Pulmonary oxygen toxicity in the adult.

Abstract

RECENTLY, there has been increasing evidence that some patients in whom oxygen administration is required in high concentration for relatively prolonged periods by means of mechanical artificial ventilation suffer gradually progressive deterioration of pulmonary function and die of pulmonary insufficiency (13). This apparently occurs as a result of an increasing reduction in pulmonary compliance and vital capacity accompanied by hypoxia. At autopsy the lungs exhibit fairly characteristic gross and microscopic changes (9). Various terms have been applied to this condition such as“respirator lung syndrome,” “pulmonary oxygen toxicity,” and “traumatic oxygen alveolopathy.” Experimental evidence indicates that prolonged administration of highly concentrated oxygen is toxic to the lungs of a variety of animals (2, 12, 15). Dogs exposed to 100 per cent oxygen generally die after approximately seventy hours (8). The lungs of these animals show damaged alveolar walls with the formation of hyaline membranes. Normal human adults are believed to be more resistant than small laboratory animals to the adverse effects of 100 per cent oxygen but are nevertheless susceptible. Pulmonary symptoms may occur after only six to seven hours of such exposure ; there is substernal pain, cough, and decrease in the vital capacity (6, 16). Cederberg et al. (3) described a fibrinous exudate in the alveoli with hyaline membrane formation in the lungs of such patients. Northway et al. (10, 11) recently reported the syndrome “bronchopulmonary dysplasia” in which there is a prolongation of the healing phase of the respiratory distress syndrome in newborn infants treated for twenty-four hours or more with warm, humidified 80 to 100 per cent oxygen via an intermittent positive pressure respirator. They believed that this was the result of prolonged high concentrations of oxygen on the developing lungs superimposed upon the healing lesions of the respiratory distress syndrome. The possible direct connection between the use of therapeutic oxygen and pulmonary hemorrhage in newborn infants has been suggested (14). The pathology of pulmonary lesions associated with oxygen toxicity has been described in detail by Nash et al. (9). Grossly, the lungs are increased in weight, frequently over 1,800 g, are deeply congested, inelastic, and noncrepitant. The cut surface shows a “beefy,” hemorrhagic consolidation. Microscopically, there appear to be 2 phases which are believed to be stages of a single progressive process. An early or exudative phase exhibits capillary congestion, an alveolar protein-aceous exudate, intra-alveolar hemorrhage, fibrinous exudate, and, prominently, hyaline membranes lining the alveolar walls. If survival is long, a second or proliferative phase occurs, in which there is marked alveolar and interlobular edema, fibroblastic proliferation, early fibrosis, and hyperplasia of the alveolar lining cells.