indeed throughout its entire course it usually escapes positive
identification. {963} Fluctuation may, however, be detected, and from
its location and concomitant symptoms may reasonably be ascribed to a
splenic abscess. The fluctuating tumor has been known to fill the whole
abdominal cavity from epigastrium to pubes. Grisolle reports such a
case where the tumor presented the appearance of ascites. In this form
of splenic abscess the progress is generally insidious. Under symptoms
of hectic fever, wasting, etc. the physical signs of splenic
enlargement are gradually manifested until the presence of fluid may be
determined. After months of suffering the patient will expire from
exhaustion or from the consequences of rupture of the abscess into the
abdominal or pleural cavity or into the lungs, lighting up
rapidly-fatal inflammation; or, discharging into the bowel or stomach
or through the abdominal wall, the abscess may temporarily improve and
allow a short prolongation of a wretched life. In the event, however,
of an escape of pus from the body, as through the abdominal wall,
bowel, etc., recovery is possible in a very small proportion of cases.
Wardell has seen such a case discharging through the abdominal
parietes. Zweifel has met a similar condition. Nasse has known of
recovery after the pus had been expectorated, and Webb, after discharge
into the intestine. Occasionally, splenic abscess may become
encapsulated and undergo caseous metamorphosis, when it may become
inactive, ultimately cicatrize, or become calcareous.
PATHOLOGICAL ANATOMY.--In abscess of the spleen, when of small size, a
non-metastatic origin may be recognized by the absence of micrococci
from its purulent contents and of concomitant signs of blood-poisoning.
When not spontaneously arrested, these abscesses attain a size not
equalled by metastatic splenic abscess. The splenic substance will then
be reduced to a semi-fluid or fluid mass of reddish pus enclosed within
a pyogenic membrane. In extreme cases all traces of true splenic pulp
and trabeculæ will be obliterated; but when the inflammatory action is
less intense the trabeculæ will extend in all directions through the
abscess cavity. The capsule, thickened and indurated, will have formed
adhesions or will have entirely disappeared before the advancing wall
of the abscess.
Embolic Abscess.
It has been shown that hemorrhagic infarction in the spleen is the
result of an embolic obstruction of the splenic blood-vessels. If the
embolus be simply a detached portion of an aseptic clot or fibrinous
vegetation or of atheromatous degeneration, the subsequent changes will
be those characteristic of the involution of hemorrhagic infarction.
Under exceptional circumstances and from not understood causes
inflammation and abscess may follow. These, however, are to be reckoned
among the rare results of simple hemorrhagic infarction of the spleen.
Altogether more frequently the embolus is derived from the ulcerative
endocarditis of septic origin or from other septic centre, and consists
of congeries of micro-organisms, themselves the infecting agents or the
vehicles of the poison that lights up the characteristic morbid
processes. A colony of these micro-organisms, lodged in and occluding
splenic arteries, by the irritation of their presence and by their
multiplication excite the inflammatory processes that accompany and
follow the hemorrhagic infarction. Embolic splenic abscess is, then,
nearly constantly a secondary result of conditions of blood-poisoning,
and as such can only play a subservient part in the train of
pathological events in which all parts reached by the blood-supply may
be engaged. The vascular distribution in the spleen is such as to
afford exceptionally favorable opportunities for the development of
metastatic abscesses, and in a large proportion of spleens of those who
have died from blood-poisoning they will be detected. They are rarely
{964} present without the appearance of similar changes in other
organs, and there is, therefore, but little difficulty in attributing
them to their true cause.
SYMPTOMATOLOGY.--Unless inflammation of the splenic capsule be excited,
these abscesses give rise to no pain, neither do they (except rarely)
produce discoverable splenic enlargement as distinct from the general
splenic enlargement always present in septic fever. Their course is
usually brief, in consequence of the usually acute course of the
disease that occasions them. When, in chronic pyæmia, splenic embolic
abscess may develop more slowly, exceptionally palpable fluctuating
tumor becomes manifest.
Fever, with all the accompanying phenomena of blood-poisoning, is
present in these cases, and commonly masks any splenic alteration that
might otherwise become apparent. Embolic abscess should always be
suspected in blood-poisoning, though in most cases its detection could
have but little influence in determining treatment.
PATHOLOGICAL ANATOMY.--Embolic abscess may develop from a hemorrhagic
infarction, in which case the necrotic central mass is surrounded by a
zone of inflammation which rapidly converts the whole area into a
broken-down, reddish, purulent, semi-fluid matter. If the abscess
supervene without the occurrence of hemorrhagic infarction, its
situation is still nearly always peripheral, the wedge-shaped embolic
area pointing toward the centre. It varies in size from that of a
pinhead to that of a pea and larger. It consists of a necrotic centre
composed of pus-cells and detritus, a surrounding mass of exudation,
and a circumscribing border of hyperæmia. Microscopic examination will
usually reveal swarms of micrococci. In the progress of the abscess the
whole mass becomes converted into a grumous brownish fluid. The
peritoneum rarely participates in the activity of the inflammation, but
may form deposits of lymph over the seats of the abscesses.
Mosler[9] summarizes Ponfick's description of a peculiar splenic
inflammatory process resulting from relapsing fever. It differs from
ordinary embolic abscess in being limited to the splenic venous system.
It may equal two-thirds of the entire spleen in bulk. It resembles in
appearance embolic abscess, but the arteries remain pervious. These
abscesses may heal or may enlarge and peritonitis may be excited. The
possibility of their originating in a venous thrombosis is entertained
by Ponfick. A peculiar inflammatory condition of the follicular tissue
of the spleen has also been described by Ponfick as a result of
relapsing fever.
[Footnote 9: _Ziemssen's Cyclop._, vol. iii.]
DIAGNOSIS.--The diagnosis of splenic abscess presents very often great
difficulties, and is frequently quite impossible. In ordinary embolic
abscess a diagnosis cannot be made with certainty. The existence of
pyæmia with enlargement and pain would make it probable that splenic
abscess had formed. In the larger abscesses of malarial, traumatic, or
unknown origin the detection of a fluctuating tumor in the region of
the spleen will suggest its true cause, but examination of the contents
will alone clear up the diagnosis between the real disease and hydatid
tumors, nephritic and perinephritic accumulations of fluids, etc. Even
where the contents of the cavity are purulent, it will often be
impossible to decide upon their splenic origin unless in the event of
portions of the splenic tissue escaping at the orifice of the abscess.
In cases of constant and increasing pain and tenderness in the splenic
region, with enlargement, associated with general failure of health,
splenic abscess may be suspected, and an exploratory puncture with the
aspirating-needle may not only be justifiable, but imperatively called
for. In all cases it must be remembered that splenic abscess of this
character is a most rare disease.
PROGNOSIS.--Splenic abscess usually terminates fatally. The
life-destroying influence, however, is not exerted through the spleen
itself, for this may {965} be converted into a simple bag of semi-fluid
contents, with complete destruction of all its tissue, and yet danger
is to be apprehended only from the effects of suppuration or of rupture
into the closed cavities or from peritonitis, etc. Of itself, embolic
abscess rarely excites alarming symptoms, because, being usually of
septic origin, the stress of the general condition is thrown more upon
the whole body, or upon a number of its parts, of which the spleen is
not the most important.
TREATMENT.--Treatment should be directed more toward prophylaxis than
toward cure. In those congestions and hyperplasias that may result in
abscess the remedies indicated for these conditions should be actively
employed. The application of ice to the splenic region, of
counter-irritants, the use of local bloodletting, the unloading of the
intestinal circulation by saline purgatives, the proper employment of
quinine, etc. in chronic malarial poisoning, seasonably adapted, may
prevent the formation of abscess. In the event of fluctuation declaring
itself, evacuation under antiseptic precautions should be practised;
ordinarily, the most effective general treatment is that directed
against the primary disease.
Perisplenitis.
Inflammation of the splenic capsule is a more common affection than
clinical observation would lead one to suppose. It consists of a more
or less localized splenic peritonitis, and its lesions are often found
at the necropsy when its existence had not been suspected during life.
ETIOLOGY.--Its commonest cause is the extension of inflammation from
neighboring parts. Chronic ulcer of the stomach may be the origin of
chronic perisplenitis, leading to the formation of dense inflammatory
deposits. Persons who have long suffered from miasmatic poisoning
frequently develop strong adhesions between the spleen and diaphragm.
And from the same cause the spleen may become closely adherent to the
neighboring viscera. Chronic enteritis, perinephritic inflammation, and
the like may excite it. It has been shown that the pain in splenic
affections is nearly always due to the capsulitis present; and it is
probable that much pain in the splenic region, stitches in the side,
etc. are really the results of this inflammation. It can only be
conjectured that in given cases one has to do with perisplenitis.
Almost all that is known about it comes from the dead-house.
PATHOLOGICAL ANATOMY.--The simplest post-mortem signs of bygone
perisplenitis are the unusually dense fibrous adhesions between the
spleen and surrounding parts. These may vary within wide limits.
Exceptionally, the spleen will be found intimately adherent to
surrounding parts throughout, and can only be separated from them by
tearing it away. Under these circumstances, mostly in chronic malarial
subjects, the capsule will be uniformly much thickened and sac-like.
The splenic tissue may be reduced to a tarry, semi-fluid pulp that
oozes through the lacerated walls. Sometimes the capsule of the spleen
will show localized thickenings of dense cartilage-like consistency,
usually on the convex surface. According to Wilks and Moxon (p. 487),
"section shows them to be laminated parallel to the surface, and the
microscope reveals a fibrinous structure, the fibres being arranged in
dense areolated lamellæ." The same authors consider these to be among
the most decisive evidences of chronic alcoholism. They may become
calcified (Orth). It is not unlikely that they may often be the effects
of syphilis. They undoubtedly often occur in syphilitic subjects. The
interest attaching to them is entirely a pathological one, as the
affection is never detected during life, and as they probably exert no
influence whatever upon the duration of life or even upon the
well-being of their bearer.
{966} Lardaceous Spleen.
The spleen is more liable to lardaceous or amyloid disease than any
other organ of the body. And, although in the further course of the
degeneration other organs and tissues inevitably become implicated
(unless the patient die of some intercurrent affection), the spleen may
in the earlier stages be alone involved. In 58 cases of lardaceous
disease compiled from the records of the London Hospital, the spleen
was the only organ in which the degeneration was detected in 28 cases,
while it remained unaffected in only 10 cases.[10]
[Footnote 10: Turner, _Transactions Patholog. Soc. Lond._, vol. xxx.]
The tendency of lardaceous disease toward generalization shows that it
is under systemic and not local influence, though whether this
influence is exerted in depositing preformed albuminoid material in the
affected parts (infiltration), or in bringing about a special
alteration in situ (degeneration), is even yet not definitely decided.
Upon the one hand, the infiltration theory is upheld by Rindfleisch,
Billroth, and others, while Fehr, Kyber, Cohnheim, and others consider
it to be a result of tissue-metamorphosis. Cohnheim concludes that the
infiltration theory could only be accepted upon the presumption that
the lardaceous material is not a soluble but a corpuscular substance,
or that it is only deposited in consequence of some acquired
predisposition of the part. He regards the process as a local
degeneration due to general causes in which the lardaceous material is
derived from the pre-existing albumen of the tissues. According to
Virchow and Kyber, there is brought to the tissue whose nutrition is
somehow lowered a substance, between which and a malarial substance
formed in loco an intimate combination occurs, the result being
lardaceous material (Ziegler).
This form of degeneration involves the spleen in one or both of two
ways. It may appear as scattered points throughout the splenic
substance, corresponding to the Malpighian bodies and presenting a
resemblance to grains of boiled sago, or in a diffused manner,
constituting true lardaceous spleen, in which the entire organ appears
to be involved.
ETIOLOGY.--As in lardaceous disease of other parts, by far the most
common causes of its development in the spleen are prolonged
suppuration, especially of bone, the suppurative processes of phthisis
pulmonalis and of scrofulosis. The next most frequent causative
influence is syphilis, whether accompanied by prolonged suppuration or
by the cachexia so often observed in this disorder. Chronic malarial
poisoning, chronic diarrhoea, chronic alcoholism, and occasionally the
less-rapidly fatal malignant new growths, may induce the degeneration.
Exceptionally, it has been observed where no other general disturbance
of nutrition had existed. The various causes of lardaceous degeneration
have in common one feature, chronicity, though Mosler quotes from
Cohnheim instances where lardaceous spleen was discovered in one case
five months after joint injuries had been received, and in another four
months after a compound fracture of the right leg.
SYMPTOMATOLOGY.--Lardaceous disease of the spleen is usually associated
with similar disease of other organs--the liver, kidneys, stomach,
intestines, heart, etc.--and its symptoms are so frequently accompanied
by those of the affection that has given origin to it that it must
always be difficult to distinguish them as attributable to the
condition of the spleen itself. Profound anæmia with an appearance of
cachexia is always present in advanced cases. Milder cases may reveal
themselves by no signs. The symptoms arising from other parts
implicated in the degeneration may completely mask those depending upon
the spleen. When the stomach is involved, vomiting and hæmatemesis even
to a fatal termination may occur, or uncontrollable diarrhoea from
intestinal changes may supervene. Splenic enlargement is not {967}
unusually accompanied by enlargement of the liver. Ascites, however, is
always a rare accompaniment.
Rarely, the spleen attains enormous size, and may then occasion
sensations of weight and tension, and occasionally acute pain from
implication of the capsule in inflammatory action. When the organ can
be felt through the abdominal walls it will generally be hardened,
painless, and with its boundaries much thicker and rounder than normal.
PATHOLOGICAL ANATOMY.--As has been already remarked, lardaceous disease
of the spleen is observed in two forms. In both the spleen is enlarged
and hardened. Its structure presents a tough, waxy consistence, and the
organ has entirely lost its friability. In sago spleen, light-brown or
grayish waxy bodies are scattered throughout the splenic structure. The
pulp may remain quite healthy, or it may also be involved. These
sago-like bodies correspond to the enlarged and lardaceous Malpighian
corpuscles, and stand out with some prominence from the general
surface. They may vary in size from that of a pinhead to that of a
small pea. The color of the spleen may shade from a pale fawn color to
a reddish-brown. In many cases where the parenchyma is involved there
will be exhibited scattered areas of semi-transparent, wax-like
material.
In the diffusely lardaceous spleen the organ is enlarged throughout,
pitting to pressure, and upon section presenting a waxy,
semi-translucent appearance, usually of a reddish-gray, but sometimes
of a deep-red, color. Instead of a pulpy, easily broken-down condition
of the splenic parenchyma, there will be found a dense tissue that can
be cut into tough, glistening slices. Minor degrees of the change
cannot be readily detected by the unaided eye, and even in advanced
cases the judgment will often be at fault. Under these, and in fact
under all circumstances a correct conclusion as to the nature of a
given change can only be reached after the employment of reagents that
exert peculiar influences over the lardaceous material. The action of
iodine upon this material is quite characteristic. If a watery solution
of iodine with iodide of potassium be applied to the cut surface of the
suspected organ, the normal portions will be stained a yellowish color,
while those parts that have undergone lardaceous degeneration will
assume a rich mahogany red or brown, which will become violet or purple
upon addition of sulphuric acid. This latter reaction is not constant,
and may usually be omitted. Cornil has recently proposed as a test a
solution of methyl-aniline-violet, which possesses the property of
staining lardaceous matter red, while ordinary tissues will be stained
a deep, bright blue. This reaction possesses the advantage of being
permanent and very delicate, and on that account preferable for
microscopic examination of specimens. According to Cohnheim, this
reagent enables one to distinguish commencing lardaceous change.
In lardaceous disease of the Malpighian corpuscles the alteration will
be found to begin in the arterial twig to which the corpuscle is
attached, soon extending to the entire tissue of the corpuscle, which
it causes to enlarge considerably. When the splenic pulp is attacked it
is said to be the vessels of the pulp that are first involved. It is
held by most pathologists (Virchow, Kyber, etc.) that the change is
chiefly seated in the muscular coat of the small arteries, but that the
intima is also very frequently affected, and that occasionally all the
coats are involved. Thence the degeneration spreads to the cells and
nuclei of the splenic tissue. Later investigations, however, seem to
make it probable that the lardaceous degeneration is mostly limited to
the connective-tissue trabeculæ and walls of the venous sinuses; that
the pulp-cells are for the most part not implicated, but that they
disappear in consequence of the pressure of the ever-increasing
lardaceous material and the consequent anæmia (Cohnheim, Ziegler).
DIAGNOSIS.--This will depend more upon the history and concomitant
{968} symptoms and general condition of the patient than upon any
positive evidence to be gained by special reference to the spleen. In a
patient predisposed to lardaceous degeneration by any of the influences
enumerated above the presumption in favor of splenic lardaceous disease
is strong if, in addition to splenic enlargement, there is evidence of
hypertrophy of the liver and albuminuria, indications of the
participation of other organs in the process, and an anæmic and
cachectic appearance of the individual always observed in advanced
degrees of the degeneration.
PROGNOSIS.--The prognosis is almost always unfavorable, not so much on
account of the splenic condition as from the general depreciation of
the powers of life. The disorder being progressive, the tendency is
toward death by complications resulting from degenerations of other
organs. And yet it seems quite probable that mild grades of lardaceous
degeneration may be entirely recovered from occasionally; but this will
be almost invariably in cases where the spleen alone is implicated. At
all events, when not advanced it may be long held in abeyance. The
duration of the disease generally is indefinite and may cover a space
of years.
TREATMENT.--The treatment of lardaceous degeneration of the spleen will
consist rather in combating its exciting causes than in efforts
directed toward the condition of the spleen itself. It may, however, be
possible to effect some good by resorting to remedies supposed to be
useful in subduing ordinary splenic enlargement.
Echinococcus of the Spleen.
Echinococci invade the human body in the United States far less
frequently than in many other countries, where the canine race occupies
much closer relations with man (as in Iceland). The echinococci are the
larval forms of Tænia echinococcus, a tape-worm of minute size
inhabiting the intestinal tract of the genus Canis, more especially
that of the dog. The ova of the tæniæ are voided in countless numbers
in the feces of their hosts. Still unhatched or in an embryonic form,
they are thence conveyed through the medium of water or otherwise to
the stomach of man, whence the embryos (scolices) escape into the
tissues and develop into ordinary hydatid cysts. Rare as is this
affection in the human body, it is relatively extremely uncommon as
implicating the spleen, and recorded instances of its occurrence are
not numerous. Hydatids of the spleen may coexist with those of other
parts, and in occasional instances are said to be secondary to these.
They are commonly encountered about the middle period of life, and
appear to affect the sexes in equal proportions.
In cases of multiple hydatid cysts in different parts of the body it
has been asserted, upon the one hand, that a single older cyst serves
as the parent cyst, germs from which become transplanted in other
localities through the blood. This view receives some support from the
fact that one cyst, usually seated in the liver, is commonly much
larger than the others. An objection to its universal acceptance,
however, as pointed out by Budd, is that it is very difficult to
imagine that a germ from a larger cyst can travel through the portal
vein, against the current, toward the spleen, mesentery, etc., to form
a secondary cyst. On the other hand, it seems likely that an individual
exposed to infection by the echinococcus would be liable to ingest many
scolices at one time or on repeated occasions, and that the differences
in development depend upon varying degrees of assimilative power on the
part of the parasite and of the conditions of its environment.