Ede R J, Gimson A E, Bihari D, Williams R
J Hepatol. 1986;2(1):43-51. doi: 10.1016/s0168-8278(86)80007-1.
Raised intracranial pressure due to cerebral oedema is a major cause of death in fulminant hepatic failure and in the present study we have carried out a controlled clinical trial of continuous hyperventilation in the prevention of this complication. Twenty patients were electively hyperventilated to maintain PaCO2 between 3.5 and 5 kPa. In the other 35 patients mechanical ventilation was instituted only if severe hypoxia or hypercapnia occurred. Cerebral oedema, diagnosed clinically or by a rise in intracranial pressure to greater than 30 mm Hg, occurred in 85% of hyperventilated patients and in 86% of those not so treated. Although there was no significant reduction in the number of episodes of cerebral oedema in the hyperventilated patients (4.8 episodes/24 h) as compared with the controls (5.3 episodes/24 h), hyperventilation did appear to delay the onset of coning but on the basis of these results could not be recommended to be used routinely as a prophylactic measure in the prevention of cerebral oedema in this condition.
脑水肿导致的颅内压升高是暴发性肝衰竭患者死亡的主要原因。在本研究中，我们进行了一项关于持续过度通气预防该并发症的对照临床试验。20例患者被选择性地进行过度通气，以维持动脉血二氧化碳分压（PaCO2）在3.5至5千帕之间。另外35例患者仅在出现严重低氧血症或高碳酸血症时才进行机械通气。经临床诊断或颅内压升高超过30毫米汞柱确诊的脑水肿，在过度通气组患者中发生率为85%，在未接受过度通气治疗的患者中发生率为86%。与对照组（5.3次/24小时）相比，过度通气组患者脑水肿发作次数（4.8次/24小时）虽无显著减少，但过度通气似乎确实延迟了脑疝的发生。基于这些结果，不建议将其作为预防此类情况下脑水肿的常规预防性措施。
