 
Gerhard, 381 
Gerhardt, 378, 379, 380, 385, 387 
Ghedini, 264 
Ghillini, 429 
Ghiron, 283 
Gies, 446, 448, 465 
Giesoro and Hahn, 14 
Girard, 30 
Girgoloff, 292 
Glaessner, 134 
Glaserfeld, 353 
Glassmer, 96 
Glassner, 134, 196 
Glassner, K. and Singer, G., 127 
Glenard, Frantz, 53, 184 
Gley, 96, 348, 359 
Glimm, 169, 246 
Glinski, 191 
Glisson, 176 
Gluck, no, 435 
Gobel, C., 135, 207, 435, 481 
Gocke, C., 64, 65 
Goebel, 312, 329, 397 
Goetzl and Israel, 283 
Goldmann, 478 
Goldschmidt, 321 
Golowieff, 122 
Goltz, 20, 24, 201, 417 
Goltz, F., 43, 201 
Goppert, 304 
Goringstein, 366 (ref. 402) 
Gosselin, 460 
Gosset, A., 61 
Gossmann, T. R., 75 
Goto, 453 
Gottlieb, 338, 339, 350 
Gottlieb and Sicher, 23 
Gottstein, 23, 24, 27, 279, 281 
Graser, F., 54, 285 
Grashey, 406 
Grassi and Munason, 344 
Gratz, 362, 363, 364, 384 
Grawitz, 243, 442, 463 
Grawitz and De Barry, 463 
Grawitz, F. and Steffen, W., 3 
Greifenberger, 476 
Greyerz, 222 
Grodel, 199 
Grodel, F. M. and Seyberth, L., 36, 206 
Groedel, F. M., 37 
Grohe, B., 66 
Grondahl, 392, 393 
Gross, 101, 279, 281, 480, 481 
Gross, O., 154 
Gross, Walter, 41 500 
INDEX OF AUTHORS 
Grossmann, 438 
Gruber, 220, 454, 459 
Grunberg, 155 
Grunert, 323 
Grunewald, 428, 437, 441, 444 
Grutzner, 5, 38, 42, 97, 194, 430 
Grutzner, P., 38 
Guelke, 359 
Guerin, 8 
Guiscz, 28 
Guiteras, 293 
Guleke, 183 
Guleke, N., ior, 104, 1x4, 363 
Gundelfinger, E., 76 
Gundermann, W., 78, 177, 287 
Gussenbauer, 64, 463 
Guyon, 309, 322 
Haab, 435 
Haberer, H., 52, 61, 63, 64, 74, 78, 116, 
286, 295, 297, 301, 351 
Haberfeld, 360, 361 
Haberland, 435 
Hacker, 28, 446 
Hadda, 181 
Hagenbach, 341 
Hagenbach and Burckhardt, 428 
Hagler, 247 
Haguenot, 250 
Hahn, 450 
Haim, 240, 256 
Hainski, 119 
Halban, 14, 480 
Haldane and Douglas, 372 
Hallendahl, 10 
Haller, 406 
Hamburger, 192, 224 
Hammar, 351 
Hammarsten, O., 4, 124, 127, 135 
Hanau, 8, 10, 329, 341 
Handel, 134 
Handley, W. S., 123 
Hansemann, 134, 388 
Hansen, 308 
Hari, 422 
Harrison, 291, 456 
Hart, 76, 342, 351, 352, 353, 356 
Hartel, F., 65 
Hartl, 383 
Hartmann, 463 
Hartmann and di Gasparo, 416, 418 
Hartmann, H. and Soupault, M., 56 
Hartmann and Mignot, 258 
Hartsemann, 256 
Hasebrock, 471 
Hasse, 378 
Hasselbach, 375, 376 
Haukin, 246 
Hauptmann, 403, 404, 407, 408, 411 
Haurrel, 12 
Hauser, G., 72, 413 
Hayem, 54 
Head, 46, 175 
Hedon, 98 
Heger, 178 
Heidelberg, 450 
Heidenhain, 1, 6, 95, 96, 221, 225, 438 
439, 444 
Heilberg, K. A., 95, 99 
Heilbronner, 418 
Heile, 193, 199, 240, 255, 256, 257 
Heine, 469 
Heineke, H., 1, 8, 9, 10, 12, 96, 100, 215, 
248, 422, 456, 479 
Heinlein, 28 
Heinsheimer, F., 57 
Heinz, 161 
Hekma, E., 97 
Helferich, 435, 466, 467 
Helfuch, 481 
Hellendahl, 9 
Heller, 23, 119, 299, 391, 475 
Heller and Weiss, 24 
Helly, 151 
Helmholtz, 434 
Hemmeter, J. C., 7 
Hendel, 134 
Henderson, L. J., 291 
Henderson, Y. and Haggard, H. W. and 
Coburn, R. C., 229, 291, 377 
Henke, 432 
Henle, 250 
Henle and Heile, 397 
Henle and Krauss, O., 199 
Henri and Portier, 125 
Hensing, 176 
Henzelmann, 373 
Herb, E., 9 
Hering, 356 
Hering and Brener, 375 
Herman and Escher, 4x9 
Hermann, 192, 295, 296, 374, 411 INDEX OF AUTHORS 
501 
Hernheimer and Hall, 292 
Herre, 56 
Hertle, 231 
Hertz, Arthur F., 206, 207, 208, 211 
Heftz, Axtel, 61 
Herz, 444 
Herzfeld and Klinger, 165 
Hess, 101, no, 176 
Hesse, 55, 180, 344 
Hesselbach, 376 
Heukelom and Siegerbeek, 130 
Heusner, 167, 177, 178 
Heuter, 429, 432 
Heyde, 227, 240, 253, 256, 295 
Heyde and Vogt, 287 
Heyrowsky, 23 
Hildebrand, 104, 298, 349, 35°, 443. 448, 
451, 452, 4ss, 466 
Hildebrand and Haga, 301 
Hildebrand, Scholz and Wieting, 449 
Hildebrandt, 435 
Hill, 403, 409 
Hill and Ziegler, 405 
Hilty, 43s 
Hippocrates, 9 
Hirsch, 224, 304, 312, 342, 365, 382 
Hirschel, 20 
Hirschel, G., 140, 162, 167 
Hiss, 456 
Hlava, 104 
Hochenegg, 79, 181, 220, 326, 327 
Hochstetter, 73 
Hoehne 170 
Hoenck, 260 
Hoessly, 409, 410 
Hofbauer, L., 3, 132, 372, 373, 378, 381, 
386 
Hoffa, 448 
Hoffmann, 72, 175, 380, 388, 459, 472, 482 
Hoffmann, A., 238 
Hoffmann, F. A., 388 
Hofmann, F., 467 
Hofmeister, 341, 474 
Hofmeister, Franz, 37 
Hofmokl, 218 
Hofstadter, 350 
Hohlweg, H., in, 135, 137 
Holder, 414 
Holmberg, 99, 100 
Holmgren, 351 
Holscher, 395, 396 
Holterhof, 361 
Holzknecht, 36, 194, 197, 209 
Holzknecht, G. and Luger, A., 38, 51 
Holzknecht and Jonas, 37, 40 
Holzknecht and Olbert, 25 
Holzmann, 404 
Homburger, 315 
Homeyer, 100 
Homeyer and Magnus, 467 
Hopfner, E., 120, 122 
Hoppe-Seyler, 395 
Hormann, 181, 183 
Hormuth, 463 
Hornborg, A. F., 42, 81 
Hornemann, 305 
Horsley, 326, 338 
Horvart, 437 
Hotz, G., 62, 70, 213, 221, 249 
Houel, 320 
Howell, 320 
Hubscher, 467 
Hunt, Reid, 339 
Hunter, 69 
Hurley, 128 
Huter, 473 
Hyrtl, 364 
Ianson, 116, 117 
Ibrahim, 50 
Ijzeren, W., 76, 79 
Ikonnikof, 241 
Ingianni, 321 
Isaac, S., hi, 157 
Isaeff, 244 
Iselin, 251, 360 
Isenschmid, 342 
Isler, 255 
Isobe, 292, 294 
Tsobeleff, 101 
Israel, 165, 292, 293, 304, 309, 478, 479 
Ito, H. and Asahara, S., 66, 419 J420 
Ito and Omi, 121 
Jackson, 417 
Jacobs, 27 
Jacobs, M. H., 377 
Jacobson, 329 
Jaffe, 164, 464 
Jager, 378 
Jagetho, 469 
Jakowski, 475 502 
INDEX OF AUTHORS 
Jamin, 441 
Janeway and Ephraim, 229 
Janis and Nakarais, 312 
Jansen, 444 
Januschke, H., 76, 77 
Jappeli, G., 3 
Jawein, 3, 6, 150 
Jeannel, 269 
Jehle, 298 
Jehn, 287, 395 
Jehn and Naegeli, 395 
Jenckel, 283 
Jensen, 242, 244 
Joachimsthal, 423, 429 
Jochmann, 385 
Jochmann and Batzner, 466 
Jonas and Rudinger, 362 
Jonas, S. and Holzknecht, G., 37 
Jordan, 264, 307, 478 
Josselin de Jong, 118, 121 
Josselin de Jong and Sax, R., 118 
Jousset, 308 
Jungling, 453 
Jungmann, 282 
Jungmann and Meyer, 282 
Justi, 192 
Kader, 213 
Kafemann, 260 
Kahler, 421 
Kahn, 19, 20, 314 
Kaiser, F. F., 66 
Kaoru, Omi, 193 
Kaplan, S., 64, 65 
Kappis, 29, 172, 283, 311 
Kapsammer, 284, 285, 301, 436 
Karlinski, 242 
Karplus and Kreidl, 315 
Kast and Meltzer, 173, 175 
Kastle, 37, 38, 39 
Kastle, C., Rieder, H. and Rosenthal, I., 
37, 38 
Kathe, H., 62 
Katschkowsky, P., 49 
Katz and Winkler, 199 
Katzenstein, M., 57, 58, 62, 70, 80, 292, 
470, 477 
Kauffman and Ruppanner, 364 
Kaufmann, 23, 24, 68, 73, 204, 474 
Kaufmann, Eduard, 73 
Kausch and Kaplan, 57 
Kausch, W., 56, 60, 79, 138 
Kavasoye, 302 
Kawamura, K., 70, 76 
Kazmelon, Helene, 21, 81 
Kehr, no, 116, 117 
Kehrer, J. K., 70 
Keller, Katharina, 374 
Kellie, 419 
Kelling, Georg, 22, 51, 55, 56, 58, 59, 61, 
181, 183, 397 
Kemp, S., 80 
Kempf, 231 
Kendall, E. C., 339 
Kepinow, 350 
Kermauner, 28 
Kertecz, 182, 217 
Kettner, 15 
Kielleuthner, 308 
Kienbock, R., 24, 74 
Killian, 17, 25 
Kimura, 445 
Kirchheim, 103 
Kirschner, 449 
Kirschner, M. and Mangold, E., 43 
Kirschstein, 228 
Kistler, 384 
Klapp, 168 
Klauber, 220, 258 
Klauser, 314, 389 
Klebs, Edwin, 12, 76 
Klebs and Welt, 474 
Klecki, 258, 304 
Klee, P., 43, 44, 46 
Klee, P. and Klupfel, O., 126, 136 
Klein, 256, 449 
Kleinschmidt, 313, 395 
Kleist and Forster, 315 
Klemperer, 463 
Klippel, 439 
Klopfstock, 121 
Klose, 342, 350, 351 
Klose, H. and Vogt, H., 152, 352, 353, 406 
Klug, 68 
Knape; W., 100, 103 
Knapp, 220, 253 
Knoll, 285 
Kobayaski, M., 76 
Koch, 463 
Koch, W., 134, 178, 298, 304, 307, 309, 
338, 463 
Koch and Filehne, 412, 413 INDEX OF AUTHORS 
503 
Kocher, 175, 214, 217, 218, 223, 225, 329, 
338, 340, 342, 344, 347, 348, 403, 4io, 
411, 413, 420, 421, 460, 468 
Kocher, A., 56, 63, 79 
Kocher and Prutz, 223 
Kocher, Thomas, 80, 363 
Koehler, 389 
Koenig, 323 
Koerte, 238 
Koerter, 238 
Kohler, 389 
Kohnstamm, 1 
Kohts, 381 
Kolb, 366 (ref. 402), 455 
Kolle and Otto, 463 
Kolliker, 459 
Kolozoff and Brunn, 161 
Kon, 157 
Kondolean, 482 
Konen, 458 
Konig, 440, 443, 447, 448, 449, 454 
Konig and Paschen, 466, 469 
Konjetzny, 207 
Koranyi, 281, 288 
Korber, 411 
Korte, W., 52, 104, 138 
Korteweg, 429 
Kostel, 345 
Kottmann, 341 
Krabbel, 363 
Krabbel, M. and Gleinitz, H., 79 
Kragelund, 448, 449 
Krall, 358 
Kramer, 310, 311, 412 
Krapp, 9 
Kraske, 179, 450 
Krasnogorski, 70 
Kraus, 12, 23, 24, 463 
Kraus, Fr., 346, 349 
Kraus and Friedenthal, 348, 350 
Krause, Fedor, 57 
Krauss, 438 
Krehl, Ludolf, 24, 50, 130, 477 
Krehl and Marchand, 372 
Kreidl, 362 
Kremer, 437, 439 
Krempelhuber, M., 54 
Kretz, 79, 128, 129, 133, 257 
Kreuter, 149, 151 
Krogh, 372 
Krogins, 242 
Kroh, 447, 450, 451, 452, 464 
Kroher, 251, 253 
Krohnlein, 412 
Kroiss, 12, 13 
Kron, 434 
Kronecker and Meltzer, 15, 16, 19, 21, 24 
Kronecker and Schmey, 365 (ref. 402) 
Kronig and Gauss, 406 
Kronlein, 403, 412 
Kruger, 456 
Kubig, G., 140 
Kuhn, 96, 388, 48r 
Kuhne and Lea, 96, 100 
Kukula, 225, 264, 266 
Kumita, 3T4 
Kummell, 28, 65, 291, 293, 295, 307 
Kunika, 131 
Kuru, 52 
Kushimura, 472 
Kusmine, 125 
Kussmaul, 53, 361 
Kussmaul and Tenner, 417, 419 
Kuster, 295, 299, 308 
Kutschera, 342, 343, 345 
Kuttner, Hermann, 6, 56, 74, 79, 148, 152, 
160, 167, 312, 394, 403, 435, 453, 455, 
469 
Kuttner and Landois, 435, 436 
Laennec, 448 
Laewen, 333, 366 (ref. 402) 
Laguesse, E., 100 
Laimer, Monro, 26 
Landau, 299 
Landau, M. and McNee, J. W., 300 
Landois, 287, 359, 419, 435, 474 
Lane, 211, 448 
Lange, 119, 355, 437 
Langemaak, 296 
Langemak, 13, 295, 468 
Langenbecks, 469 
Langenbuch, 118, 120 
Langendorff, 97, 381 
Langendorff and Mommsen, 314 
Langerhans, R., 101, 102 
Langley, 6, 171 
Langley, J. N., 43, 3*4 
Langley and Magnus, 194, 197 
Langmak, 296 
Lannelogue, 461 
Lanz, 180, 256, 341, 346, 363, 364, 482 504 
INDEX OF AUTHORS 
Larguier des Bancels, 97 
Larrey, 365 
Larroche, 132 
Latarjet, A. and Cade, A., 81 
Lattler, 346 
Latzko, 292 
Laubenheimer, 134 
Laudenbach, 152 
Lauenstein, 220 
La wen and Sievers, 389, 391 
Lawson, and Tait and Heidenhain and 
Vogel, 162 
Lebedeff, 113 
Leber, 462 
Ledderhose, 164, 378, 468, 471 
Legg, 438 
Leggett, N. B. and Maury, J. W. D., 56 
Leguen, 52 
Lehmann, G., 78, 433 
Leichtenstern, 213 
Lendorf, 321, 322 
Lengemann, 395 
Lenk, 298 
Lennander, K. G., 47, 162, 172, 283, 291, 
436 
Lennander and Nystrom, 242 
Lennander and Wilms, 172 
Lenormant, 269 
Lepehne, G., 151, 153 
Lepine and Barral, 97 
Leporski, 366 (ref. 402) 
Lequen, 277 
Leriche, R., 1 
Leser, 450 
Lesser, 472 
Lesshaft, 447 
Letienne and Hanot, 124 
Letulle, 74 
Leube, 6, 297, 319 
Leueberger, 319 
Leuenberger, 228, 319 
Leverenz and Schoenwerth, 160 
Levi and Ludloff, 455 
Levy, R., 9 
Lewandowsky, 171, 404, 459 
Lewin, 127, 307 
Lewin and Goldschmidt, 301, 303, 310 
Lewis, 365 (ref. 402) 
Lexer, 393, 461, 467, 469 
Lexer and Kuliga and Turk, 461 
Leyden, 407 
Lichtenbelt, J. W., 76 
Lichtenberg, 248, 301, 395, 396, 397 
Lichtenstern, 324 
Lichtheim, 372, 378, 381, 386 
Lichtwitz, L., 132, 313 
Licini, C., 70, 77 
Liebermeister, 129 
Lieblein, 148 
Lieblein, V., 265 
Liek, 292, 293, 455 
Lindemann, 288, 289, 395 
Linser, 407, 473 
Lintbeck, 287, 288 
Lissauer, 117, 119, 121, 124, 128 
Litten, 233 
Litthauer, 77 
Lob, 474, 475 
Lobenhofer, 282, 293, 344 
Loeb, A., 125, 311 
Loeschke, 322, 323, 388 
Lohmann and Muller, 379, 388 
Lombroso, U., 99, 100, 101 
London, 265 
Longuet, 230 
Looser, E., 135 
Lorenz, 220, 429, 445 
Lorin, 302 
Lossen, 217, 218 
Lovett, 438 
Lowenstein, 470 
Lowit, 395 
Lubarsch, 121 
Luciani, 4, 154, 428, 429, 433 
Lucke, 443, 460 
Luckhardt, A. B. and Henn, S. C. and 
Palmer, W. L., 96 
Ludakeevitsch, 153 
Ludloff, 267, 268, 269, 449 
Ludsucki, 389 
Ludwig, 1, 280 
Luscher, 20 
Luschka, 199 
Lusk, Graham, 115 
Luter, 284 
Luthi, 338 
Maas, 295, 435 
Maas and Pinner, 318 
Macleod, J. J. R., 37 
Madelung, 328 
Mafucci, 167 INDEX OF AUTHORS 
505 
Magendie, 19, 405 
Magendie and Longet, 18 
Magnan, 418 
Magnus and Alsleben, 119, 225, 226 
Magnus and Levy, 342, 346, 348 
Magnus, R., 43, 97, 127, 194, 373, 435, 
446, 463 
Malassez and Ponchet, 155 
Malchol, 454 
Malcolm, 229 
Mall, 170 
Manasse, 50 
Manfredi, 480 
Mangold, E., 52, 65 
Mann, 229 
Mansfeld and Muller, Fr., 346 
Manteuffel, 213 
Maragliano, D., 105 
Marburg and Ranzi, 416, 422 
Marchand, 54, 161, 364, 395, 435, 472 
Marchand and Krehlschen, 165 
Marckwald, 17 
Marcus, 303, 306, 307, 310 
Marek, 234 
Marey, 429, 476 
Marine, D. and Kimball, O. P. and 
Rogoff, J. M., 347 
Marinesco and Minea, 341 
Marion, 322 
Martens, 448 
Martin, 435 
Martin, Sidney and Dawson, 127 
Martini, 292 
Martius, F., 77, 78 
Marwedel, 461 
Marzocchi and Bizzozero, 13 
Masius, 283 
Massland, 413 
Mathieu, 209 
Mathieu, A. and Roux, J. C., 53 
Mathiew, A. and Savignac, R., 61 
Mathiew and Roger, 59 
Matsuoka, 329 
Matthes, M., 54, 60, 62, 66, 69, 233 
Matti, 201, 351, 356, 392, 427, 431, 455 
Mauthner and Pick, 229 
Maximore, 6 
May, W. P., 44 
Maydl, 222 
Mayer, Aug., 180 
Mayer, Fritz, 74 
Mayer and Gottlieb, 5, 9 
Mayersbach, 457 
Mayo, W. J., 63 
Mayo-Robson, 124, 126, 135 
McCallum, 359, 363, 364 
McCosh, 233 
McLean, 227, 259 
McMaster, P. D. and Rous, P., 128 
McNee, J. W., 128, 132 
Meaugedis, 295 
Meckel and Helmsbach, 131 
Medwedew, 363 
Meinert, 360, 361 
Meinertz, 308 
Meisel, 170, 241, 245, 256, 258, 416 
Melchior, 326, 328, 346, 354 
Melchior and Loser, 263 
Melchior and Suter, A. O., 318 
Melnikow and Montuori, 154 
Meltzer, 16, 17, 21, 137 
Menge, 293 
Menzels, 441 
Mering, 64, 95, 98 
Mering and Aldehoff, 40, 44, 49 
Merkel, 72 
Merrem, 64 
Merten, 412 
Merzbacher, 202, 208 
Messerer, 4x1, 4x3, 421 
Mestrezet, 404 
Metschnikoff, 168, 245, 246 
Metzger, 152 
Metzner, 314 
Meyer, A. W., 148,151,152, i54, i55> 173, 
414 
Meyer and Betz and Gebhardt, 202 
Meyer and Gottlieb, 171 
Meyer, H., 428 
Meyer and Jungmann, 282, 283, 284 
Meyer, O. B., 314 
Meyer, R., 181 
Michaelis, 366 (ref. 402) 
Michaud, 421 
Miflet, 328 
Mikulicz 21, 22, 25, 27, 251, 452 
Miller, Fr., 192 
Miloslavich and Namba, 262 
Minkowski, 98, 125, 129, 372, 375, 378 
Minkowski and Naunyn, 128 
Mobius, 346, 347 
Moeckel, 420 506 
INDEX OF AUTHORS 
Moeckel, K. and Rost, F., 97 
Mohr, 7, 9 
Molitoris, 365 (ref. 402) 
Moll, 442 
Moller, 361 
Molnar, 191 
Momburg, 419 
Monakow, 281 
Monari and Umberto, 66, 265, 266, 267 
Monckeberg, 162, 364 
Monro, 26, 448 
Monroe, 407 
Mora, Henri, 101 
Morandi and Sisto, 151 
Morano, G. P. and Baccarani, W., 7 
Morawitz, 115 
Morawitz, P. and Bierich, 130 
Morawitz and Siebeck, 441 
Morgagni, 18, 230, 365 
Moricke, 9 
Morison, 179 
Moritz, 181, 182 
Moro, 185, 362 
Morpurgo, 287 
Morris, 253 
Mosengeil, 464, 465 
Moskowitz, 246 
Mosler, 152 
Mosse, 157 
Mosso, 430, 439 
Most, 464, 480 
Motschutkowsky, 423 
Moty, 230 
Mouton, 30 
Moynihan, 263 
Muck, 478, 479 
Muhsam, R., 157, 196, 257 
Muller, 8, 71, 205, 292, 314, 316, 465, 466 
Muller, Albert, 37, 47, *95, 3°7, 3r4 
Muller, Fr., 101, 281, 284, 287, 303, 358 
Muller, Johannes, 40, 434 
Muller, L. R., 43, 66, 174, 175, 201, 208 
Muller, P., S3 
Mummery, 229 
Munk, 127,, 417 
Muralt, 384 
Murphy, 467 
Muscatello, 161, 167 
Musculus, 319 
Myers, 134 
Mylard, 254 
Naegeli, 150, 354, 361 
Nagamori and Hikohachi, 76 
Nagano, 266, 267, 321 
Nakahara, 297 
Nakahara and Dilger, 454 
Narath, II, 116, 192, 215 
Narath, II, 116, 117 
Narath, II and Steckelmacher, S., 117 
Nasse, 130, 136 
Natus, M., 100, 101, 103 
Naumann, 132 
Naunyn, 124, 131, 165 
Naunyn and Schreiber and Falkenheim, 
403, 405. 407 
Nauwerck, C., 74 
Nauwerk, C. and Lubke, 139 
Neisser, 242 
Neisser and Wechsberg, 463 
Nelaton, 164 
Nencki and Pawlow, 112 
Nepper, 127 
Nesbieth, 225 
Neu and Hermann, 405 
Neuber, 364 
Neugebauer, 24, 452 
Neuhaus, 63, 464 
Neuhaus and Hildebrand, 56, 464 
Neumann, 172, 220 
Neumann, A., 232 
Neumann, E., 69, 74 
Neumann, R., 233 
Newton, 421 
Nicol, 8 
Nicoladoni, 181 
Nicolletti, 116 
Niebergall, 478 
Niederstein, 234 
Nigrisoli, 264, 266 
Nikolaysen, 225 , 
Nissen, 355 
Nitsche, E., 73 
Nobl, 469 
Nocard, 305 
Noetzel, 251 
Noguchi, 463 
Nolf, P., 1x6 
Nonne, 409, 482 
Nonnt and Apelt, 405 
Nordmann, 351 
Nothnagel, 173, 174, 176, 194, 212, 223, 
250, 253, 417, 437, 477 INDEX OF AUTHORS 
507 
Notkin, 339 
Notzel, W., 140, 149, 166, 183, 244, 397, 
398, 463, 465, 480 
Nowatski and Arndt, 420 
Nussbaum, 251 
Nystrom, 242, 436 
Oberdorfer, 262 
Oberndorffer, 23 
Oddi, 126, 136 
Oehlecker, 321 
Offergeld, 396 
Ogata, M., 67 
Ohlecker, 176 
Ollier, 435, 469 
Olshausen, 216 
Openchowski, 22, 43, 45 
Opitz, 304 
Oppenheim, 96, 224, 415, 447 
Oppenheim and Loew, 311 
Oppenheimer, 97, 319 
Oppler, 203 
Ore, 122 
Orfila, 318 
Orlow and Heidenhain, 168 
Orth, Johannes, 9, 73, 308 
Orthmann, 463 
Ortner, 174 
Orzechowski, 362, 416 
Osborne, T. B. and Mendel, L. B. and 
Ferry, E. L., 312 
Oser and Pribram, 154 
Osthoff, 288 
Ostwald, Adolph, 124 
Oswald, 338, 346, 348 
Otto, E., 40 
Pagenstecher, 164, 166, 464 
Paget, 449 
Paine, 257 
Pal, 170 
Palmer, W. W. and Van Slyke, D. D., 291 
Paltauf, 23, 355, 364 
Pansini, 242, 247 
Panum, 72 
Parlavecchio, 292 
Partsch, 458 
Passavant, 16 
Passler, 348 
Passler and Heinecke, 286 
Passow, 363 
Pasteur, 462 
Paterson, 264 
Patrion, 62 
Pauchet, 264, 266 
Pavy, 71 
Pawlow and Boldireff, V. N., 39 
Pawlow, I., 2, 11, 41, 43, 47, 49, 59, 95, 
96, 97, 126, 135 
Pawlow, J. P. and Schumowa-Siman- 
owskaju, 43, 49 
Pawlowski, 243 
Payr, 72, 73, 162, 180, 237, 253, 254, 263, 
393, 408, 434, 464, 465, 467, 468, 469 
Payr, A. and Martina, E., 104 
Pean, 64 
Pearce, 286 
Pearce, R. M. and Krumbhaar, E. B and 
Frazier, C. H., 149 
Peiser, 167, 169, 243, 245 
Pels, Leusden, 309 
Pelschinsky, 13 
Pennington, 207, 230 
Penzoldt, 163 
Peres, 148 
Perez, 154, 464 
Peritz, 362, 364 
Pernice and Scagliosi, 304 
Perrier and Hartmann and Monprofit, 55 
Perthes, G., 65, 207, 248, 384, 422, 441, 
458 
Petersen, Walther, 37, 59, 60, 380 
Petren, 30 
Petry, 231, 232 
Pettavel, 351 
Pfaff and Balde, 125 
Pfaundler, 285 
Pfeifer, 314 
Pfeiffer, 348 
Pfeiffer and Kolle, 244 
Pfeiffer, R., 247, 287, 289 
Pfeiffer and Wassermann, 247 
Pflanz, 209 
Pflaumer, 282, 284. 315 
Pfluger, in 
Phleps, 359 
Pick, 129, 255 
Piktin, 153 
Pinkus, 208 
Piorry, 436 
Pirogoff, 412 
Pirone, 178, 179 508 
INDEX OF AUTHORS 
Placzek, 365 (ref. 402) 
Plaschke, S. and Schur, H., 80 
Pletnew, 125 
Pochhammer, 454, 459 
Pohl, 155 
Poirier, 277 
Polya, E., 103 
Pommer, 214, 445 
Poncet, 449 
Ponfick, 110, 285, 301 
Popielski, L., 2, 41, 43, 44, 95, 96, 97, 155, 
172 
Popper, 352, 458 
Poppert, 395 
Porter, 366 (ref. 402) 
Posner, 297, 301, 305, 313, 314, 316, 320, 
329 
Posner and Lewin, 306 
Preiser, 446, 447 
Pretsch, 181 
Prettin and Leibkind, 389 
Pribram, 373 
Primbs, 302 
Propping, 172, 220, 251, 252, 253, 379. 406 
Propping and Dieterichs, 220 
Prutz, 233 
Prutz and Ellinger, 196 
Purkhauer, 432 
Quarta, 154 
Quenu, 458, 476 
Quenu and Hartmann, 207 
Quenu and Walter and Routier, 277 
Quervain, 222, 339 
Quincke, 120, 123, 130, 138, 284, 314, 404, 
406, 415 
Quincke, H. and Dettweiler, 77 
Qurin, 224 
Rabe, 124 
Raiser, 197 
Ramstroem, 176 
Ranke, 217 
Ransohoff, I., 120 
Ranzi and Tandler, 351 
Ranzier, 14 
Rashford and Southgate, 127 
Rautenberg, 301, 302 
Ray and Sherrington, 410 
Raymond, 438 
Reach, F., 126 
Real, 450 
Recklingshausen, 72, 167, 234, 391, 477 
Redlich, 362, 416 
Redlich and Binswanger, 416, 418 
Redwitz, 65, 72, 79, 210, 261 
Reerink, 322 
Regnier, 441, 442 
Rehfisch, 3x4, 317, 321 
Rehn, 251, 252, 255, 319, 351, 365 (ref. 
402), 468 
Reich, 24, 434 
Reich and Blauel, 346 
Reichard, 73 
Reichardt, 403, 408, 409 
Reichel, 192, 2x5, 228, 243 
Reichmann, M., 54, 406 
Reifs, 287 
Reimann, S. P. and Bloom, G. H. and 
Reimann, H. A., 378 
Reineboth, 374, 382, 384 
Reiner, 392, 393 
Reiniger, Clara, 135 
Reinsbach, 482 
Remak, 481 
Renner, 282, 283 
Renton, 458 
Retzius, 22 
Reyher, 442 
Rheinbolt, M., 49 
Ribbert, 71, 119, 257, 389, 391, 392, 472 
Ribbert and Kruse and Fischer, B., 465 
Richards, A. N., 280 
Richet, Ch., 81, 154 
Ricker, G., 103, 104, 298 
Riedel, 101, 137, 164, 181, 205, 256, 263, 
300, 392, 464, 476 
Rieder, 36, 194, 197 
Riedinger, 442 
Riegel, 365 (ref. 402) 
Riegner, 152, 155 
Rimann, 448 
Rio Branco, 116 
Rippert, 262, 304 
Risel, 140, 391 
Ritter, 293, 355, 480 
Ritter, A., 73 
Ritters, 444 
Riva-Rocci, 278 
Rivington, 320 
Rivinus, 177 
Rjesanoff, 210 INDEX OF AUTHORS 
509 
Robinson, 255, 383, 384 
Robson, Mayo, 124, 126, 135 
Rochet, 319 
Rockwitz, C., 60 
Rodet, 461 
Roessle, 76, 350 
Roger, 127, 178, 226, 461 
Rogoszinsky, 305 
Rogowitsch, 341 
Rohde and Ellinger, 282, 285, 379 
Rohleder, 325 
Rohr, 242 
Rohrbach, 407 
Roith, 193, 254 
Rokitansky, 253 
Rolando, 13 
Roily, 308 
Romanoff, 380 
Romberg and Passler, 248 
Romer, 462 
Ropke, 463 
Rose, 21, 365 (ref. 402) 
Rosenbach, 104, 372, 375, 384, 385, 460 
Rosenbach and Schschterbak, 421 
Rosenbaum, 18 
Rosenberg, 97, 99, 100, 125, 127, 136 
Rosenheim, 23, 254 
Rosenow, E. C., 75 
Rosenstein, P., 119, 122, 180 
Rosenthal, 375 
Roser, 178, 217, 384, 385, 445, 460, 467 
Rosier, 77 
Rossolino, 207 
Rost, F., 2, 6, 8, 19, 29, 58, 105, 123, 125, 
126, 136, 140, 154, 178, 179, 193, 207, 
209, 210, 221, 222, 223, 253, 267, 301, 
302, 314, 317, 321, 322, 357, 451, 
457, 463, 466, 472, 474, 481 
Rotschild, 322 
Rotter, 251, 252, 253 
Roubaix, 218 
Roubitschek, 305, 306 
Rouotte, 123 
Rous, P. and McMaster, P. D., 137, 139 
Roussi and Rossi, 201 
Roux, 427, 429, 440, 441 
Roux, J. C. and Riva, A., 68 
Roux and Roger and Sosne, 257 
Rouxeau, 359 
Rovsing 184, 185, 293, 310, 318 
Rovsing and Niels and Thorkild, 54 
Roy, 28, 155 
Roy and Sherrington, 410 
Rubaschow, S., 140 
Rubin, 179 
Rudinger, 341, 359, 360, 361 
Ruge, 291, 293, 294, 301 
Rumpf, 421 
Runeberg, 240, 256 
Runge, 322 
Rutimeyer, 78 
Ruttermann, 9 
Rydigier, 236, 481 
Rywosch, 130 
Saar, 380, 381 
Sab razes, J. and Faguet, C., 8 
Sachs, 97 
Sackur, 379, 381 
Sagimura, 305 
Sahli, 478 
Saito, 463 
Sakata, 305 
Salis, 347, 388 
Salis and Vogel, 347 
Salkowski, E., 5, 6, 468 • 
Salou, 96 
Samuel, 461 
Sanarelli, G., 3 
Sarbach, 340 
Sasse, F., 66 
Sattler, 349 
Sauerbruch, 25, 227, 230, 232, 351, 359, 
365 (ref. 402), 372, 373, 375, 376, 379, 
380, 382, 383, 384, 386, 403, 407, 413, 
419 
Sauerbruch and Haecker, 23, 24 
Sauerbruch and Heyde, 287 
Savo, 307 
Sawamura, 309 
Scarpa, 185 
Schablowsky, 465 
Schade, H., 11, 12, 131, 132, 313 
Schall, 389 
Schambacher, 470 
Schanz, 443 
Schattenfroh, 246 
Schatz, 181, 183 
Schede, 384 
Scheidemantel, 304 
Scheidtmann, 253 
Scheier, 15 510 
INDEX OF AUTHORS 
Schenker, 388 
Schepelmann, 386, 468 
Schepowalnickow, 191 
Scheuerlen, 463 
Schiefferdecker, 176, 177, 180 
Schievelbein and Ritter, 139 
Schiff, 18, 24, 76, 122, 125 
SchifI and Contejean, 41 
Schiff and Zack, 438, 439 
Schifferdecker, 422 
Schifone, 415 
Schischko, 302 
Schittenhelm and Weichardt, 204, 344 
Schlagenhauer and Wagner and Jouregg, 
342, 344 
Schlagintweit, E. and Stepp, W., 96 
Schlange, 322, 323, 324 
Schlatter, C., 67 
Schlayer, 281, 289 
Schlesinger, 383, 395 
Schlesinger, E., 56, 2x0 
Schlesinger, W., 97, 222 
Schloessman, 453, 458 
Schloffer, 236 
Schmaus, 421 
Schmerz, 468 
Schmid, 17, 171 
Schmidt, 18, 165, 202, 217, 364, 481 
Schmidt, A., 97, 101, 191, 192, 206 
Schmidt, Ad. and Strassburger, 203 
Schmidt and Aschoff, 307 
Schmidt, G. B., 436 
Schmidt and Lohrisch, 210 
Schmidt, Mulheim, 165 
Schmidt, J. E. and Betke, 329, 364 
Schmidt, J. H., 47 
Schmidt, M. B., 153, 469 
Schmieden, V., 241, 297, 450, 469 
Schmincke, 148, 154 
Schmorl, 337 
Schmorl and Ingier, 356, 392, 405, 463 
Schneider, 363 
Schnitzler and Ewald, 167, 169 
Schoemaker, T., 56, 58 
Schoenfeld, 154 
Schonborn, 348 
Schoppe, 458 
Schott, 178 
Schottmuller, 10 
Schrader, 170, 247 
Schramm, 5 
Schreiber, 15, 21, 182, 293, 474 
Schroder, 112, 135 
Schrottenbach, 415 
Schrumpf, 256 
Schrunder, 162, 166 
Schuchardt, 68 
Schuller, L., 38, 55, 56, 59, 6r, 64 
Schulten, 15 
Schultz, 476 
Schultze, 463 
Schultze, F., 149 
Schultze, W., 104 
Schulz, Emma, 185 
Schulze, 100, 348 « 
Schumm, 96 
Schupbach, 127 
Schuppel, 119 
Schuster, 366 (ref. 402) 
Schutz, R., 203 
Schwalbe, 473 
Schwartz, 285, 314, 317 
Schwarz, G., 17, 37, 79, 194, i97, 200, 
209 
Schwarz, K., 79 
Schwenkenbecker, 20 
Scott, R. W., 303, 377 
Seelig and Lyon, 229 
Seeliger, 308 
Segale, 318, 467 
Seggel, 449 
Seidel, H., 105, 135, 298, 383, 388 
Selter, 305 
Senator, 297 
Seringer, 56 
Sherington, 432 
Shimodeira, 223 
Shingu, 384 
Short, 230 
Shulten, 15 
Sick, 139, 225, 264 
Siebeck, 375, 386 
Sievers, 390 
Silbermann, O., 77, 474 
Silhol, 764 
Simmonds, Morris, 37, 105, 296, 310, 312, 
328 
Simon, 296 
Singer, 209 
Singer, C., 74 
Singer, G., 76 
Sinnhuber, 24 INDEX OF AUTHORS 
511 
Sittmann, 304 
Sjubimowa, 75 
Skzreczka, 375 
Smirnow, 282, 283 
Snel, 396 
Soli, U., 351 
Solowieff, 118 
Sonnenburg, 54, 256, 260, 261, 262 
Soulie, 155 
Soyesima, 265, 266 
Spalteholtz, 17, 365, 476 
Spemann, 457 
Spiess, 459 
Spitzy, 457 
Sprengel, O., 72, 234, 238, 239, 247, 249, 
255, 256, 259, 260, 262 
Ssolowjeff, 67 
Stadelmann, 125, 128, 129 
Stadler, 224 
Staehelin, 372, 381 
Stark, 23, 24, 25 
Starlin, 194 
Starling and Bayliss, 95 
Starling and Tubby, 168 
Stassoff, 266 
Stawraky, W., 99 
Steenhuis, 118 
Steinach, 325, 329 
Steiner, 138, 329, 456 
Steinert, 456 
Steinharter, E. C., 74 
Steinlein, 341 
Stempel, 446, 453 
Stern, R., 162, 247, 398 
Sternberg, 482 
Steudel, 59 
Stewart, 305 
Stewart and Barbes, 302 
Steyrer, 285 
Sthamer, E., 72 
Stich, 474, 478 
Stier, 441 
Stierlin, E., 65, 194, 202, 209, 211 
Stierlin and Rieder, 198 
Stiller, 36, 53, 78, 184, 299, 329 
Stiller and Glenard, 208 
Stilling, 329 
Stintzing, 459 
Stoeber and Dahl, 257 
Stoerk, 297 
Stoffel, 422, 457 
Stovesand, 375 
Strangury, 379, 383 
Strassburger, 202, 203 
Strasser, 438, 444 
Strassmann, 303 
Straub, 289 
Straup, 206 
Strauss, 200, 287, 318, 319 
Strauss and Gernout, 301 
Strehl, 172, 248, 249 
Strieker, 5 
Strohmeyer, F., 74, 412 
Strubell, 294 
Strumpell and Vulpian, 438 
Stuber, 59, 71 
Stuberauch, 136, 151, 320 
Studensky, 313 
Stursberg, 292, 395 
Sturtz, 373, 386 
Sturtz and Sauerbruch, 209 
Stuzer, 178 
Sudeck, 436, 440, 453, 454 
Sultan, 13, 220 
Sulzer, 438, 439 
Sumita, 368, 467 
Suter, 307 
Suzuki, T., 178 
Svehla, 352 
Swanson, 7 
Sweet, J. E., 105, 228 
Szymanowsky, 19 
Takoyusu, 265 
Talke, 475 
Talma, S., 47, 75, I22, 2I5 
Tandler, 328 
Tandler and Gross, 324, 325 
Tappeiner, 117, 119, 125, 467 
Tarulli and Pascucci, 154 
Tashiro, 445 
Tavel, E., 58, 59, 60 
Tavel and Lanz, 243, 256, 257 
Teevan, 411 
Teleky, 437 
Telemann, 22, 27 
Tendeloo, 309, 374, 380 
Ten Horn, 257 
Tenner, 417 
Terrier, 277 
Teutschlander, 311, 392 
Thaler, 360 512 
INDEX OF AUTHORS 
Thelemann, 292 
Thiery, 14, 17, 190 
Thiessch, 384 
Thoele, 111 
Thole, 116, 119, 421 
Thoma, E., 66 
Thommen, 230 
Thorspecken, 124 
Thran, 119 
Tiedemann, 152 
Tiegel, 383, 384, 394 
Tietze, Allen, 62 
Tigerstedt, 378 
Tigerstedt and Bergmann, 289 
Tillmann, 24, 122, 295, 397, 4”, 4*3, 437, 
464 
Tilmann and Bungart, 418, 420, 439 
Tischner, 130 
Tizzoni, 151, 152, 155 
Tobler, L., 40, 41, 42 
Toldt, 199 
Tomsa, 328 
Torek, 253 
Trager, 268 
Trappe, 453 
Traube, 288, 372, 381 
Treindlsberger and Schlagintweit, 312 
Trendelenberg, 194, 238, 339, 389, 460, 
47i, 475 
Treskin, 318 
Trinkler, N., 66 
Tromberg, 392, 393 
Tronyl, 1 
Trousseau, 360 
Trousseau and Leblanc, 163 
Trzebicki, 265, 266, 267 
Tschekunow, J. S., 42 
Tsunoda, T., 130 
Tuffier, 52, 301 
Tuffier and Ehrhardt, 292 
Tuffier and Rosenbach, 314 
Turck, F. B., 74 
Turk, 157 
Uffenheimer, A., 42 
Ujeno, 161 
Ullmann, 320 
Umber, 42 
Umbreit, 119 
Unger, E., 66, 291 
Ury, 192, 203 
Uskoff, 463 • 
Uxkull, 430 
Van Braam and Honckgeest, 44 
Van de Kamp, 394 
Van Roojen, P. H., 61 
Van Slyke, 112, 290 
Vanghetti and Sauerbruch, 434 
Vaquez, 475 
Vassale, 360, 363 
Vassale and Generali, 359 
Vazin, 439 
Veil, 285, 286 
Venus, 398 
Verlicae, 293 
Verneull, 269, 476 
Verse, 118, 133 
Verth, 478 
Viborg, 13 
Vignolo, 478 
Vincent, 338 
Viola, 480 
Viola and Gaspardi, 70 
Virchow, 8, 22, 70, 234, 253, 388, 391, 392, 
414, 473 
Virgli, 321 
Voelecker, 244, 251, 303, 310, 452, 454 
Vogel, H., 148, 161, 162, 277, 347 
Vogt, 459 
Voisin and Petit, 419 
Volcker, 301, 474 
Volhard, 279, 281, 282, 287, 288, 292 
Volkmann, 429, 435, 440, 442, 445, 450, 
4Si, 459, 460, 465 
Von Bramann, 13 
Von Eiselberg, 20 
Vulpian, 439, 440, 441 
Vulpius, 148, 149, 152, 154 
Wagner, 8, 9, ix 
Wahl, 413, 478, 479 
Walbaum, 249 
Waldeyer, 267, 460 
Waldeyer and Volckmann, 460 
Wolkoff and Delitzin, 299 
Walkhoff and Ewald and Preiser, 445, 447 
Wallgreen, 244 
Wallney, 320 
Walthard, 243 
Walther, F. K., 97, 341 
Walther and Hosemann, 348 INDEX OF AUTHORS 
513 
Walz, 356 
Wasserthal and Epstein, 305, 306 
Wassilief, 19 
Wearn, J. T., 280 
Weber, E. F., 428, 429, 443 
Weber, O., 392, 476 
Weber, Th., 478 
Wegner, 166, 170 
Wehrmann, C., 4 
Weichselbaum, A., 99, 445, 448 
Weidenreich, 178 
Weil, 15, 169, 239 
Weinland, 190, 240 
Weintraud, 124 
Weisker, 181 
Weiss, 222 
Weissgerber, 384 
Weissgerber and Peris, 293 
Weitz, 385 
Wells, 251, 289 
Wendel, 23, 415 
Wendelstadt, 346 
Wendt, E. C., 8 
Wenkebach, 373 
Wenzel, 269 
Wertheim, 479 
Werzejewki, 392 
West, 374 
Westphal, 417 
Westphal, K. and Katsch, 76, 77 
Wettstein, 56 
Wheelon, H. and Thomas, J. E., 40, 46 
Whipple, G. H. and Sperry, J. A., 114, 228 
Wickmann, 362 
Widmer, 24 
Wiebrecht, 363 
Wiedemann, 138 
Wiedhopf, 183, 185 
Wieland, 254 
Wiener, 363 
Wiesel, 354, 355, 356 
Wieting, 478 
Wilbrand and Sanger, 410 
Wildboltz, 284, 309, 310 
Wilkie, D. P. D., 54, 64 
Wilms, M., 50, 75, 98, 135, 175, 209, 212. 
216, 220, 228, 235, 238, 253, 260, 
283, 300, 323, 344, 388, 404, 420, 421, 
454, 455, 459 
Wilms and Posner, 324 
Windboltz, 296' 
Winiwarter, 64, 481 
Winkler, 152, 257 
Winternitz, M. C. and Smith G. H. and 
Robinson, E. S., 396 
Wirth, 359, 361 
Witzel, 177 
Wohlgemuth, J., 96, 97, 112, 113, 124, 126 
Wolf, 394, 395 
Wolff, 295, 296, 428, 430 
Wolff, A., 22 
Wolff, J., 428 
Wolfler, A., 59 
Wollenburg, 445, 446, 447, 448 
Wossidlo, 296, 303 
Wrede, 435 
Wreden, 306 
Wright, 475 
Wroblewski, 67 
Wunderlich, 298 
Wundt, 434 
Wunschheim, 307 
Wurster, 307, 334 
Wurttenberg and Altburg, 312 
Wurtz, R. and Lendet, R., 74 
Yanase, 362 
Yatsushiro, T., 73 
Zadyier, 292 
Zagari, 6 
Zahn, 118, 472, 473, 474 
Zahn and Chandler, 165 
Zander, 381 
Zangemeister, 288 
Zehnder, 480 
Zeidler, 277 
Zeissl, 314 
Zencker, 20, 29, 393, 435, 437 
Zesas, D. G., 152, 241, 355, 380, 381 
Ziegenspeck, 269 
Ziegler, 156, 161, 445 
Ziehen, 417 
Ziemssen, 25, 29, 474 
Ziesch, 266 
Zietzschmann, 341 
Zigerus, 177 
Zimmermann, 14, 20, 27, T75, 316 
Zollner, 317 
Zondek, 292, 293 
Zuckerkandl, 262, 268, 3r6, 322 
Zuntz, 477 
Zuntz and Tacke, 213 
Zuppinger, and Christen, 431 
Zurhelle, 473 SUBJECT INDEX 
Abdomen, 161; and pain, 173; pendulous, 
183; reflex rigidity, 238; in pneu- 
monia, 239 
Abdominal cavity, see peritoneum, 161; 
sensitivity of its organs, 172; and 
pain, 172; regulation of blood supply 
by omentum, 177; infection and 
omentum, 178; intraabdominal pres- 
sure, 181, 200; enteroptosis, 183; 
hernias, 185; hemorrhage, 233; ab- 
scesses, 238; and bacteria, 240; 
drainage, 244 
Abdominal muscles and abdominal pres- 
sure, 183; and ‘defecation, 208; 
reflex rigidity in peritonitis, 238; 
rigidity in pneumonia, 239 
Abscess, tropical liver a., no; multiple a. 
of liver and thrombophlebitis, 237; 
in abdominal cavity, 238; perinephri- 
tis, 239; abscesses secondary in peri- 
tonitis, 245; appendiceal abscess, 
drainage, 247; secondary pelvic ab- 
scesses, drainage, 254; encapsulation 
of appendiceal abscess, 262; in toxic 
nephritis, 304; paranephritis, 307; 
of brain, 414; tuberculous, 466 
Absorption, absorption fever, 166; and 
temperature, 168; pathological condi- 
tions, 168; absorptive power of peri- 
toneum, 170; from bowel, 192; 
disturbances, 204; ileus, 214; from 
bowel ileus, 221; intestinal of gas, 
225; in ileus, 226; and peritonitis, 
243; danger of irrigation with saline 
solution from increased absorption, 
245; delay by camphor oil, 246; differ- 
ence of indifferent bowel segments, 
266; of bladder, 318 
Acapnia, 377 
Acetabulum and pressure on head of 
femur, 447 
Acetone bodies, 113 
Acholia, 124 
Achylia and diarrhea, 203 
Acid-base equilibrium, 290, 377 
Acidosis, 290, 376 
Acids HC1 and Ptyalin, 5; HC1 secret, 
stomach, 41, 69; amino acids, 96, in; 
nucleic a., 100, 112, 246; fatty acids 
in fat necrosis, 103; uric a., 112; 
bile acids, 124; cholic acid, 130; 
oleic in bone marrow, 392 
Acromegaly and hypophysis, 327; and 
club fingers, 482 
Actinomycosis and enteritis, 205 
Addison’s disease, 350 
Adhesions about liver, 117; protective, 
122; peritoneal, 161; preventatives, 
162; of colon, 210; peritoneal, 247, 
253 
Adrenal gland shock, 230, 297; and Base- 
dow’s disease, 350; and thymus, 352 
Adrenalin, 297; adrenalin symptoms in 
Basedow, 350 
Agglutinins, spleen, 154 
Air embolism, 398; danger of, 394; death 
from, 395; brain death, 395 
Air, pressure in chest cavity, 374; residual 
and complementary, 375; in lungs, 
378; in pneumothorax, 379; intra- 
alveolar, 380; in pleuritis, 385; and 
changes in respiration, 387; Valsalva’s 
pressure test, 387; in pleural cavity, 
390; and divers, 395 
Albumen in spinal fluid, 404 
Albuminuria and tuberc. kidney, 295; 
orthostatic, 297; lordotic, a., 298; 
from slight palpation of kidney, 301; 
permanent after ureteral injury, 303; 
in constipation, 306 
Alkaloids and liver action, 113 
Alkalosis, 291, 377 
Ammonium salts in blood of portal vein, 
112 
Ampula of vater, 126 
Amputation stump and muscle sense, 433 
515 516 
SUBJECT INDEX 
Amylolytic ferment, 97; of bile, 127 
Anaphylaxis, 78; and shock, 229, 474; 
and uremia, 289 
Anasarca, 465 
Anastomosis of renal art. and portal vein, 
117 
Anemia and gastric ulcer, 77; and spleen 
preparations, 150; anemia pernicious, 
129; and splenectomy, 148, 155; 
myelocytes and myeloid transform., 
159; cerebral, 407 
Anerobic organisms, 240 
Anesthesia and salivation, 3; and vomit- 
ing, 46; with chloroform and icterus, 
114; and thymol ymphaticus, 356; 
and cyanosis, 390; chloroform, a. 
and embolism, 391; and lung lesions, 
396; spinal, 404; local anesthesia and 
inflammation, 459 
Aneurysm, 478; arteriovenous, 478; aneu- 
rysmal bruit, 478 
Ankylosis of a limb, partial, 434 
Anoxemia, 377 
Anthrax and duodenal ulcer, 75; and 
thrombophlebitis, 238 
Antibodies and spleen, 153; and peritoni- 
tis, 239, -246; nucleic acid in gyne- 
cology, 246; and bone marrow, 463 
Antipepsin, 70 
Antiperistalsis, 196, 212 
Antitrypsin, 99 
Antrum pylori, 38 
Anuria and jaundice, 131; reflex a., 283, 
295; decapsulation, 291 
Anus, 194-197; sphincter musculature 
and innervation, 201; Houston’s 
folds, 207; spasms, 207; fissure, 207; 
prolapsus, 267 
Aorta, 30 
Apnea, 375 
Apoplexy and meteorism, 216; traumatic 
secondary a. in brain concussion, 
414 
Appendicitis, duodenal ulcers, 74; suppu- 
rat. and liver abscess, 135; omentum, 
179; and cecum, 223, 255; and 
thrombophlebitis, 238; peritonitis, 
238; its flora, 240; and blood agglu- 
tination, 240; early stage, 246; 
appendiceal abscess drainage, 247; 
meso appendicitis, 256; peri-appendi- 
citis, 256; bacterial flora, 256; ulcers, 
257; fecal concretions, 258; causes 
racial and local, 258; perforating a., 
260; chronic appendicitis, 262; treat- 
ment, 263 
Appendix perforation, 238; and pleura in 
direct lymphatic communication, 239; 
gangrene of and putrefactive bac- 
teria, 240; embolic destruction, 257; 
valve of Gerlach, 257; position, 258 
Appetite and gastric stimuli, 80 
Arachnoidea, changes in epilepsy, 4x9 
Arcades, 235 
Arginase, 190 
Arteries of stomach, 71, 46; hepatic, 
no; sup. mesent. 233; coronary 
injuries, 365 
Arteriosclerosis, 73; and gastric ulcer, 77; 
hepatic artery, 117; and cholesterin, 
132; and embolism, 237; and vene- 
section, 294; gnd circulation, 478 
Arteriovenous aneurysms, 478 
Arthritic habitus, 454; arthritis de- 
formans, 445; secondary, 446; and 
neuropathic bone and joint disease, 
459; arthritis suppurative, 463; and 
gonococcus, 464 
Ascaris in liver, 134; in intestinal spasms, 
221 
Ascites and salivation, 6; and stasis 
portal circulation, 120; and peri- 
tonitis, 122; puncture and permanent 
drainage, 123; peritoneum, 170; 
polyserositis, 255; and dyspnea, 
386 
Asialia idiopathic, 6 
Asphyxia, 379; from narrowing of respira- 
tory channels, 389; acute asphyxia, 
389; and cyanosis, 390; artificial 
respiration, 390 
Asthenic constitution, 184 
Asthma, 388 
Atelectasis circumscribed, 385, 391 
Atony of esophagus, 24 
Atrophy acute yellow, 114; of muscles 
from rest, 436; of muscles from 
overstretching, 439; of muscle and 
bone after nerve section, 441 
Auto-digestion, gastric, 68; pancreatic, 
103 
Auto-intoxication, 224 SUBJECT INDEX 
517 
Babies nursing, digestion, 42,190; thymus 
death, 354 
Bacteremia ileus, 227, 244 
Bacteria and gastric ulcer, 74; and 
exudate, 121; and spleen, 153; in- 
testinal, 204; in peritonitis, 239; 
anerobic (toxin formers) 240; infec- 
tion from contaminated food, 242; 
peritonitis phagocytosis, 245; pre- 
dilection for special areas, 257; in 
toxic nephritis, 304; in blood and 
tissues, 305; tuberc. in kidneys, 308; 
in normal lung, 396; and osteomye- 
litis, 461; and thrombosis, 475 
Bacteriolysins, 463 
Bandages, plaster corset, 52; airtight in 
pneumothorax, 384. 
Banti’s disease, 156 
Banti’s disease of infantilism, 157 
Basedow’s disease and spleen, 156, 347; 
War Basedow, 350; and hypophysis, 
350; and growth, 351; and islands of 
Langerhans, 351; and thymus, 353; 
death, 357 
Bauhins valve, 198-221; cecal distension, 
222, 256 
Bile, 58; regurgitation, 58, 1x3; formation 
and secretion, 123; bile acids, 124; 
bile pigments, 124; cholesterin, 124; 
colorless b., 124; quantity, 124; 
absence, 124; stimuli, 125; bile acid 
salts, 125, 127; and digestion, 126; 
amylolytic enzyme, 127; and peristal- 
sis, 127; stasis, 128; pigments absent; 
128; icterus, 130; calculi, 131, 
ascaris, 134; as culture medium, 134; 
osteoporosis, 135; concentration, 
137; white bile, 138; dilution, 139, 
bile periontitis, 139; bile pigments, 
150 
Bile cylinders, 156 
Bile discharge, 126 
Bile ducts, 123; mucin, 124; disinfection, 
124; pressure, 129; ligation, 130; 
calculi, 133, 134; after cholecystec- 
tomy; 136; obstruction, 138 
Bile formation and secretion, 123 
Bile stasis, 128 
Bile thrombi, 129 
Bilharzia, 312 
Biliary calculi, 124-135 
Black and blue marks, hematoidin, 128, 
479 
Bladder, urinary innervation, 176, 3r4; 
omentum, 179; transplanted intes- 
tine, 190; kidneys, 284; extrophy, 
285; in hydronephrosis, 3or; tuber- 
culosis, 308; calculi, 312; bilharzia, 
312; function, 314; innervation, 315; 
centrum, 315; sensitivity, 316; tra- 
beculated, 3x7; automatism, 3x7; 
absorption, 3x8; infection, 318; pol- 
lakisuria, 319; vesical irritation, 319; 
carcinoma, 319; colds, 319; injuries, 
319; regeneration in wounds, 321; 
sphincter action, 321; prostate, 321 
Bleeders, 73 
Bleeding, parenchymatous, 73 
Blood circulation icterus, t28; shock, 229; 
interruption by air embolism, 394; 
obstruction to, 470 
Blood coagulat., 115; destruction of r.b.c. 
icterus, 128; after splenectomy, 148; 
destruction of spleen, r5o; fluidity 
in serous cavities, 168; antithrombin, 
165; fibrinogen, 165; colloids, crystal- 
loids, 167; agglutination in appendix, 
240; blood residual nitrogen, 287; 
H-ion concentration, 29x5 increased 
viscosity in gastric tetany, 361; 
increased acidity, 376; anemic anox- 
emia, anoxic anoxemia, 377 
Blood coagulation, liver, 115; delayed in 
icterus, 130, 162; mesenteric throm- 
bosis, 237; eclampsia, 237; agonal, 
473> crystallization center, 473; 
blood enzymes, 474 
Blood concentration, 286 
Blood distribution respiration, 377, 390; 
changes of position, 390; in Tren- 
delenburg pos., 390 
Blood pressure depression and ligation 
port, vein, 119; foramen of Winslow, 
120; ileus, 224; fall of in shock, 229; 
infection, 248; kidney function, 280; 
in heart lesions, 365 
Blood serum, spleen, 154 
Blood supply, spleen, 154; liver and 
spleen, 156; regulated in abdomen by 
omentum, 177; intestinal distension, 
223; insufficient and intestinal ulcers, 
236; of brain and thyroid, 340; of 518 
SUBJECT INDEX 
Brain pressure, 403-405; choked disk, 410; 
dilatation of pupils, 410 
Brain tumor, 403 
Branchial clefts, 26 
Breathing C02 impoverishment, 229 
Bright’s disease, 280, 293 
Bronchial catarrh, 386; enlarged bron- 
chioles and emphysema, 389 
Bruit aneurysmal, 478 
Burns thrombosis, 473 
Bursae origin trauma, 468 
Buttermilk auto-intoxication, 225 
Cachexia strumipriva, 338 
Calcium balance thymus, 352; para- 
thyroid, 364 
Calculi salivary, 2; biliary obstruction, 
128; biliary, 131; urinary and ureters, 
302; of kidney, 312; vesical, 312 
Callous healing of fractures, 435; marrow 
callous, 435 
Camphor oil in peritonitis, 246 
Caput medusae, 118-122 
Carbon dioxide concentration, 376; im- 
poverishment shock, 229; accumula 
tion and asphyxia, 389 
Carcinoma saliva, 6; of stomach, 60; 
gall bladder, icterus, 128; spleen 
pulp, bone carcinoma, 150; rectum 
and constipation, 207; intestinal, 
212; from vesical irritation, 319; 
of hypophysis, 327; after thyroidec- 
tomy, 360 
Cardia, 21, 22 
Cardiac failure from bacterial toxins, 248 
Cardiospasm, 23, 68 
Carotid gland, 364 
Cartilage from joints and epiphysis 
insensible, 436; necrosis, 445; joint 
mice, 448; cartilage necrosis and 
osteochondritis, 449 
Casein, 190 
Castration, prostatic hypertrophy, 323; 
hypophysis cerebri, 325 
Cataract parathyroid tetany, 360 
Catarrh bronchial, 386 
Cathartics and distended bowel, 195, 202; 
action, 202 
Catheterization, 307; catheter fever, 307 
Cecum, 66; distension, 222; ileocecal 
junction and adhesions, 254; typhia- 
brain, 404-407; of brain and epi- 
lepsy, 419; of bone and cartilage, 446 
Blood transfusion, 474 
Blood vessels of peritoneum, 170 
Bloody vomit, 73, 250 
Bone carcinoma and spleen pulp, 150; 
goiter changes, 352; carotid gland, 364 
Bone fractures, fat emboli, 392; muscle 
tonus, 428; treatment and functional 
result, 432; and extension, 432; 
healing, 435; callous formation, 435 
Bone growth cretinism, 342, 429; repair, 
455 
Bone marrow, 129; splenectomy, 149- 
152; tumors of myelocytes, 150; 
splenic disease, 157; fat emboli, 392; 
callous, 435; antibodies, 463 
Bone tuberculosis, 466 
Bones, 427; fracture, 427; muscles and 
tendons, 428; changes in form, 429; 
functional adaptation, 429; bone 
fracture healing, 435; transplanta- 
tion, 435; pain sensation, 436; 
atrophy, 430; after nerve section, 
441; b. changes and contracture, 444; 
and cartilage, 446; escaping from 
joints, 450; bone formation ab- 
normal, 453; overgrowths, 455; osteo- 
myelitis, 460; necrosis, 463; tuber- 
culosis, 466 
Bradycardia, 358 
Brain abscess, 414 
Brain injury and hypophysis cerebri, 328; 
regulat. of blood supply by thyroid, 
340; death from air embolism, 395; 
brain, 403-426; increase of pressure, 
403; function, 403; circulation, 404- 
407; cerebrospinal fluid, 404; ven- 
tricular dilatation, 405; fracture of 
skull, 407-409; brain pressure and 
choked disk, 410; dilatation of 
pupils, 410; concussion, 410; elastic- 
ity, 4x1; contracoup fracture, 412; 
commotio cerebri, 413; hyperemia, 
413; traumatic secondary apoplexies, 
414; acute inflammation, 414; en- 
cephalitis, 414; prolapsus, 415; men- 
ingitis, 415; epilepsy, 415; trephin- 
ing, 420; operat. surgery, 420; 
spastic paralysis, 422; literature, 
423-426 SUBJECT INDEX 
519 
tony, 264; antiperistalsis, protogenic 
constipation, 209 
Cells, ganglion cells of intestines, 193, 221; 
in anus, 201; in bladder, 314 
Cerebellum, closure of foramen magnum, 
408 
Cerebrospinal fluid, 404 
Chaga’s disease goiter trypanosome, 346 
Chest type, 184; tight lacing and enter- 
op tosis, 184; chest cavity, 372-402; 
gas exchange, 372; pulmonary em- 
physema, 373; respiratory muscles, 
373; diaphragm, 373; tension dif- 
ference, 374; lungs, 375; respirat. 
problems, 377; pulmonary vessels, 
378; exudates, 379; pleural reflex, 
381; enlargement in exudative pleu- 
risy, 385; and pulmonary emphysema, 
386; barrel chest, 387; asthma, 388; 
asphyxia, 390 
Child birth and trauma, 208 
Children and the young, appendicitis, 
262; anal and rectal prolapse, 268; 
pyelitis, 304; myxedema, 342: gastric 
tetany, 360 
Chloroform poisoning liver, 114 
Chlorosis and gastric ulcer, 77 
Cholecystectomy and gastric juice, 41, 
52, 135; and pancreatic secretion, 136 
Cholecystenterostomy, 59, 137 
Cholecystitis lymphadenitis, 102; calcu- 
lous, 128; and pain, 139; and throm- 
bophlebitis, 237 
Cholesterin-calculi, 131 
Cholesterin-content of bile, 113, 124 
Cholic acid poisoning, 130 
Cholin, 338 
Chondrodystrophy and dwarfism, 328 
Chorda tympani, 1-5 
Choroid plexus and spinal fluid, 404 
Chromaffin system, 341; and status 
thymolymphaticus, 356 
Chyle, chyle channels, 113, 126 
Chyme, 40-55; chyme cleavage, 266 
Cicatricization of lung cavity, 383 
Circle viscious, 59; in renal complications, 
304; in respiration, 377 
Circulation stasis of portal, 120; biliary, 
125-128; and disturbances in hernia, 
219; and peritonitis, 244; pulmonary, 
378; capillary and exudates, 379; 
circulatory disturbances due to in- 
creased pressure of r. ventricle, 
382; and brain pressure, 403; circu- 
latory disturbances due to weak 
myocardium, 383; circulation of 
brain, 404; collateral circulation, 476; 
circulatory disturbances due to 
chronic cough, 387 
Club fingers in chronic chest conditions, 
390, 482; peripheral nerve injury, 
390; in cardiac lesions, 482 
Coccyx and anal prolapse, 268 
Cold and pneumonia, 319; colds and 
bladder, 319 
Colitis, 204; pericolitis, 253 
Collagen and bursae, 468 
Colloid chemistry, n; and gall stones, 
131; of bile, 139; in urine, 313 
Colon secretion, 191; and food, 193; and 
motility, 193-197; and defecation, 
200; fermentation, 203; strictures 
congenital gonorrheal, 206; and 
constipation, 209; and adhesions, 
210; kinking of splenic flexure, 211; 
splenic flexure and adhesions, 254; 
stenosis due to gas blocking, 255 
Compression of vessels, 390 
Concussion of brain, 410 
Connective tissue formation, 253; (adhe- 
sions abdominal) in thoracoplasty, 
384 
Consciousness loss of in brain affections, 
403; and brain lesions, 409 
Constipation after gastric operation, 67; 
and splenectomy, 155; chronic, 206; 
proctogenic, 206; and rectal car- 
cinoma, 20,7; constipation muscularis, 
208; and hernia, 208; and cecum, 
209; spastic, 209; and gastric ulcer, 
210; due to pericolitis, 254 
Constriction of limb and venous stasis, 451 
Contortionists and omentum, 180; and 
muscle relaxation, 428 
Contracture muscular and pain, 176, 444; 
its influence on bone changes, 444; 
ischemic, 450; and peripheral nerves, 
45i 
Convulsions uremic, 286; in brain affec- 
tions, 403; in epilepsy, 419 
Corpora cavernosa and suppuration hema- 
togenous, 461 520 
SUBJECT INDEX 
Corpus striatum and operations, 421 
Cough and dyspnea, 380; reflex cough 
from pleura, 381; and circulatory 
changes, 387; in fat embolism, 393 
Courvoisiers sign, 128 
Coxitis, 443 
Cretinism, 342; and myxedema, 342; 
and goiter, 343 
Cryoscopy, 282 
Cryptorchism, 329 
Crystalloids, n; and gall stones, 131; in 
bile, 139; in urine, 313; in spinal 
fluid, 404 
Cyanosis, 382; in emphysema, 387; in 
asphyxia, 390 
Cylindruria, 298; and constipation, 306 
Cystitis, 304; post-operative, 318 
Cystoscopy, 283; in hydronephrosis, 
302 
Cysts echinococcus, m; of hypophysis, 
327; cysts and tumors of brain, 421; 
formation in joints, 468 
Decapsulation of kidney, 291 
Defecation, 197, 200; involuntary, 201; 
tenesmus, 206; muscles, 208; and 
spinal cord, 208; and diaphragm, 209; 
and rectal prolapse, 269 
Deformities from muscular contractures, 
445 
Degeneration fibrinoid, 161; yellow of 
rib cartilages in emphysema, 387 
Deglutition, 13-15 
Diabetes melitus and parotitis, 8; and 
pancreatic extirpation, 98; and liver 
metabolism, hi; and cholesterin, 
132; diabetes insipidus and hypo- 
physeal extract, 328 
Diaphragm esophagus, 23; hernia, 74; 
and peritoneal absorption, 167; in- 
nervation, 176; and intraabdominal 
pressure, 182; hernia, 182; and em- 
physema, 184; defecation, 209; 
spasm, 215; and singultus, 250; chest 
cavity, 373; paralysis, 373~386; 
movements, 374; low position, 382; 
in pleuritis, 385; and dyspnea, 385; 
and emphysema, 386 
Diarrhea and gastroenterostomy, 60; and 
lactose, 191, 202; pathological, 202; 
egg albumen, 204; and ulcers, 205; 
and pneumococcus 244; 
after bowel resection, 265 
Diastatic enzymes of intestines, 191 
Digestion and saliva, 4; and bile, 126; 
intestinal and bile in stomach, 138; 
and spleen, 154; bowel digestion, 
192; and diarrhea, 203; of fat, 266 
Disc choked in brain affections, 403, 410; 
in war wounds, 410 
Divers air embolism, 395 
Diverticuli of esophagus, 25; congenital, 
26; Meckel’s, 257 
Douglas’ cul de sac, 53; and bowel rup- 
ture, 232; pus collection in, 257; 
drainage, 253; in rectal prolapse, 261; 
in children, 268 
Drainage, 251; 253 
Ducts of Stenson, 10; Wharton’s, 10; their 
ligation, 13; of pancreas, 95, 102; 
thoracic, 98; ligation, 244; common 
d., 102; Thoracic and bile, 128 
Duodenum, duodenal cap, 40; ulcers, 40, 
68; fistula, 40; duodenal back flow, 
59; ulcers, 74; from appendicitis, 
from tonsilitis, 75; tubercle bac., 75; 
hunger pain, 78; and bile flow, 126; 
stasis, 137 
Dysentery, tropical, 135 
Dyspepsia, fermentation, 203; intestinal, 
204-224; and appendicitis, 263 
Dysphagia of valsalva, 18 
Dyspnea lusoria, 30; fermentation dysp., 
203; thymus complication, 354; 
and cough, 380; dyspnea and pneu- 
mothorax, 381; and diaphragmatic 
paralysis, 386; and emphysema, 386; 
inspiratory, 389; and goiter, 389 
Dysthyreosis, 348 
Dystrophy adipose genital, 327 
Ecchinococcus cyst, in 
Eck’s fistula and pancreat. necrosis, 105; 
liver activity, no-in; and urine, 
112; chloroform, 113; liver eliminat., 
119 
Eclampsia and blood coagulation, 237; 
convulsions, 286; edema of brain, 
288; hypertension theory, 288; fat 
emboli, 392 
Edema of bowel, 217; and thyreopriva, 
340; edema of brain and eclampsia, SUBJECT INDEX 
521 
288; tendency to, 289; of neck and 
Stock’s collar, 358; and venous stasis, 
451; edema of nephritis, 451; of 
syringomyelia, 481 
Effusions' and tension, 443 
Elbow luxation, 454 
Elephantiasis Arabian and Graecorum, 
481 
Embolism gastric ulcers, 72; bacterial, 74; 
and thrombosis differentiated, 237; 
pulmonary fr. appendicitis, 260; 
pulmonary emboli, its operation, 390; 
retrograde, 391; fat emboli, 392; 
their course, 392; paradox embolism, 
392; air embolism, 394; cerebral, 
407 
Emphysema diaphragm, 184; pulmonary, 
386; and heart, 386; Valsalva’s pres- 
sure test, 387; cyanosis, 387; and 
rib, 387; vicarious, 388; marginal 
emphysema, 389; occupation factors, 
389; from narrowed respiratory 
channels, 389 
Empyema of gall bladder, 186; opened 
empyema and air embolism, 395 
Encephalitis, 414 
Endocarditis and emboli, 392; murmurs, 
478 
Endotoxins in acute osteomyelitis, 462 
Enema and margin current, 194 
Enteritis, 204; and poisons, 204; acute 
enteritis, 205; renal, 205; and bac- 
terial infect, of peritoneum, 242 
Enterokinase, 96, 104, 190 
Enteroptosis and abdominal pressure, 
183; origin, 184; filling of arm, 184; 
chest cavity, 373 
Enterostomy, 225 
Enzymes gastric, 42-69; pancreatic, 9650!' 
liver, no; uricolytic ferments, 112; 
inhibition, 115; amylolytic of bile, 
127; tryptic enzyme in bile, peri- 
tonitis, 139; adhesions, 162; leuco- 
cytes as enzyme carriers, 162; intes- 
tinal, 190; entero kinase, 190; erepsin, 
190; arginase, 190; nuclease, 190; 
lactase, 191; in suppurative peri- 
tonitis, 243 
Epididymitis, tuberc., 311-329 
Epigastrium blunt trauma, 230 
Epiglottis, 16-20 
Epilepsy and edema of brain, 288; tetany, 
363, 415; true and traumatic, 416; 
and poisoning, 418; from bacterial 
toxins, 418; syphilis, 418; following 
puncture of ventricle, 420 
Epiphyseal osteomyelitis, 461 
Epiphyses changes after thymectomy, 
352 
Epityphlitis, 255 
Erepsin, 190 
Ergot-poisoning tetany, 361 
Erosions gastric, 38, 73; uremic, 79 
Esmarck bandage and spina bifida, 460; 
and hyperemia, 477 
Esophagus care, and salivation, 2-13; 
innervation, 19-44; deglutition, 21; 
narrowing, 22; sphincter, 22; and 
cardiospasm, 23; paralysis, 24; atony, 
25; diverticula, 25; disturbances, 27; 
organic stenosis, 27; perforation, 28; 
scarlet fever, 28; ulcers, 28; esophago- 
malacia, 29; rupture, 29; esophago- 
tomy, 30; dysphagia, 30; esophageal 
stenosis and gastrostomy, 80; litera- 
ture of saliv. glands and esoph., 30- 
35; esophageal varices fr. cirrhosis 
of liver, 122 
Ether, 2, 3; and saliva, 2; in peritonitis, 
473 
Eunuch, 325; and geroderma, 327 
Exhaustion and nerve shock, 229 
Exner’s needle reflex and intestinal 
contractions, 194 
Exophthalmic goiter, 347; nervous signs, 
349; and adrenalin, 350; differentia- 
tion, 353 
Exostosis and esophag. ulcers, 28 
Extension and bone fracture, 432 
Extremities, 427-492 
Extrophy of bladder, 285; and pain, 316 
Exudates, transudates, ascites, 121; and 
chest cavity, 379; in pleuritis, 385 
Eyes from ectodermic cells, 457 
Fasting and nitrogen loss, 1x4 
Fat absorption, 113, 126, 266; in yessels 
saponified, 393 
Fat embolism, 126, 392; in eclampsia, 392; 
in greater and in lesser circulation, 
393 
Fat necrosis, 102 522 
SUBJECT INDEX 
Fat synthesis, 193 
Fatigue and partial paralysis, 434 
Fecal fistula and skin irritation, 191; 
action of fistula, 221; and tamponade, 
f*1 , . 
Fecal impaction, 219 
Fecal obstruction, 209 
Fecal retention incarcerat., 217; fecal 
stasis, 210; ileus, 212-219; fecal 
toxicity, 225 
Fecal vomiting, 212 
Feces acholic, 124-128; decomposition, 
126; bile stained with icterus, 128; 
composition, 191; starvation, 192; 
quantity, 192; involuntary evacua- 
tion, 201 
Fermentation dyspepsia, 203 
Ferments, lab ferment, 41; uricolytic, 112; 
of thymus, 353; tryptic of poly- 
morph leucos., 466; in synovial 
fluid, 468 
Fibrinogen, 115, 165 
Fibrinuria, 314 
Filaria, Bancroft’s and Arabian ele- 
phantiasis, 481 
Fingers, club fingers, 390, 482; webbed 
fingers, 416; polydactylism, 416 
Fissure in ano, 207; and intest, spasms, 
222 
Fistula salivary, 1-13; from neck to 
stomach, 21; pancreatic, 96; gall blad- 
der, 101, 124, 135; Eck’s, see there, 
intestinal, 190; discharge, 203; intes- 
tinal in surgery, 221; tuberculous 
and difficult healing, 466 
Flat foot leading to atrophy of leg mus- 
cles, 439; contractures, 443 
Food defective evacuation, 51; and bowel 
absorption, 193 
Foramen of Winslow and blood pressure, 
120; foramen ovale and emboli, 392; 
f. of Magendi’s, 405; foramen mag- 
num, 408 
Foreign bodies, see calculi, in fracture of 
skull, 411 
Fracture of skull, 407-409; and foreign 
bodies, 411; of bones, 427; of patella, 
431; treatment and functional result, 
432; of bone and rest position, 432; 
of metastarsals, 444 
Furunculosis, 304 
Gall bladder, galactose, x 11; and liver, i io; 
cholecystenterostomy, 59, 137; and 
chr. pancreatitis, 101; and lympha- 
dentitis, 102; and bile, 123; cho- 
lesterin, 124; movements • and its 
innervation, 126; and icterus, 128; 
shrunken, 128; and pancreatic tum- 
ors, 128; Courvoisier’s sign, 128; 
hydrops., 129, 133, 138; gall Stones, 
124, 131; and surgery, 135; chole- 
cystectomy, 135; function of, 185; 
Oddi’s sphincter, 102, 105, 136; 
enlargement of stump after removal, 
136; and bile concentration, 137; bile 
peritonitis, 139; rupture, 140, 240; 
literature of liver and gall bladder, 
141-147; gall bladder operations 
and omentum, 180; cholelithiasis 
and meteorism, 215; and peritonitis; 
240 
Gall stones, 124-131; gall stone colic, 133; 
and diet, 134; and surgery, 135 
Ganglion, Jackson’s, 5; Gasserian, 14; of 
cardia, 24; intragastric, 41 
Gangrene and ileus, 215; and hernia, 219; 
and retrograde incarceration, 220; 
after bowel injury, 233; from cold, 
473 
Gas exchange, absence in pneumothorax, 
358, 372; decrease and resection of 
spinal cord, 422 
Gastric crises, 49 
Gastric diseases, 495 
Gastric juice, 41, 47, 61; and splenectomy, 
i54 
Gastric mucus and antienzyme, 62 
Gastric resection, 642 
Gastric secretion, 39 
Gastric ulcer pain irrad., 47; and trypsin, 
59, 61, 68, 71; and arteriosclerosis, 77; 
and chlorosis, 77; reflex ischemia, 79; 
and constipation, 209 
Gastric wounds, 63 
Gastrin, 42, 96 
Gastritis, 48 
Gastroduodenostomy, 56 
Gastroenterostomy, 54, 55; and diarrhea, 
60; and healing of gastric ulcer, 79 
Gastrointestinal inflammation and throm- 
bophlebitis; 238 
Gastrointestinal innervation, 44 SUBJECT INDEX 
523 
Gastroptosis of Glenard, 53, 79 
Gastrostomy, 80 
Genitalia female and peritonitis, 240; 
pneumococcus peritonitis, 242; and 
cystitis, 318; and thyreopriva, 340; 
generative glands and thymus, 352 
Genu valgum, 447 
Geroderma, 326 
Giantism and hypophysis, 327, 482 
Glands, endocrine and exophthalmus, 350; 
and thymus, 352 
Glands, salivary, 1; salivary and sexual 
glands, 7; literature, 30; digestive, 
39; Brunners, 58; emptying action, 
125; lymph glands and splenectomy, 
149; parotid gland, 257; pineal, 326; 
hypophysis cerebri, 326; endocrine 
glands in exophthalmus, 350 
Glaucoma of kidney, 292 
Glottis and inspiration, 182, 187 
Glycogen, 111; decrease, 130 
Glycosuria, 98; in exophthalmus, 350 
Goiter, 20, 338; and cretinism, 343; 
cause, 343; distribution, 344; due to 
a Brazilian trypanosome, 346; ex- 
ophthalmic, 347; and thymus, 353; 
death, 357; and respiratory diffi- 
culty, 389 
Gonorrhea strictures of colon, 206; and 
occlusion of efferent ducts, 330; and 
suppurative arthritis, 464 
Gout, renal and true, 112; urine in gout, 
313; and arthritis deformans, 448 
Grafe’s sign, 349 
Harelip, 18 
Head lesions, 407, 409, 414, 420 
Healing of aseptic operative incisions, 454 
Heart, 364-366; heart failure, 224; 
cardiac disease and embolism, 237; 
surgery, 364; bundle of Hiss, 365; 
pericardial hemorrhage, 365; in- 
juries to coronary arteries, 365; peri- 
carditis, 366; blunt force, 366; dilat. 
r. ventricle and dyspnea, 380; pleura 
reflex, 380; heart condition and 
cyanosis, 382; myocardial weakness 
and circulatory disturbance, 383; 
and emphysema, 386; heart action 
in acute asphyxia, 389; and air 
embolism, 394; heart sounds, 479 
Hematemesis and gastric ulcer, 72; and 
peritonitis, 250 
Hematoidin, 128 
Hematoma, icterus, 129 
Hemoglobin iron free, 129; regenerat. after 
splenectomy, 148 
Hemolymph nodes, 151 
Hemolysins in osteomyelitis, 463 
Hemolytic diseases, 157 
Hemorrhage in serous cavities, 163; mas- 
sive in kidney bed, 298; and brain 
concussion, 414 
Hemothorax, 163 
Hepatitis, see liver 
Hepato-cholangio-enterostomy, 138 
Hernia and omentum, 181; diaphragma- 
tic, 182; development, 185; umbilical, 
186; and constipation, 208; meteor- 
ism, 216; incarcerated, 218; rupture, 
232; reduction of, leading to trauma 
of intestines, 233; strangulation, 237; 
and peritonitis, 241; sliding hernia, 
269; perineal hernia, 269; scrotal, 
329 
Hirschsprung’s disease, 207 
Hormones gastric, 41; pancreatic, 98; and 
splenectomy, 152-155; and renal 
stimuli, 282 
Houston’s folds, 207 
Hunger mechanism, 48; and gastric 
operat., 66,78 
Hydrocephalus, 403; and spinal fluid, 405 
Hydrogen ion concentration saliva, 2; in 
renal conditions, 290; of blood, 376 
Hydronephrosis cause of death, 287, 291, 
300 
Hydrops of gall bladder etc., 129-138 
Hydrothorax and salivation, 6 
Hygroma, 468 
Hyoid bone, 16, x8 
Hyperemia of relaxation, 183, 234 
Hyperesthesia and brain lesions, 175 
Hyperglycemia, 98 
Hypernephroma, 297 
Hyperpnea, 377 
Hyperthyroidism, 346 
Hypophysis cerebri castration, 325; physi- 
ology, 326; action, 327; acrome- 
galy, 327; menopause, 327; adipose 
genital dystrophy, 327; tumors, of 
327; obesity, 327; extracts in treat- 524 
SUBJECT INDEX 
ment, 228; enlargement after total 
thyroidectomy, 341; Basedow, 350 
Hypospadias hydronephrosis, 301 
Icterus galactose, in; following chloro- 
form anesthesia, 114; bile flow, 128; 
obstruction, 128; hemolytic or toxe- 
mic icterus, 128; Kupfer’s star cells, 
129 ;*catarrhal, familial, neonat., 129; 
hematoma, 129; results of icterus, 
130; delayed coagul. of blood, 130; 
subarachnoid fluid, 405 
Ileocecal junction and adhesions, 254 
Ileocolic muscle, 198 
Ileum, 42, 45, 61, 191; invagination, 199; 
weakness, 203; resection, 265 
Ileus arteriomesenteric, 51; abdomin. 
pressure, 183; rectal carcinoma, 207; 
chr. intestinal intoxicat., 212; pain, 
212; dynamic, obturation ileus, 212; 
paralysis of bowel, 214; retrograde 
incarceration, 220; invagination, 220; 
paralytic ileus, 221; spastic, 221; 
due to lead, 221; ascaris ileus, 222; 
distension, 223; auto-intoxication, 
225; enterostomy, 226; bacteremia, 
227; acute pancreatitis, 228; in- 
testinal noises, 228; and peritonitis, 
249; necrosis of kidney, 306 
Iliac fossa and intestinal trauma, 230 
Immunization, 246 
Inactivity muscular atrophy, 436 
Incarceration elastic, 216; fecal, 217; 
relaxed inc., 219; retrograde, 220- 
237; renal, 300 
Infarcts red. liver, 118; hemorrhagic, 234; 
anemic infarction, 234 
Infection omentum, 178; direct hemato- 
genous, 257; of kidneys, 305; tetany, 
361 
Innervation of salivary glands, 1; of 
tongue, 13; esophagus, 19; stomach, 
41; pancreas, 95; of hepat. vessels, 
125; gall bladder movements, 126; 
intestinal bacteria, 176; bladder, 
176, 314; diaphragm, 176; intestines, 
198; of distal end of intestines, 201; 
anus, 201; crossed, 315 
Intestinal absorption of food, 193 
Intestinal catarrh, 203 
Intestinal contents toxicity, 225 
Intestinal fistula, 190 
Intestinal gases, 213 
Intestinal infarct, 234 
Intestinal juices regurgitation, 59, 190; 
secretion, 191 
Intestinal tract innervation, 176 
Intestinal ulcers, 61 
Intestinal wall, 55 
Intestines, law of, 44; strength, 45; opera- 
tion sutures, 55; intestinal juice 
regurgitation, 59, 172; intestinal 
mucosa, 62; bile, 123; fecal decom- 
position, 126; jaundice, 128; sensi- 
tivity operations, omentum, 180; 
enteroptosis, 184, 190; length, 190; 
transplantation, 190; secretions, 190; 
enzymes, 190; lactase, diarrhea, 191; 
secretory stimuli, 191; paralytic secre- 
tion, 191; pancreas, 191; hormonal 
stimuli, 191; feces, 191; sensitive 
bowel, 192; absorption, 192; food, 193; 
in test, movements, 193; mixing move- 
ments, 193; marginal current, 194; 
peristaltic wave, 195; cathartics, 195; 
rolling movement, 195; anti-peristal- 
sis, 196; motion, its nerve supply, 
198; sphincters, 198; invagination, 
199; defecation, 200; anal innervation, 
202; diarrhea, 202; bowel weakness, 
203; enteritis, 204; poisoning, 204; 
chronic inflammation, 205; ulcer, 
205; tenesmus, 206; chronic constipa- 
tion, 206; rectal carcinoma, 207; 
anal fissure, 207; covered sensitivity, 
208; constipation surg. of colon, 211; 
intestinal intoxication, 212; ileus, 212; 
paralysis of bowel, 214, 249; meteor- 
ism, 215; trauma, 216; incarceration, 
216; edema, 217; hernia, 218; paralyt. 
ileus, 221; evacuation before surgery, 
221; lead colic, 221; ascaris ileus, 222; 
tabetic crises, 222; stercoreal ulcers, 
223, 231; auto-intoxication, 225; ileus 
intestinal noises, 228; manipulation 
of, 1; shock, 228; blunt trauma, 230; 
rupture, 231; injury from reducing a 
hernia, 233; gangrene o.f, 235; ulcers, 
236; stenosis, 236; peritonitis, 238; 
chr. peritonitis, 250; resection, 263; 
chyme cleavage, 266; fat digestion, 
266; literature, 269-278; permea- SUBJECT INDEX 
525 
bility of walls to bacteria, 286; renal 
disease, 305 
Intestines, large, secretion, 191; sigmoid 
flexure, 193; movements, 197; defeca- 
tion, 197; constipat., 206; surgery, 
211; vascular supply, 236; pericolitis, 
253; typhlatony, 264; rectal pro- 
lapse, 267; sliding hernia, 269; 
perineal hernia, 269 
Intoxication intestinal, 225 
Intraabdominal pressure, 181; and defe- 
cation, 200 
Intussusception, 198-220 1 
Invagination of bowel ileocecal, 198-220 
Iodine Basedow, 347' 
Iodothyreoglobulin, 338, 363 
Iodothyrin, 338, 348 
Iron content of food, blood regeneration 
148 
Iron metabolism splenectomy, 149, 152; 
Band’s disease, 137 
Ischemic contracture, 450 
Jaundice obstr. galactose, hi, 128; toxic, 
130; anuria, 131; spleen, 156 
Jejunum, 53; prosecretin, 57; ulcers, 62- 
68; food, 193; tearing of, 232; resec- 
tion, 265 
Joint capsule muscle tonus, 428; joint 
cartilage insensibility, 436; shrinkage, 
442; joint mice and arthritis defor- 
mans, 450; to prevent refilling and 
shrinking, 466 
Joints, 427; muscle tonus, 428; muscle, 
equilibrium, 432; joint mice, 436, 
448; joint disease, 438; stiffening and 
contracture, 441; air mobilization. 
442; rheumatism, 442; arthritis 
deformans, 445; joint movements, 
447; osteochondritis dissecans, 449; 
infection in suppurat. arthritis, 464; 
destruction of, 465; artificial mo- 
bilization, 467; formation of 467; 
synovia, 468; resection, 469; trans- 
plantation, 469 
Keloid formation, 453 
Kidney hyperglycemia, 98; and peritoneal 
absorption, 167; renal calculi meteor- 
ism, 215; gunshot wounds, perineph- 
ritic abscess mistaken for peritonitis, 
239; inflamm., 257; bladder, male 
genitalia, hypophysis, 279-337; uni- 
lateral renal disease, 279; threshold, 
279; microscopic function, 279; reab- 
sorption, 280; functional tests, 280; 
Bright’s disease, 280-293; nephritis, 
281; polyuria, 281; nerve supply, 
282; salt puncture, 282; hormones, 
282; pain, 283; reflex anuria, 283; 
cystoscopy, 283; normal secretion, 
283; polyuria, 284; pollacissuria, 284; 
tubercul. nephritis, 284; retention, 
285; uremia, 286; concentration, 
286; kidney wasting, 287; para- 
biotic tests, 287; eclampsia, 287; 
acid base equilibrium, 290; acido- 
sis, 290; H-ion concentration, 290; 
alkalosis, 291; decapsulation, 291; 
renal insufficiency, 291; uranium, sub- 
limate poisoning, 292; glaucoma of 
kidney, 292; transplantation, 293; 
relations between the two kidneys, 
294; blunt injury, 295; healing of 
wounds, 295; and adrenals, 297; mas- 
sive hemorrhage in kidney bed, 298; 
floating kidney, 298; fixation of 
kidney, 299; Dietl’s crises, 300; tor- 
sion, 300; pelvis, pain, 300; hydron- 
ephrosis, 301; dilatation of pelvis, 303; 
pyonephrosis, 304; toxic nephritis, 
304; infections, colon bacilli, 305; 
relat. of kidney to bowel, 305; necro- 
sis of kidney, ileus, 306; paraneph- 
ritic abscess, 307; tuberculosis, 308; 
calculi, 312; literature for kidney, 
bladder, male genit. hypophysis, 330- 
337 
Knee joint contracture, 444 
Kupfer’s star cells, 129, 151 
Kyphosis respiration, 388 
Lacing, enteroptosis, 184; renal ptosis, 299 
Lactase diarrhea, 191 
Langerhan’s islands and diabetes, 99; 
Basedow’s disease, 351 
Laparotomy scars, bone formation, 453 
Larynx, 16 
Lead colic, 207, 221 
Lecithin fat synthesis, 193 
Leg ulcers varicose veins, 475; nervous 
origin, 476; nerve stretching, 476 526 
SUBJECT INDEX 
Leg wounds difficult healing, 470; lepra, 
elephantiasis graecorum, 481 
Leukocytosis phagocytosis in peritonitis, 
245; in appendicitis, 260; in spinal 
fluid, 404; phagocytosis in suppura- 
tive arthritis, 465; lymphatic in 
tuberculosis, 466 
Leukourobilin, 124 
Ligamenta varioforma, 210 
Ligamentum hepato duodenal venous 
dilat., 118; hemorrh. of liver, 120; 
phrenico-colic, 254 
Ligation of hepatic art., 117; portal vein, 
118 
Lipase, 41, 97 
Liver, no; thrombosis in after ligation of 
omentum, 72; physiology, no; tropi- 
cal abscess, no, 135; cirrhosis, no; 
independence of lobes, no; regenera- 
tive power, no; echinococcus cysts, 
in; carbohydrate metabolism, in; 
glycogen, in; galactose, in; purin, 
nucleoprotein metabolism, 112; urico- 
lytic ferments, 112; fat absorption, 
113; acetone bodies, 113; detoxifying 
property, 113; phosphorus poisoning, 
113; chloroform poisoning, central 
necroses, 113; trypsin, 114; acute 
yellow atrophy, 114; protein sparing, 
115; repair, 115; blood coagulation, 
115; antithrombin, 115; surgery, 
115; ligat. and anastomoses of 
vessel, in; red infarcts, 118; caput 
medusse, 118, 122; closure portal 
vein, 118; Eck fistula, 119; obstruct, 
hep. vein, 119; checking of hemor- 
rhage, 119; ascites, stasis port, 
circul., 120, 170; cirrhosis, 121; 
splenic tumor, 121; Talma’s operat., 
122; esoph. varices, 122; permanent 
drainage, 123; bile formation, secre- 
tion, 123; bile acids, 124; cholesterin, 
124; acholic stools, 124; white bile, 
124; curve of secret., 125; biliary 
circulation, 125; icterus, 128; Kup- 
fer’s star cells, 129, 151; hepatic 
insufficiency, 130; hematogenous in- 
fection, 135; suppur. appendicitis, 
135; injuries, 140; literature, 141- 
147; liver and spleen, 150-152; 
bile cylinders, 156; omentum, 178; 
thrombophlebi tis, 23 7; Pick’s pseudo- 
cirrhosis, 255; Zuckergussleber, 255 
Local anesthesia and inflammation, 459 
Lordosis, 53, 298 
Lumbar anesthesia, 404 
Lumbar puncture uremia, 288 
Lung paranephritic abscess, 307; oscilla- 
tion, 358; expansion, wounds in 
heart, 365; elasticity, 373; collapsed 
1., 375. 384; lung activity, body 
position, 375; respiratory movements, 
375; respiratory center, 375; respira- 
tory innervation, 375; CO2 content of 
venous blood as respiratory stimu- 
lant, 375; apnea, 376; H-ion con- 
centration, 376; pulmonary circula- 
tion, 378; pneumothorax, 379; intra- 
alveolar pressure, 380; pneumo- 
thorax, 381; dyspnea, 381; pendulum 
air, 382; cyanoses, 382; increased, 
decreased pressure, 383; pleuritis, 
383; closed pneumothorax, 383; 
thoracoplasty, 383; paradox respira- 
tion, 380; obliteration of cavity in 
pneumothorax, 384; redistension of 
hilus, 385; exudative pleuritis, 385; 
atelectasis, 385; diaphragmatic par- 
alysis, 386; pulmonary emphysema, 
386; bronchitis, 386; emphysema, 387; 
changes in thoracic cavity, kyphosis 
etc., 388; enlargement due to dy- 
namic causes, 388; asphyxia, 389; 
artificial respiration, 390; pulmonary 
emboli, 390; air emboli, 393; post- 
operative lung complications, pneu- 
monia, 395; from anesthesia, 396; 
bacteria in 1., 396; war gases, 396; 
hemorrhages, 397; edema, 397; trau- 
ma, 398; literature, 398-402 
Luxation of elbow, 454 
Lymph, colloids, 167 
Lymph glands, spleen, 149-152; of omen- 
tum, 178; mesenteric bacilli, 305; 
enlargements and status thymo- 
lymphaticus, 355 
Lymph vessels of omentum, 179; col- 
lapsed lung, 384; of lung, 396; flow of 
lymph, 480; regeneration, 480; tuber- 
culosis, syphilis, 481 
Lymphadenitis, 102 
Lymphangitis, 102 SUBJECT INDEX 
527 
Lymphatic diseases, stasis, elephantiasis, 
481 
Lymphatic edema, 481 
Mediastinal palpitation, 358 
Mediastinum compression, 357; emphy- 
sema, 358; tumors, 358; lymph 
channels, 358; kinking, 382; oscilla- 
tions, 383; after pneumothorax, 385; 
in pleuritis, 385 
Medulla oblongata deglutition center, 20; 
vomiting center, 45; paralysis of 
vaso-motor center by bacterial tox- 
ins, 248; respiratory center, 375; 
increased pressure, 403, 409; brain 
concussion, 443; in epilepsy, 417 
Meningitis sacculcated, 404, 415; menin- 
gitis serosa, 415 
Menopause hypophysis, 327 
Mercury poisoning enteritis, 204; renal 
activity, 292 
Mesenteric veins kinking, 219 
Mesenteric vessels kinking, 219; injury 
from pressure, 233; aneurysm, 237 
Mesentery, 233; tears, 236 
Mesocolon ligat. of veins in thrombophle- 
bitis, 238 
Metabolism of carbohydrates, 98; fat, 99; 
protein, 100; and liver, no; cellular, 
ascites, 121; cholecystectomy, 136; 
iron metabolism, 149, 152, 157; 
spleen, 154; disturbances from resec- 
tion of bowel, 265; thyroid, 340; 
thymus gland, 351; calcium metab- 
olism, 352, 448 
Metastasis, tumor spleen, 154 
Meteorism splenectomy, 155; ileus, 2x2; 
differentiation, 213; diaphragm, 215; 
nerve involvement, 215; abdominal 
tumors, 215; renal and biliary calculi, 
215; hysteria, 216; tabes, 216; in 
apoplexy, 216; after blunt trauma, 
216; localized Bauhin’s valve, 222; 
solar plexus, 249 
Milk digestibility for adults, 191 
Momburg’s belt compression of vessels, 
39i 
Momburg’s tube, 233 
Mouth hygiene, 4; wounds, 4 
Murmurs of endocarditis, 478; venous 
murmur, 479; arterial, 479 
Murphy button, 55, 63 
Muscles of tongue, 15; orbicularis, 18; of 
deglutition, 19; of defecation, 208; 
427; fracture of bones, 428; tension, 
428; muscle tonus, 428; contortion- 
ists, 428; muscle anlagen, 429; form 
of muscle and skeleton, 429; develop- 
ment, 429; muscle fibers, 430; 
muscles of spine of sea urchin, 430; 
threshold of muscle tension, 430; 
nerves in muscle, 430; peripheral 
stimuli, 430; injury, 430; atrophy, 
431; deformity, 431; muscle equilib- 
rium, 432; paralysis, 432; muscle 
sense, 432; deep sensations, 433; 
muscle transplantation, 434; learn- 
ing a new function, 434; regeneration, 
43 5; size and strength, 437; endur- 
ance muscle, 437; atrophy from 
overwork, 437; internal and external 
work, 438; joint disease, 438; kinetic 
chains, 440; atrophy after nerve 
section, 441; ischemic contracture, 
451; venous stasis, torticollis 452; 
myositis ossificans, 453; traumatic, 
454; neurotisation, 456 
Myasthenia, parathyroid, 362 
Myelocytes spleen, 150 
Myositis, ossificans, 453; traumatic, 454 
Myotonia and parathyroids, 362 
Myxedema, 338, 340; in adults, 341; 
cretinism, 342 
Necrosis, focal after omental thrombosis, 
72; pancreatic, 102; central of 
liver, 113 
Nephrectomy, 294 
Nephritis, 9; enteritis, 205, 284; tuber- 
culous, 284; eclampsia, 286; acute 
and eyeground, 288; decapsulation, 
292; from floating kidney, 301; 
toxic, 304; suppurative, 304; edema, 
45i 
Nephrolysins, 287 
Nerve degeneration, 456 
Nerve disease bone overgrowths, 455 
Nerve injury peripheral and club fingers, 
390; brain pressure, 403; healing, 
456; pain, 458 
Nerve resection muscular atrophy, 441; 
neuroma, 456 528 
SUBJECT INDEX 
Osteochondritis dissicans, 449 
Osteomalacia parathyroids, 362; muscle 
contracture, 445 
Osteomyelitis, 460; infection, 461; causes, 
463; hemolysins, 463 
Osteoporosis, absence of bile, 124, 135 
Ovariotomy and parotitis, 9 
Oxamid calculi, 314 
Oxygen, 376; respiration, 376 
Pacchionian bodies and spinal fluid, 405 
Pacinian corpuscles, 4; pleura, 380 
Pain in gastric ulcer, 47, 174; in chole- 
lithiasis, 139; in subcutaneous hemor- 
rhage, 166; intestines, 173; in ulcera 
tive processes, 174; muscul. con- 
traction, 175; enteroptosis, 185; in 
anus, 207; abdominal and ileus, 212; 
appendicitis, 223; anesthesia, 229; 
in peritonitis appendiceal, 260; in 
renal affections, 283; in renal ptosis, 
300; in urethra, 315; pleura, 380; 
muscle sense, 432; bone, 436; nerve 
injury, 458 
Palate and taste, 14; cleft, 18 
Palpation slight of kidney and albuminu- 
ria, 301 
Pancreas, 95; enzymes, 57; secretion and 
secretin, 57, 96; function, 95; ducts, 
95; innervation, 95; secretin and 
gastrin, 96; stimuli, 96; juige, 96; 
fistula, '96; lipase, 97; trypsin, 97, 
amylase, 97; nuclease, 97; steapsin; 
102; extirpation, 98; diabetes, 98; 
pancr. hormone, 98; islands of 
Langerhans, 99; ligation of ducts, 99; 
internal secretion, 100; chronic pan- 
creatitis, 101; lymphangitis, 102; 
bile, 102; pancr. necrosis, 102-105; 
intravital self digestion, 103; entero- 
kinase, 96, 104; sphincter of Oddi, 
102-105; literature, 106-109; bile, 
127; pancreat. secretion and cho- 
lecystectomy, 136; and intestinal 
secretion, 191; acute and ileus, 228; 
superior mesent. vein, 235; islands of 
Langerhans in Basedow’s disease, 351 
Papilla of Vater, 57; innervation, 126; 
Oddi’s sphincter, 102, 105, 136, 140 
Paracentesis for exudative pleuritis, 385 
Paradox embolism, 392 
Nerve severance, 456 
Nerve stretching of motor nerves, 457; 
neuralgia, 458; neurolysis, 459; neuro- 
kynese, 459; and freezing of nerve, 458 
Nerves of salivary glands, 1; of tongue, 13; 
of esophagus, 19; stomach, 41; pan- 
creas, 94; hepatic vessels, 125; gall 
bladder, 126; of peritoneum, 171; 
intestinal tract, 176; bladder, 176; 
diaphragm, 176; splanchnic in gastr. 
innervation, 44; vagus in gastr. 
innervation, 44; sympathetic, 44; 
pain, 174; constipation, 209; in 
respiration, 376; nutritive stimulus, 
376; muscle tonus, 430; paralysis, 
432; transplantation, 452,457; anas- 
tomosis, 457; trophic and muscular 
atrophy, 459 
Neuralgia, 458 
Neurasthenia and auto-intoxication and 
sphincter tonus, 207 
Neuritis, 458 
Neuroma, 456; prevention of, 456 
Neuropathic arthritis, 459 
Neurotization, 456 
Nitrogen renal elimination, 285; residual, 
286 
Nuclease, 97, 190 
Obesity, hypophysis cerebri, 327 
Obstruction of flow of bile, 128; see also 
under ileus. 
Occupation tetany, 361 
Omentum resection and gastric ulcer, 72; 
resection and vomiting, 148; ab- 
sorption, 168; gastr. ulcer pain, 174; 
greater function, 176; liver necroses, 
177; regulator of abdom. blood 
supply, 177; protective function, 177; 
lymph nodules, 178; foreign bodies, 
178; wounds, 179; gall bladder 
operations, 180; its removal, 181; 
torsion, 181; strangulation, 215; 
in decapsulation of kidney, 292 
Oral cavity, 1 
Orchitis tuberculous, 312 
Osmosis of intestinal wall, 192; renal 
activity, 288 
Ossification cretinism, 340; thymus endo- 
chondral, 352; osteoarthropathy of 
Pierre Marie, 482 SUBJECT INDEX 
529 
Paradox respiration, 359, 383 
Paralysis of tongue, 17; of esophagus, 24; 
ileus, 51; bulbar p., 20; in strangula- 
tion ileus, 214; reflex p., 216; of 
bowel in hernia, 219; intestinal and 
peritonitis, 249; diaphragm, 386; 
respiratory, brain affection, 403; 
spastic, 422; infantile p., nerve trans- 
plantation, 457; of a limb and pain, 
458 
Paraplegia, 421 
Parasites, echinococcus cysts in liver, hi; 
ascaris in liver, 134; ascaris ileus, 222 
Parathyroids, 341, 359; tetany, 359; 
Chvostek’s phenomenon, 359; ac- 
cessory p., 360; trophic disturbances, 
360; latent tetany, 360; epilepsy, 362; 
myotonia, 362; myasthenia, 362; 
detoxifying action, 363; transplan- 
tation, 363; calcium metabolism, 364 
Parotid gland, 1; inflammat., 257 
Parotitis, 8; saliva, 7; and diabetes, 8; 
post-operative suppurative, 8; orchi- 
tis, 9; ovariotomy, 9; Stenson’s duct, 
10; Wharton’s duct, 10 
Passavant’s cushion, 16 
Patella fracture, 431 
Pellagra veins, 472 
Pelvis renal, 303; infection, 304; tuberc., 
3°9 
Pendulum, air, 382 
Pepsin, 52, 57; after splenectomy, 154 
Peptids, splitting of food, 192 
Perforation peritonitis, 240; of stomach 
difference whether by ulcer or 
carcinoma, 241 
Pericarditis, 365 
Pericardium, 162; hemorrhage, 365 
Pericolitis, 253; pneumonia, 254; cause of 
constipation, 254 
Perihepatitis, 255 
Perinephritic abscess, 239 
Periosteum bone transplantation, 435; 
pain, 436; myositis ossificans, 454 
Periostitis, occupational, 454 
Peristalsis of esophagus, 21; gastric, 37; 
stimul. by bile, 127; absorption, 169; 
reverse p., 45; omentum, 176; ab- 
domin. pressure, 182; hernial loops, 
216; of ureters, 302; in vas deferens, 
311 
Peritoneal shock, 166; resistance, 185 
Peritoneum infection, gastr. ulcer, 72, 
161; embryology, 161; anatomy, 161; 
function, 161; adhesions, 161; en- 
capsulation of foreign bodies, 162; 
similarities of diff. serosa, 163; 
hemorrhage, 163; shock, 166; total 
surface, 166; process of absorption 
and exudation, 166, 178; and urine, 
167; colloids and crystalloids, 167; 
diaphragm, absorption, 168; omen- 
tum, 168; absorption and heat and 
cold, 168; peritonitis, 169, 238; 
eventration, 170; blood vessels, 170; 
lymphatics, 170; vegetative nervous 
system, 171; sensitivity, 172; pain, 
173; ulcerative processes, pain, 174; 
diaphragm, 176; omentum, 176; in- 
traabdominal pressure, 181; dia- 
phragm. hernia, 182; tumors, 183; 
enteroptosis, 183; hernias, 165; peri- 
tonitis, 186; literature, 186-189; peri- 
tonitis, 238; parietal perit. and reflex 
action, 239; resistance of, 241, 247; 
difference of absorption power be- 
tween parietal and visceral p., 245; 
bactericidal property, 246; peritoneal 
irritation, 248; polyserositis, 255 
Peritonitis, 238; resistance of bowel, 55; 
Murphy button, 55; ascites, 122; 
bile peritonitis, 139; and food, 169; 
post-operative preventatives for, 170; 
abdominal adhesions, 210; ileus, 213; 
paralytic ileus, 221; bowel contents, 
221; cecal distention, 222; absorption, 
226; fr. trauma to bowels, 233; 
nerve involvement, 238; bacterial p., 
239; gangrenous p., 240; chronic p., 
240; streptococcus p., 240; pneumo- 
coccus p., 242; suppurative p., 243; 
course of the disease, 244, 245; danger 
of saline solution, 245; secondary 
abscesses, 245; phagocytosis, 245; 
leukocytosis, 247; death from p., 248; 
intestinal paralysis, 249; singultus 
and vomiting, 250; hematemesis, 250; 
drainage, 251; tamponade, 251; op- 
erations, 252; chronic p., 253; adhe- 
sions, 254; polyserositis, 255; ap- 
pendiceal p., 260; pain, 260; renal 
abscess, 306; tetany, 361 530 
SUBJECT INDEX 
Phagocytosis, 245 
Pharynx sphincter of, 25; diverticuli, 26 
Phlebosclerosis, 237 
Phlegmon in esophagus, 28; of bone 
marrow, 460, 481 
Phosphorus poisoning, 113 
Phthisis, phthisical habit, 184; urine, 308 
Pineal gland sexual precocity, 326 
Pituitrin, 328 
Placental circulation, 376 
Pleura, 162; abdomen in bacterial infec- 
tion, 242; capillary adhesions, 374; 
pleura, reflex, 380; Paccini bodies, 
380; pain, 380; pulmonary tonus, 386 
Pleural cavity serosa, 162, 374; oblitera- 
tion in pneumothorax, 384 
Pleural reflex, pneumothorax causing 
death, 381 
Pleuritis, 383; exudative, 385; death due 
to kinking of vessels, 385; atelecta- 
sis, 385 
Plexus of Auerbach, 22, 43, 53, 198; 
Meissner’s, 43, 198; choroid plexus, 
404 
Plexus solar, inhibitory center, 44; injury, 
gastr. ulcer, 76; chr. pancreatitis, 101; 
peritoneum, 171 
Pneumatocele, 11 
Pneumonia, abdominal rigidity, 239; 
pericolitis,. 254; post-operative, 373, 
395; colds, 319; trauma, 398 
Pneumothorax mediastinum, 358, 362, 
379, 382 
Poisoning effecting liver, 113; phosphorus, 
chloroform, 113; enteritis, 204; by 
lead, 221; kidney fr., sublimate, 
uranium, 292; from alcohol increase 
of spinal fluid, 408; epilepsy, 418 
Poliomyelitis, 459 
Pollacissuria, 284, 319 
Polyserositis, 255 
Polyuria, 281; prostatic hypertrophy, 285; 
pollacisuria, 319; hypophyseal ex- 
tract., 328; Basedow, 351 
Portal vein Eck’s fistula, no; anastomosis 
with renal art., 117; ligat., 117; 
thrombosis, 118; occlusion, 118; 
infection of liver, 135 
Portal system, spleen, 155 
Position sense of muscle, 432 
Precipitins antibodies, 246 
Precocity, sexual, 326 
Pregnancy, salivation, 5; cholesterin, 132; 
extrauterine pr., 166; intraabdom- 
inal pressure, 183; renal ptosis, 299; 
enlarged renal pelvis, 303; cystitis, 
318; tetany, 360; dyspnea, 386 
Pressure in esophagus, 28; in bile ducts, 
129; intraabdominal, 181; in rectum, 
182; garrulitis vulvae, 182; dia- 
phragm hernia, 182; peristalsis, 182; 
and tumors, 183; enteroptosis, 183; 
intraabdominal in ileus, 223, 268; 
upward pressure, 252; hydraulic in 
kidney trauma, 295; in urination, 
317; tension difference in chest 
cavity, 374; in lungs, 378; pneumo- 
thorax, 379; intraalveolar, 380; in 
pleuritis, 385; changes in respiration, 
387; pressure test of Valsalva, 387; 
in pleural cavity, 390; low venous 
pressure and air embolism, 394; in 
brain conditions, 403; in subarach- 
noid space, 405; brain pressure and 
choked disk, 410; dilatation pupils, 
410; hydrodynamic in bullet wounds 
of head, 412; in spinal column, 421; 
spastic paralysis, 422 
Prolapsus of rectum, 267; brain prolapse, 
4i5 
Prostate inflamm., 257; hypertrophy and 
polyuria, 285; hydronephrosis, 302; 
tuberc., 311, 322; hypertrophy, func- 
tion, 323 
Prostatectomy, 324 
Proteins metabolism, hi; nucleoproteins, 
112; carbohydrates, 114 
Pseudoarthrosis healing of, 435 
Pseudotuberculosis, 263 
Psychical disturbances thyroid, 349 
Ptosis, 37, 53; of kidney, 299 
Ptyalin, 4, 5, 42 
Pulmonary circulation, 377 
Pulse-rate in brain affection, 403; pulse in 
cerebrospinal fluid, 404 
Puncture salt p., 282; lumbar, uremia, 
288; in pleuritis, 385; for spinal 
fluid, 404 
Pupils dilatation in asphyxia, 389; in 
brain lesions, 410 
Purin metabolism of liver, 112 
Pyelitis, 203 SUBJECT INDEX 
531 
Pyelography, 303 
Pyemia, thrombophlebitis, 237 
Pylorospasm, 50, 78 
Pylorus, 37-39; movements, 40; acid 
control, 40; duodenal cap., 40; 
stenosis, 42; resection, 64 
Pyonephrosis, 302 
Rachitis, 352; (Rosary) relaxation of 
muscle, 428 
Rectal feeding, 81 
Rectal neuralgia, 207 
Rectal prolapse, 267; defecation, 269 
Rectum pressure, 182; margin, current., 
195; defecation, 200; tenesmus, 206; 
proctogenic constipation, 206; car- 
cinoma and constipation, 207; recto- 
scopy, 223; rupture of, 232; in 
drainage of Douglas’s cul de sac, 253; 
prostate, 267 
Reeducation of muscles, 434 
Reflexes, myenteric, 44; pleural reflex, 
381 
Reichmann’s disease, 54 
Renal artery and portal vein, anast., 117; 
renal disease, 279; r. colic, 283, 300; 
insufficiency, 291; renal incarcera- 
tion, 300 
Rennin, 42, 57 
Residual air, 375 
Residual urine, 318 
Respiration, gall bladder tracings, 137; 
chest cavity, 372; thoracic, 373; 
respiratory center, 375; stimulant 
CO2 in venous blood, 375; increase, 
376; blood distribution, 377; pres- 
sure change, 387; passages and their 
chronic narrowing, 389; artificial in 
asphyxia, 390; brain lesions, 409 
Respiratory center, 375 
Respiratory failure from bacterial toxins, 
248; in asphyxia, 389; artificial 
respiration, 390; respiratory paralysis 
and brain affections, 403 
Retention, 285 
Retrograde embolism, 391 
Rheumatism joint disease, 442; rheumatic 
diathesis, 454 
Ribs after pneumothorax, 385; rib carti- 
lages, yellow degeneration in emphy- 
sema, 387; in kyphosis, 388; in 
senile spondylarthritis, 388; in tuberc. 
spondylitis, 388 
Rupture of bowel, 231; of bladder, 319 
Saline solution as irritant in peritoneum, 
243; renal activity, 292 
Saliva, 1; in fever, 3; composition, 3; 
function, 3; and digestion, 4; inhibi- 
tion, 5; stimulation, 6; changes, 6; 
asialia idiopathic, 6; absence of, 6; 
anesthesia, n. 
Salivary glands, 1; innervation, 1; stimu- 
lation, 2; genital glands, 7; ducts, 10; 
stomatitis, trauma, 10; parotitis, 8; 
pneumatocele, n; saliv. calculi, 11; 
and foreign bodies, 12; salivary 
colic, 13; tumor salivarium, 13; 
degeneration, 13; ligation of ducts, 
13; saliv. fistula, 13; literature of 
saliv. gl., esoph., 30, 35 
Salivation, 2, 5; in stomatitis, 2; from 
poisons, 5; in disease, 5; pregnancy, 
5; paralytic secretion, 5 
Salpingitis leucocytosis, 260 
Scar tissue sarcoma, 154 
Scrotal hernia, 329; scrotal swelling in 
elephantiasis, 481 
Secretin, 57, 95, 125; and bile, 136 
Secretion paralytic, 5; stomach, 41; pan- 
creatic regurgitation into stomach, 58; 
of pancreas, 95, 191; of endothelium, 
121; format, bile, 123; pancreat. 
seer, cholecystectomy, 136; of intest, 
juices, 191; paralytic secretion, 191; 
of large intestines, 191; absence of 
pancreatic and diarrhea, 205 
Sensitivity of abdomin. organs, 172 
Sepsis peritonitis, 243 
Septicemia toxic nephritis, 304 
Sequestrum formation bone necrosis, 
463 
Serosa infection, 243 
Sexual characteristics secondary, 328 
Shock from manipulat. of intestines, 228; 
from anaphylaxis, 229, 289; from 
exhaustion, 229; CO2 impoverish- 
ment, 229; adrenals, 230 
Sialolithiasis, 11; sigmoid flexure, 193; 
defecation, 200; kinking, 207; rup- 
ture, 231 
Sialogogues, 5 SUBJECT INDEX 
532 
Singultus and peritonitis, 249; diaphragm, 
250 
Skeleton readjustment, muscle anlagen, 
429 
Skin bronzing after thyroidectomy, 363 
Skull contents, 407; pressure, 407; frac- 
ture, 407; and foreign bodies, 4x1; 
depressed, 409; elasticity, 411 
Spasmophilia, 360-362; epilepsy, 362 
Spasms, pylorospasm, 50, 78; of anal 
sphincter, 207; diaphragm, 215; 
intestinal lead colic, 221; ascaris, 221; 
ulcers, 222; of tetany, 359; tetacin 
from ventricular hemorrhage, 417 
Spastic paralysis, 422 
Speech, 7, 13 
Spermatogenesis, 329 
Sphincter of cardia, 22; pharynx, 25; 
sphincter antri, 38; of Oddi, 102, 
105, 134; of intestines, 198; defeca- 
tion, 200; of anus, 201; of bladder 
innervation, 315; urinary function, 
321 
Spina bifida trophic changes, 459 
Spinal column and intestinal trauma, 230; 
injury with abdominal rigidity, 239; 
cerebrospinal fluid, 404 
Spinal cord, conus terminalis and anal 
innervation, 201; and defecation, 
208; sensory roots, 238; resection 
and abdominal reflexes, 239; bladder 
innervation, 315; surgical diseases, 
421; tuberculosis, gun shot wounds, 
421; resection, 422; spastic paralysis, 
422 
Spinal fluid, origin, albumen leucocytosis 
in syphilis, 404; quantity, 405; 
hydrocephalus, 405; compared to 
ascites, 408; brain tumors and 
trauma, 408 
Splanchnoptosis, 184 
Spleen, 70, hi, 121, 129; splenectomy, 
148; blood picture, 148; increased 
resistance of r.b.c. after splenectomy, 
149; embryonic spleen, 150; erythro- 
poetic, 150; Malpighian follicles, 
150; myelocytes, 150; destruction of 
blood corpuscles, 150, 155; macro- 
phages, 1507 splenic tumor, 150; 
hemolymph nodes, 151; splenoids, 
151; accessory spleens, 151; regenera- 
tion, 152; iron metabol., 153, 157; 
infections, 153, 158; metastasis, 154; 
digestion, 154; rhythmic changes, 
155; splitting of its capsule, 155; 
psychoses, 15s; severe anemia, 155; 
Band’s disease, 156; splenomegaly, 
Basedow, 156; jaundice, 156; liver, 
156; injuries, 158; literature, 158- 
160 
Splenectomy, 148; blood increased resis- 
tance r.b.c., 149; leucocytic changes, 
149; bone marrow, 149, 152, 157; 
lymph glands, 149; eosinophilia, 149; 
iron metabolism, 149, 152, 153; 
thymus hyperplasia, 152; infectious 
diseases, 153; digestion, 154; con- 
stipation, 155; psychoses, 155; ane- 
mias, 156; Band’s disease, 156 
Splenic tumor, 150 
Splenomegaly, 156; Basedow, 156 
Spondylarthritis, senile, respiration, 388 
Sprain-fracture, 466 
Status, thymolymphaticus, 355 
Steapsin, 102 
Sterility and thyroid gland, 340 
Stock’s collar, 358 
Stomach ptyalin, 5, 36; movements, 36; 
motor function, 36, 81; divisions, 37; 
peristalsis, 37, 65; sphincter antri, 38; 
fasting, 38; defense reflex, 38; food, 
38; juice, 38; erosions, 38, 73; antrum, 
38; systole, diastole, 39; stimuli, 39; 
secretion, 39; pylorus, 39; chyme, 
40, 56; secretory function, 41; gastric 
hormone, 41; ganglia, 41; gastr. 
juice, 41, 47; enzymes, 42; absorp- 
tion, 42; water, 42; nervous mech- 
anism, 42; pathological changes 
in gastric motility, 45; vomiting, 45; 
sensory tract, 46; contractions, 47; 
hunger, 48, 66; gastric crises, 49; 
pylorospasm, 50; defective evacua- 
tion of food, 51; acute dilatation, 51; 
arteriomesenteric ileus, 51; gastropto- 
sis, 53; chronic motor insufficiency; 
53; asthenia, 53; Reichmann’s dis- 
ease, 54; operation sutures, 54, 63, 
66; gastroenterostomy, 54, 57; nar- 
row pass; 56; back flow of intestinal 
juices, 57, 80; regurgitation, 59; 
vicious circle, 59; lavage, 60; marginal SUBJECT INDEX 
533 
ulcers, 6x; hyper-, hypoacidity, 62; 
pyloric resection, 64; transverse 
section, 65; total resection, 66 
gastrointestinal ulcers, 68; protec- 
tion against auto-digestion, 62, 69; 
antipepsin, 70; trypsin causing gastr. 
ulcers, 51, 71, 76; ligation of blood 
vessels, 71; capillary thrombosis, 72; 
hematemisis, 72; bacterial embolism, 
74; displacement, 74; constitutional 
weakness, 78; gastrostomy, 80; secre- 
tin, 57, 95; literature, 81-94; cho- 
lecystectomy; 137; cholecystenteros- 
tomy, 137; slowing of gastric motility, 
138; perforation stomach, 166, 172; 
pain in gastr. ulcer, 174; intra- 
abdom. pressure, 182; marginal 
current, 194; achylia and diarrhea, 
203; poisoning, 204; tetania gastrica, 
361 
Stomatitis and salivation, 2, 10 
Stools, retention, 217; acholic, 124, 128; 
bloody, 177 
Strangulation ileus, 212 
Streptococcus peritonitis, 240 
Stroma, 27, 448 
Subarachnoid space, 404 
Succus entericus, 97 
Sugars, monosaccharides and intestinal 
absorption, 193; galactose, in 
Swallowing, 15 
Synovial fluid, nature, 468 
Synovin in artificial mobilized joints, 468 
Synovitis and synovial cells, 442; absorp- 
tion, 465 
Syphilis, duodenal ulcers, 75; enteritis, 205; 
spinal fluid in late, 404; epilepsy, 4x8 
Syringomyelia, 459; edema, 481 
Tabes, 49; meteorism, 216; tabetic 
crises, 222, 459 
Tachycardia in exophthalmus, 349, 358 
Talma’s operation, 65 
Tamponade of abdomen differentiated 
from drainage, 251 
Taste, 13; suspension, 14 
Teeth, growth in extirpation of para- 
thyroid, 360 
Tendons, 427; bone fracture, 428; of 
Achilles and development of calf 
muscle, 429 
Tenesmus, 206 
Testicle parotitis, 9; tuberc., 311; castra- 
tion, 324; internal secretion, 328; 
injury, 329; transplantation, 329; 
undescended, 329 
Tetany, 359; latent, 360; in pregnancy, 
360; spasmophilia, 360; in infections, 
361; occupation, 361; ergot, 361 
Thirst, saliva, 3; after bowel resection, 265 
Thoracic duct, 98; colloids, 167; enlarge- 
ment, emphysema, 386 
Thoracoplasty mediastinum, 358; ex- 
trapleural, 383; connective tissue 
growth, 384 
Thorax, chest cavity, 373; emphysema, 
387 
Threshold values, 279 
Thrombokinase, 131 
Thrombophlebitis, 237 
Thrombosis, capillary in gastric ulcer, 72; 
venous in acute pancreatitis, 104; 
portal vein, 118; after splenectomy, 
148; intestinal distention, 223; after 
mesenteric injury, 233; embolism 
differentiated, 237; after appendicitis, 
238; varicose veins, 472; infection, 
475 
Thymus, 351; hyperplasia, splenectomy, 
152; complete thyroidectomy, 341; 
in Basedow’s disease, 351; gland, 
morphology, 351; metabolism, 351; 
removal and adipose stage, 352; 
rickets, 352; calcium balance, 352; 
function, 352; its ferments, 353; 
thyroidectomy, 353; death, 354; 
status thymolymphaticus, 355; chro- 
maffine system, 356; seconds heart 
death, 356 
Thyroid gland splenectomy, 152; func- 
tion, 338; thyroidectomy conse- 
quences, 339; regulating blood supply 
to brain, 340; sex, 340; nerve influ- 
ence to thyroid, 340; metabolism, 
340; cachexia thyreopriva, 340; sex 
organs, 340; ossification, 340; results 
of complete thyroidectomy, 341; 
implantation, 342; cretinism, 342; 
hyperthyroidism, 346; Basdow’s dis- 
ease, 347; exophthalmus, 347; dys- 
thyroidism, 348; nervous system, 
349; acute Basedow, 350; thymus, 534 
SUBJECT INDEX 
Typhoid peritonitis, 240; muscle regenera- 
tion, 435 
Ulcers of esophagus, 28; gastric pain, 47; 
marginal, 61; jejunal, 62; gastro- 
intestinal, 68, 74; leg ulcers, 71; 
duodenal, 74; intestinal, 205, 236; 
intestinal spasms, 222; stereo real, 
223; appendiceal, 259; peptic, 260 
Uranium poisoning, 292 
Urea, 279, 287; decomp, into ammonia in 
cystitis, 319 
Uremia, 286; lumbar puncture, 288; surgi- 
cal, 288; venesection, 294; after 
vesical rupture, 321 
Ureters, 284; back flow in hydronephrosis, 
301; peristalsis, 302; tuberculosis, 
308 
Urethra, 319, 321; prostatic, 322 
Urine and peritoneum, 167; urine, 284; 
innervation, 285; concentration, 286; 
albuminuria, see there, stagnation, 
304, 319; difficulty in voiding, in 
prostatitis and pregnancy, 304, 323; 
in phthisis, 308; composition, 313; 
in gout, 313; bilharzia, 313; fibrinu- 
ria, 314; impulse to void, 316; 
retention in children, 317; bacteriuria, 
318; alkaline, 318; residual, 318; 
pollakisuria, 319; absorption in blad- 
der injury, 320 
Vaginal drainage of Douglas’s cul de sac, 
253 
Vagotony, 50; gastr. ulcer, 78 
Vagus, 20, 40, 50; intussusception, 221 
Valsalva’s dysphagia, 18; pressure test, 
387 
Varices esophageal, cirrhosis liver, 122; of 
syphilis, 472 
Varicose veins, 472; leg ulcers, 475 
Vas deferens, peristalsis, 311; prostate, 323 
Veins, 469; portal vein lig. and Eck 
fistula, no; saphenous and femoral 
for permanent drainage for ascites, 
of mediastinal space, 357, 382; 
impeded outflow, 382; of the leg 
and pulmonary emboli, 391; of neck 
congestion, 406; pressure in, 469; 
arterial pulse, 471; thrombosis, 472 
Venesection and uremia, 294 
351; parathyroid, 359; complete 
removal and bronzing of skin, 363; 
literature, 366-371 
Tongue, 13; function, 13; nerves of taste, 
13; taste, 14; speech, 14; removal, 
14; deglutition muscles, 15; paralysis, 
17 
Tonsils duodenal ulcers, 75 
Tonus of muscles, 428 
Torsion of viscera, 215; of kidney, 300 
Torticollis, 452 
Toxemia due to peritonitis from toxin 
forming and putrefactive bacteria, 
240; urinary, 287 
Toxins, bacterial and paralysis of vaso- 
motor center, 248; intestinal, 225 
Trachea, 30 
Tracheal stenosis and thymus, 355 
Traction diverticuli, 25 
Transfusion of blood, 474 
Transudate ascites, 121 
Tremor in -Basedow’s disease, 350 
Trendelenburg posit., circulatory changes, 
390; operat. for pulmonary emboli, 
39° 
Trypanosome causing goiter in Brazil, 346 
Trypsin, 57; gastric ulcers, 59, 71, 96, 
104; enterokinase, 190; treatment of 
tuberculous fistula, 466 
Trypsinogen, 97 
Tuberculosis of lymph nodes of neck and 
dry mouth, 7; of epiglottis, 20; duod. 
ulcers, 75; acholic stools, 124; spleen, 
156; enteroptosis, 184; enteritis, 
205; intestinal stricture, 236; renal, 
294, 307; congenital, 310; erotism, 
311; of parathyroid, 361; closed 
pneumothorax. 383; encapsulating 
pulmonary, 384; spondylar, 388; of 
vertebrae, 421; of bone, 466; fistula, 
466 
Tumors, submaxillary, 6; parotid, 6; 
tumor salivarium, 13; splenic and 
cirrhosis liver, 121; splenic, 150; 
intraabdominal pressure, 183; intra- 
abdominal-twisting, 215; prostatic; 
323; of hypophysis, 327; of mediasti- 
num, 357; brain tumors, 403; brain 
tumors, increase of cerebrospinal 
fluid, 408; of cerebello-pontine, 
angle, 420 SUBJECT INDEX 
535 
Venous stasis, 408, 451; venous circula- 
tion, 460; murmur, 479 
Ventricles cerebral, 405; puncture and 
epilepsy, 420 
Vertebrae tuberculosis, 421; caries and 
laminectomy, 421 
Vertebral fracture, 404 
Vesicles seminal tuberc., 311; optic 
vesicle, ectoderm cells, 457 
Vomiting, 44, 45; innervation, 46; after 
gastric resection, 67; vomito negri, 
73; after splenectomy, 148; fecal 
and ileus, 212; peritonitis, 249 
War gases, 396 
War wounds, peritonitis, 241; of head, 
choked disk, 410; to spinal cord, 422 
Wounds in stomach, intestines, 63, 233; 
in abdomen and omentum, 179, 233; 
in kidney, 295; of heart, 364; of 
spinal cord, 421; near spinal cord, 
pain, 458 
Yellow fever, black vomit, 73 
Zuckerguss leber, 255 
Zymogen, 42, 96