Symptoms. Most observations of inflammation of the spleen and its results have been made only post mortem, so that we must allow that the simple forms occur and undergo resolution without obvious symptoms. In the perisplenitis supervening on another disease also in infective cases there will be the antecedent symptoms of such primary diseases. In those resulting from traumatic injury, bruises, swellings or wounds, cutaneous or subcutaneous, there will often be suggestive features. In the more purely idiopathic cases symptoms are only shown when the lesions are extensive and acute. In oxen, Cruzel has noted the initial chill, followed by disturbance of the respiration, more or less hyperthermia, and a swelling of the left flank and hypochondrium in the absence of tympany of the rumen. The nature of this swelling is the most characteristic feature, as it gives a flat instead of a drumlike sound on percussion, and does not bulge outward and downward over the whole left side of the abdomen, pit on pressure, nor crepitate uniformly all over from fermentation, as in overloading of the stomach.
If abscess should form, chills and high febrile reaction are marked symptoms. In vomiting animals, anorexia, nausea, vomiting, constipation, and even diarrhœa may appear.
Prognosis. Unless in extreme cases and those due to traumatism or infection, the result of splenitis is usually favorable.
Treatment would consist in depletion from the portal system and spleen by rectal injections, and laxatives which like castor oil, will operate without extensive absorption. Cold water or ice applied to the left flank and induction currents of electricity may also be resorted to. General blood-letting is strongly advised by Cruzel, and Friedberger and Fröhner. In infective cases quinia, salicylates, salol, and the sulphites, or iodides would be indicated.
HÆMORRHAGIC INFARCTION OF THE SPLEEN.
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.