REPORT 
ON THE 
CAUSES AND PATHOLOGY OF PYJIMIA (SEPLEIIA). 
BY 
J. J. WOODWARD, M. D., 
ASSISTANT SURGEON AND BREVET MAJOR U. S. ARMY, ETC. ETC. ETC. 
EXTRACTED FROM THE 
TRANSACTIONS OP THE AMERICAN MEDICAL ASSOCIATION. 
PHILADELPHIA; 
COLLINS, PRINTER, 105 JAYNE STREET. 
1866. REPORT ON THE CAUSES AND PATHOLOGY OF 
PYiEMIA (SEPTiEMIA). 
The American Medical Association, at its last annual meeting, 
did me the honor to appoint me chairman of a committee to report 
on the “ Causes and Pathology of Pyaemia.” This appointment 
was made, as I understand, at the request of my friend, Brevet 
Col. Chas. S. Triplek, Surgeon U. S. Army, and was not known 
to me until after the Association had adjourned. It was the more 
unexpected, as for several years my best efforts have been directed 
quite away from the domain of surgery, to which the subject as- 
signed is generally supposed to belong. Nevertheless, the same 
disordered condition of the system which modem surgeons indicate 
by the word Pyaemia occurs so frequently in connection with dis- 
ease that it has been a topic of earnest thought with me, especially 
in its relations to the ulcerated colon of camp dysentery; and I 
have thought that perhaps its discussion from the medical point of 
view would not be without interest. 
The affection to be considered is a peculiar constitutional condi- 
tion, which may come on after wounds and operations, during puer- 
peral convalescence, or the progress of certain diseases; which is 
characterized by febrile symptoms of a typhous character, and in 
fatal cases is frequently accompanied by multiple abscesses, by 
gangrenous foci, or by patches of parenchymatous congestion and 
degeneration, though, indeed, these local phenomena are far from 
being uniformly present. 
The term Pyaemia, contracted from the Pyohasmia of Piorry, sig- 
nifying pus blood, appears at the present moment to be no longer 
proper, since there is no good reason to believe that the presence 
of pus in the blood has anything to do with the disease. "Virchow 
has proposed the word Ichorhaemia, which is much better. I must 
express my own preference for the designation Septaemia, literally 
putrid blood (aynros and ’ai.ua) as expressing more sharply the idea 
of an alteration in the circulating fluid under the influence of a 6 
REPORT ON THE 
septic poison. The appellation Pygemia is, however, in such gen- 
eral use that I shall retain it in the present paper with this pre- 
liminary protest. 
I by no means propose to offer here an extensive essay on the 
subject. The burthen of other duties places this quite out of my 
power at present. I hope indeed to return to the theme at no very 
distant day, with the purpose of handling it more in detail. All 
that I shall now attempt is to bring together a few considerations 
in connection with the literature of the subject, to offer a brief 
summary of the leading explanations of the phenomena which have 
been propounded, and a criticism of the basis on which they rest— 
perhaps to venture on a few hints in further explanation—after 
which I shall conclude with a sketch of some of the more promi- 
nent forms of non-surgical pyaemia, and especially of uterine 
pygemia, the pygemia of new-born infants, pyaemia originating in 
intestinal ulcers and other lesions of the portal system, and the so- 
called idiopathic or spontaneous pyaemia. It will be convenient, 
however, to introduce the subject by a brief description of the 
chief phenomena of pyaemia in general, by which needless repeti- 
tion will be avoided in subsequent portions of the paper. 
The disease may begin abruptly with a chill followed by fever, 
or with rigors alternating with febrile flushes. During the late 
war I have noticed in wound-pyaemia that generally the first symp- 
toms are malaise, with loss of appetite, restlessness at night, and 
pallor of the skin, sometimes verging on an icteroid condition. 
The patient frequently complains of a peculiar unpleasant taste in 
the mouth, which communicates itself to all articles of diet. After 
several days of this condition, rigors or chills make their appear- 
ance for the first time. Fever once established may present an 
intermittent or remittent form, but usually in the course of a very 
few days becomes continuous and typhoid in its character, with hot, 
dry skin, frequent, feeble pulse, mental disturbance soon amounting 
to low delirium or stupor, a red, dry tongue, which after a time 
becomes brown or coated with sordes, meteorism, diarrhoea, in 
short the symptoms of the fevers of the typhoid grade. Icterus 
more or less pronounced is a frequent accompanying phenomenon. 
These constitutional conditions, when dependent upon a visible 
local lesion, are accompanied by local phenomena of equal signifi- 
cance. If the point of departure be a wound, it will be found to 
have lost its healthy character, the formation of normal pus ceases, 
the lips of the wound become dry and livid, and often after ampu- CAUSES AND PATHOLOGY OF PYAEMIA. 
7 
tations or gunshot injuries, sloughing or phagedaena sets in. The 
superficial veins leading from the wound are often swollen, hard, 
and tender ; occasionally abscesses form in their track. Sometimes 
an erysipelatous condition of the integument commences at the 
wound and spreads with great rapidity. In many of these cases 
brought under my notice, during the late war, the erysipelatous 
blush was modified by a yellowish or brownish tinge intermixed 
with the deeper shades of red, and sloughing of the integument 
was not uncommon (erysipelas gangrenosa). In the cases which 
occur after parturition the lochia become at first fetid, then nearly 
or quite suppressed, the vagina is hot and dry, the lower portion 
of the abdomen tender, and the phenomena of metritis or metro- 
peritonitis are usually present. The progress of the affection is 
often complicated with symptoms attributable to the secondary ab- 
scesses or foci, such as difficulty of breathing, more or less cough, 
pain in the side, dulness on percussion, with rude or bronchial 
respiration, if the lungs have become their seat; jaundice, and 
pain or tenderness in the right hypocbondrium, if the liver; swell- 
ing and tenderness in the articulation affected in the case of ab- 
scesses in the joints, etc. 
The time after an injury at which the disease appears varies 
greatly with the nature of the injury. I have known pyaemia to 
set in months subsequent to a compound fracture of the femur. 
In the case of parturient women it usually begins during the first 
fifteen days; after venesection, dissecting wounds, and similar acci- 
dents, still earlier. 
The duration of the disease may vary from a few days to several 
weeks, and in either case it is very apt to prove fatal. Where 
secondary foci can be recognized, a fatal result may almost always 
be anticipated; not invariably, however, as some have assumed; I 
have myself seen at least one case of recovery after the commence- 
ment of metastatic foci in the lungs. There is a class of cases re- 
markable for the intensity of the constitutional phenomena which 
prove fatal within forty-eight hours or a few days, and in which no 
secondary foci are found after death; while many mild cases occur 
unaccompanied by symptoms of such foci during life, presenting 
simply a typhoid depression of the system under the influence of a 
foul or phagedenic condition of the wound or injury, and terminate 
in recovery. 
The conditions observed after death may be divided into two 
groups; those connected with the local morbid affection in which 8 
REPORT ON" THE 
the disease originated, and those existing in the blood or in distant 
organs. The essential part of the local affection is the condition of 
the veins which has been described by almost all writers since the 
time of Hunter under the name of phlebitis, and this again has been 
subdivided into two varieties, adhesive phlebitis and suppurative 
phlebitis. The conditions actually to be observed are as follows: 
The veins involved are more or less distended with blood-coagula, 
which may be quite red and firm like ordinary freshly-coagulated 
blood, or mixed with a yellowish or grayish pus-like fluid. Exa- 
mination of the coagula in those cases in which this yellowish 
fluid is not abundant shows that it originates in the centres of the 
clots. If carefully examined with the microscope it will be found 
to consist simply of decomposing blood. Granules, often in a state 
of active molecular movement, altered red blood-corpuscles with 
a few scattered white corpuscles, are all that is to be seen. There 
is here no true pus; and the name of suppurative phlebitis is 
therefore a misnomer. Whether or no pus is ever to be found in 
such situations lam not prepared positively to assert. I certainly 
have never seen it, although I have examined a number of cases. 
It is to be borne in mind that the white corpuscle of the blood is 
not distinguishable from the pus corpuscle; and as the debris of the 
softened clot must contain a number of these proportioned to the 
amount of blood which has undergone alteration, it might readily 
happen that some of them seen microscopically should induce an 
observer to characterize the yellowish fluid in which he saw them 
floating as pus. This would be especially apt to be the case if he 
commenced the investigation expecting to find pus in the site exam- 
ined. To justify the application of the name of pus to such a fluid, 
however, it should be shown either on the one hand that there is 
some distinctive mark by which the white corpuscle can be dis- 
tinguished from the pus cell, or, on the other hand, that the number 
of corpuscles is too great to be accounted for by supposing them 
to belong to the altered blood. Neither of these possibilities can 
be proven. The two kinds of corpuscles have no anatomical dis- 
tinctive marks, and in all the cases in which I have examined the 
pus-like fluid under consideration, the recognizable white corpus- 
cles were so few as to compel the supposition that a large part of 
those belonging to the softened clot had undergone degradatibn 
into the same granular debris into which the fibrin and most of the 
red corpuscles had been transformed. 
The credit of first showing the real nature of the pus-like fluid CAUSES AND PATHOLOGY OF PYASMIA. 
9 
in these cases, is usually assigned toYirchow, but very incorrectly. 
Long before the publication of his Essays, Gulliver, in England, 
had pointed out the errors which existed in the previous descrip- 
tions of suppurative phlebitis, and had arrived at the following 
conclusions;— 
“ Ist. That coagulated fibrin, when removed from the body and 
subjected to a blood heat, commences to soften in about forty 
hours, assuming the color and consistency of pus, but easily dis- 
tinguishable from it by microscopic and chemical examination. 
“2d. That the purulentdike fluid found in the fibrinous clots of 
the heart and arteries, and so frequently in the veins, is essentially 
distinct from pDs, and analogous, if not identical, with softened 
fibrin. 
“3d. That the softening of coagulated fibrin is an elementary 
pathological condition of frequent occurrence, distinct from suppu- 
ration, and constituting a considerable proportion of the cases 
generally denominated suppurative phlebitis.”1 
The transformation of the coagulated blood into a puriform fluid, 
commencing at the centre of the clot, may ultimately involve its 
whole substance and the vessel is then found filled with a fluid 
which, in its appearance, more or less closely resembles pus, but 
which, in its origin and microscopic characteristics, differs radically 
from it. Where the disease is associated with a gangrenous sur- 
face, as in certain sloughing wounds, the peculiar decomposition of 
the clot here described may pass into a form of putrefaction not 
unlike that occurring in the gangrenous part itself; and the puri- 
form fluid in the bloodvessels is found to possess a putrid smell, 
and to consist of a mass of extremely minute granules in a state 
of active molecular movement. 
The foregoing remarks will serve to indicate the basis upon which, 
in my opinion, the usual doctrine of suppurative phlebitis rests. 
The condition described as adhesive phlebitis, is simply the stage 
of the process in which the clots fully formed have not yet begun 
to undergo degradation. 
'These criticisms are not to be understood as denying the pos- 
sibility of a true phlebitis, which indeed may coexist with any of 
the stages of clot formation or degradation I have sketched. True 
phlebitis is characterized by a thickening of the coats of the affected 
1 “ On the Softening of Coagulated Fibrin,” by George Gulliver, F. R. S., Assist- 
ant Surgeon to the Royal Regiment of Horse Guards. (Medico-Chirurgical Trans- 
actions, vol. xxii. p. 136. See also London Medical Gazette, March, 1839.) 10 
REPORT ON THE 
vessel, due to multiplication of their elementary forms, sometimes 
even by abscess formation in the substance of the vascular walls 
or in the surrounding connective tissue. I am not prepared to 
assert positively that lymph or pus formation can, under no cir- 
cumstances, occur on the inner surface of the veins; but the very 
class of cases relied upon to prove such “ exudative processes” 
fail, as has been just shown, to bear analysis. 
The alterations existing in the blood or in organs at a distance 
from the primary seat of the disease, have next to be considered. 
The blood, to which naturally attention has been earnestly directed, 
affords little information of significance. Observations have chiefly 
been directed to the question of an admixture of pus, whether pro- 
ceeding from phlebitis or introduced from without by absorption 
or through the patulous orifices of open veins. For a long time it 
was supposed that this question had been settled in the affirmative. 
Not only was a fluid supposed to be pus found in connection with 
the so-called phlebitis, as has already been mentioned, but accumu- 
lations of corpuscles, believed to be pus-corpuscles, were found in 
the sinuses of the dura mater and elsewhere; and the presence of 
numerous similar corpuscles, in the blood was clearly demonstrated 
by many microscopical observers. Unfortunately this pus-blood 
did not always or even generally coexist with suppurative phlebitis 
or with any of the secondary phenomena of pyaemia; on the con- 
trary, its most exquisite development was generally in cases in 
which none of the symptoms of pyaemia were observed during 
life and none of its pathological appearances after death. This 
naturally drew attention to the comparative morphology of pus and 
of white blood-corpuscles; and this comparison, with a careful 
analysis of cases, resulted in the doctrine of Lukaemia, which re- 
cognizes in these cases simply an abnormal increase of the number 
of the white corpuscles of the blood coincident with enlargement 
of the spleen or of the lymphatic glands. The credit of this doc- 
trine undoubtedly belongs to Virchow; although it has been claimed 
by Bennett, whose argument in favor of his own priority seems 
to have been generally admitted in this country and in Great 
Britain. The argument by which Bennett has attained this repu- 
tation requires some comment. 
In November, 1845, Virchow published in Froriep’s Neue Noti- 
zen, under the designation, “Weisses Blut,” a case in which the 
blood contained immense numbers of white blood-corpuscles. He 
not only described the corpuscles, but he recognized their nature. 11 
CAUSES AND PATHOLOGY OF PYAEMIA. 
“When I. therefore, speak of white blood,” he says, “I mean, in 
fact, a blood in which the proportion between the red and colorless 
corpuscles is reversed, without any noticeable admixture of foreign 
chemical as morphological elements.” In the same paper he quotes 
a case of so-called general pyaemia observed in Vienna,1 of which 
he suggested that it is probably erroneously so-called, and is in fact 
a case similar to his own. 
On the other hand, Bennett claims that he had published a simi- 
lar case six weeks before in the Edinburgh Medical and Surgical 
Journal, for 1845, page 413, and in his “Clinical Lectures”2 he gives 
what purports to be a “verbatim” reprint of the original paper. 
A comparison of this reprint with the original paper shows, how- 
ever, not only that it does not describe an increase of the white 
corpuscles of the blood, the possibility of which is indeed expressly 
excluded from the interpretation of his case, but that it differs in 
several important particulars from the original paper, as may be 
shown by a few parallel passages;— 
Original paper in the Edinburgh Medical 
and Surgical Journal. 
Reprint of the same in the Clinical Medi- 
cine. 
“ Case of hypertrophy of the spleen and 
liver in which death took place from 
suppuration of the blood.” 
“ Leucocythemia discovered after death. 
Hypertrophy of the spleen, liver, and 
lymphatic glands. Absence of phle- 
bitis and of purulent collections in 
any part of the body.” 
“ The yellow coagulum of the blood was 
composed of coagulated fibrin in fila- 
ments, intermixed with numerous pus 
corpuscles, which could be readily 
squeezed out from it when pressed be- 
tween glasses.” 
“ The yellow ooagulum of the blood was 
composed of coagulated fibrin in fila- 
ments, intermixed with numerous color- 
less corpuscles, which could be readily 
squeezed out from it when pressed be- 
tween glasses.” 
“ The red portion of the coagulum con- 
tained a large number of these pus-cor- 
puscles mixed, however, with a multi- 
tude of normal yellow corpuscles.” 
“The pus-corpuscles above described 
were found in the blood throughout the 
system.” 
“ The red portion of the coagulum con- 
tained a large number of these colorless 
globules, mixed, however, with a multi- 
tude of normal yellow corpuscles.” 
“ The colorless corpuscles now describ- 
ed were found in the blood throughout the 
system.” 
“ The enlarged lumbar glands, on being 
pressed, exuded a fluid that was crowded 
with corpuscles; some resembling those 
of pus already alluded to; others oval, 
containing a distinct nucleus.” 
“ The enlarged lumbar glands, on being 
pressed, exuded a fluid crowded with 
corpuscles; some resembling the color- 
less corpuscles already alluded to, others 
oval and round, containing a distinct 
nucleus.” 
“ Acetic acid produced the same 
changes in these as in the pus-corpuscles 
the blood. 
Omitted in the reprint. 
1 From the Zeitschrift der K. K. ges. der Aertze zu Wien, 1845; Band 11. s. 488. 
2 Clinical Lectures on tlie Principles and Practice of Medicine. American edi- 
tion of 1860, page 814. By John Hughes Bennett, M. D. 12 
KEPORT ON THE 
It will be seen, by comparing the above,-that in the reprint the 
words colorless corpuscles are substituted for the words pus-cor- 
puscles in four different places, which are all in which they occur 
in the original, except in the sentence which is omitted in the 
reprint, and that the title of the paper is changed. After present- 
ing this reprint, Dr. Bennett continues as follows;1— 
“In the remarks originally appended, I observed; ‘The points 
connected with this case that require discussion are, Ist. The con- 
nection between the symptoms and morbid appearances ; 2d. Were 
the corpuscles contained in the blood really those of pus? and 3d. 
If so, how were they produced.’ The discussion of these theoreti- 
cal points, it appears to me, has nothing whatever to do with the 
correctness or incorrectness of the facts above detailed, which, it 
will be observed, are studiously separated from everything of a 
hypothetical character.” How studiously this separation was made 
may be learned not only from, the frequent repetition of the words 
“pus-corpuscles” in the “microscopic examination,” and the head- 
ing of the case “in which death took place from suppuration of 
the blood,” but in such passages as the following, which I quote 
from the original article in thq Edinburgh Journal. “In the pre- 
sent state of our knowledge, then, as regards this subject, the fol- 
lowing case seems to me particularly valuable, as it will serve to 
demonstrate the existence of true pus, formed universally within 
the vascular system, independent of any local purulent collection 
from which it could be derived.” “I think there can be little 
doubt that pus in the blood was the cause of death, and that it pro- 
duced the febrile symptoms.” “ When, then, we take into con- 
sideration the existence of these corpuscles throughout the vascular 
system, their general size and appearance, and, above all, the changes 
they underwent on adding water and acetic acid, there can be little 
doubt that they were true pus-globules.” “ But can we explain the 
production of pus independent of inflammation? We reply in the 
affirmative. The corpuscles of pus arise in the blastema formed of 
liquor sanguinis. This fluid, when exuded through the blood- 
vessels, does not thereby in itself undergo any change. If any cir- 
cumstances, therefore, should arise by means of which it could be 
separated from the red corpuscles within the vessels, there is no 
reason why these pus-cells should not be formed in it.” And 
finally, “ Positive facts, therefore, indicate that pus can form in 
liquor sanguinis within the vessels independent of inflammation.” 
1 Clinical Medicine, p. 819. CAUSES AND PATHOLOGY OF PYJSMIA. 
Such is the tenor of all the “remarks,” and the possibility that 
these “pus-corpuscles” might after all be the “colorless corpuscles” 
of the blood is only alluded to, to be positively rejected. “With 
regard to the colorless corpuscles of the blood, we know of no in- 
stance where they existed in the amount, or ever presented the 
appearance described.” 
It is thus seen that Bennett’s case was believed by himself to be 
simply one of pus in the blood. He himself, in his modern argu- 
ment, admits nearly as much, but seems to think that the actual 
observation of a pus-like substance in the blood, with enlarged 
spleen, and without local inflammation, was, after all, the point of 
originality, and that his erroneous interpretation should not rob 
him of the credit of the observation. But the presence of pus in 
the blood played a conspicuous part in all the notions of pyaemia 
current at that day, and not only Craigie, as Bennett himself ad- 
mits, but others, had observed precisely similar cases. Duplay,1 
for example, more than ten years previously had described a case 
of the presence of pus in great quantities in the arterial and venous 
system, without appreciable origin. In this case there was enor- 
mous enlargement of the liver and spleen. Like Bennett’s, it was 
undoubtedly a case of leuksemia erroneously understood. 
lieturning after this digression, demanded by the truth of his- 
tory, it is to be remarked that the failure to establish the contami- 
nation of the blood with pus in cases of pyaemia has left us without 
any definite information as to what alterations of this fluid are 
really present. Some have laid great stress upon the disposition 
of the blood to coagulate, and inferred thence an increase in the 
quantity of its fibrin, which, however, could usually be admitted 
only in the earlier stages of the disorder. A deficiency of fibrin 
has been assumed on the other hand. A condition of the cor- 
puscles like that seen in the earlier stages of putrefaction has also 
been mentioned. But on none of these heads has sufficient testi- 
mony been offered to render the doctrines based upon them 
plausible. And the same may be said of the notion of Mackenzie/ 
which attributes the phenomena, in women after parturition, at 
least, to the accumulation of lactic acid in the blood. 
1 Observation d’une alteration tr£s-grande du sang. Presence d’une quantite tres- 
grande de pus dans le systeme arteriel et veineux sans origine appreciable. Par 
M, A. Duplay. Arcbiv. Gen., 11. serie, t. vi. p. 223. 1834. 
2 Researches on the Pathology of Obstructive Phlebitis and the Nature and REPORT ON THE 
Of the secondary formations in distant organs by far the most 
frequent exist in the lungs. They are sometimes true abscesses, 
containing ordinary pus-cells; this, however, I have only seen 
occasionally. Much more frequent are hard, yellowish, irregular 
nodules, sometimes softened in the centre into a pus-like fluid, in 
which the microscope detects only granules and amorphous debris 
of the lung tissue in various stages of granular degeneration.' Asso- 
ciated with these yellowish nodules are often others, which present 
on section a reddish color with small ecchymosed spots. These 
exhibit on microscopical examination, an appearance similar to the 
yellowish, except that the normal lung elements are not so com- 
pletely obliterated, and that a large number of normal or more or 
less altered red blood-globules are plainly observable in the scrap- 
ings from the surface of sections. The reddish nodules frequently 
exist in cases in which there are no yellowish ones, and often pre- 
sent in their centres a larger or smaller portion of yellow sub- 
stance, quite like that of the yellow nodules. On the whole, it ap- 
pears probable that the reddish nodules are the primary formation, 
that they are converted by a peculiar form of breaking down 
(similar to that which occurs in the blood clots, already described) 
into the yellowish ones, and that where true pus is found it is due 
to ordinary inflammation in the tissues surrounding the nodule. 
In view of these considerations, and especially of the frequent 
absence of all true pus, I prefer the term secondary foci to the more 
usual designation, metastatic abscess. 
The foci in the lungs vary in size from that of a millet seed to 
masses of considerable bulk; their shape almost always corresponds 
to that of some individual lobule or group of lobules. Generally 
they are situated on the periphery of the organ, just below the 
pleura; sometimes, however, they are scattered through its sub- 
stance. They are said to be more frequent in the left lung than in 
tbe right,1 and in the lower than in the upper lobes.2 Associated 
with them is usually a certain degree of pleurisy, with serous 
effusion, and the formation of a yellowish or opaque lymph, which 
coats the foci on the lung surface, or extends beyond them over the 
Proximate Cause of Phlegmasia Dolens. By F. W. Mackenzie, M. D. (Med.- 
Chirurg. Trans., vol. xxxvi. p. 169.) 
1 Callender. In Holmes’ System of Surgery, vol. i. p. 276. London, 1860. 
2 Dance. De la plilebite uterine et de la plilebite en generale. (Archiv. gene- 
rales, t. xix. p. 167.) CAUSES AND PATHOLOGY OF PYJSMI A. 
15 
pleura. Sometimes the pleural sac is more or less distended with 
pus. 
The description above given of secondary foci in the lungs 
applies in the main to those observed in the liver, spleen, and kid- 
neys. In all these organs there may be reddish indurations, with 
or without a yellowish central spot, yellowish indurations, or true 
abscesses; of course on microscopical examination the characters 
of the debris are found to vary with the organ involved. Similar 
foci are sometimes observed in the subcutaneous connective tissue, 
also in the muscles and skin, but more rarely. In the latter situa- 
tion they give rise to the formation of peculiar small carbunculous 
foci, to a peculiar pustular eruption, or to gangrenous spots.1 
Besides foci of the character described, accumulations of true pus 
may take place in the ventricles of the brain, or in the joints. 
The larger joints are generally involved; the knee most frequently 
—next the shoulder. The accumulation of pus in the joints is 
often associated with tumefaction, and even heat and redness of 
the surrounding parts. 
After this brief survey of the symptoms and pathological anatomy 
of the disease, the various attempts at its interpretation have 
next to occupy our attention. These efforts largely refer to the 
secondary foci, which, however, it must be distinctly understood, 
though frequent concomitants, are not essential to the existence of 
pyasmia. 
The occurrence of multiple abscesses in the liver, lungs, and other 
parts of the body after injuries had long been known in medicine. 
Such observations had been placed on record by Massa,2 Meekren,3 
Pacchioni us,4 Schmucker,5 Morgagni,6 Desault,7 and many others. 
Especially had attention been drawn to the occurrence of abscesses 
in the liver after injuries of the head, for which various explana- 
tions were offered. Of these the most important was that of Mor- 
gagni, who regarded them as due to the translation of pus from' the 
seat of primary injury by means of the bloodvessels. He relates 
four cases of wounds of the head followed by abscesses in the 
1 Dance. Loc. cit., t. xix. p. 30. 
2 Nicbolai Massse, Anatomise Liber Introdnctorius. Yenetiis, 1559, p. 56. 
3 Observations Medico-Chirurgical. Amstelodami, 1682, p, 23. 
4 Opera. Romse, 1741, p. 63. 
5 Chirurgische Wabrnebmungen. I. Tbeil, Berlin, 1774, p. 55. 
6 De Sedibus et Causis Morborum, lib. iv., epist. 51. 
7 Desault. Jour, de Cbirurgie, t. ii. p. 11. Paris, 1791. 16 
REPORT ON THE 
lungs, in one of which there were also abscesses of the liver, and 
quotes from Bonnet’s “Sepulcreturn” to show that other organs may 
be involved, as the spleen, the mesentery, and the heart. This 
doctrine of actual metastasis was generally accepted for a time; it 
found a supporter as late as 1832, in no less a person than Velpeau,1 
and the terras metastatic abscesses and metastatic foci derived from 
it are still current in medical literature. One of the circumstances 
which strengthened the opinion was the alleged absence of the 
marks of inflammation around the margin of secondary abscesses; 
it was hence argued that the pus found could not be of local origin. 
Arnott2 quotes a passage from the pathological observations of 
Chester, published in 1766, which shows that this apparent absence 
of inflammation had attracted notice even at that early period. 
Velpeau3 particularly insists upon the doctrinal importance of this 
point, declaring that he had seen in these cases “abscesses around 
which the most attentive and minute observation did not permit 
the recognition of the least lesion of the organic elements.” 
Practical difficulties, however, arose with further investigation. 
More accurate observation showed on the one hand that whenever 
true pus was found in the secondary foci, it was formed by an in- 
flammatory process quite like that by which pus is formed elsewhere, 
and on the other hand that very often the foci contain no pus, but 
merely granular matter, commingled with the broken down debris 
of the normal tissues involved. A correct knowledge of the size 
of the pus-corpuscles moreover demonstrated the impossibility of 
pus being taken up by absorption, or of its exudation into the tissues, 
supposing it to be introduced into the blood through the open 
orifices of wounded veins. These considerations would undoubtedly 
have ultimately overturned the doctrine of metastasis had it not 
earlier become obsolete through the influence of the Hunterian 
theory of phlebitis. The essay of John Hunter on inflammation of 
the veins,4 although containing no reference to multiple abscesses 
of the internal organs, was followed by other efforts in the same 
direction, in which the Hunterian doctrine of phlebitis was made 
to play a conspicuous part in the explanation of all the constitu- 
tional and anatomical phenomena of pyaemia. Prominent among 
1 Noveaux Elements de Medecine Operatoire. Paris, 1832, t. i. p. 39. 
2 Med.-Chir. Trans., vol. xv. p. 62. 
3 Loc. cit., p. 50. 
4 Observations on the Inflammations of the Internal Coats of the Veins. Trans- 
actions of a Society for the Improvement of Medical and Chirurgical Knowledge, 
toI. i. p. 18. 1793. Also Hunter’s works by Palmer. CAUSES AND PATHOLOGY OF PYAEMIA. 
these may be mentioned the essays of Abernethy,1 Hodgson,2 
Travers,3 Carmichael,4 Rose,sand Arnott.6 
Hunter’s essay referred simply to the morbid condition which 
occasionally follows venesection, and he proposes two possible 
modes of accounting for fatal cases. “It may either be that the 
inflammation extends itself to the heart, or that the matter secreted 
from the inside of the vein passes in considerable quantity to the 
heart and mixes with the blood.” Both Abernethy and Hodgson 
adopted this twofold opinion, with little modification. Travers, 
however, rejected both possibilities, and attributed the constitu- 
tional symptoms merely to the extent of the venous surface in- 
volved. “If we consider,” he says, “ the importance of the veins 
in the economy, the extent of the surface which the collective area 
of the venous tubes affords, larger, I imagine, than any of the shut 
sacs of the body, and the diffused and disorganizing character of 
the inflammation, we can surely be at no loss to account for the 
disturbance of the system.” This suggestion, however, failed to 
command confidence, and after Arnott had shown that the ex- 
tension of inflammation from the seat of the primary affection 
along the veins to the heart could not be demonstrated in the 
autopsy, the opinion advocated by him that the constitutional 
symptoms and the secondary lesions were due to the admixture of 
pus or other inflammatory secretions with the circulating fluid, was 
very generally received. Arnott’s elaborate paper was not based 
merely on the sequelae of wounds, but an important part of his 
observations referred to the so-called uterine phlebitis. The same 
may be said of the essay of Dance,7 published nearly simultaneously 
1 On the 111 Consequences sometimes succeeding Venesection. (Surgical Obser- 
vations by John Abernethy, F. R. S. Philada. ed., 1811, pp. 83-104.) 
2 Hodgson on Diseases of the Arteries and Veins. London, 1815. 
3 Surgical Essays by Astley Cooper, F. R. S., and Benjamin Travers, F. R, S. 3d 
edition, London, 1818, vol. i. p. 286. 
1 Carmichael. Observations on Varix and Venous Inflammation. (Transactions 
of King’s and Queen’s College of Physicians in Ireland. Dublin, 1818, vol. ii. p. 
355.) 
5 Observations on Deposition of Pus and Lymph occurring in the Lungs and other 
Viscera, after Injuries of different parts of the Body. By Thomas Rose, Esq. (Med.- 
Chir. Transv, vol. xiv. p. 251.) 
6 A Pathological Inquiry into the Secondary Effects of Inflammation of the Veins. 
By James M. Arnott. Read Oct. 1828. (Med.-Chir. Trans., vol. xv. pp, 1-131.) 
7 Dance. De la phlebite utexine et de la phlebite en general considerees princi- 
palement sou le rapport de leurs causes et de leurs complications. (Archiv. Gene- 
rales, t. xviii. p. 472, and t. xix. pp. 5 and 161.) 18 
RETORT ON THE 
in Paris, which advocated similar views, and continued to be the 
chief French authority in this direction for the next twenty years. 
The subject had previously attracted the attention of several French 
physicians, and cases and remarks have been published by Bres- 
chet,1 Velpeau,2 Bouillaud,3 Andral,4 and Louis.5 
But the precise manner in which the pus thus introduced produced 
its effects, and especially how the secondary foci arose, was not so 
easily settled. The coarser mechanical explanation of metastasis 
derived from the earlier observers was not readily reconciled with 
the fact that the foci did not always contain pus, or with the large 
of pus sometimes found in them where the original local 
condition was comparatively trifling. Both Arnott and Dance simul- 
taneously abandoned this explanation as untenable. “I think it 
right, however, to state,” says Arnott,6 “ that I must not be consid- 
ered as regarding the matter so deposited to be actually that which 
has been brought into the circulation from the inflamed vein or veins.” 
“ The question is no longer one of a translation of matter merely, but 
one which involves the very difficult subject of the pathology of the 
blood.” 
“The word purulent metastasis,” says Dance,7 “is insufficient to 
express what occurs in the formation of the lesions consecutive to 
phlebitis. Before penetrating the organs, the pus mingles first 
with the blood, which it alters in a special manner; from this 
alteration result equally special inflammations; and the suppura- 
tions which then follow are not the result of a transportation of 
pus in substance as some have thought.” 
It will be seen that these opinions tend to the speculative idea 
that the secondary lesions are to be regarded as the special dynamic 
effects of a peculiar alteration of the blood; an idea which subse- 
quently received its development in the doctrine of a pyasmic dys- 
1 Breschet. De I’inflammation des veines et de la Phlebite. (Jour. Comp, du 
Diet, des Sci. Med., t. ii. p. 325, t. iii. p. 317.) 
2 Yelpeau. Recherches et observations sur la Phlegmatia alba dolens. (Arch.. 
Gen., t. vi. p. 220, 1824.) 
3 Bouillaud. Recherches clinique pour servir a I’histoire de la Phlebite. (Revue 
Medicale, 1825, p. 424.) 
4 Andral. Clinique Medicale, t. iv. p. 667. 
5 Louis. Observation de Metrite sub-aigue avec inflammation des veines uterines. 
(Archiv. Gen., t. x, p. 338, 1826.) 
6 Loc. cit., p. 123. 
7 Loc. cit., t. xix. p. 180. CAUSES AND PATHOLOGY OF PYJSMIA. 
19 
crasis taught by Eokitansky in the first edition of his pathological 
anatomy.1 
Such was still essentially the state of the question at the time of 
the publication of the work of Sedillot,2 whose elaborate volume con- 
tains a good resume of the principal labors of his predecessors, with 
much valuable personal observation and experiment, and may be 
regarded as the most complete and modern exposition of the doc- 
trine of pus-blood. In this work he endeavors to show that pyaemia 
is always preceded by suppurative phlebitis; that the presence of 
pus in the blood can be made the subject of actual observation, and 
that the symptoms and pathological alterations of can be 
experimentally produced in animals by the injection of pus into the 
veins. Each of these statements has been attacked by Yirchow, who, 
commencing in 1846, with the study of the obstruction of the pul- 
monary artery by blood clots, was led thence to the consideration 
of the general question of clot-formation in the bloodvessels during 
life, the anatomical history of inflammation of the arteries and veins, 
and finally the question of the phenomena of pyaemia. Virchow’s 
papers on this subject are republished in his Collected Essays,3 and 
an excellent summary of the opinions to which he was led is to be 
found in his lectures on The Cellular Pathology.4 
The originality and clearness of his doctrine of thrombi and 
emboli have drawn too exclusive attention to it. Virchow distinctly 
recognizes the possibility of a very different class of cases from 
those in which mere thrombous formation is the chief phenomenon. 
“To these kinds of metastasis in which definite substances, though 
' O 
not in a palpable form, but in solution, find their way into the mass 
of the blood, careful attention must at all events be paid when we 
endeavor to unravel the complex mass of conditions which are 
comprehended under the term pyaemia. I see at least no other 
possibility of explaining certain more diffuse processes, which do 
not present themselves in the form of ordinary circumscribed 
metastatic deposit. To this class belongs that metastatic pleurisy, 
which develops itself without any metastatic abscesses in the lungs 
—that seemingly rheumatic articular affection in which no distinct 
deposit is found in the joints—that diffuse gangrenous inflamma- 
tion of the subcutaneous connective tissue which cannot be ac- 
1 A Manual of Pathological Anatomy, by Carl Rokitansky. Sydenham So- 
ciety’s Translation, vol. i. p. 381. 
2 Sedillot. De I’infection purulente. 1849. 
3 Virchow. Gesammelte Abhandlungen. Zweite Ausgabe. Hamm, 1862. 
4 Die Cellular Pathologie. Zweite Auflage. Berlin, 1859. 20 
EEPOET ON THE 
counted for unless we suppose a more chemical mode of infection. 
Here we have, as may be seen in cases of variolous and cadaveric 
infection, to deal with a transference of corrupted, ichorous juices 
into the body; and we must admit the existence of a dyscrasia 
(ichorous infection) in which this ichorous substance, which has 
made its way into the body, displays its effects in an acute form in 
the organs which have a special predilection for such matters.”1 
The general view presented in this paragraph forms the subject 
of careful discussion in his essay on Emboli and Infection, and 
nine carefully described instances are presented in illustration of 
the group of cases in which, on the one hand, “ no primary thrombo- 
sis is to be discovered, and, on the other, where the condition of the 
vessels leading to the metastatic focus is not of such a kind that one 
can thence conclude a primary obstruction of it,”2 A careful 
perusal of the essay referred to will show clearly that Yirchow had 
found the doctrine of embolism inadequate to account for many of 
the phenomena of pyaemia, and that although he attributed to it 
the formation of metastatic foci in the majority of cases, he is not 
to be taxed with that exclusiveness on this point which some have 
attributed to him. 
Yirchow’s doctrine of embolism may be briefly summed up as 
follows; The starting-point is coagulated blood, contained in some 
one or more of the veins. The coagulum once formed fills the vein 
up to the next branch through which the circulation is going on; so 
long as this is the condition present, no constitutional harm results, 
but soon “new masses of coagulum deposit themselves from the 
blood upon the end of the thrombus, layer after layer, the tkrombus 
is prolonged beyond the mouth of the branch into the trunk in the 
direction of the current of the blood, shoots out in the form of a 
thick cylinder farther and farther, and becomes continually longer 
and longer.” “It is these prolonged plugs that constitute the 
source of real danger.” “ The stream of blood may detach minute 
.particles, hurry them away with it, and wedge them tightly into 
the nearest system of arteries or capillaries,”1 
The part whose nutritive supply is thus cut off undergoes chem- 
ical changes, and the metastatic focus is the result. We have to do 
in such cases “with fragments of coagula in a more or less altered 
condition, and according as this alteration has assumed this or that 
1 Die Cellular Pathologic, Lecture X. 
2 Gesammelte Abhandlungen, p. 668. 
s Die Cellular Pathologie, Lecture X. CAUSES AND PATHOLOGY OF PYEMIA. 
21 
character, the nature of the processes which arise in consequence 
of the obstruction may also be very different. If, for example, a 
gangrenous softening has taken place at the original site of the 
coagulum, the metastatic deposit will also assume a gangrenous 
character.” 
Eelying upon the process of embolism to explain most of the 
phenomena of metastasis, and supplementing this by the doctrine 
of ichorous infection to account for those cases which embolism 
fails to interpret, Virchow denies each one of the principal state- 
ments of Sddillot, He asserts that suppurative phlebitis, as under- 
stood by Hunter, Arnold, Dance, and their followers, has no exist- 
ence; that the pus-like fluid found in the veins is softened fibrin, 
and not pus; that pus has not been observed in the blood in cases 
of pyaemia; and that the experimental injection of pus into the 
blood is not followed by the constitutional symptoms or anatomi- 
cal alterations of that disease, unless some complicating circumstance 
interferes, such as the accidental introduction of coagulated frag- 
ments, which might act as emboli. 
The question of the existence of a suppurative phlebitis has 
already been referred to as far as comports with the purposes of 
this paper. Let us for a moment consider the other two questions. 
Has pus been observed in the blood in pyaernic cases ? Can pyaemic 
symptoms be produced by injections of pus or other substances into 
the circulation ? 
First, has pus been observed in the blood in pyaemic cases ? It is 
quite evident that in attempting to answer this question, we must 
lay aside the statements of observers who used the naked eye alone, 
since we have seen that decomposing blood-clots may simulate the 
appearance of pus. But some excellent microscopical observers 
also have asserted that they have actually seen pus-corpuscles in 
great numbers, both in the pus-like fluid in the so-called inflamed 
veins and in the general torrent of the circulation. Hasse1 says, 
for example, in discussing the puriform fluid in the veins, “I have, 
however, likewise found great numbers of genuine pus-globules in 
inflamed veins,” Gluge,2 who in his “Pathological Histology” 
teaches that it is generally impossible to distinguish the pus cor- 
puscles from other similar cells, gives several instances in which 
1 An Anatomical Description of the Diseases of the Organs of Circulation and 
Respiration. Sydenham Society’s Translation, page 16. 
2 Atlas of Pathological Histology, by Dr. Gottlieb Gluge. Translated by J. 
Leidy, M. D., Philadelphia, 1853, p. 54, note. 22 
REPORT ON THE 
he states that he observed pus in the blood, and especially in the 
venous blood. Of such instances he says, “It has already been 
mentioned that although pus-corpuscles have no absolute distinc- 
tive characters, yet they are readily recognized, when they possess 
several nuclei, from the smoother, indistinctly nucleated lymph 
corpuscles, in which view I entirely correspond with Dr. Lebert.” 
In one of Gluge’s cases he gives a figure of the pus-cells found by 
him in the crural vein after an amputation,1 In the text he says: 
“ These pus-corpuscles were about a third smaller than normally, 
although their nuclei were visible, and they were mixed with a few 
oil-globules.” The figure is stated to be magnified 550 diameters, 
which is certainly an exaggeration, and the corpuscles represented 
in it are not sufficiently well drawn to enable a definite opinion of 
their nature and structure to be formed. 
Sedillot claims that the pus-corpuscles have a more granular sur- 
face, a more distinct outline, are more opaque, and of larger size 
than the white blood-corpuscles. 
Lebert adds that the pus corpuscles have a more yellowish tinge 
and larger nuclei. Stress has also been laid upon the presence in 
pus corpuscles of several nuclei. 
In answer to these and similar statements, Virchow5 shows that 
although perhaps the pus corpuscles of typical pus are somewhat 
larger than the white corpuscles of the blood, and have somewhat 
larger nuclei, yet neither possess invariable characteristics. As to 
size, not only are pus-corpuscles frequently met with quite as small 
as the smallest white blood-corpuscles, and the latter quite as large 
as the largest in pus, but abscesses may be met with in which the 
mass of the corpuscles are larger or smaller than usual, and the 
same variation in size is true of the white blood-corpuscles. As 
for a more granular or yellowish appearance or sharper outlines in 
the pus-corpuscles, these may or may not be present; and, in fact, 
the appearances of both sets of corpuscles vary greatly with the 
variations in the composition of the fluid in which they float. 
Virchow quotes from Becquerel and Rodier3 to show that even in 
puerperal fever and anaemia, the blood contains less water than is 
usually present in pus. He argues that the blood serum is usually 
denser than the pus serum, and accounts in this way for the usually 
smaller size of the white corpuscles. He hence concludes that the 
1 Loc. cit., Plate 1., fig. 12. 
2 Gresaramelte Abhandlungen, p. 646. 
3 Traite de Chim. Path., pp. 122, 154, 570. CAUSES AND PATHOLOGY OF PYEMIA. 
diagnosis of pus in the blood is difficult, if not impossible, and shows 
that those cases in which the whole blood has appeared under the 
microscope to be mixed with pus, are really cases of leukaemia, the 
corpuscles being in fact white blood-corpuscles in abnormally in- 
creased numbers. My own observations have satisfied me that in 
the main these statements are quite correct. I have frequently ob- 
served and measured white blood-corpuscles, mucous corpuscles 
from the mouth, vagina, and mucous surfaces, and pus-corpuscles, 
collected under the most varied circumstances, and have not been 
able to satisfy myself that a single constant peculiarity exists by 
which a diagnosis can be made. All these bodies when recently 
formed are spherical granular cells, which may vary considerably in 
size, and which contain most frequently from one to four nucleus- 
like bodies also of variable size. Perhaps the average diameter of 
the pus and mucous corpuscles is slightly greater than that of the 
white blood-corpuscles; but pus is frequently to be met with contain- 
ing corpuscles no larger than those of the blood, and not only are 
individual corpuscles as large as any in pus often to be met with 
in the blood, but sometimes great numbers of them are present, 
especially in the blood of leuksemic patients. 
Perhaps it is true that corpuscles, with single nuclei, are more 
frequent in the blood and mucus, those with several in pus ; but 
the reverse occasionally takes place, and I have seldom examined 
a sample of either of the liquids without finding specimens of each 
kind. In March, 1866, I compared carefully the white corpuscles 
of my own blood, with the mucous corpuscles of my saliva, and the 
corpuscles of a drop of pus from a small alveolar abscess with which 
I was at that time annoyed. The majority of the white blood-cor- 
puscles observed, measured eight or nine thousandths of a milli- 
metre; a number were as large as ten, and a few eleven. The 
majority of the pus-corpuscles were nine to ten, many of them reach- 
ing eleven, and a few twelve. The majority of the mucous corpuscles 
measured ten to nearly eleven. On the addition of acetic acid, the 
majority of the cells in all the fluids were found to contain from 
one to four nuclei. But it happened that the double and triple 
nuclei were most numerous in the blood and least so in the pus. 
Next day most of the pus-cells from the same abscess contained 
double and triple nuclei. 
On the whole, therefore, it may be concluded that the diagnosis 
of blood, pus, and mucous corpuscles, is to be founded in any case REPORT ON THE 
on the situation in which the corpuscles are found, the nature of the 
fluid in which they float, and the careful consideration of all the cir- 
cumstances of the case, rather than upon the size or character of 
the corpuscles themselves. 
Secondly, can pycemic symptoms he produced by injections of pus or 
other substances into the circulation f From a very early period in 
the history of the discussion, attempts were made to produce metas- 
tatic foci, and the symptoms of putrid infection, by artificial means; 
and the introduction chiefly in the veins, but sometimes also into 
the arteries, of various solid substances, of pus, and of putrid liquors 
of different kinds, has been experimented on by a number of ob- 
servers with variable results. 
Gaspard and Cruveilhier injected quicksilver into the veins, and 
produced thus tubercle like foci in the lungs, some of which con- 
tained globules of mercury in their centres. This experiment was 
subsequently repeated by various persons, among others, by Vir- 
chow, who failed to obtain the tubercle-like foci. Still later the 
matter has been investigated by Panum,1 who obtained results op- 
posed to Virchow, and similar to those of Cruveilhier. Panum 
explains that Virchow killed his animals within forty-eight hours 
after injecting the mercury, while Cruveilhier and himself waited 
usually several days to give time for the foci to form, Cruveil- 
hier attributed the results observed in his experiments simply to 
obstruction of a branch of the pulmonary artery. But Virchow 
showed that, like obstructions produced by the introduction of 
pieces of India-rubber into the jugular vein, which were carried 
into the circulation, to be impacted in the small pulmonary arteries, 
created no similar local irritation, and Panum found that little balls 
of wax, similarly introduced, simply become encysted, Panum 
hence concludes with reason that the mercury globules, once fixed, 
act in some way as an irritant to the surrounding lung tissue, and 
not merely as a mechanical obstruction. 
More positive results were obtained by the injection of organic 
liquids in a state of septic alteration. After such injections, Gas- 
pard2 obtained gangrenous foci in the lungs. Trousseau and Dupuy 
injected into the veins of two horses a putrefying liquid obtained 
by the maceration of flesh. Grave constitutional disturbances were 
produced in both cases; in one, red foci were found in the lungs; 
1 Experimentelle Beitrage zur Lelire von der Emboli. Prof. Dr. P. L. Panum 
in Kiel. (Virchow’s Archiv, Band xxv, s. 449 ; 1862.) 
2 Journ. de Phys., par Mageudie, 1822, t. ii. p. 1 ; 1824, t. iv. p. 1. CAUSES AND PATHOLOGY OF PYEMIA. 
25 
in the other, petechia and ecchymoses in all the organs of the body.1 
Nearly similar results were obtained by Leuret, by the transfusion 
of the blood of a horse affected by charbon into a healthy mare.2 
Sedillot also gives a number of cases in which he obtained well- 
marked gangrenous foci in the lungs after putrid injections. On the 
other hand, Castelnau and Ducrest asserted that putrid injections 
prove fatal without leading to the formation of abscesses, and Stich3 
explains the results of Sedillot by supposing his experiments to have 
been made without sufficient precautions against small solid frag- 
ments which might act as an emboli. Panurn agrees with Stich in 
his opinion that metastatic foci will not be formed after putrid in- 
jections, if the fluid injected is carefully filtered. He quotes several 
experiments of his own in proof of this opinion. In these the 
fluid injected was obtained by letting dog’s flesh putrefy in distilled 
water, and afterward filtering it. He obtained, however, metastatic 
foci, and the general sj'mptoras of pyaemia, by introducing into 
the veins solid fragments in a state of decomposition or thoroughly 
soaked in the putrid fluid. 
Yirchow obtained in the main similar results, but, more mode- 
rate than Stich and Panurn, does not hold the experiments hitherto 
performed quite conclusive. On the one hand, he objects that most 
of them have been performed either on dogs, which are extremely re- 
sistant to putrid and purulent affections, or on rabbits, which perish 
under comparatively trifling lesions, and so give little opportunity 
for prolonged experiment; on the other hand, he calls attention to 
the fact too generally overlooked that the products of putrefaction 
depend so closely upon the temperature and other circumstances 
under which it occurs, that the fluid obtained by letting flesh 
putrefy in water in the open air at ordinary temperatures, is 
scarcely to be regarded as the equivalent of any of the products 
of the putrefactions or decompositions which actually go on within 
the human body in diseased conditions. He therefore regards the 
question as one which demands further investigation before a satis- 
factory conclusion can be reached. 
Like contradictions exist in the statements of experimenters with 
regard to the effects of injections of pus into the blood, on which 
1 Trousseau and Dupuy. Experiences et observations sur les alterations du sang 
considerees comme causes ou comme complications des maladies locales. Archiv. 
Generates, t. xi. p. 373, 1826. 
2 Leuret. Recberches et experiences sur I’alteration du Sang. Arcbiv. Gene- 
rales, t. xi. p. 98, 1826. 
3 Stich. Anualeu des Charite-Krankenhauses, iii. s. 192, 1852. 26 
REPORT ON THE 
indeed the experimental proof of the doctrine of pyaemia depends. 
Dupn vtren1 failed to produce metastatic abscesses by the injection 
of pus into the veins. Trousseau and Dupuy, by repeated injec- 
tions of pus into the veins of a horse, obtained constitutional dis- 
order and the production of a peculiar inflammation of the subcu- 
taneous cellular tissue of the thorax. Gunther2 failed to produce 
any anatomical alteration by the injection of healthy pus. The 
same failure attended Sedillot in many single injections of pus. 
Castelnau and Ducrest3attempted to imitate the conditions supposed 
to occur in purulent phlebitis more closely by repeating the injec- 
tions so that a constant purulent supply might be maintained. 
Under these circumstances, they succeeded in developing metastatic 
foci. Similar success attended Sedillot and more lately Gamgee4 
and Lebert.5 
On the other hand, Beck6 attributes all successes of this kind to 
a want of due precaution on the part of the experimenters, which per- 
mitted the introduction of solid or semi-solid fragments capable of 
acting as emboli, and gives fourteen cases of pus injections by him- 
self in which no abscesses were produced. Virchow takes essentially 
similar grounds; he points out that Sddillot, by leaving the canula 
tied in the vein for several days, for the purpose of facilitating 
repeated pus injections, greatly favored the probability of the acci- 
dental introduction of small coagula or other fragments, and arrives 
at the following conclusions as the results of his experiments: 
First, the injection of undecomposed, normal, non-specific pus into 
the veins, if performed with proper precautions, produces generally 
no considerable anatomical alteration, and especially no metastasis 
even when the injection is frequently repeated in the same animal. 
Secondly, the careless injection of unfiltered or very coherent pus, 
especially when frequently repeated through the same vein, pro- 
duces manifold foci of inflammation and suppuration. Thirdly, if 
putrid or specific pus is used, the foci assume a putrid or specific 
character. Fourthly, injections into the arteries give similar re- 
sults. 
We have finally to mention the experiments of Virchow and 
1 See Sedillot, p. 66. 
2 Rust’s Magazin, Band xxx. s. 332, 1834. 
3 Mem. de PAcad. de Med. 1846, t. xii. 
4 Gazette Med. de Lyon, 1855. 
5 Krankheiten der Blut- und Lymph-Gefasse, by H. Lebert, in Virchow’s Hand- 
bach. der Speoiellen Pathologie und Therapie, t. v. p. 90. 
6 [lnters. u. Studieu im Gebiete der Anat. Phys. u. Chir. s. 45, 1852. CAUSES AND PATHOLOGY OF PYiEMIA. 
Panum on the introduction of artificial emboli into the vein?. 
Virchow placed in the jugular vein of dogs, fibrin clots from various 
sources, coagulated blood from human thrombi, and small frag- 
ments of muscle; violent pneumonic affections, with pus-formation 
or necrosis of parts of the lung tissue, and other disturbances 
followed these experiments. 
Panum’s paper, already quoted, also contains an ingenious series 
of experiments. Having shown that small wax balls introduced 
into the jugular vein become merely encapsuled in the lungs, like 
Virchow’s fragments of India rubber, but did not produce abscesses; 
that the injection of the putrid liquid from meat, if carefully filtered, 
killed, but produced no secondary foci; even if wax balls were 
simultaneously introduced to obstruct the pulmonary vessels; he 
adduces two series of observations, in one of which solid animal 
substances, in a state of decomposition, or infiltrated with putrid 
fluid, in the other quite fresh coagula of healthy blood were intro- 
duced into the veins. In the first class of cases foci of inflamma- 
tion and suppuration were uniformly found in the lungs. The 
same occasionally occurred in the second series, but generally no 
considerable alteration of the lung tissue was noticed, except minute 
fibroid points resembling miliary tubercle, the precise nature and 
origin of which are not clearly made out. Panum had previously 
published a paper on transfusion of blood,1 in which he lays great 
stress on the dangers of transfusion unless performed with defi- 
brinated and carefully strained blood. Further experiments on 
the consequences of the introduction of the fresh blood coagula 
are necessary, however, to explain the irregularity of these results. 
In concluding this sketch of the general pathology of pyaemia, I 
may be permitted to state briefly how far the views hitherto 
sketched, and especially those of Panum and Virchow, correspond 
with my own personal observations. And first I must freely admit 
that careful examination of the secondary foci has usually failed to 
show me emboli impacted in the arterial twig, by which the region of 
the focus is supplied. On the contrary, the vessel continues gener- 
ally quite patulous even after it is involved in the substance of the 
morbid nodule. This I have observed in a case of foci in the lungs 
consecutive to syphilitic suppuration of the tibia, as well as in a 
number of similar cases due to wounds and amputations. I have 
investigated the branches of the portal vein leading into similar 
1 Exper. Unter. über die Transfusion. (Virchow’s Arcb. Band xxvii. s. 240,433.) REPORT ON THE 
foci in the liver in cases of ulcerative dysentery with like results. 
On the other hand, how frequently has it occurred to me to see the 
most diverse coagula in the veins leading from an amputated limb 
where death has occurred from other causes, without any pyaemic 
symptoms, and where the most critical examination of the body has 
failed to discover any secondary foci. 
Next, I may mention that so far as my own personal observation 
has gone, the pyaemic phenomena have been invariably connected 
with the primary occurrence of local septic processes. I do not 
mean to lay this down as an unchangeable law. My observations 
have not been as yet sufficiently numerous to make me positive of 
more than that this is at least an important and frequent group of 
cases. In cases of wounds the local conditions brought under my 
notice were chiefly sloughing of the edges of the wound, and the 
peculiar gangrene of the marrow which has so generally been mis- 
called osteo myelitis. This latter word has played so conspicuous 
a role that it is impossible to pass it by without notice. That there 
is an osteo-myelitis—a true inflammation of the marrow—is beyond 
a doubt. It gives rise to the changes which accompany the round- 
ing of the bone after amputations; it is connected with the repara- 
tive-effort after fractures; in unfavorable cases it terminates in sup- 
puration, When it spreads along the bone the affected marrow 
becomes reddened, often indurated, occasionally a series of discrete 
abscesses forms; occasionally the whole marrow is bathed in pus. 
But this condition, to which alone the term osteo-myelitis properly 
belongs, is usually unaccompanied by formidable constitutional dis- 
turbances, and is very generally overlooked entirely by the practi- 
tioner. The peculiar gangrene of the marrow which in armies and 
great general hospitals plays so formidable a part, may set in before 
any true inflammation has occurred in the marrow, or at any stage 
whatever of the inflammatory process, and taking its origin in the 
sloughing flaps or edges of the wound may involve the inflamed 
portion of the marrow, and thence' spread rapidly beyond along the 
healthy marrow which it speedily reduces to a greenish-yellow or 
brownish-green stinking pulp. This condition I have seen extend 
to the head of the femur after amputations at the lower third ; I 
have known it to spread throughout the whole length of the femur 
in cases of contusion of the bone by balls without fracture. 
Where death has taken place before the whole marrow has been 
involved, the region of transition between the healthy marrow and 
the gangrenous part affords the opportunity for studying the steps CAUSES AND PATHOLOGY OF PYiEMIA. 
29 
of the process. The gangrene is not preceded by redness, by effu- 
sion, by cell multiplication, by anything that can be construed into 
inflammation. The first phenomenon noted is the peculiar coagula- 
tion of the blood in the bloodvessels, and the granular aspect of the 
tissues under the microscope, which shows that the part is already 
dead, and that decomposition has commenced. The subsequent 
changes are purely chemical, and the normal elements become less 
and less recognizable amidst the host of actively moving molecules 
set free by the putrefactive alteration. The process is in fact only 
to be compared with the most destructive and rapidly progressing 
form of gangrene of the external soft parts. Energetic as it is, how- 
ever, it does not always prove fatal, especially in the cases which 
follow amputations. A line of demarcation may be formed by a 
true inflammatory process, and the dead tissue may separate as a 
slough, the prominent part of which is a cylindrical tube of bone of 
variable size, representing usually the whole shaft at the point di- 
vided by the saw, and from the eighth of an inch to an inch above 
it; thence an irregularly eroded cylinder of variable length. I have 
seen these tubes seven or eight inches long. 
But in the cases which prove fatal by inducing pysemia, no line 
of demarcation, no barrier of inflammation limits the gangrenous 
portion, and the veins leading from the affected bone are usually 
full of coagula which have entered into a form of putrefaction quite 
similar to that going on in the marrow. The ultimate result of this 
change is a yellowish or greenish-yellow fetid fluid, in which the 
microscope recognizes nothing but actively moving molecules with 
bright centres and dark borders. I have once or twice seen the veins 
leading from the flaps of a sloughing stump in a similar condition, 
but in most of the cases to which my attention was drawn the veins 
affected proceeded directly from the diseased bone itself. The putre- 
factive change going on in the marrow is transmitted through the 
coagulated blood mass in the veins by actual continuity. The 
femoral vein, the saphena and their branches were sometimes stuffed 
with thrombi throughout a part of their extent, but in all the cases 
I found the veins from the bone, filled with their fetid contents, 
were clearly traceable to the point where the trunk with which 
they were connected discharged into the femoral, or one of the 
larger branches with no thrombi intervening on the cardiac side. 
The granular yellowish fluid could sometimes be traced some little 
distance towards the heart. In short, there was clear anatomical 
proof of the introduction into the torrent of the circulation of the 30 
REPORT ON THE 
putrefying debris of the coagula which had formed in the veins 
leading from the affected bone. 
As for the detaching of larger fragments which should deserve 
the name of emboli, I found no actual anatomical proof, though 
abundant possibility for such an occurrence existed. What was to 
be seen discharging into the femoral vein was simply the putrefying 
liquid described, a liquid more viscid than blood, which could not 
be expected to circulate as readily as blood, which might readily, I 
admit it, although I saw nothing of the sort, carry with it more 
coherent fragments of the involved coagulurn, but which, in any 
case, might be expected to be arrested in the capillaries of the lungs, 
and if so arrested, to set up there, by actual contact, a similar form 
of change. It is also easier to conceive how a part of such a viscid, 
putrid fluid, which had passed through the capillaries of the lungs, 
might subsequently bs arrested in the systemic capillaries, than it 
is to account for the frequent occurrence of foci in the liver and 
kidneys after amputations of the thigh on the supposition of solid 
emboli. 
I do not offer this summary of my own observations as a solu- 
tion of the question of pyaemia; rather as a statement of facts, diffi- 
cult to account for on the supposition of emboli, impossible to ac- 
count for on the supposition of suppurative phlebitis, which must yet 
be fully embraced by any satisfactory explanation of the disease. 
The general series of phenomena here sketched, as observed in con- 
nection with wounds, perfectly accords with what I have been able 
to observe in puerperal pyaemia, and in the pyaemia connected with 
dysentery. In the inflamed womb of the first group of cases, and 
the colon ulcers of the second, all the autopsies I have witnessed 
or made, demonstrated the existence of gangrenous or phagedenic, 
that is, septic processes in connection with the local lesion. With- 
out insisting upon any exclusiveness for the opinions which must 
necessarily spring from such cases, it is difficult to avoid the con- 
clusion that local septic processes have a significant connection 
with the genesis of pyaemia, and that viscid septic liquids derived 
from the degenerating primary coagulum may at times play the 
part which Yirchow ascribes only to solid emboli. 
These considerations assume still more importance when an at- 
tempt is made to arrive at some definite notion with regard to the 
causes of pycemia. Truly it must be admitted that our knowledge 
of these causes is yet more unsatisfactory than our knowledge of 
the pathology of the disease. It is well known, however, that the CAUSES AND PATHOLOGY OF PYEMIA. 
31 
conditions under which it most certainly develops itself are those 
under which almost all zymotic diseases attain their greatest malig- 
nancy ; and it will readily be understood, if the views I have hinted 
are correct, that whatever favors the occurrence of septic processes 
in the local lesion may become a cause of pyaemia. Hence it is in 
crowded hospitals, where ventilation, cleanliness, and diet are com- 
paratively neglected, and among patients debilitated and disordered 
by previous exposures and privations that pyaemia secures most 
victims, whether among wounded soldiers or parturient women. 
Under the same circumstances, erysipelas, hospital gangrene, and 
sloughing of wounds and sores become common, very often indeed 
appear to stand in direct genetic connection to the subsequent 
pyaemia. Whether besides such hygienic conditions, to which in 
modern times attention has been most exclusively directed, there 
lurk yet other and more obscure momenta; whether above all, as 
has been especially claimed by the obstetricians, there is a peculiar, 
pyaernic, epidemic influence which exists at certain times and places, 
and is absent at othqrs, is a question which can be first intelligently 
approached when an epidemic of pyaemia shall have been observed 
under circumstances which completely fulfil every well-known 
hygienic requirement; until then to insist upon this aspect of the 
question tends to encourage and excuse the neglect of conditions 
whose influence is beyond question. 
After the foregoing remarks on the general relations of pyaemia, 
it remains to consider briefly its more important varieties. Passing 
by the strictly surgical relation of the subject, I shall first speak 
of puerperal pycemia. Puerperal-pyaemia embraces the group of 
cases which occur in parturient women in connection with the local 
changes which have been most generally described under the name 
of uterine phlebitis. The disease constitutes one of the most 
formidable types of the so-called puerperal fever. The general 
symptoms during life do not differ from those of pyaemia as already 
described, and after death the metastatic foci often found, especially 
in the liver and lungs, and the state of the veins leading from the 
uterus, particularly those connected with its placental region, differ 
in no essential particular from what is seen in pyaemia consecutive 
upon wounds. The condition of the womb itself in these cases 
requires a more exact anatomical investigation than appears as yet 
to have been bestowed upon it. It is generally spoken of as in- 
flamed ; often abscesses are said to exist in the substances of its REPORT ON THE 
walls. In the cases which have been brought within my own per- 
sonal investigation, I have found no satisfactory anatomical proof, 
either of inflammation or abscesses. On the contrary, what was to 
be observed in the general tissue of the womb itself was merely 
the usual retrograde metamorphosis (fatty degeneration of the mus- 
cular tissue) which follows parturition. A putrid condition of the 
inner surface of the organ, however, existed, extending to a vari- 
able depth, and coagula filled the uterine veins, especially those 
corresponding with the placental surface. Septic metamorphosis 
existed in these precisely as in the similar coagula in the veins 
leading from bones affected with gangrene of the marrow. 
In the earlier periods of medical literature the cases now under 
consideration were confounded under the general designation of 
puerperal fever, but immediately after the essay of Hunter on 
phlebitis, the English obstetricians began to discriminate a class of 
cases which they supposed to be best described under the name of 
uterine phlebitis, Clarke1 found what he considered to be pus in 
the uterine veins of a woman who had died after labor, and Wil- 
• 7 
son2 described the morbid appearance of one case, and alluded to 
others in which inflammation of the uterine veins had existed and 
even extended to the cava. Both Arnott and Dance drew from 
uterine pyaemia the most important of their illustrative cases, and 
subsequently there are few writers on phlebitis and pyaemia who 
fail to refer to the puerperal form. Virchow, in his “ Cellular Pa- 
thology” (Lecture X.), appeals to the facts observed in an epidemic 
of puerperal fever in Berlin to support his doctrine of emboli, and 
H. Meckel3 and Kiwisch4 in the main adopt his views of the part 
played by thrombi and emboli in the production of the secondary 
lesions. 
It is not very easy to separate the consideration of puerperal 
pyaemia from that of phlegmasia dolens; an affection of the lower 
extremities, which, although chiefly met with in the parturient 
female, is not always confined to this condition or indeed to the 
female sex. It is characterized by the development of a peculiar 
oedema, the affected limb becoming painful to the touch, with swell- 
2 Transactions of a Society for the Improvement of Medical and Chirurgical 
Knowledge, vol. iii. p. 65. 
1 Practical Essays on the Management of Pregnancy. London, 1793, p. 70, 
3 H. Meckel, Annalen des Charite-Krankenhauses, v. s. 276. 
4 Kiwisch, Klinisohe Vortrage liber spec, Pathologie u. Tberapie der Krankb. 
des weiblichen Geschlechtes, 1851, Band 1., s. 630. CAUSES AND PATHOLOGY OF PYAEMIA. 
33 
ing and induration in the course of the veins. It may affect one 
limb or both; in the latter case either successively or simultane- 
ously. It may produce comparatively little constitutional disturb- 
ance, or may be accompanied by the usual symptoms of pyaemia 
with a fatal result. In the latter case, degenerating coagula in the 
uterine as well as the crural veins, pelvic abscesses, abscesses in 
the femoral subcutaneous tissue, and secondary foci of the viscera 
are the conditions most frequently observed. Bouillaud' was among 
the first to connect this peculiar swelling with obstruction of the 
veins, and Dr. Davis, in the same year published an able paper in 
which he makes the attempt to connect the condition with phlebitis 
of the crural veins.2 According to Dr. Davis four different theories 
had previously been propounded ; that of Mauriceau3 that it was 
due to a reflex “of humors which ought to be evacuated by the 
lochia;” that of Puzos4 “ that it was due to the metastasis of milk,” 
which was also adopted by Levret;5 that of White and Trye, that 
it was due to obstruction or other morbid states of the lymphatics, 
and that advocated by Dr. Hull in his essay on phlegmasia dolens, 
published in 1800, that it “ consists in an inflammatory affection, 
producing suddenly a considerable effusion of serum and coagulable 
lymph from the exhalants into the cellular membrane of the limb.” 
The next year Velpeau published a paper on the same subject, in 
which he arrived at essentially the same conclusions as Davis had 
done.6 And still further development was given to the idea by the 
labors of Dr, Kobert Lee,7 who particularly insisted upon the exten- 
sion of inflammation from the uterine veins to the crural as explain- 
ing the origin of the affection. On the other hand, Mackenzie8 dis- 
1 De I’obliteration des veines, etc. M. Bouillaud. (Archiv. Gen., t. ii. p. 188. 
1823.) 
2 An Essay on the Proximate Cause of the Disease called Phlegmasia Dolens, hy 
David D. Davis, M. D. (Medico-Chirurg. Trans., vol. xii. p. 419. 1823.) 
3 Traite des Maladies des Femmes Grosses et de celles qui sont accoucliees, sme 
edit., t. i. p. 446. 
4 Puzos. Memoire sur les depot laiteux. 
5 Levret. L’art des accouchements. 
5 Recliercbes et observations sur la Phlegmatia alba Dolens. M. Velpeau. (Ar- 
cliiv, Gen., t. vi. p. 220. 1824.) 
7 Robert Lee. A Contribution to the Pathology of Phlegmasia Dolens. (Med. 
Chir. Trans., vol. xv. p. 132. 1829.) Pathological Researches on Inflammation 
of the Veins of the Uterus, with Additional Observations on Phlegmasia Dolens. 
(Ib., vol. xv. p. 369.) Further Researches on Phlegmasia Dolens. (Ib., vol. xxxvi. 
p. 281. 1853.) 
8 Researches on the Pathology of Obstructive Phlebitis and the Nature and REPORT ON THE 
puted the general correctness of the popular doctrine of phlebitis, 
and especially its application to the interpretation of phlegmasia 
dolens, which he regarded as due to non inflammatory clot forma- 
tion; a view also adopted by Yirchow in his account of this affection. 
Of course, the ultimate interpretation of phlegmasia dolens will be 
determined by the prevalent doctrines on phlebitis, thrombosis, and 
infection; at present, however, the uniform existence of thrombi 
in these cases, and the comparative rarity of pysemic symptoms 
may be particularly mentioned as of doctrinal importance. Ac- 
cording to Mackenzie, of sixty cases of puerperal phlegmasia dolens 
only twenty proved fatal. 
The pyaemia of new-horn children connected with erysipelatous 
and gangrenous conditions of the naval, which is generally described 
under the head of phlebitis of the umbilical vein, may next be 
briefly mentioned. Described early in the present century by 
Breschet, Duplay, and Trousseau, this affection has comparatively 
recently been carefully studied by H. Meckel1 in La Charitc at 
Berlin. The affection is seldom observed except in hospitals and 
among the squalid children of the poor. It begins as a suppurative, 
erysipelatous or gangrenous affection of the navel, followed by 
thrombus formation in the umbilical vein, occasionally in the por- 
tal vein; secondary foci in the liver, lungs, etc., result. According 
to H. Meckel, abscesses in the lungs and subcutaneous tissue occa- 
sionally occur without foci in the liver. Peritonitis often accom- 
panies the disease, and jaundice and diarrhoea are frequent symp- 
toms, The course of the affection does not differ from other cases 
of pyaemia. It almost always terminates fatally. 
Of more general significance to the medical practitioner than any 
group of pyaemic cases, except those connected with the puerperal 
state, are those which spring from ulceration of the bowels and 
other conditions connected with the parts whose venous branches 
terminate in the portal vein. These cases have been the subject 
of numerous essa}7s and studies, and after the memoir of Francon- 
neau Dufresne,2 and the publication of Lambron’s3 remarkable case 
Proximate Cause of Phlegmasia Dolens. F. W. Mackenzie, M. D. (Med.-Chirg, 
Trans., vol. xxxvi. p. 169. 1853.) 
1 H. Meckel. Ueber die Entztindung des Nablevenen. Annalen der Charite, 
1854. 
2 De I’inflammation du systeme veneux abdominal, par le Docteur Franconneau 
Dufresne. (Gazette Medicale de Paris du 16 Novembre, 1839.) 
3 Observations d’inflammation de veins du foie, par Ernest Lambron. (Arcbiv. 
Gen. 3me serie, t. xiv. p. 129. 1842.) CAUSES AND PATHOLOGY OF PYASMIA. 
in which a fish bone swallowed by an old man found its way 
through the walls of the stomach, transfixed the portal vein, and 
gave rise to a fatal pylephlebitis, numerous cases and remarks on 
pylephlebitis were published by different observers, among others 
by Frey, of Manheim,1 Waller,2 and Oppolzer,3of Prague, and Hen- 
noch,4 of Berlin. The excellent paper of Leudet5 may also be 
mentioned. All these, and most of the subsequent essays, includ- 
ing the section on inflammation of the portal veins in Budd’s work 
on the liver,6 describe phlebitis of the portal vein as consisting of 
two varieties, the adhesive and the suppurative, and in the details 
of the local description agree with the general account of phlebitis 
as received by their contemporaries. More modern views are ex- 
pressed in the treatise on diseases of the liver by Frerichs,7 who, 
while still speaking of adhesive and suppurative pylephlebitis, 
clearly recognizes the frequency of thrombus formation in the por- 
tal vein without inflammation, and especially in his description of 
suppurative pylephlebitis, shows his understanding of that process 
to be much more in accord with modern doctrines than the names 
he still employs would indicate. “ The thrombus in the interior of 
the vein undergoes destruction at an early period. It softens from 
the centre into a dirty greenish-red pulp, and afterwards dissolves 
more or less completely into a purulent fluid.” “ Not unfrequently 
metastatic deposits are developed, as in other forms of phlebitis, by 
particles of thrombi being floated by the blood into the liver; these 
deposits are found in various stages of development, from reddish- 
brown infarctions to yellow cavities of pus.”8 
The affection usually described under the name of pylephlebitis, 
is characterized by abdominal pain, usually in the epigastrium or 
right hypochondriac region, with rigors, fever, enlargement of the 
liver and spleen, followed by jaundice, symptoms of diffuse peri- 
tonitis, delirium, and a fatal typhoid condition with or without evi- 
1 Heidelb. Annal., t. x. 1844, in Archiv. Gen., 4me serie, t. vii. p. 483. 
2 Wiener Zeitung, 1846, in Archiv. Gen., 4me serie, t. xviii. p. 462. 
3 Prager Vierteljahrschrift, t. i. p. 110. 1849. 
5 Recherches sur la Phlebite de la veine porte. (Archiv. Gen., sme serie, t. i. 
p. 145.) 
4 Klinik der Unterleihs-Krankh., p. 188. Berlin, 1852. 
6 On Diseases of the Liver. By George Budd, M. D. 3d ed. London, 1857, p. 170. 
7 A Clinical Treatise on Diseases of the Liver. By Dr. F. T. Frerichs. Edit, of 
New Sydenham Society, Loudon, 1861. 
8 Loc. cit., vol. ii. p. 408. 36 
REPORT ON THE 
dence of metastatic foci in the lungs and joints. It usually runs its 
course in from four to six weeks, but may prove fatal earlier, or 
may be protracted longer. It may be due to ulcerations of the 
alimentary tract, abscesses of the spleen or mesenteric glands, dis- 
turbances due to gall-stones, etc. Here, as elsewhere, it is necessary, 
however, to distinguish between mere thrombus formation and 
those cases which terminate in pyaemia. In the cases which result 
from chronic dysenteric ulcers of the colon, the patient, alter having 
suffered from dysentery for a variable period, suffers a chill, or a 
series of chills, followed by the usual constitutional symptoms of 
pyaemia with fatal issue. After death metastatic foci in various 
stages of development are found in the liver, the lungs, the spleen, 
or elsewhere. A similar form of pyaemia occurs in connection 
with typhoid ulcers of the small intestines. 
Intimately allied to the question of pyaemia originating in dysen- 
tery, is the special subject of abscess of the liver occurring in 
that disease. Budd, in his treatise on the liver, attributes all ab- 
scesses of this organ, except those resulting directly from blows or 
injuries, to “suppurative inflammation of some vein, and the con- 
sequent contamination of the blood by pus.” Bristow1 attacked 
the exclusiveness of this explanation, speaks of tubercular ab- 
scesses, abscesses due to hydatids, to obstruction of the hepatic 
ducts by gall-stones, etc., but admits the occasional applicability 
of Budd’s views, and regards the hepatic abscess of dysentery as 
due to phlebitis of the mesenteric veins. Frerichs2 enumerates as 
causes contusions or other traumatic agencies, metastatic or pysernic 
inflammation of the liver, inflammatory and ulcerative processes in 
the gastro-intestinal canal, and inflammation and ulceration of the 
bile ducts. The whole matter possesses great interest, but at pre- 
sent I must be content with this passing notice. 
Besides the foregoing more important varieties, pyaemia may 
result from a great number of other morbid conditions, among 
others from syphilitic or other diseases of the bones, and from 
rheumatism, as in the cases of Habershon3 and Bennett.4 Haber - 
1 On the Connection between Abscesses of the Liver and Gastro-intestinal Ulcera- 
tion, (Trans, of Path. Society of London, vol. ix. p. 241,1858.) On the Modes in 
which Hepatic Abscesses may be formed, etc. (Ib., p. 273.) 
2 Loc. cit., vol. ii. p. 110. 
3 Guy’s Hospital Reports, 1859. 
1 Clinical Lectures, Am. ed., 1860, p. 847. CAUSES AND PATHOLOGY OF PYiEMIA. 
37 
shon, indeed, goes so far as to suggest that gonorrhoeal rheumatism 
is generally a form of pyaemia. 
Finally, we have to consider the so called idiopathic or spontane- 
ous pyaimia of the Vienna school,1 to which attention has recently 
been drawn by Wunderlich. Wunderlich2 indicates by the idiopa- 
thic pyaemia simply those cases in which the cause is hidden and 
cannot be traced to the local lesion in which it originated. But 
this moderate view has not always prevailed. I will not attempt 
to trace the full history of the confused statements that have been 
made. It is sufficient to state that a pyaemia which is without 
typhoid symptoms, and without secondary foci—which is predi- 
cated wholly upon the presence in the blood of bodies believed 
from their microscopical appearances to be pus-corpuscles, is not 
pyaemia, but leukaemia, or white blood. The existence of true cases 
of pyaemia for which no local cause can be found cannot, how- 
ever, be denied, though their appearance is comparatively rare. 
Cases which take their origin in idiopathic erysipelas or gangrene 
are much more frequent, and are properly embraced in the notion 
of spontaneous pyaemia. Among these latter cases there is an in- 
teresting;: form in which metastatic foci occur in the skin. Dance 
gives two cases of this sort; the first,3 a true case of spontaneous 
pyaemia; the second, originating in idiopathic gangrene of the right 
little finger. In both the history of pyaemia was undoubted, and 
metastatic foci were found in the lungs as well as in the skin. I 
have myself had my attention drawn to a similar case taking its 
origin in idiopathic erysipelas. 
In concluding this paper, I have to express my regret that other 
engagements have not permitted me to bestow upon the subject the 
time and labor it so well deserves. But a detailed criticism of its 
literature, with an attempt to throw further light on the open ques- 
tions by experimental researches, would occupy a volume, .and I 
have been compelled to content myself with this brief survey of 
the present state of our knowledge, which I trust may not be found 
devoid of interest. 
1 Rokitansky, Path. Anat. Sydenham Soc. Edit., vol. i. 
2 Wunderlich, from Archiv. fiir Phys. Heilkunde, in Gazette Medicate de Paris 
vol. xxx. p. 422. 1858. 
3 Loc. cit. Archiv. Gen., t. xii. p. 30.