In congestive conditions. Absence of free capillary anastomosis and
contraction, absence of valves in splenic veins. Embolism of splenic
artery. Clots in pulp spaces. Wedge shaped infarcts, first black,
later yellow, later caseated, or cicatrized. Abscess. Prognosis good
in non-infective forms. Treatment as for hyperæmia, or infection, or
both.
This condition appears in hyperæmia, hypertrophy, splenitis, and splenic
infection and largely because the structure and circulation in the organ
conduce to such trouble. The splenic arteries terminate in open vascular
spaces filled with splenic pulp and where all trace of a freely
anastomosing capillary network is lost. The splenic veins in the same
manner originate from these open vascular spaces. There is, therefore,
an absence of the free communication of capillary network, which
virtually acts as a safety valve in other vascular tissues, and the
vascular cavities connected with each terminal artery are independent of
those belonging to another, and find no way of ready relief when they
become over distended, or when there occurs obstruction (thrombosis) of
their afferent or efferent vessels. From blocking of arteries or veins
there is at once produced a wedge shaped area of stagnation which cannot
be relieved through any collateral circulation. Again the splenic veins,
being destitute of valves, offer no obstacle to the reflux of blood into
such vascular spaces whenever the further access of blood has been
arrested by the blocking of the artery. The blocking may occur in the
afferent artery through embolism by clots carried from the lungs or left
heart, or formed within the vessel by the colonization of microbes on
its walls. Even more likely is the formation of coagula in the vascular
spaces themselves as the result of the introduction of pus, or
septicæmic microbes, which are long detained and have ample time for
multiplication in these cavities. In either case the result is
obstruction to the sanguineous current, the filtering of blood backward
from the veins and the engorgement of the cavity with blood. The plugs
consist of fibrinous matter enclosing colonies of micrococci, and the
result is not only black infarction of the spleen, but a subsequent
general infection of the system at large.
The wedgeshaped infarcts are usually situated at the surface of the
organ, the base turned outward and forming a dark projection on the
surface, and the apex turned inward. The aggregation of two or three in
one group may considerably alter the outline. If recent they are of a
dark red color. Later from absorption of the coloring matter and fatty
degeneration of the mass they assume a pale yellow hue and the swelling
flattens or disappears. Later still through complete fatty degeneration
they may be transformed into caseated masses, or through organization
into fibrous tissue they may form thick white cicatrices. If pus cocci
are present suppuration and abscess may be the outcome.
The simpler forms recover like cases of simple hyperæmia while the
severe infecting forms may become the point of departure for the
formation of multiple abscesses in other organs, and of more or less
fatal general infections.
These conditions can only be discovered post mortem, and any symptoms
directing attention to the spleen could only suggest such treatment as
would be indicated in hyperæmia. Any purulent or septic disease which
might coexist would of course serve to indicate a germicide line of
treatment.