FIG. XLIII. THE ALVEOLAR WALLS ARE THIN AND THE EXUDATE OF RED BLOOD CELLS AND DESQUAMATED EPITHELIUM IS IN PART HYALINIZED. ]
The advent of red blood cells where grossly the exudate is red can hardly be explained by the simple process of diapedesis. Indeed, there is ample evidence that they escape by rhexis through lesions of the vascular wall. This phenomenon cannot be demonstrated in areas where a compact mass of red cells obliterates the alveolar space (Fig. XXV), but in the less firmly consolidated alveoli where red blood cells predominate (Fig. XXVI) the picture of the alveolar wall is very instructive. The capillaries may be prominent and contain red cells almost exclusively. Often the epithelium of the air space is exfoliated so that there is nothing to minimize the prominence of the engorged vessels. These capillaries, covered by such a delicate wall that rupture seems imminent, may protrude like saccular aneurysms (101) into the alveolar space (Fig. XXVI). In all probability, these sacs do rupture and this result would be one explanation for the escape of large numbers of red blood cells. In several instances such a picture was encountered, where with little reaction at the point of rupture, red cells within the vessel were continuous with an accumulation of similar cells in the alveolus. Further evidence for such rupture is offered where the vessel is collapsed. Here there is accumulation of polymorphonuclear leucocytes in the area of destruction in contrast to the well preserved red corpuscles in the remainder of the vessel (Fig. XXVI). The above pictures may be utilized in the interpretation of the outspoken foci of red hepatization which may assume infarct-like proportions. As has been said, it is impossible to conceive that these hemorrhagic areas where the alveoli are packed with red cells ever change to a grey type of consolidation. Consequently, it seems more probable that the color of red hepatization in the usual types of pneumonia depends upon the marked engorgement of the vessels seen through a relatively acellular, transparent, serofibrinous, alveolar mass and not upon the number of red cells in the exudate.
The absence of cellular elements in the alveolar exudate is frequently observed in influenzal pneumonia (Figs. XXI, XXII, XXIII). This picture has been reproduced experimentally in animals which have been rendered aplastic with benzol, especially with reference to their myeloid elements (160). Pneumonia produced by intratracheal insufflation is more rapidly fatal in aplastic animals, and it is conceivable that the absence of cellular reaction is an explanation for the lack of resistance demonstrated by the high mortality of influenzal pneumonia. Frequently the fibrinoserous mass scattered diffusely throughout the lung is rich in bacteria. In the absence of cells of the polymorphonuclear series, the bacterial development seems to be unrestricted. The aplastic exudate is associated clinically with an absence of a myeloid reaction in the peripheral circulation. The leucocytic count may be definitely decreased, even though the tissues have been invaded by pyogenic organisms to which the usual response is a definite leucocytosis. The only explanation is that the myeloid structures have been injured, probably by the unknown virus of the disease.