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The pathology of influenza

Chapter 35: A. THE EXTENT OF THE INITIAL PULMONARY LESION
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The authors present a systematic pathological study of cases from the 1918 influenza epidemic, based on eighty-two autopsies, detailing gross and microscopic findings. They describe necrotizing hemorrhagic lesions of the trachea and bronchi and several pulmonary patterns including acute diffuse fulminant hemorrhagic pneumonia, localized necrotizing pneumonias, and organizing bronchiolar/alveolar exudates. The work documents extrarespiratory effects on lymphoid tissues, spleen, bone marrow, blood vessels, the alimentary and urinary tracts, central nervous system structures, and changes observed in pregnancy. A comparative analysis contrasts these lesions with those produced by inhaled poisonous gases and emphasizes peculiar histologic features such as hemorrhagic and hyaline necrosis and patterns of organization. Bacteriological findings and their relation to pleural involvement and pneumonic types conclude the study.

V. PECULIARITIES OF THE HISTOLOGY OF INFLUENZAL PNEUMONIA

A. THE EXTENT OF THE INITIAL PULMONARY LESION

One of the features differentiating the pneumonic process in influenza from the usual types of inflammation of the lung, is diffuseness (90). In the early cases especially, or in cases which terminate fatally at an early period, both lungs are often involved, and, on histological examination, only a small portion of the pulmonary parenchyma is found unaffected. The exudate, largely acellular, presents serum as its most conspicuous feature. The picture is one of a patchy pneumonia with intermediary areas of what might be called edema, although fibrin is often demonstrable in the coagulated, albuminous material. So little attention has been paid to earlier stages of the usual types of pneumonia, for example lobar, that it is impossible to say whether or not diffuse involvement of the pulmonary parenchyma initiates the process which later becomes localized in one or more lobes. The initial edema of influenzal pneumonia is the expression of a widespread irritation. If the injury has not extended deeply, the edema may disappear within a relatively short time, and exfoliated lining cells fill the alveoli; those remaining in their normal position are frequently in process of division (Fig. XLVII). It is conceivable—and the view has already been announced—that this edema is a disseminating factor and perhaps responsible for the diffuseness of the pneumonic process which may follow. If the fluid is simply a serous exudate, it may play no essential rôle in the severe acute symptoms manifested by these patients, for it has been shown, both in the experimental lesions induced by pulmonary irritating gases and by pulmonary irrigation through which extensive artificial edema of the lungs may be attained, that the presence of fluid in the lung in itself is not harmful (161).