OF SPLENIC AND LYMPHATIC HYPERTROPHY WITH- 
OUT LEUCOCYTHAEMIA (HODGKINS’ DISEASE — 
A DFNIE—PSE UDO-LE UCAE Ml a ). 
ON A" CASE 
IN the month of August I was asked by Dr. Fricke to see, 
with him, a case in the northern part of the city. Mr. 
, aged about 30 years, had served in the army during the 
last six months of the rebellion, chiefly in Virginia, much 
of the time in malarious districts, during which he suffered 
severely from camp-diarrhoea or dysentery, but never had any 
distinctly malarious disease. After his return, he resumed his 
occupation, that of a confectioner. At this time, he states, he 
was an exceedingly powerful man, lifting a barrel of flour with 
ease. His habits were in every respect moral; strictly tem- 
perate ; never had syphilis or gonorrhoea. His work was very 
heavy, consisting chiefly in kneading and handling immense 
pound-cakes, and was done altogether with his right hand, his 
body being bent sharply to the left in a constrained position. 
To this he himself attributed his attack. His wife, after his 
death, stated that ever since she had known him—three years 
—he had been troubled with looseness of the bowels and sud- 
den attacks of diarrhoea. Four months ago, in April, he was 
taken with pain in back and left side; this pain was chiefly 
dragging and heavy. During the next two months he had occa- 
sional attacks of diarrhoea, but was treated chiefly for the 
persistent pain, which was believed to be rheumatism. During 
the last two months he has lost flesh and strength rapidly, and 
a few days ago sent for Dr. Fricke, who at once determined the 
case to be one of diseased spleen. The following is taken 
from my note-book: 
August 15. Man very thin and weak, but able to walk about 
the room. Skin natural in color but pale, and temperature 
normal. Tongue clean. Heart and lungs normal. Abdomen 
enlarged, apparently free from fluid. Spleen very much en- 
larged; the area of decided percussion dulness 5 inches 
DR. H. C. WOOD. ■vertically, b]/2 transversely; its surface smooth, hard, its 
■ edges rounded; decided tenderness when strong pressure is 
made upon it. Liver enlarged, its smooth edge reaching 
about an inch below the ribs; vertical percussion dulness 5]/2 
inches. Urine normal, save only that it contains some minute 
crystals of phosphates and a good deal of mucus. 'Has not 
either sexual desire or power, nor has he had for two months. 
Legs slightly oedematous. Has had iron and quinine, and 
an ointment of iron and belladonna over region of spleen. 
Examined, with Dr. Fricke, blood microscopically: cer- 
tainly no increase in white blood corpuscles. 16. Has 
decided fever this morning. Ordered tr. iodin. comp. gtt. 
v, t. d. 17. Has some fever; skin hot and dry. 25. Patient 
worse since last entry; feet very much swollen; is weaker 
and more emaciated; has had fever occasionally; a good 
•deal of irritation of the stomach, possibly caused by iodine, 
and also diarrhoea. Examined blood carefully microscopic- 
ally-; the white blood corpuscles found were very few in 
number, certainly below rather than above the normal pro- 
portion. Ordered tr. ferri chi. gtt. xxxv and cinchon. sulph. 
grs. ii, t. d,; also decoction of broom (Scoparium). 28. No 
decided change, but marked increase in flow of urine. 30. 
No especial change since last entry. Patient has had no 
fever for several days, September 12. Not very much changed, 
"but decidedly paler and weaker; hardly able to walk a few 
steps; occasionally has fever, no regularity perceptible in its 
attacks; spleen, by palpation and percussion, %]/2 inches 
transversely by 6 vertically, apparently not quite so hard as 
before, smooth; vertical liver-dulness 5 inches; pulse 96, ex- 
cessively dichrotic; a very decided basal systolic murmur, 
anaemic in character of its sound; tongue clean; appetite 
■pretty good; legs very oedematous. 29. No change since last 
entry; merely a steady advance in severity of symptoms; 
more or less frequent attacks of diarrhoea and of fever; pro- 
gressive emaciation; great loss of strength, so that he is not 
able to stand alone now; general hue of skin that of intense 
anaemia; lips almost white ; nothing like cancerous cachexia; 
no oedema now (probably partly from his being constantly re- 
cumbent) ; decided ascites; spleen very hard; lymphatics of 
neck, axilla, and groin decidedly but not greatly enlarged. 
October I. Examined blood microscopically: certainly dimi- 
nution, rather than excess, in proportionate number of white 
blood corpuscles; not more than one field of an y&th in three 
contained any, and only once, out of a number, were two found in a single field; red corpuscles pale, showing no tendency to 
adhere in rouleaux. 8. Man died quietly of exhaustion. 
Autopsy, about 36 hours after death.—Body emaciated, pale. 
Thorax.—Pleura containing a large quantity of serous fluid. 
Lungs healthy. Blood-vessels normal. Heart small, pale, 
somewhat soft; valves healthy. Abdomen.—Liver very much 
enlarged, fatty, nutmeg; no heterologous deposits in it; con- 
sistence much firmer than normal. Pancreas large, hard. 
Stomach normal. Intestines thin; their mucous membrane 
pale; no enlargement perceptible of the simple glands; Pey- 
er’s glands a little more prominent than usual; not ulcerated; 
suprarenal capsules normal. Kidneys rather small, normal; 
no heterologous growths discovered. Spleen very much en- 
larged and hardened; as laid on a plate, eight inches long, 
five and three-quarters broad, and nearly four thick; color 
very bright red, almost scarlet, mottled with numerous dark 
spots and with some yellowish ones; capsule readily detach- 
able ; showing on section a narrow external zone of bright red; 
internally, darker red, a sort of reddish liver-colored, with 
numerous very dark spots or masses closely placed. There were 
also a few masses of a straw-yellow color scattered through the 
spleen. These masses were of various shapes and sizes; not 
very numerous. The largest was of a wedge-shape, the base 
against the surface of the spleen; the edges irregular in places, 
folded in, with one or two lines of deep red external to them 
and everywhere following their contour. This patch is one 
and a quarter inches long and three-quarters of an inch across 
the base. The whitish material appeared to be formed in 
centre of the dark patches; at least, quite a number of such 
spots exhibited a minute central whitish spot, similar in appear- 
ance to the larger whitish ones. Lymphatics enlarged both in 
thorax and abdomen, and still more so in the axilla, neck, and 
crural regions. The only superficial glands taken out were 
from the groin. These were about an inch in length, and 
were larger than the internal glands. 
Microscopic Examination.—Spleen.—Pulp containing usual 
elements, fibrous tissue, nucleated trabecular cells, and pulp 
cells. The latter appeared more granular and less distinctly 
nucleated than normally. Red Spots.—These appeared to be 
chiefly colored by an intense hyperaemia; not so much, how- 
ever, by the distinct presence of blood as by an excessive over- 
plus of coloring-matter. The latter was not contained so much 
in distinct globules, as it appeared to penetrate everything. 
There were a very few pigment granules. The red spots could be in great measure washed out, and, under the microscope, 
presented no other elements than such as were found in the 
pulp elsewhere; only everything intensely red. A very few 
pigment granules were seen, and in one place was found, in 
the centre of a dark spot, a somewhat cylindrical, dark-green, 
hard, flattened mass of nearly a line long. Nowhere else 
were any indications found of masses of blood having existed. 
Whitish Spots.—Composed almost entirely of cells similar to 
those of the pulp, but smaller to shrunken, 
a little more inclined to be globular, never nucleated, and 
filled with granules; some oil, but not much. Malpighian 
corpuscles were not at all evident. I dissected one out of the 
centre of one of the dark spots. It appeared normal, save 
that it was of an intensely red color. 
Among the first distinct recognitions of a disease 
whose anatomical characters were great enlargement of 
the lymphatic glands and of the spleen, with which I 
am acquainted, is that of Dr. Hodgkins {Medico-Chi- 
rurgical Review, vol. xvii.). In this paper, however, 
there were no microscopical examinations of the blood, 
and it is therefore uncertain whether the affection was 
actually the disease since known as Hodgkins’ disease, 
or whether it was leucocythsemia. In a paper published 
in Recueil des Travaux de la Societe Me die ale d' Ob- 
servation, 1857-58, to which I have not, however, had 
access, Dr. Bonfils appears to have described for the 
first time what have been considered since as the chief 
characters of the disease,—namely, glandular enlarge- 
ment without increase of the white corpuscles of the 
blood. Since this time there have been some half a 
dozen papers upon this affection ; and in the Archives 
Generates for 1865 there is a good resume by Dr. 
Cornil of our knowledge upon the subject, with one 
or two excellently observed cases. In the last edition 
of the Clinique Medicale, by Professor Trousseau, there 
is a brilliant lecture upon this affection, its clinical his- 
tory and pathology. The doctor gives to the disease 
the name of Adenie, and assigns to it, as clinical char- 
acteristics, great and progressive enlargement of the 
lymphatic glands, without any tendency to suppuration 
or resolution, and finally death of the patient, some- 
times from intercurrent accidents, as suffocation from the pressure of the enlarged glands upon the respira- 
tory passages, or, escaping these, from intense anaemia, 
with diarrhoea, hectic fever, colliquative sweats, etc. 
In only three out of twelve observations was there any 
enlargement of the spleen, and in these this was pre- 
ceded by enlarged lymphatics, and belonged, Professor 
Trousseau states, strictly to the second stage of the dis- 
ease. The disease was chronic in its nature, lasting 
from twelve to eighteen months, or even longer; and in 
several cases the patient was apparently in excellent 
health, although enormously enlarged lymphatics had 
already existed for months. 
In the cases described by Dr. S. Wilks, in Guy s Hos- 
pital Reports, 1865, under the name of Hodgkins’ dis- 
ease, the enlargement of the spleen was a more con- 
stant and more striking feature; but in other respects 
the agreement is complete,—the same enlarged glands 
and the same peculiar whiiish masses found in the 
spleen. There is, therefore, a disease described by 
these authors closely allied to leucocythaemia,—so 
closely, that it is impossible to distinguish between the 
two, either before or after death, save by the micro- 
scopic examination of the blood, their clinical history 
and post-mortem appearances being otherwise exactly 
similar. In leucocythaemia, however, there are, as is well 
known, two sets of cases,—namely, the lymphatic and 
splenic, — in the one of which the glands are chiefly, 
or even solely, affected; whilst in the other the spleen 
bears the brunt of the disorder. 
The splenic variety is certainly the most common ; 
but that there are certain cases of leucocythaemia in 
which the spleen remains healthy whilst the lymphatic 
ganglia become enormously enlarged, is attested, from 
personal experience, by both Virchow and Niemeyer. 
All the cases of the allied adenie hitherto published 
have corresponded more closely to the rarer form of 
leucaemia, the glands being very greatly and primarily 
affected. 
The case herein detailed, I conceive, presents hith- 
erto unnoted clinical characteristics, in that the affection 
of the spleen was primary, and the enlargement of the 
lymphatics was manifested late in the disorder and was at no time sufficient to attract attention. The paral- 
lelism between the two diseases is therefore now com- 
plete, both of them exhibiting a splenic and a lymphatic 
form; although it is worthy of remark that, so far as I 
am aware, no case of Hodgkins’ disease has been re- 
ported which ran its full course, with death from anaemia 
without accident, in which the spleen was not finally 
enlarged. 
There is one anatomical change, occurring not infre- 
quently in leucocythaemia, which has as yet scarcely 
been noted in adenie, namely, the formation of masses 
of lymphatic tissue in the liver, kidneys, etc. I do not 
think this, however, can at present be allowed to be a 
point of difference. The masses alluded to are not 
new tissue formation. Von Recklinghausen and other 
German histologists have demonstrated, or at least ren- 
dered extremely probable, the existence of minute lym- 
phatic masses or cells in all these glandular organs ; 
and the interpretation of the appearances alluded to is 
simply that such minute portions of the lymphatics have 
partaken in the general hypertrophy. Friederich, to 
be sure, claims to have demonstrated that these for- 
mations take their origin in the connective tissue cor- 
puscles ; but I do not think, at present, this can be ac- 
knowledged. I see, therefore, nothing more than was 
to be expected in the leucaemic tumors of the liver and 
kidneys, and believe the reason that they have not been 
more frequently found in Hodgkins’ disease is the ex- 
ceedingly small number of the cases that have been 
well observed. According to Dr. Cornil, moreover, M. 
Herarcl has observed this formation of apparently new 
lymphatics in a case of adenie, in the lungs, ovaries, 
and mucous membranes of the stomach: so that I do 
not see how the exact parallelism between the two 
affections can be denied. 
In regard to the nature of Hodgkins’ disease, Dr. 
Wilks advances the opinion that it is a constitutional 
disorder, closely allied to tubercle and cancer, charac- 
terized by a peculiar exudation in the spleen tissue. 
This is evidently an erroneous theory. It is hardly 
possible to conceive a disorder of the same class as 
tubercle in which the deposit is always confined to a single organ ; and, moreover, similar masses are found 
in the spleen in leucocythaemia, more rarely in chronic 
malarial hypertrophy, and also in ulcerative endocar- 
ditis. They are, in truth, not deposits at all, but are 
the results of arrest of circulation, and are the so-called 
“hemorrhagic infarctions.” In heart-disease, they are 
often directly traceable to the presence of emboli 
stopping up the smaller splenic arteries. In the case de- 
scribed in the present paper, their method of formation 
was very clearly shown. The first step was evidently 
a damming of the circulation in the intertrabecular 
spaces by the rapid multiplication of cells. In this way 
were formed the very numerous and prominent dark 
spots. The changes into whitish tissue evidently com- 
menced in the centre of these dark masses, as the result 
of a complete arrest of the circulation, and gradually 
spread as the effect of this arrest widened. Where a 
large triangular mass of tissue was involved, there was, 
without doubt, a secondary formation of a thrombus in 
a large vessel by coagulation taking place owing to the 
impeded blood-current. The microscopical examination 
bore out entirely this view, as the cells of the “ deposit” 
consisted simply of shrunken splenic pulp cells, with 
oil granules and debris, and a small proportion of trabe- 
cular tissue. 
The post-mortem study of the case fully carried out 
the view held by Trousseau, Cornil, and Niemeyer, that 
the changes in the spleen consist principally in a hyper- 
trophy of the pulp of the organ, the cells, as I think, 
being less fully developed than normally, exhibiting, in 
a word, the characters found wherever there is excess 
of formative at the expense of developmental action. 
The theory that leucaemia is owing to an overaction 
in the lymphatics and spleen, resulting in the pro- 
duction of an overplus of white corpuscles, which, 
from being imperfectly developed, are unable to pass 
into red corpuscles, although by no means proven, 
seems to me to be the best that our present knowledge 
will allow. The physiology of the spleen is certainly 
not finally settled. Indeed, Dr. Flint, Jr., in his great 
work, asserts that our knowledge of it amounts to 
nothing ; yet its connection with formation of the blood seems to me very plainly shadowed forth. It is well 
known that two theories have been advanced,—the one 
of which attributes to the spleen the function of forming 
white blood corpuscles ; the other, the destruction of the 
red. It is by no means impossible that both of these are 
true; for the idea of such a double function involves no 
absurdity. If it be so, the two affections leucaemia and 
pseudo-leucaemia, connected as they are with apparently 
identical changes in the spleen, represent respectively 
abnormal states of the two functions,—in the former, 
an excess of imperfectly developed white corpuscles 
resulting; in the other, a rapid destruction of the red 
corpuscles, and consequent deterioration of the blood. 
In this connection, it is interesting to observe that no 
case is as yet recorded* in which the patient died of 
the characteristic anaemia without splenic hypertrophy. 
There have been, it is true, several instances in which 
the disease proved fatal without marked implication of 
the spleen; but the cause of death was not anaemic 
exhaustion, but gradual suffocation from pressure upon 
the trachea or bronchi by the enlarged glands. More- 
over, there have been cases in which the lymphatics 
were enormously hypertrophied, and had been so for 
years, the general health of the subject remaining good, 
until, the spleen commencing to enlarge, the charac- 
teristic anaemia appeared. 
These clinical facts or coincidences are certainly very 
interesting; but a much greater number of well-observed 
cases and more complete knowledge of the healthy 
organs are requisite before any permanent theory of 
the disease can be made out. 
As to the etiology of the affection, our ignorance is at 
present absolute, and the case here reported is in strict 
agreement with most of those hitherto observed, in hav- 
ing no tangible cause. Professor Trousseau endeavors, 
it is true, to connect adenie with a prolonged irritation 
of some mucous membrane; but I do not think he at 
all establishes this. There have been several cases re- 
ported in which no such irritation had existed; and 
* Perhaps this is asserted too positively; I certainly have not been able 
to find such case. some of the cases upon which Professor T. relied as 
establishing his theory were observed so loosely that it 
is not certain. they represented the disease. In the 
present instance the previous camp-diarrhoea had too 
long passed away to bear any direct relation to the fatal 
disorder. It is true, there was an indistinct history of 
subsequent disorder of the bowels made out after the 
death of the patient; but, from close cross-questioning 
of his friends, it appeared to have been more of the 
nature of relaxation than irritation. The circumstance 
that no affection of the bowels in the years previous to 
the attack was spoken of by the patient, although closely 
and frequently questioned on his history, would appear 
to forbid any importance to be attached to the after- 
statement of friends. 
B1BL10GRA PHY. 
The following list comprises all the more important papers upon the 
subject which I know of. Although making no pretensions to complete- 
ness, it may be of value to some desirous of following the subject. 
Hodgkins. 1 Medico-Chirurgiral Transactions, Vol. xvii.) 
Bonfils.—Hypertrophie ganglionnaire generate, fistules lymphatiques, 
cachexie sans leucemie. (Recueil des Travaux de la Societe Medicale 
d’ Observation, t. i., 1857-58.) 
Wilks.—Hodgkins’ Disease. (Guy’s Hospital Reports, 1865.) 
Pauy.—Case of Anaemia lymphatica, a New Disease characterized by 
Enlargement of the Lymphatic Glands and Spleen. (London Lancet, vol. 
ii., 1859.) 
Potain.—Double tumeur lacrymale ; engorgement lymphatique sous- 
maxillaire considerable; erysipele de la face, etc. (Bulletin de la Societe 
Anatomique, 1861.) 
PenrIn.—Double fistule lacrymale, hypertrophie generalisee de tout le 
systeme ganglionnaire, ramollissement du tissu osseux. (Idem, 1861.) 
Cossy.—Memoire pour servir 4 l’histoire de l’hypertrophie simple plus 
ou moins generalisee des ganglions lymphatiques sans leucemie. (Echo 
Medicale, Neuch4tel, 1861.) 
Halle.—Alteration des ganglions lymphatiques. (Bulletin de la Societe 
Anatomique, 1862.) 
Billroth.—Schmidt’s Jahrbiicher, vol. cxxiii. Sydenham’s Year- 
Book, 1864. 
Trousseau.—De l’Adenie. (Clinique Medicale de l'Hdtel-Dieu, 2dedi- » 
tion, vol iii. p. 555.) 
Coknil.—De l’Adenie ou hypertrophie ganglionnaire suivie de cachexie 
sans leucemie. (Archives Generates de Medecine, 6e ser., tome vi., 1865.) 
LakoulbLne.—Cas de l'Adenie. (Memoires de la Societe de Biologie, 
1864.) 
Niemeyer.—Hypertrophy of Spleen ; Text-Book of Practical Medi- 
cine, vol. ii. 
Black.—Progressive Enlargement of the Lymphatic Glands. (American 
Journal ojthe Medical Sciences, 1868, p. 382.)