The alveoli adjacent to the distended septa are filled by inflammatory products; edema is almost invariably present and the alveoli may contain serum and desquamated epithelial cells; fibrin is often present, but more frequently polynuclear leucocytes are predominant. Not infrequently, abscess formation, recognized microscopically, has occurred in contact with septa most often immediately below the pleura. Polynuclear leucocytes are present in immense number and alveolar septa have disappeared; occasionally, with abscess formation there is more or less widespread necrosis of tissue, cells both of the exudate and of the alveolar walls having lost their nuclei.
Lymphatics in many places are distended and plugged by fibrinous thrombi, whereas elsewhere softening of the thrombus has been brought about by suppuration. Suppuration, both within the lymphatic and in adjacent alveoli, appears to be secondary to lymphatic obstruction. In some instances the lymphatic appears to have undergone distention after the thrombus has formed, for between the thrombus and the wall of the lymphatic a channel is occasionally found containing uncoagulated lymph.
Fig. 14.—Endophlebitis occurring in association with suppurative pneumonia; the intima contains lymphoid cells in great number; at one spot there is a small thrombus adherent to the intima. Autopsy 325.
Acute endophlebitis has been repeatedly observed in association with interstitial suppurative pneumonia (Fig. 14). The lesion usually occurs in veins situated within the septa which are the site of intensely acute inflammation associated with necrosis. The wall of the vein appears to be so injured by the surrounding changes that polynuclear leucocytes and small mononuclear cells accumulate below the endothelium. Throughout the circumference of the veins, often 0.5 to 1 mm. in diameter, the endothelium is separated from the underlying media by polynuclear leucocytes which form a conspicuous zone encircling the lumen. Some cells of lymphoid type are usually present among the polynuclear leucocytes. Polynuclear leucocytes are often adherent to the endothelial lining of the vessel and are not infrequently fixed in the process of passing through the endothelium. The lesion may be more severe (Autopsy 325), so that the endothelium has disappeared, and upon the exposed surface fibrin is deposited; within this fibrin polynuclear leucocytes are numerous and nuclear fragmentation has occurred. The middle coat of the vessel usually contains few cells; some polynuclear leucocytes within it may be stretched out as if in process of wandering through the wall.
In other instances the accumulation of cells below the endothelium is almost wholly mononuclear. Cells of the type of lymphocytes occur, but more abundant are slightly larger cells with more abundant cytoplasm. These cells may form a thick zone below the intima throughout the entire circumference of the lesion. It seems probable that these cells, like the polynuclear leucocytes, are derived from circulating blood within the lumen of the vessel, for small cells of the type of lymphocytes are not infrequently found adherent to the lumen and occasionally one is fixed in process of passing through the endothelium.
This endophlebitis appears to be the result of changes outside the vessel; there is usually necrosis of the adjacent tissue and the production of the lesion is favored by lymph stasis; as the result of injury to the vessel wall, polynuclear leucocytes in response to chemotaxis, or with milder irritation, mononuclear cells, wander through the endothelium and accumulate below it perhaps on account of the greater impermeability of the middle coat to the passage of cells.
The lesion described does not occur exclusively with interstitial suppurative pneumonia caused by hemolytic streptococci, but has been found in association with abscess formation (Autopsies 354 and 383) caused by hemolytic streptococci or (Autopsy 322) caused by staphylococci. In 1 instance it has been found with lobar pneumonia (Autopsy 320) caused by atypical Pneumococcus II and in 2 instances with combined lobar and bronchopneumonia (Autopsy 357 with Pneumococcus IV; Autopsy 392 with Pneumococcus II). In these 3 instances there has been interstitial inflammation, edema and lymphangitis without suppuration.
Interstitial suppurative pneumonia of long standing may occasionally be accompanied by chronic changes which bring about thickening of the interlobular tissue. In the following autopsy acute suppurative inflammation in the left lung has been associated with conspicuous thickening of interlobular septa in the right lung.
Autopsy 474.—I. H., white, aged twenty-one, was a native of Oklahoma and had been in military service one month. His illness began with influenza thirty-six days before death; he was admitted to the base hospital thirty-one days before his death with signs of pneumonic consolidation of the right lower lobe. Evidence of fluid in the right pleural cavity was obtained two weeks before death, and from 100 to 700 c.c. of thick purulent fluid were aspirated on five occasions. Hemolytic streptococci were found in the aspirated fluid.