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The pathology of influenza

Chapter 38: D. THE HYALINE NECROSIS OF THE PULMONARY TISSUE
By M. C. Winternitz
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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.

D. THE HYALINE NECROSIS OF THE PULMONARY TISSUE

The hyalinization of the epithelium lining the ducti alveolares (47, 48) also merits special attention (Figs. V, XV, XVI). This process may extend through the wall of the duct and is often seen in the alveolar walls throughout the involved lung. The entire alveolar wall may be homogeneous in appearance, but, occasionally, the thrombus alone, which has formed in its vessels (41), presents this change (Fig. XVII). The alveolar as well as the bronchiolar wall is thickened by a homogeneous material in which cell-body and exudate cannot be differentiated. This acute necrosis, as has been mentioned, is encountered in gas poisoning but is unusual in other known types of respiratory infection. Doubtless, it is a precursor to the more destructive lesions commonly found in later stages of the disease—abscesses which extend through the bronchiolar walls (Fig. XXXI), necrotizing areas of pneumonia in which huge clumps of bacteria are found (Fig. XXXII), and true gangrene (Figs. XXXIII, XXXIV, XXXV). The destruction of the alveolar wall in the early stages of the disease plays a causal rôle in the production of subcutaneous emphysema (Figs. XVIII and XIX). This important phase of the histological change in influenzal pneumonia has received but little attention and, with one or two exceptions, is not mentioned in the literature (8, 162).

In the interpretation of this necrotization, the only helpful analogy is offered by the acute respiratory lesions following the inhalation of poisonous gases. With the aid of vital stains, it has been demonstrated that chlorine quickly initiates necrosis due to the direct action of the gas. Since necrosis also occurs with phosgene,—in the decomposition of which hydrochloric acid is probably liberated,—there is presumptive evidence that the halogen is responsible for the process. Studies are now in progress to determine the relation of the acid-producing properties of the different strains of organisms to the type and fate of the pneumonic exudate.