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.
[Illustration:
FIG. XLIV. THE ALVEOLAR WALLS ARE IN PART OBLITERATED. THE ALVEOLAR
EXUDATE IS ORGANIZED BUT THE FIBROUS TISSUE STRANDS ARE SPREAD APART
BY EDEMA.
]
[Illustration:
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.