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.
E. THE ORGANIZATION PROCESS
The similarity between the acute lesions of influenzal pneumonia and those following the inhalation of poisonous gases led to the prediction, in the early studies, that if the process were not terminated by death, the bronchiolar and alveolar changes would not result in a restoration of the tissue to normal, but in an organization which would in its turn bring about mechanical changes in the pulmonary tissue. This prediction has been fulfilled; obliterating bronchiolitis (Figs. [XI] and [XLVIII]), bronchiectasis (Figs. [L] and [XII]), and organizing pneumonia (47, 92, 156, 162) (Figs. [XXXIX], [XL], [XLI], [XLIV], [XLV]) have been encountered despite the fact that the time interval for fatalities from extraneous or subsidiary causes has been short.
FIG. XLIV. THE ALVEOLAR WALLS ARE IN PART OBLITERATED. THE ALVEOLAR EXUDATE IS ORGANIZED BUT THE FIBROUS TISSUE STRANDS ARE SPREAD APART BY EDEMA.
FIG. XLV. AUTOPSY NO. 163. ORGANIZATION OF THE ALVEOLAR EXUDATE AFTER THE SUBSIDENCE OF THE ACUTE PROCESS. COMPARE FIGURE [XLIV].
Resolution of the exudate in pneumonia, with the restoration of the tissue to normal, is a result at such variance with the usual fate of an inflammatory exudate, that it has attracted a great deal of attention. Perhaps the most striking results of the study of this subject have been published recently by Kline (69). Arguing from previous experiments (70) in which it was demonstrated that the circulation of the pneumonic lung is impaired, and that for this reason sufficient serum cannot reach the exudate to inhibit the proteolytic action of leucocytic ferments, Kline introduced normal serum into the consolidated lung by the tracheal route, and showed conclusively that this resulted in an organization of the alveolar exudate. This, of course, might explain resolution, but it is difficult to see without further study how serum can reach the exudate to inhibit autolysis, and in this way stimulate organization, in one case of pneumonia and not in another.
Comparison with certain processes in other portions of the body suggest the nature of this stimulus to organization in pneumonia. For example, it is well known that epithelial necrosis of the liver that results from chloroform is followed by a restitution of the organ to normal. On the other hand, if the liver necrosis is produced by a chemical agent plus a bacterial one, the destructive lesion not only involves the liver cell, but extends to the framework of the organ and terminates in a cirrhosis. Unquestionably, the difference between the reaction after the chemical alone and that after chemical plus bacterial injury is a more extensive destruction in the latter case resulting in a stimulation of all the elements of the organ, including liver cell, connective tissue, and blood vessel. The connective tissue and vascular elements have a greater capacity to regenerate than has the liver cell; consequently, granulations form which impede the less active reparative process of the hepatic cell. If this comparison be applied to the pulmonary changes in influenza and after the inhalation of poisonous gases, it will be seen that in both processes the initial damage is extensive, as has been indicated in the discussion of necrotization. Where the lesion is superficial, tracheal, bronchial, and alveolar epithelia rapidly regenerate and restore the injured surface. Where, however, the lesions are more extensive, alveolar and bronchiolar exudates are transformed into granulation tissue, even though the epithelium may manifest unusual activity in its attempt to repair a denuded area.