Incidence and pathophysiology of pulmonary edema in fulminant hepatic failure.
Thirty-seven of 100 consecutive patients with fulminant hepatic failure had clinical and radiological evidence of pulmonary edema. None of them had clinical evidence of left heart failure, and the pulmonary artery wedge pressure measured in 12 patients was normal. Similarly, there was no evidence to incriminate renal failure, endotoxemia, or hypoalbuminemia. However, there was a significantly higher incidence of pulmonary edema in patients with cerebral edema, suggesting either a central origin for the pulmonary edema or common factors predisposing to edema in both sites. An additional local factor may have been the presence of intrapulmonary vasodilatation. Detailed isotope studies in 11 patients showed a significantly increased pulmonary extravascular water volume in the patients with pulmonary edema which was in keeping with the severity of the radiological changes. Although the over-all mortality was higher in those patients with pulmonary edema than in those without, the difference was not significant, and early ventilation with positive and expiratory pressure achieved adequate oxygenation in all but 3 patients.
D001794:Blood Pressure; D001929:Brain Edema / Q000150:complications / Q000209:etiology; D002199:Capillary Permeability; D002302:Cardiac Output; D006501:Hepatic Encephalopathy / Q000150:complications; D006801:Humans; D008107:Liver Diseases / Q000150:complications*; D011175:Positive-Pressure Respiration; D011312:Pressure; D011654:Pulmonary Edema / Q000150:complications / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D012964:Sodium / Q000378:metabolism; D014664:Vasodilation; D014867:Water / Q000378:metabolism
D014867:Water; D012964:Sodium