SYMPTOMATOLOGY.—Hemorrhagic infarction of the spleen, as such, reveals its presence by no signs during life. Its importance depends almost entirely upon the nature of its exciting cause. When this is of simple origin there is hardly ever any deleterious influence exerted upon the health of the individual. That hemorrhagic infarction was present in any given case can only be ascertained by the evidences of it discoverable after death. Rarely by its presence localized inflammation and abscess may be excited. Far different, however, is the result where the embolic material has been derived from an ulcerative endocarditis or other septic centre. In this event the infarction serves surely as the starting-point for metastatic abscess.
PATHOLOGICAL ANATOMY.—Hemorrhagic infarctions of the spleen may vary in number from one to many, and in size from that of a large shot to a bulk nearly equal to that of the spleen itself. They are usually situated at the surface of the organ in a wedge-shaped distribution, the base looking toward the capsule and causing a slight projection, the apex pointing toward the deeper portions. Infarctions, however, may also occasionally occur in the central parts of the spleen. A definite wedge-shape may be destroyed by the coalescence of several neighboring infarcts.
The appearance and density of the infarction will depend very much upon its age. When recent it is of a dark-red color, of firm consistency, and of homogeneous aspect, and is surrounded by a zone of hyperæmia. As it grows older the dark color gradually fades to a paler hue, in consequence of the absorption of the color-elements of the hemorrhage, and a yellowish shade appears, from fatty degeneration of the cellular constituents. With the fading in color the infarction decreases in size; contractions and scar-formations are developed, later to become converted into bands of dense fibrous tissue. Occasionally complete fatty metamorphosis of the cellular elements may ensue and caseation of the infarct take place. The caseous mass may soften and form a cavity, or may ultimately undergo calcareous degeneration. Not very infrequently one may detect at necroscopic examinations of spleens these calcareous nodules, equal to shot or peas in size, witnesses of the bygone metamorphoses of which we are speaking. When, instead of being of simple origin, the infarct is the result of septic changes, the course is different. Coincident with or immediately preceding the hemorrhagic infarction inflammatory symptoms will develop around the embolic masses (consisting principally of fibrinous material imprisoning multitudes of micrococci), and metastatic abscess rapidly becomes established. Pus will then be commingled with the softening mass, and the microscope will reveal the swarming organisms. In the latter event the changes of the hemorrhagic infarction are much more rapid than in simple infarction, when they may be very protracted.
Splenitis.
Although it is impossible to separate acute splenic tumor and chronic splenic enlargement from the processes of inflammation, for practical purposes it is convenient to consider as splenitis only those morbid conditions in which the tendency is toward suppuration. Simple idiopathic splenitis is undoubtedly very rare, and, although formerly its symptoms were described with great detail, most recent writers are content to acknowledge an almost complete ignorance of them. Indeed, splenic abscess is often detected after death when it had not even been suspected during life.
Diffuse Splenic Abscess.—In the rare cases of idiopathic splenic inflammation the exciting cause will commonly have been a fall or blow or other violence by which the spleen has been injured, or it may have followed chronic malarial poisoning or an extension of inflammation from the capsule or neighboring parts.
SYMPTOMATOLOGY.—The rarity of this affection makes accurate description of its symptoms almost impossible. Mosler has never seen it. The descriptions of it are based, at best, upon observation of but few cases. Its onset may be sudden; more commonly it is insidious, the patient complaining of weight and dull pain in the left hypochondrium, irradiating to the left shoulder. The presence of pain depends upon the participation of the capsule in the process. Cough and dyspnoea may be present, and febrile phenomena are constantly to be observed. Vomiting, want of appetite, furred tongue, etc. will be noticeable. After a time a tumor will be detected that will, at first, almost certainly show no sign of fluctuation. Coincidently with the development of the tumor a small degree of ascites and of anasarca of the lower extremities may appear.
Up to this point the presence of abscess may only be conjectured, and indeed throughout its entire course it usually escapes positive identification. 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.