Pulmonary edema is a relatively common problem facing most physicians. Its separation into cardiogenic and noncardiogenic or high-permeability variants is crucial to its proper early management. Our understanding of the disease processes producing noncardiogenic pulmonary edema has greatly expanded in the last 2 decades. Upper airway obstruction (UAO) is one of many recently recognized mechanisms which can produce noncardiogenic pulmonary edema. The UAO may be subtle in some patients, making its association with the subsequent pulmonary edema difficult especially for the physician unaware of this entity and the potential risk factors contributing to it. A high index of suspicion for this diagnosis is required in the right clinical settings. Our clinical results support a noncardiogenic basis for pulmonary edema occurring after UAO. Five of our 7 patients had at least 1 identifiable risk factor for the development of peri-intubation UAO and pulmonary edema. Additionally, the onset of pulmonary edema following UAO and the duration of the pulmonary edema varied considerably in our patients. Individuals with additional risk factors for the development of noncardiogenic pulmonary edema developed a more severe form of pulmonary edema associated with other organ-system disease. However, in most individuals, UAO-associated pulmonary edema appears to be a self-limited reversible process once it is recognized and properly treated.