Trewby P N, Warren R, Contini S, Crosbie W A, Wilkinson S P, Laws J W, Williams R
Gastroenterology. 1978 May;74(5 Pt 1):859-65.
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.
100例暴发性肝衰竭患者中，37例有肺水肿的临床和影像学证据。他们均无左心衰竭的临床证据，12例患者测得的肺动脉楔压正常。同样，没有证据表明肾衰竭、内毒素血症或低白蛋白血症与此有关。然而，脑水肿患者中肺水肿的发生率显著更高，这表明肺水肿要么起源于中枢，要么存在导致两个部位水肿的共同因素。另一个局部因素可能是肺内血管扩张的存在。对11例患者进行的详细同位素研究显示，肺水肿患者的肺血管外水容量显著增加，这与影像学改变的严重程度相符。虽然肺水肿患者的总体死亡率高于无肺水肿患者，但差异不显著，除3例患者外，早期采用正压呼气通气均能实现充分氧合。
