With few exceptions, the gases studied have their most marked effect
upon the respiratory tract. They differ, however, in the localization of
the lesions and in the extent of the damage. For instance, mustard gas,
in high concentrations, has a necrotizing effect upon the entire
respiratory tract even to the pulmonary parenchyma itself. Inhaled in a
more dilute form it involves the larynx and the trachea and has spent
itself before the lung is reached. With phosgene, the opposite is true.
The upper respiratory tract is only slightly involved. The outspoken
lesions involve the bronchioles, the ducti alveolares, and extend to the
alveolar walls of the lung. Chlorine, while it produces a less severe
lesion of the upper respiratory tract, extends more often through all of
the ramifications of the tracheal tree to the lung.
With vital stains (trypan blue), it may be readily demonstrated that
these gases kill the epithelium of the respiratory tract and extend
through this superficial cellular coat to the deeper tissues of the
bronchiolar wall and to the lung tissue, killing it entirely, just as a
corrosive chemical destroys the wall of the stomach.
When chlorine and phosgene reach the lung, an intense reactive process
follows immediately. The congestive changes, the hemorrhage into the
pulmonary parenchyma both in the alveoli and in the subpleural and
interstitial tissues, and the albuminous rich, serous exudates occupy
the foreground of the acute picture and are associated clinically with
intense cyanosis, great dyspnœa, hemorrhage, bronchorrhea, and also with
pulmonary and subcutaneous interstitial emphysema. The microscope
reveals a hyalinization of the walls of the bronchioles or ducti
alveolares which are distended during this acute period and form a
picture that is very unusual in the more frequent types of respiratory
inflammation. It shows also a hyalinization of the alveolar walls,
usually those in direct continuity with the larger air passages. The
interstitial edema and hemorrhage, often perivascular in distribution,
is only overshadowed by the thick, almost colloid-like material within
the alveolus itself. Fibrin stains at this stage show this exudative
element in surprisingly large amounts. Fibrin not only covers the
alveolar wall, but crosses this structure and often forms intracapillary
plugs. In fact, besides the red blood cells, the serum and the fibrin,
one often sees, not only an excess of polymorphonuclear leucocytes in
the vessels of the lung, but these appear in process of migration within
a few hours after the animal has been exposed.
Animals surviving this stage often succumb later with a typical
pneumonic process. Although frequently pseudolobar, the process may
be lobar in extent, and as time goes on more definite lobular
involvement is frequently encountered. With the localization of the
inflammatory process, the general edema, congestion and milder
reactions in other portions of the lung tend to subside, and may be
entirely absent in a few days. The clinical picture, in the
experimental animal at least, also assumes a more typical expression
of respiratory infection,—leucocytosis, chlorine retention, etc.,
appear. Often the pneumonias, both lobar and lobular, are
complicated, grossly, by softening, and histologically, by
necrotization of the bronchiolar and alveolar walls. Recrudescence
of the active pulmonary infection is not uncommon, and perhaps is
associated with these focal necrotizing areas.