Noncardiac pulmonary edema precipitated by tracheal intubation in patients with inhalation injury.

Ten patients with body surface burn and clinical evidence of inhalation injury developed transient, reversible pulmonary edema within 5 min after endotracheal intubation. Hemodynamic studies within 1 hr after intubation revealed normal cardiac output and pulmonary artery wedge pressure (WP). Additionally, in the latter 4 patients, protein concentration of edema fluid (EF) aspirated from the trachea was 58-104% of plasma (P) total protein. These findings suggest that altered capillary permeability was responsible for this transient pulmonary edema. It is postulated that glottic generated expiratory retard may increase alveolar pressure, thus preventing pulmonary edema. Bypass of glottis by tracheal intubation may render alveolar pressure atmospheric and facilitate edema formation.