B. LESIONS OF THE BLOOD VESSELS AND ELSEWHERE IN THE BODY Here, as in the discussion of the involvement of the lymphadenoid tissue, the most outspoken changes are in the thorax. Frequently thrombi are encountered in the vessels of the lung (34, 138). This does not include the capillary thrombi associated with damage to the alveolar walls already discussed. It has not been possible to demonstrate an association between the hemorrhagic, infarct-like foci in the lung and these vascular complications (47). The thrombi, histologically, are most frequently propagated, but occasionally an indication of their etiology is found in a destructive lesion of the vessel wall (19, 47, 50, 108, 156). This arteritis or phlebitis may be embedded either in a pneumonic zone or in relatively normal lung. The vessel wall may be obscured by a cellular infiltrate throughout its circumference or only at one point. The cells, on account of karyorrhexis often difficult to identify, are, partly at least, polymorphonuclear leucocytes, and the thrombus which forms upon the inflammatory nucleus, as a rule, is fairly rich in these cells (Fig. LII). This vascular lesion may involve either artery or vein and may be found either within the lung or at distant points. Not infrequently, pulmonary embolus terminates influenza. One instance of this is incorporated in the group of chronic influenzal cases detailed above (Fig. LIII). In this instance, the thrombus originated in the right iliac veins; and, although no attempt was made to demonstrate the primary vascular lesion, so many similar cases are recorded (7, 82), and vascular damage is so frequent in this disease, that the hypothesis attributing pulmonary embolus to a thrombus initiated by a phlebitis is strongly supported. Parenchymatous and skeletal lesions of hemorrhagic type, although variable quantitatively, are frequent and involve the muscles, the parenchymatous organs,—the adrenal especially,—and the mucosa of the alimentary canal. They have been described already with regard to the pleural surface and they may occur in other serous membranes. [Illustration: FIG. XXXII. AUTOPSY NO. 100. A HIGHER MAGNIFICATION OF THE LESION ILLUSTRATED IN FIGURE XXXI. THE ALVEOLAR WALL IS ENTIRELY NECROTIC: BACTERIA AND POLYMORPHONUCLEAR LEUCOCYTES ARE ABUNDANT. ] [Illustration: FIG. XXXIV. AUTOPSY NO. 87. CROSS SECTION THROUGH THE AREA OF GANGRENE SHOWN IN FIGURE XXXIII. ] [Illustration: FIG. XXXV. AUTOPSY NO. 160. MICROSCOPIC DRAWING OF THE GANGRENOUS CAVITY ILLUSTRATED IN FIGURES XXXIII AND XXXIV. ]