Hashim S W, Kay H R, Hammond G L, Kopf G S, Geha A S
Am J Surg. 1984 Apr;147(4):560-4. doi: 10.1016/0002-9610(84)90022-9.
Nine episodes of fulminant noncardiogenic pulmonary edema after cardiopulmonary bypass were observed in eight patients between September 1977 and December 1982. All these catastrophic reactions occurred during administration of fresh frozen plasma 30 minutes to 6 hours after discontinuation of cardiopulmonary bypass. In one patient, two episodes of noncardiogenic pulmonary edema occurred 4 hours apart. In each instance, fresh frozen plasma was being administered. In all patients, pulmonary artery diastolic pressure became elevated during the administration of fresh frozen plasma while left atrial pressure or pulmonary capillary wedge pressure progressively decreased, and cardiac output deteriorated markedly in all but one patient. Corticosteroids, positive end-expiratory pressure, and catecholamines were administered to all patients. All deaths were due to a decrease in cardiac output. Cardiac output did not increase substantially with the use of an intraaortic balloon pump or the administration of catecholamines. The last two patients in the series showed a steady and remarkable improvement in cardiac output when the wedge pressure was increased to a level above 15 mm Hg with the administration of normal saline solution. Our data suggest the following: (1) noncardiogenic pulmonary edema after cardiopulmonary bypass is most probably an anaphylactic reaction to fresh frozen plasma. (2) The syndrome is reversible within hours; in only one patient (who suffered noncardiogenic pulmonary edema twice) did adult respiratory distress syndrome develop. (3) The three deaths were not related to hypoxia but to the deleterious effects of low cardiac output associated with hypovolemia secondary to fluid loss through the lungs and possibly across other capillary beds. Therefore, treatment should include restoration of adequate left-sided filling pressures to achieve satisfactory cardiac output.
1977年9月至1982年12月期间,在8例患者中观察到9次体外循环后暴发性非心源性肺水肿。所有这些严重反应均发生在体外循环停止后30分钟至6小时输注新鲜冰冻血浆期间。1例患者在间隔4小时的时间内发生了2次非心源性肺水肿。每次发生时,均正在输注新鲜冰冻血浆。所有患者在输注新鲜冰冻血浆期间肺动脉舒张压升高,而左心房压力或肺毛细血管楔压逐渐降低,除1例患者外,所有患者的心输出量均显著恶化。所有患者均接受了皮质类固醇、呼气末正压通气和儿茶酚胺治疗。所有死亡均归因于心输出量下降。使用主动脉内球囊反搏或给予儿茶酚胺后,心输出量并未显著增加。该系列中的最后2例患者在输注生理盐水使楔压升高至15 mmHg以上时,心输出量出现了稳定且显著的改善。我们的数据提示如下:(1)体外循环后非心源性肺水肿很可能是对新鲜冰冻血浆的过敏反应。(2)该综合征在数小时内可逆转;仅1例患者(该患者发生了2次非心源性肺水肿)发生了成人呼吸窘迫综合征。(3)3例死亡与缺氧无关,而是与低心输出量的有害影响有关,低心输出量与因肺内液体丢失以及可能通过其他毛细血管床导致的血容量减少继发的低血容量有关。因此,治疗应包括恢复足够的左心充盈压以实现满意的心输出量。