Another striking feature of the inflammatory process in this disease is the extensive hemorrhagic exudate expressed clinically in the fresh, red blood of the abundant sputum. In the tissues the blood is always fairly well preserved. It may be scattered diffusely through the cellular exudate (Fig.XXIV) or so abundantly that the area resembles an infarct (Fig.XXV). These hemorrhagic foci, which vary considerably in size, are found not only in the cases that terminate fatally within a few days, but may occur at any time during the acute manifestation of the disease. They are an exaggerated form of red hepatization and it is difficult to see how such red foci could ever change to areas of grey pneumonia. It is a widely accepted statement, in textbooks of Pathology at least, that the stage of red hepatization in pneumonia follows the period of engorgement and precedes the grey form. This interpretation is open to question concerning the lesions that are encountered in influenza, as well as in those that are seen after gas inhalation. Unquestionably, in the stage of engorgement the lung has a red appearance, enhanced by the acellular, serofibrinous exudate in the alveoli through which the greatly congested vessels are seen. At this stage, the lung has a translucency on gross examination, which is not the case when the cellular content of the alveoli is increased. This picture is not the one spoken of most commonly as red hepatization; for, although it appears as a relatively red lung in the gross, difficulty is encountered in its histological correlation, for the exudate is composed, not of red cells, but largely of serum and fibrin. The red color may persist even when numerous polymorphonuclear leucocytes and desquamated alveolar wall cells are within the alveoli, the walls of which are markedly engorged. Later, as the circulation in the pneumonic zone is impaired, the alveolar exudate determines the tone of the gross color, and a considerable number of red blood cells may be overshadowed by the larger percentage of white ones.
FIG. XLII. AUTOPSY NO. 133. IS A MUCH LATER STAGE OF THE PROCESS SHOWN IN FIGUREXXXI. ASSOCIATED WITH THE ENCAPSULATED BRONCHIOLAR AND PERIBRONCHIOLAR ABSCESS, THERE IS A DIFFUSE ORGANIZATION OF THE EXUDATE IN THE SURROUNDING ALVEOLI.
FIG. XLII. AUTOPSY NO. 133. IS A MUCH LATER STAGE OF THE PROCESS SHOWN IN FIGUREXXXI. ASSOCIATED WITH THE ENCAPSULATED BRONCHIOLAR AND PERIBRONCHIOLAR ABSCESS, THERE IS A DIFFUSE ORGANIZATION OF THE EXUDATE IN THE SURROUNDING ALVEOLI.
FIG. XLII. AUTOPSY NO. 133. IS A MUCH LATER STAGE OF THE PROCESS SHOWN IN FIGUREXXXI. ASSOCIATED WITH THE ENCAPSULATED BRONCHIOLAR AND PERIBRONCHIOLAR ABSCESS, THERE IS A DIFFUSE ORGANIZATION OF THE EXUDATE IN THE SURROUNDING ALVEOLI.
FIG. XLIII. THE ALVEOLAR WALLS ARE THIN AND THE EXUDATE OF RED BLOOD CELLS AND DESQUAMATED EPITHELIUM IS IN PART HYALINIZED.
FIG. XLIII. THE ALVEOLAR WALLS ARE THIN AND THE EXUDATE OF RED BLOOD CELLS AND DESQUAMATED EPITHELIUM IS IN PART HYALINIZED.
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.