hyperæmia of the portal circulation from cirrhosis of the liver. It is,
however, certainly not a necessary consequence of cirrhosis, since this
may exist to a pronounced degree and yet the spleen remain normal--a
condition that is probably favored by extensive distribution of
muscular and elastic fibres to the viscus, that enable it to a great
extent to regulate its own circulation. On the other hand, the spleen
may be atrophied by a fibrotic contraction of its trabeculæ, the result
of long-standing hyperplasia. Chronic engorgement and enlargement of
the spleen may also result from mechanical obstruction to the systemic
venous circulation, especially that due to insufficiency of the mitral
valve, whereby obstruction to the portal circulation arises
secondarily. (The ulcerative endocarditis of septic origin is
associated with splenic congestion, which is, however, always of the
acute active variety, and complicated for the most part with embolic
abscess and hemorrhagic infarction.)
SYMPTOMATOLOGY.--Long-continued or frequently-recurring attacks of
splenic hyperæmia, occurring under the stimulus of chronic malarial
poisoning or of leucocythæmia or pseudo-leucocythæmia, will ultimately
induce those structural changes that result in new formation.
Enlargements from the two latter diseases will be more appropriately
considered elsewhere. After repeated attacks of remittent or
intermittent fever or other forms of malarial intoxication the symptoms
of acute will gradually merge into those of chronic congestion. They
will usually prevail to a more intense degree. The dragging weight of
the tumor will excite pain, and may render rest upon the right side too
uncomfortable to be indulged in. Hemorrhage from the stomach and bowels
may occur, and at times will be excessive. The patient may be reduced
to an extreme degree by the profuse and repeated losses of blood. In
the intervals of the malarial attacks the temperature will be
unelevated, and the pulse may be slow and irregular, though oftener
feeble and rapid. All the symptoms will be, however, commingled with
those from other causes. Those of malarial cachexia will sometimes be
very pronounced. The pale, sallow complexion, the pallid lips, the
extreme anæmia and generally unhealthy aspect, and the general symptoms
accompanying such states, the history of miasmatic fevers, of
characteristic neuralgias, etc., will generally be present. Oedema may
be observed, but will usually be hydræmic in origin. Anomalous symptoms
due to the systemic condition will be often developed when the
enlargement arises from other than malarial causes.
Under the influence of the latter cause the spleen may acquire many
times its normal dimensions, and may easily be felt below the border of
the ribs, where its irregularly curving and notched border will serve
to identify it. The tumor sometimes becomes so large that it reveals
its presence by causing a bulging and asymmetry appreciable by the
patient. Here, however, congestion will have been supplanted by
hypertrophy. The tumor may vary greatly in size. It may fill the left
part of the abdominal cavity, reaching to the pubes and distending the
belly-wall with its dense enlargement, dull upon percussion, and
perhaps moving within narrow limits under the hand of the examiner.
This tumor may attain a size and weight many times greater than the
normal. Hypertrophy once established, it may remain more or less
pronounced for years, directly occasioning unimportant symptoms. It is
difficult to determine the exact influence exerted by these tumors upon
the duration of life.
PATHOLOGICAL ANATOMY.--In simple hypertrophy there is both hyperplasia
of the pulp and of the trabecular connective tissue. The spleen is
{958} enlarged, sometimes to an extreme degree, equalling fifteen or
sixteen times its normal weight.[3] Such enlargement is not observed in
any other form of splenic disorder, excepting in some rare cases of
leucocythæmia and tumor. Its density is also increased. The capsule is
thickened, and adhesions to the surrounding parts may be quite
intimate. The color of the surface is darker than normal. Upon section
the structure appears dense, smooth, of a dark color (from deposit of
pigment), and showing to the naked eye great increase of the trabecular
tissue. The pigmentation more especially observed in malarial
intoxication occurs in the intervascular cords of the pulp
(Rindfleisch), where it can be seen as black, flaky masses of hæmatin
(the origin of melanæmia). According to Friedreich,[4] there may be a
circumscribed splenic hypertrophy, consisting of little points of
granulation imbedded in the pulp. In ordinary diffuse hypertrophy all
the elements are involved, though the trabeculæ show the greatest
increase and encroach more or less upon the pulp. The Malpighian
corpuscles may show little or no enlargement. The processes are
indistinguishable from those of chronic inflammation. In hypertrophy
from obstructed portal circulation the organ will be dark red and very
full of blood. It sometimes happens that obstructive hypertrophy
terminates in fibrotic contraction, when the connective tissue will be
found to have almost completely crowded out the pulp.
[Footnote 3: Hertz, _Ziemssen's Cyc._, vol. ii.]
[Footnote 4: _Virchow's Archiv_, xxiii., 1865; _Ziemssen's Cyc._,
viii., Mosler.]
DIAGNOSIS.--Decided enlargement will usually be recognized with but
little difficulty. A tumor in the left hypochondrium, occupying and
transgressing the normal splenic boundaries, will probably be of
splenic origin. Occasionally enlargement may be simulated by a spleen
of normal size displaced downward by intra-thoracic growths or
effusions or by that remarkable abnormality known as wandering spleen.
The course of the primary affection in the one case, and the free
movability of the organ in the other, will suffice generally to guard
against error. Rarely, the tumor may be due to cancer of the stomach,
enlargement of the left kidney or of the left lobe of the liver,
omental tumors, fecal accumulations in the colon, or ovarian tumors.
The concomitant symptoms will suffice to distinguish cancer of the
cardiac end of the stomach. Percussion will reveal the presence of
subjacent gases, and palpation will detect the greater hardness of the
gastric tumor. Enlargement of the left kidney may be due to cancer,
abscess, or other causes, and may simulate splenic hypertrophy. The
renal tumor may be traced farther backward, and will not present the
characteristic outline of the spleen. The clinical history and symptoms
will here, again, prevent error. Omental tumor is usually separated
from the splenic region by an area of resonance. Enlarged liver may be
traced toward the right side of the body, becoming more noticeable as
the spleen is receded from. Fecal accumulation may closely resemble
splenic tumor, as it does other abdominal enlargements. The doughy
consistency of enlarged spleen may be like that of the fecal mass, but
one may often permanently alter the shape of the latter by the pressure
of the fingers, and in any case doubt may be dispelled by the use of
purgatives. Ovarian tumors may be traced into the pelvis, as may also,
for the most part, fibro-cystic and fibroid tumors of the uterus and
its appendages.
On the other hand, recognition of splenic tumors may be prevented by
gaseous distension of the stomach and bowels, by abdominal dropsy,
diffuse or encysted, by fecal distension of the colon, and may, indeed,
be impossible until these conditions have been remedied. Enlargement of
the spleen from simple hyperplasia must also be distinguished from
other forms of splenic enlargement--from splenitis, from lardaceous
degeneration, from tumors, from leukæmia and pseudo-leukæmia, from
syphilitic and tuberculous {959} spleen, etc. In such cases the
diagnosis will rather depend upon concomitant symptoms than upon the
physical characters of the enlarged organ. Percussion and palpation
will not seldom enable one to determine the presence of tumor (cancer),
hydatids, etc. Pressure will often serve to elicit expressions of great
tenderness in splenitis; enlargements with fluid contents will be
revealed by fluctuation. In the greater number of cases where the
enlargement is evident, but is without distinguishing characteristics,
the general condition of the patient and the history of his illness
will disclose its true nature. Lardaceous degeneration will have been
anteceded by prolonged suppuration, by tubercle, by scrofula, or by
syphilis, and will generally be associated with the same processes in
other parts. Syphilitic disease may be indicated by the history of the
patient, though in this case, of course, lardaceous degeneration could
only with difficulty be excluded. Tubercle, rarely giving rise to an
appreciable tumor, can only be conjecturally diagnosticated from the
history and general condition of the patient. The condition of the
blood and of the lymphatic system in leukæmia and pseudo-leukæmia will
suffice to determine the nature of the splenic enlargement. The
ague-cake of chronic malarial poisoning is usually accompanied by a
degree of cachexia, as is shown in the earthy pallor of the complexion.
This is often sufficient to enable one to discriminate between several
forms of enlargement, for it differs from the intense pallor of
leukæmia by its sallow hue, and is not at all like the hue of the
complexion in lardaceous disease. The cancerous cachexia, it is true,
may closely resemble it, but here the history and symptoms assist in
avoiding mistakes.
PROGNOSIS.--When the hyperplastic processes have amounted to true
connective-tissue formation, a complete return to normal conditions
will not occur after the removal of the stimulus. The permanence of the
enlargement will be proportionate to the extent of organization of the
hyperplastic elements. In ague-cake some reduction in size will follow
the exhaustion of the malarial influence, though the spleen probably
never ceases to be appreciable as a distinct enlargement. At the same
time, the enlarged organ may not, of itself, exert any specially
unfavorable effect upon its bearer. Not a few persons will live for
years with it, and eventually die from other causes. It may be assumed,
however, that the presence of ague-cake is indicative of profound
malarial cachexia, by which the powers of life are much less resistant
to unfavorable influences. It may be said, in a general way, that the
larger the spleen the less favorable is the prognosis. It should be
remembered that a considerable proportion of persons suffering from
leucocythæmia have also suffered from chronic malarial poisoning, and
that the enlarged spleen of this affection may possibly have begun its
morbid course under the influence of malaria.
TREATMENT.--In passive congestion relief is often secured through the
use of remedies that diminish portal engorgement or enable the heart to
find compensation for a damaged mitral valve--conditions in which the
splenic disorder is really an unimportant concomitant. In the
enlargement that has for its cause chronic malarial intoxication
cinchona and its alkaloids are preferable to all other remedies, not
only in arresting the new growth otherwise progressive under the
stimulus of the poison, but by neutralizing the latter and facilitating
the absorption of the hyperplastic elements that have not already
become converted into more highly-developed tissue. To effect these
objects the agents must be given in fair doses (twenty grains of
sulphate of quinia daily) until the malarial cachexia shall have been
overcome--until the bulk of the enlarged spleen shall have been reduced
to the smallest possible proportions. To bring about the desired result
the treatment may have to be continued during several months,
occasionally suspended upon the supervention of symptoms of cinchonism.
A drug of deserved repute {960} (probably through its anti-malarial
influence) is arsenic. This should be given for protracted periods.
Many remedies possessing anti-malarial properties have also been
recommended and employed in these conditions. Eucalyptus and eucalyptol
have recently been used with promising results, though the sanguine
expectations of some will hardly be realized. Iron, preferably as a
sulphate or as the tincture of the chloride, is invaluable in
correcting the profound anæmia always present in these cases, though
its influence in reducing the splenic bulk immediately is, at best,
doubtful. Remedies competent to reduce hepatic and portal engorgement
will often prove beneficial. Salines and vegetable cathartics may more
especially be employed, but the use of mercurials, except for
occasional administration, is almost universally condemned as
productive of evil consequences.
Local Treatment.--The systematic application of cold by effusion or by
ice-bags will at times undoubtedly reduce the size of an enlarged
spleen. Alleviation will often be afforded by solutions of nitric acid
to the splenic region, and counter-irritants are of occasional service,
either by means of the tincture of iodine persistently employed or by
blistering fluids or plasters. These, however, should be used with
great caution in debilitated subjects, as gangrene has been known to
follow their application. Mosler thinks that the practice of injecting
tincture of iodine, carbolic acid, etc. into the substance of the
spleen is sufficiently promising to justify further experiment. The
continuous electric current and electrolysis have also been recently
recommended as of advantage in reducing the splenic bulk. In cases of
excessive enlargement, where accompanying or consequent cachexia
threatens to end in death, extirpation of the spleen has been advised
and practised. While the removal of the leucocythæmic spleen is so
constantly followed by death that the operation cannot be considered
justifiable, it seems that the spleen enlarged from other causes may
sometimes be removed with safety. In the _Lancet_ of Feb. 11, 1882,
Herbert Collier tabulates all (until then) known cases of removal of
the spleen for disease, 29 in number: 16 of these operations were upon
leukæmic subjects, and had a fatal termination; 8 of the remaining
cases recovered. Crédé[5] concludes from an analysis of 30 cases of
extirpation of splenic tumor that the adult spleen may be removed
without detriment; that its removal causes temporary derangement of the
blood-making function; and that this is compensated for by activity of
the thyroid body and red marrow of the bones. As bearing further upon
the question of the practicability of splenectomy, should surgical art
succeed in reducing the dangers immediately dependent upon the
operation, are the highly interesting experiments of Tizzoni[6] and
Griffini,[7] wherein extirpation of the spleen in dogs was followed by
reproduction of true splenic tissue.
[Footnote 5: _Centralbl. f. d. med. Wissensch._, June 23, 1883.]
[Footnote 6: _Arch. Ital. de Biologie_, 1883, iii. 2, and i. 1.]
[Footnote 7: _Ibid._, 1883, iii. 2.]
In chronic congestion and enlargement of the spleen from malarial
poisoning the removal of the patient to a non-malarious locality will
always materially assist in the recovery of health.
Hemorrhagic Infarction of the Spleen.
The investigations of Virchow, and more recently of Cohnheim, into the
pathogenesis and pathology of hemorrhagic infarction have afforded an
easily intelligible explanation of the causes of the frequency of this
morbid process in the spleen. A moment's reference to the anatomy of
the splenic blood-vessels will show that the conditions most favorable
to the production of hemorrhagic infarction in the presence of an
exciting cause are here afforded. Instead of terminating in a capillary
network with free and abundant {961} anastomoses, the splenic arteries
end in fine pencils, opening, not into capillaries leading to venous
radicles, but into vascular spaces in which traces of both afferent and
efferent blood-vessels gradually become effaced. These arterioles have
no other vascular communications than with the small arteries, the
terminal extremities of which they are. This arrangement may be very
perfectly demonstrated in injected spleens where the material has been
imperfectly driven through the vascular system of the organ, so that
wedge-shaped areas of successful injection become sharply defined. This
distribution of the blood-vessels renders the area supplied by each
almost completely dependent upon it for efficient nutrition, and almost
certain to become structurally altered if its lumen should become in
any manner obstructed. To this arrangement of the arteries and
arterioles upon one side is added, upon the other, a valveless
condition of the splenic veins, whereby regurgitation may readily
occur. We have here, therefore, evidently conditions most favorable to
the development of hemorrhagic infarction.
The process through which hemorrhagic infarction occurs has been
definitely observed by Cohnheim. The area of the distribution of the
obstructed artery or arteriole, receiving no blood-supply from
anastomosing branches, undergoes disintegration. The walls of the
blood-vessels as far as the nearest communicating branch participate in
the process of disorganization. After a while a backward movement of
the blood-current begins in the nearest still pervious vessels, and is
continued into the obstructed vessels, through whose disintegrating
walls the blood escapes and the hemorrhagic infarction is established.
The future course of the infarct depends almost entirely upon the
nature of the causes that brought it about.
In the spleen, as in other organs, the causes of hemorrhagic infarction
may be widely different, though an essential condition of each is that
it be competent to produce plugging of the blood-vessel. The most
important cause is probably ulcerative endocarditis, in the course of
which minute fragments of the endocardium or of the vegetations that
have formed upon it, especially of the neighborhood of the valves, in
consequence of inflammation, constitute the emboli. The plugs largely
consist of fibrinous matter enveloping colonies of micrococci, or they
may be derived from detached portions of thrombi, or from solid
particles that may have in any way gained access to the circulatory
current, as from endarteritis, from atheroma, primary emboli in the
pulmonary circulation, etc.
Hemorrhagic infarction has also been described by Ponfick[8] as
occurring in relapsing fever and originating in the veins, and not to
be referred to any of the already-mentioned causes. It is thrombotic in
origin, and due to some peculiarities of the morbid processes of the
affection.
[Footnote 8: _Virchow's Archiv_, Bd. lx.; Mosler, _Ziemssen's Cyclop._,
viii. p. 443.]
SYMPTOMATOLOGY.--Hemorrhagic infarction of the spleen, as such, reveals
its presence by no signs during life. Its importance depends almost
entirely upon the nature of its exciting cause. When this is of simple
origin there is hardly ever any deleterious influence exerted upon the
health of the individual. That hemorrhagic infarction was present in
any given case can only be ascertained by the evidences of it
discoverable after death. Rarely by its presence localized inflammation
and abscess may be excited. Far different, however, is the result where
the embolic material has been derived from an ulcerative endocarditis
or other septic centre. In this event the infarction serves surely as
the starting-point for metastatic abscess.
PATHOLOGICAL ANATOMY.--Hemorrhagic infarctions of the spleen may vary
in number from one to many, and in size from that of a large shot to a
bulk nearly equal to that of the spleen itself. They are usually
situated at the surface of the organ in a wedge-shaped distribution,
the base looking toward the capsule and causing a slight projection,
the apex pointing toward {962} the deeper portions. Infarctions,
however, may also occasionally occur in the central parts of the
spleen. A definite wedge-shape may be destroyed by the coalescence of
several neighboring infarcts.
The appearance and density of the infarction will depend very much upon
its age. When recent it is of a dark-red color, of firm consistency,
and of homogeneous aspect, and is surrounded by a zone of hyperæmia. As
it grows older the dark color gradually fades to a paler hue, in
consequence of the absorption of the color-elements of the hemorrhage,
and a yellowish shade appears, from fatty degeneration of the cellular
constituents. With the fading in color the infarction decreases in
size; contractions and scar-formations are developed, later to become
converted into bands of dense fibrous tissue. Occasionally complete
fatty metamorphosis of the cellular elements may ensue and caseation of
the infarct take place. The caseous mass may soften and form a cavity,
or may ultimately undergo calcareous degeneration. Not very
infrequently one may detect at necroscopic examinations of spleens
these calcareous nodules, equal to shot or peas in size, witnesses of
the bygone metamorphoses of which we are speaking. When, instead of
being of simple origin, the infarct is the result of septic changes,
the course is different. Coincident with or immediately preceding the
hemorrhagic infarction inflammatory symptoms will develop around the
embolic masses (consisting principally of fibrinous material
imprisoning multitudes of micrococci), and metastatic abscess rapidly
becomes established. Pus will then be commingled with the softening
mass, and the microscope will reveal the swarming organisms. In the
latter event the changes of the hemorrhagic infarction are much more
rapid than in simple infarction, when they may be very protracted.
Splenitis.
Although it is impossible to separate acute splenic tumor and chronic
splenic enlargement from the processes of inflammation, for practical
purposes it is convenient to consider as splenitis only those morbid
conditions in which the tendency is toward suppuration. Simple
idiopathic splenitis is undoubtedly very rare, and, although formerly
its symptoms were described with great detail, most recent writers are
content to acknowledge an almost complete ignorance of them. Indeed,
splenic abscess is often detected after death when it had not even been
suspected during life.
Diffuse Splenic Abscess.--In the rare cases of idiopathic splenic
inflammation the exciting cause will commonly have been a fall or blow
or other violence by which the spleen has been injured, or it may have
followed chronic malarial poisoning or an extension of inflammation
from the capsule or neighboring parts.
SYMPTOMATOLOGY.--The rarity of this affection makes accurate
description of its symptoms almost impossible. Mosler has never seen
it. The descriptions of it are based, at best, upon observation of but
few cases. Its onset may be sudden; more commonly it is insidious, the
patient complaining of weight and dull pain in the left hypochondrium,
irradiating to the left shoulder. The presence of pain depends upon the
participation of the capsule in the process. Cough and dyspnoea may be
present, and febrile phenomena are constantly to be observed. Vomiting,
want of appetite, furred tongue, etc. will be noticeable. After a time
a tumor will be detected that will, at first, almost certainly show no
sign of fluctuation. Coincidently with the development of the tumor a
small degree of ascites and of anasarca of the lower extremities may
appear.