General anæmia, debility, wasting diseases, starvation, hæmorrhage, stimulus to formation of red globules, asphyxia, electricity, cold, quinine, eucalyptus, ergot. Symptoms: lack of eosinophile leucocytes in the blood of a debilitated subject may lead to suspicion. Treatment: tonic, light, sunshine, pure air, exercise, nutritive food, iron, bitters.
In cases of general anæmia the spleen is liable to be small, shrunken, wrinkled, and when cut the surface is drier and lighter colored than in the normal condition. This condition may be seen after old standing debilitating diseases, but is common in animals that have been reduced by starvation, just as the opposite condition of hyperæmia and enlargement comes of abundance of rich food and an active digestion. It may shrink temporarily as the result of profuse hemorrhage, but Bizzozero and Salvioli found that several days after such loss of blood it became enlarged and its parenchyma contained many red nucleated hæmatoblasts. The result of hemorrhage is therefore to stimulate the organ to enlargement and to the resumption of its embryonic function of producing red blood globules. Contraction of the spleen further occurs under asphyxia, the deoxidized blood being supposed to operate through the medulla oblongata. As already noted the spleen shrinks under stimulation of the central end of a sensory nerve (vagus, sciatic). An induced current of electricity applied to the skin over the spleen causes marked contraction (Botkin). Cold, quinine, eucalyptus, ergot and other agents also induce contraction. In the normal condition there is an inverse ratio between the bulk of the spleen and the liver, the enlargement of the one entailing a diminution of the other, but in certain diseased states, such as anthrax, ague, etc., both are liable to enlargement at the same time.
Symptoms of splenic anæmia are wanting, through a lack of eosinophile leucocytes, in the blood of a starved or otherwise debilitated animal, may lead to suspicion of the condition.
The treatment of such a case would be addressed rather to the general debility which induced the splenic contraction than to the contraction itself. Light, sunshine, pure air, exercise, grooming, nourishing food and the avoidance of all debilitating morbid conditions would indicate the principles of therapeutic management.
HYPERÆMIA—CONGESTION OF THE SPLEEN.
Four hours after full meal in splenic diastole. In well fed, high conditioned. From obstruction of splenic or portal vein or vena cava, heart, liver, or pulmonary disease, inhibition from encephalon acting through splanchnics or vagi, microbes, ptomaines, toxins, paresis, albuminoid diet. Spleen may be seven times its normal weight. Lesions: simple blood engorgement: proliferation of pulp cells: increased friability; rupture; dark color; hyperplasia of trabeculæ—hypertrophy. Symptoms: none; or colic; palpation in ruminants; tenderness. Treatment: directed against the causative disease; quinine, cinchonine, eucalyptus, ergot, cold douche, electricity, puncture.
Considerable hyperæmia of this organ takes place physiologically in connection with active digestion in the first four or five hours after an abundant meal, and especially at intervals of a minute, during what may be called the diastole of the viscus. The supply of blood is also much greater in the well fed animal, than in the emaciated and impoverished one.
Pathological hyperæmias of a passive kind may occur as the result of obstructions in the veins leading from the spleen, such as the splenic veins, the posterior vena cava, or that part of the portal vein comprised between its junction with the splenic and the liver. Diseases of the right heart or its valves, of the lungs (emphysema), or of the liver which hinder the onward flow of blood and increase the blood tension in the vena cava or portal vein have a similar action. Perhaps we should include inhibition of the nerves (splanchnic, vagi) and nerve centres (medulla oblongata, cerebral cortex) which preside over the contraction of the splenic vascular walls, and of the capsular and trabecular muscles. There is reason to believe that the ptomaines and toxins of several microbian diseases, operate through these centres, while other such microbes and toxins operate directly on the spleen itself.
Active congestions of the spleen are most commonly associated with microbian diseases and may be attributed partly as above stated to the action of the toxic products on the contraction nerve centres, and on the splenic vessels and parenchyma, but also in no small degree on the active proliferation of the germs themselves in the splenic pulp, and of the splenic cells. Among the most notable instances of this kind are, in man, malarious, yellow and typhoid fevers, and, in animals, anthrax, and Southern cattle fever. In most febrile diseases, however, there is a tendency in this direction, which may be fairly attributed to the paresis of the organ and the delay of the blood in its pulp channels and spaces with the consequent local increase of microbes and toxins. The microörganisms can usually be found abundantly in such cases, in the liquid of the pulp, and in the interior of the leucocytes and other cells that go to make up its solid constituents.
It has been long recognized by veterinarians that acute congestion often arises in connection with a sudden transition from a poor or insufficient diet to an abundant and nutritious one and especially to one that is rich in albuminoids (beans, peas, vetches, lucerne, sainfoin, clover, trefoil, in the fresh or preserved condition). If these are not in themselves the direct causes of acute and fatal engorgements of the spleen, they at least contribute in no small degree to the overdistension of the pulp spaces, the paresis of the organ and its successful invasion by pathogenic microbes.