暴发性肝衰竭的治疗

【关键内容】·暴发性肝衰竭 (ＦＨＦ)是指过去无肝病史者 ,在短期内发生严重的肝功能衰竭和肝性脑病。病因大多为药物性和病毒感染 ,其他病因少见 ,约 2 0 %病因不明。·一旦本病诊断成立 ,应立即将患者置于强化监护病房 (ＩＣＵ) ,密切观察病情 ,调整治疗方案。·脑水肿是主要的并发症之一 ,可用脱水剂或巴比妥类药物治疗 ,后者可引起低血压 ,故主要用于并发肾功能衰竭者。如发生其他并发症 ,如低血糖、感染、出血等 ,需及时处理 ;多脏器功能衰竭是ＦＨＦ的高死亡率的主要原因 ,即使经积极处理 ,也常难逃死亡的厄运 ,故处理要着重于预防其…     

暴发性肝衰竭

暴发性肝衰竭王耆煌，乐祥东暴发性肝衰竭（ＦＨＦ）是指原无肝病的患者突然发生大量肝细胞坏死或出现严重的肝细胞功能损害并在起病８周内出现肝性脑病的一种综合征。主要临床表现是肝性脑病和肝肾综合征。根据起病至肝性脑病出现的时间不同，有几种不同的分类方法，通常...     

免疫抑制诱导性暴发性肝衰竭

免疫抑制诱导性暴发性肝衰竭 (ｆｕｌｍｉｎａｎｔｈｅｐａｔｉｃｆａｉｌｕｒｅ,ＦＨＦ) ,是指由纤维淤胆性肝炎 (ｆｉｂｒｏｓｉｎｇｃｈｏｌｅｓｔａｔｉｃｈｅｐａｔｉｔｉｓ,ＦＣＨ )迅速发展的肝功能衰竭。ＦＣＨ是一类新的临床病种 ,有着独特的发病机制和临床病理特征 ,发生于各种原因引起的严重免疫抑制状态下 ,特别是器官移植后大量使用免疫抑制剂的肝炎病毒感染者 ;临床经过凶险 ,病人多在起病后数月甚至数周内因ＦＨＦ而迅速死亡。在此对ＦＣＨ作一系统介绍。一、ＦＣＨ的发现和发病背景1991年 ,英国学者Ｄａｖｉｅｓ和Ｏ′Ｇｒ…     

免疫抑制诱导性暴发性肝衰竭1例

病例　患者男,72岁。2002年5月因双下肢水肿在某医院诊断为“肾病综合征”,给予强的松60mg/d、雷公藤多甙片、中草药等治疗。2003年3月开始出现恶心、腹胀,ALT237U/L,按“药物性肝炎”治疗,予“护肝片”、“联苯双酯滴丸”等口服效果不明显,并出现黄疸,后又静滴“茵栀黄针剂、泰特针剂”月余,病情无好转。2003年5月6日查ALT449U/L、AST284U/L、TBil110μmol/L、DBil72μmol/L、HBVDNA( )、HBsAg( )、抗HBe( )、抗HBc( )。入住某医院肾内科,强的松片减为5mg/d,静滴“茵栀黄针、泰特针、强力宁针”等,黄疸进行性加重,伴腹胀、恶…     

免疫抑制诱导性暴发性肝衰竭一例

患者 ,男 ,6 8岁。因乏力、纳差、中上腹饱胀不适 3个月 ,巩膜、皮肤黄染、尿少 2 0ｄ入院。入院前肝功能 :丙氨酸转氨酶 (ＡＬＴ) 2 30Ｕ/Ｌ ,天门冬氨酸转氨酶 (ＡＳＴ) 340Ｕ/Ｌ ,清蛋白 (ＡＬＢ) 2 3ｇ/Ｌ ,球蛋白 4 1ｇ/Ｌ ,总胆红素 (ＴＢＩＬ)187.4 μｍｏｌ/Ｌ ,直接胆红素 (ＤＢＩＬ) 12 3.1μｍｏｌ/Ｌ ,Ｂ超示肝硬化腹水 ,门诊以“肝硬化失代偿”收入院。既往无肝炎病史 ,但发现ＨＢｓＡｇ阳性 10年 ,6年前因双肾积水 ,多囊肾 ,肾功能衰竭行肾移植手术 ,术后一直服用泼尼松和硫唑嘌呤至今。体检 :体温 37.4℃ ,脉搏 78次 /ｍｉｎ…     

血液净化治疗暴发性肝衰竭的疗效

【《Braz J InfectDis》2013年7—8月报道】题：血液净化治疗暴发性肝衰竭的疗效（作者Pu Y if）     

暴发性肝衰竭病人颅内改变的最佳治疗

脑水肿和颅内高压在暴发性肝衰竭病人(FHF)中的发病率很高，尽管令人难以接受，但由其造成的死亡率也非常高。不幸的是，只有少量小规模随机对照试验用于这种人类FHF并发症的研究，并且其中大部分研究结果并不确定。因为临床上采用了其它危急病症的治疗方案，所以是根据     

血浆置换治疗暴发性肝衰竭的研究进展

近年来，国内外多家相继开展了血浆置换治疗暴发性肝衰竭的研究，取得了较大的进展。本文介绍血浆置换治疗暴发性肝衰竭的原理、临床应用情况及存在问题。     

Antithrombin III concentrate in the treatment of fulminant hepatic failure

Twenty-six patients with fulminant hepatic failure were treated with daily infusions of antithrombin III concentrate until recovery of consciousness or death. Seven patients were alive (group A), 7 survived 17 to 47 days after treatment (group B), and 12 died within 9 days (group C). Decreased plasma antithrombin III levels increased on the day after treatment, irrespective of the pretreatment levels in all patients. Continuous or temporary normalization was seen in all patients in groups A and B, but in only 5 in group C patients whose bleeding was extensive (p less than 0.05). An abrupt drop in peripheral platelet counts occurred when plasma antithrombin III levels were below normal. General bleeding accompanied this drop. These results suggest that maintained normal plasma antithrombin III levels are beneficial for prolonged survival time in fulminant hepatic failure, probably through controlling intravascular coagulation, and that antithrombin III infusion may be useful for such treatment.     

Antithrombin III concentrate in the treatment of fulminant hepatic failure

Twenty-six patients with fulminant hepatic failure were treated with daily infusions of antithrombin III concentrate until recovery of consciousness or death. Seven patients were alive (group A), 7 survived 17 to 47 days after treatment (group B), and 12 died within 9 days (group C). Decreased plasma antithrombin III levels increased on the day after treatment, irrespective of the pretreatment levels in all patients. Continuous or temporary normalization was seen in all patients in groups A and B, but in only 5 in group C patients whose bleeding was extensive (p<0.05). An abrupt drop in peripheral platelet counts occurred when plasma antithrombin III levels were below normal. General bleeding accompanied this drop. These results suggest that maintained normal plasma antithrombin III levels are beneficial for prolonged survival time in fulminant hepatic failure, probably through controlling intravascular coagulation, and that antithrombin III infusion may be useful for such treatment.     

Bioartificial liver support for fulminant hepatic failure

ＯＲＩＧＩＮＡＬＡＲＴＩＣＥＥｆｅｃｔｓｏｆａｂｉｏａｒｔｉｆｉｃｉａｌｌｉｖｅｒｓｕｐｐｏｒｔｓｙｓｔｅｍｏｎａｃｅｔａｍｉｎｏｐｈｅｎｉｎｄｕｃｅｄａｃｕｔｅｌｉｖｅｒｆａｉｌｕｒｅｃａｎｉｎｅｓ．ＭＡＪＯＲＰＯＩＮＴＳＯＦＴＨＥＣＯＭＭＥＮＴ...     

Sulfasalazine-induced fulminant hepatic failure.

We report two cases of massive hepatic necrosis associated with sulfasalazine. Both patients had underlying inflammatory bowel disease. One of the patients had a history of an ill-defined autoimmune disorder (Sj?gren's syndrome). Symptoms and signs of a generalized hypersensitivity reaction were present in both patients. One patient died of a subarachnoid hemorrhage while awaiting transplant, the second died 2 weeks after transplant from disseminated aspergillosis. These two cases remind us of one of the potential hazards of sulfasalazine at a time when alternative therapies are now available.