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 theinflammatory 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.