Neurogenic Pulmonary Edema in Fatal and Nonfatal Head Injuries

Impaired pulmonary function is a frequent but poorly understood complication of acute head injury (HI). A potential early contributor to the pulmonary dysfunction seen in HI patients is neurogenic pulmonary edema (NPE). We hypothesized that NPE would occur early after HI and that it would have a continuum of clinical severity depending on the severity of the HI and associated intracranial hypertension. A large autopsy data base and inpatient HI data base were used to search for cases of NPE. Patients in the autopsy data base were stratified according to injury type and whether they died at the scene or within 96 hours of injury. There were significant (p < 0.0001, analysis of variance) elevations in lung weights in patients dying at the scene and within 96 hours from HI, compared with those dying from other noncentral nervous system injuries. No other organs studied showed significant weight increases. The incidence of NPE in isolated HI patients dying at the scene was 32%. In patients with isolated HI dying within 96 hours, the incidence of NPE was 50%. We found an inverse correlation (r = 0.62; p < 0.0014) between the initial cerebral perfusion pressure and the Pao2 /FIO2 ratio despite a normal-appearing chest x-ray film. We conclude that NPE occurs frequently in HI patients. The process of edema formation begins early in the clinical course and is isolated to the lung. Furthermore, surviving HI patients manifest a significantly decreased Pao2 /FIO2 ratio in the presence of a normal chest x-ray film, which seems to be related to a decrease in cerebral perfusion pressure and may be caused, in part, by NPE.