Pulmonary edema that follows upper airway obstruction may occur in a variety of clinical situations. The predominant mechanism is forced inspiration against a closed or occluded glottis, inducing large intrapleural and transpulmonary pressure gradients favoring the transudation of fluid from the pulmonary capillaries into the interstitium. Postanesthetic laryngospasm has been implicated as the most frequent cause of this syndrome in adults. Risk factors for development of postlaryngospasm pulmonary edema include difficult intubation; nasal, oral, or pharyngeal surgical site; and obesity with obstructive apnea. The syndrome is recognized by development of hypoxia shortly (1-90 min) after a laryngospasm. A chest radiograph will reveal a symmetric bilateral infiltrate with normal heart size. Cardiogenic pulmonary edema and aspiration must be ruled out. Treatment is directed at correction of hypoxia with supplemental oxygen and use of diuretics (furosemide). Occasionally patients may require intubation.