The sequelæ after exposure to gas may be markedly delayed. They occur,
not only in animals which have exhibited characteristic acute symptoms,
but also, and especially with phosgene, where no serious immediate
clinical effects followed exposure to the gases. They are dependent upon
the fact that the pneumonic process has a very striking tendency to
undergo organization, a process which involves not only the exudate in
the alveoli, but also that within the bronchioles. The organizing
process may be present in both these portions of the lung or may be
confined to the bronchiole alone, and lead to a progressive interference
with the ingress and egress of alveolar air, so that atelectasis and
emphysema become permanent, and in turn lead to narrowing of the
vascular bed, ultimately producing right-sided cardiac decompensation.
Bronchiectases also occur; they may be tubular, associated with
organization of the pneumonic process in their vicinity, or saccular if
death has not followed the destruction of the bronchiolar wall.
Compare this picture with that of influenzal pneumonia and its sequelæ;
in both there is, first the acute diffuse involvement of the lung,
initiated by, or occurring simultaneously with, an acute
tracheobronchitis and presenting clinically dyspnœa, cyanosis,
blood-stained, abundant sputum, and even interstitial emphysema; next,
the tendency for the pneumonic process to localize and to necrotize; and
finally, if the acute period is survived, organization of the pneumonic
and bronchiolar exudates with resulting bronchiolitis and
bronchiectasis. With even more minute comparison, the resemblance is
sustained. The initial or early dilatation of the ducti alveolares, so
characteristic in gas poisoning, also occupies the foreground of the
histological picture in influenza. These dilated structures are the more
prominent on account of the red, ribbon-like strands that cover the
surface and often involve the walls. Similar necrotization, varying in
its depth even to involve the whole of the alveolar walls, occurs in
both of these conditions. Similar hemorrhages in the early stage,
rupture of the alveolar wall with interstitial and subcutaneous
emphysema, necrotization, gangrene, and organization in the same
localities, characterize the two lesions, and are not found with the
same uniformity in any other type of respiratory disease.
D. THE IMPORTANCE OF THE TRACHEA AND ITS RAMIFICATIONS AS A PROTECTIVE
MECHANISM AGAINST INFECTION OF THE PULMONARY PARENCHYMA
In gas poisoning it has been demonstrated that the initial damage to the
epithelium of the larger air passages is followed by an invasion of the
pulmonary parenchyma by the bacteria of the mouth. Repeated cultures
from the mouth before the exposure of the animal to gas have been
followed by the recovery of the same organisms, including the
pneumococci, the streptococci, the staphylococci, and a gram-negative,
hemoglobinophilic, small bacillus from the pneumonic lung. They find
their way into the lung after the destruction or incapacitation of the
protective mechanism (70) of the upper respiratory tract,—into a lung
which has been so damaged by the irritative gas that bacteria innocuous
in the normal pharynx now find a favorable medium for their development.
The inflammatory reaction which develops into pneumonia, perhaps
necrotizing, perhaps later organizing, can only be explained by the
combined action of the corrosive gas and the organisms saprophytic in
the normal mouth, but now pathogenic in varying degrees in the lung
whose vital reactions have either been inhibited or impaired by the gas.
[Illustration:
FIG. XL. AUTOPSY NO. 140. LEFT LUNG. THE HISTOLOGY OF THE PULMONARY
CHANGES IN THIS CASE IS ILLUSTRATED IN FIGURES XI, XLI, AND XLIV.
THESE PROCESSES, ILLUSTRATED IN FIGURE XXXIX, ARE ACCENTUATED AND
THERE IS ALSO AN ORGANIZATION OF THE EXTENSIVE PURULENT PLEURISY TO
BE MADE OUT IN THE ABOVE FIGURE.
]
There is no reason why this analogy should not be drawn, no reason why
we should not consider that the unknown etiological agent in influenza
produces a similar injury to, or even destruction of, the protective
mechanism of the respiratory tract. Similarly, gas and influenza damage
the pulmonary parenchyma itself, so that the bacteria of the air and of
the mouth which find their way into the damaged lung[16] initiate
processes and produce complications which may not be distinguished.