We have already seen that an active hyperemia of the spleen occurs physiologically during digestion. It is met with as a distinctly pathological condition, and frequently in a very exaggerated form, in a variety of acute febrile diseases. The spleen seems a favourite seat of at least some of the infective agents which have to do with the acute fevers, and this may partly explain the special proclivity to congestion and inflammation in such diseases. Thus the bacilli of typhoid fever and the haematozoa of malaria are found in particular abundance in the spleen. Enlargement of the spleen in these diseases forming the Acute splenic tumour is often seen in the highest degree in typhus fever, but it is found also in other specific fevers as well as in pyaemia, pneumonia, diphtheria, erysipelas, etc. In this group of diseases the blood contains morbid products, and we know that the various parenchymatous organs, the muscles and the glands, are enlarged as a result of cloudy swelling, which is to be traced to the condition of the blood. But the enlargement of the spleen is from hyperaenria rather than the result of a direct tissue change. Consistently with this the eidargement may be very rapid, so much so as to cause rupture of the capsule, as observed in some cases of typhus and of intermittent fever. It will be inferred that in this condition the splenic tissue is exceedingly soft, sometimes almost diffluent, and the colour of the cut surface is a dark red.
But the condition does not continue as a pure hyperaenria. The cells forming the honeycomb structure of the pulp enlarge, the bloodvessels and the meshes of the pulp come to contain more round cells or white blood-corpuscles. These are all indications of inflammation, and a further indication is sometimes afforded by the deposition of fibrine on the capsule of the spleen. The Malpig-hian bodies sometimes undergo enlargement at this stage, but not in all the diseases named. It is most frequently seen in the later stages of Typhoid fever and Small-pox, and when it occurs the consistence of the organ is firmer than is usual in the acute splenic tumour. At this stage, in which more definite inflammatory processes are superadded to the congestion, the spleen is even larger than in the earlier stage, and it may reach two, three, or even four times the normal size. The organ is unduly soft, and on section may look half-diffluent, although it is firmer than in the cases without enlargement of the Malpighian bodies. The colour of the cut surface is considerably paler than in the earlier period, being more of a greyish or whitish red. On scraping the surface a thick juice is obtained which is not unlike pus mixed with blood. There is not infrequently haemorrhage in the substance of the spleen so affected, and it may take the form of the wedge-shaped haemorrhagic infarction.
As a general rule the acute splenic tumour diminishes as the primary disease passes off, and the spleen may be left soft and loose with wrinkled capsule and unduly prominent trabecular. Sometimes there results a chronic inflammation with thickening of the trabecule, but this hardly occurs unless there have been repeated attacks of hyperemia as in malarial fevers, and occasionally in typhoid fever.
It is a very, rare circumstance for suppuration to occur in the inflamed spleen, but this has been met with in intermittent fever. In such cases the pus appears in numerous little points which represent the Mal-pighian follicles, or there is a more diffuse suppuration of the spleen. If the abscesses burst a fatal peritonitis results.
Among the cases of suppurative inflammation of the spleen "should be mentioned those in which Ulcerative endocarditis or Pyaemia is the primary disease. Minute emboli are carried to the spleen as to other structures, and being of a septic nature they each form the focus of an acute inflammation, which has at first a hsemorrhagic character, and afterwards passes on to suppuration. The spleen as a whole is enlarged by active hyperemia.