No matter what the portion of the lung from which the sections are derived, the fundamental changes found are the same. The subpleural sheets are spread wide apart, now by empty spaces, now by coagulated fluid. The process extends from the surface through the interlobular septa (Fig. XX), and is accentuated where the connective tissue is more prominent around vessels and bronchi. The nature of the infiltrate in the subpleural and interstitial tissues becomes more evident in the alveoli, which likewise are filled. The material varies somewhat in appearance, probably dependent upon its proteid content. Not infrequently the alveoli contain a homogeneous, pink-staining mass, which resembles the colloid of the thyroid gland. Again, it may be simply a coarse granular precipitate (Fig. XXIII), and in still other instances, small sticks and strands form the bulk of the alveolar content (47, 92, 140, 156). This subpleural, interstitial, perivascular, peribronchial, and alveolar edema, which is a term applicable to this collection of fluid, is very prominent, and although its intensity varies in different portions of the lung; and although it may be replaced in some areas by other types of exudate, unquestionably, this is the dominating expression of the inflammatory process in the early stage of the disease.
As might be expected from the gross appearance, the alveoli vary in size. At times slightly collapsed and at other times overdistended, their lumina are still the seat of the inflammatory exudate, although the mechanical change may allow of some variation in the appearance of their walls. As a rule, however, the alveolar wall is prominent and owes its conspicuousness to the tortuous, engorged vessels within. These vessels contain red blood cells almost exclusively, and on account of the partial, occasionally complete, loss of the lining epithelium, the alveolar wall appears as a huge, dilated arteriole (101) separating the lakes of coagulated material in the spaces (Fig. XXIII). There are areas, as indicated above, where the alveolar content may be more definitely arranged in the form of beaded or homogeneous strands of different caliber; the smallest resemble delicate threads. They tend to converge toward the alveolar wall like wheat in a sheaf, and often pass through this wall by way of the so-called pores of Cohn; as soon as the body of the neighboring alveolus is reached, they again present a fan-like expansion into innumerable, fine strands (Fig. XXII). Where the exudate is more fibrinous, the alveolar wall is less likely to be distended, its vessels are not so prominent, and their content of red blood cells is definitely decreased. Still this is not the most extreme type of alveolar exudate met with at this stage. Perhaps, the most striking, although not the most frequent, exudate has a superficial resemblance to a huge, red blood clot, and it may be difficult to make out the alveolar walls separating the masses of well preserved red blood cells that fill the alveolar spaces. These areas are indistinguishable from infarcts and may be associated with thrombotic arteritis in near-by pulmonary vessels (47) (Figs. XXIV and XXV). Among the red blood cells an occasional strand of fibrin, a desquamated alveolar epithelial cell, and rarely a polymorphonuclear leucocyte may be encountered. The alveolar wall itself varies in the definition of its outline. When its vessels are greatly distended, when its alveolar epithelium is gone, and when its content consists largely of red blood cells, it is difficult to distinguish from the exudate which it encloses. However, when it is more compressed or when its epithelial lining cells are still more or less intact, it may be seen as a blue-staining strand under the low power of the microscope, for the well preserved nuclei lend it prominence.
