Liver transplantation in a case of fulminant liver failure after exertion
Liver transplantation in a case of fulminant liver failure after exertion
复制标题
劳累后暴发性肝功能衰竭的肝移植一例
作者：
J. Saissy
先生：预防性中暑（EHS）被定义为由于在严重和长时间的肌肉努力过程中发生的中心温度的极端和长时间的升高而引起的细胞攻击。在EHS病例中几乎总是观察到肝损害，但暴发性肝衰竭（FLF）是一个例外。Hassanein等人[1]首次报道了一例患者在EHS后需要进行原位肝移植（奥尔特）。我们描述了第二种情况。在加蓬的一次突击队行军中，一名30岁的士兵，体格健壮，对热带气候适应良好，突然昏倒并昏迷（格拉斯哥昏迷评分= 9），伴有抽搐、高热（直肠温度= 40 ~轻度横纹肌溶解（血清肌酸磷酸激酶= 557 IU/1））、动脉低血压（血压= 60/40 mmHg）和大量腹泻。他被插管和人工通气，然后飞往法国。20小时后，他的直肠温度正常，没有黄疸或出血，但患者始终处于昏迷状态，格拉斯哥昏迷量表评分为4分。生物学检查显示FLF，丙氨酸氨基转移酶为5200 IU/l，凝血酶原水平低于5%，因子V低于5%，中度横纹肌溶解，血清肌酸磷酸激酶为5900 IU/l。入院后36 h行奥尔特。肉眼检查发现肝脏小、苍白、失血，重量为1400 g。组织学检查结果显示中央小叶坏死伴结膜组织解体。术后第2天，患者完全清醒;凝血酶原水平为68%，因子V为102%，丙氨酸氨基转移酶为625 IU/l。然而，在术后第4天，患者完全清醒时，发生了重度横纹肌溶解症，血清肌酸磷酸激酶为34000 IU/l，急性肾衰竭，血清肌酐为788 gmol/l。因此，患者需要血液透析，肾衰竭在3周内完全克服。此后，他的病情恶化，胆汁性腹膜炎，需要另外两次手术，他在奥尔特后11个月死于慢性排斥反应。在其最严重的形式中，EHS是一种多器官功能障碍综合征，其病因仍然知之甚少[1]。其血浆肿瘤坏死因子和白细胞介素1 a水平高[2]，可能与全身炎症反应综合征有关[3]。这种综合征的特征性链式炎症过程可能是由于EHS中内脏缺血继发于热环境中体力活动期间发生的再分布引起的细菌移位[4，5]。报告的病例中未观察到毒性、感染性或血管病因，表明体力活动期间发生的中暑可导致FLF，这是由于热对肝实质的直接影响或由于热适应受试者中发生的抗利尿激素（一种强效门静脉血管收缩剂）分泌过多导致再分布现象恶化而导致的急性肝缺血[4]。总之，EHS可能是复杂的FLF，和低的肝脏缺血耐受性的主题适应热带气候可能是一个促进因素。
Sir: Exertional heat stroke (EHS) is defined as a cellular aggression due to an extreme and prolonged increase in the central temperature that occurs during the course of severe and prolonged muscular effort. Liver damage is almost always observed in cases of EHS, but fulminant liver failure (FLF) is an exceptional occurrence. Hassanein et al. [1] were the first to relate the case of a patient requiring orthotoptic liver transplantation (OLT) after EHS. We describe a second case. During a commando march in Gabon a 30-year-old soldier, athletic and well acclimated to the tropical climate, collapsed and became comatose (Glasgow Coma Scale = 9) with convulsions, hyperthermia (rectal temperature = 40 ~ mild rhabdomyolysis (serum creatine phosphokinase = 557 IU/1), arterial hypotension (blood pressure = 60/40 mmHg), and profuse diarrhea. He was intubated and artificially ventilated and then flown to France. Twenty hours later his rectal temperature was normal, and there was no 9 icterus or hemorrhage, but the patient was always comatose, with Glasgow Coma Scale Score at 4. Biological examination revealed FLF with alanine aminotransferase at 5200 IU/1, prothrombin level below 5%, factor V below 5%, and moderate rhabdomyolysis, with serum creatine phosphokinase at 5900 IU/1. OLT was performed 36 h after admission. Macroscopically the liver was small, pale, and exsanguinate, weighing 1400 g. The histological findings revealed central lobular necrosis with disorganization of the conjunctive tissue. On the 2th day after surgery the patient was completely conscious; and the prothrombin level was at 68%, factor V at 102%, and alanine aminotransferase at 625 IU/1. However, severe rhabdomyolysis with serum creatine phosphokinase at 34000 IU/1 and acute renal failure with serum creatinine at 788 gmol/1 developed on the 4th day after surgery while the patient was perfectly alert. Therefore the patient needed hemodialysis, and the renal failure was completely overcome in 3 weeks. His condition thereafter deteriorated, with biliary peritonitis which required two other operations, and he died 11 months after OLT in a context of chronic rejection. In its most serious forms EHS is a multiple organ dysfunction syndrome whose pathogeny is still poorly known [1]. With its high plasma tumor necrosis factor and interleukin l a levels [2] it could be associated With the systemic inflammatory response syndrome [3]. The chain inflammatory process which characterizes this syndrome may be due in EHS to the translocation of bacteria by splanchnic ischemia secondary to the redistribution which occurs during physical exertion in hot environments [4, 5]. The reported case, in which no toxic, infectious, or vascular etiology was observed, suggests that heat stroke occurring during physical exertion can cause FLF, resulting either from the direct effect of heat on the hepatic parenchyma or from acute hepatic ischemia due to the phenomenon of redistribution made worse by the hypersecretion of antidiuretie hormone, a potent portal vasoconstrictor, which occurs in the heat-acclimated subject [4]. In conclusion, EHS may be complicated by FLF, and the low hepatic tolerance to ischemia in the subject acclimated to the tropical climate could be a promoting factor.
肝功能衰竭是劳力性中暑的一个组成部分。
影响因子：
29.4
作者：
Hassanein,T;Perper,JA;Tepperman,L;Starzl,TE;VanThiel,DH
通讯作者：
VanThiel,DH