Lidofsky S D, Bass N M, Prager M C, Washington D E, Read A E, Wright T L, Ascher N L, Roberts J P, Scharschmidt B F, Lake J R
Department of Medicine, University of California, San Francisco 94143.
Hepatology. 1992 Jul;16(1):1-7. doi: 10.1002/hep.1840160102.
Cerebral edema and intracranial hypertension, commonly present in fulminant hepatic failure, may lead to brainstem herniation and limit the survival of comatose patients awaiting liver transplantation before a donor organ becomes available. Also, they are likely responsible for postoperative neurological morbidity and mortality. Although intracranial pressure monitoring has been proposed to aid clinical decision making in this setting, its use in the prevention of brainstem herniation preoperatively, in the selection of patients for liver transplantation who have the potential for neurological recovery and in the maintenance of cerebral perfusion during liver transplantation has not been examined in detail. To address these issues, we established a protocol for intracranial pressure monitoring in comatose patients with fulminant hepatic failure as part of their preoperative and intraoperative management. Twenty adults and three children underwent intracranial pressure monitoring. Ten patients required preoperative medical therapy with mannitol, barbiturates or both for a rise in intracranial pressure above 25 mm Hg. Four patients had a sustained lowering of intracranial pressure, three of whom survived hospitalization. Six patients had intracranial hypertension refractory to medical management, were removed from a waiting list for a donor organ and died with brainstem herniation. Of the remaining 17 patients, 3 died of other causes while awaiting a donor organ, 2 recovered spontaneously without neurological sequelae and 12 underwent liver transplantation. All but one patient undergoing liver transplantation had transient intraoperative intracranial hypertension develop, requiring medical treatment. The 12 patients who had transplants recovered neurologically and were discharged from the hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
脑水肿和颅内高压常见于暴发性肝衰竭,可能导致脑干疝形成,并限制等待肝移植的昏迷患者在获得供体器官前的生存。此外,它们可能是术后神经并发症和死亡的原因。尽管有人提出颅内压监测有助于在此种情况下的临床决策,但术前预防脑干疝、选择有可能神经功能恢复的肝移植患者以及肝移植期间维持脑灌注方面其应用尚未得到详细研究。为解决这些问题,我们制定了一项针对暴发性肝衰竭昏迷患者的颅内压监测方案,作为其术前和术中管理的一部分。20名成人和3名儿童接受了颅内压监测。10名患者因颅内压升至25mmHg以上,术前需要用甘露醇、巴比妥类药物或两者进行药物治疗。4名患者颅内压持续降低,其中3名存活出院。6名患者颅内高压对药物治疗无效,被从供体器官等待名单中除名,死于脑干疝。其余17名患者中,3名在等待供体器官时死于其他原因,2名自发康复且无神经后遗症,12名接受了肝移植。除1名患者外,所有接受肝移植的患者术中均出现短暂颅内高压,需要药物治疗。12名接受移植的患者神经功能恢复并出院。(摘要截选至250字)