肝硬化腹水处理指南.doc
http://www.100md.com
参见附件(209KB)。
肝硬化腹水处理指南(2006年英国)
K P Moore, G P Aithal
1.0 INTRODUCTION
Ascites is a major complication of cirrhosis,1 occurring in 50% of patients over 10 years of follow up.2 The development of ascites is an important landmark in the natural history of cirrhosis as it is associated with a 50% mortality over two years,2-5 and signifies the need to consider liver transplantation as a therapeutic option.3 The majority (75%) of patients who present with ascites have underlying cirrhosis, with the remainder being due to malignancy (10%), heart failure (3%), tuberculosis (2%), pancreatitis (1%), and other rare causes.6 The true prevalence and incidence of cirrhosis of the liver and its complications in the UK are unknown. Mortality from cirrhosis has increased from 6 per 100 000 population in 1993 to 12.7 per 100 000 population in 2000.7 Approximately 4% of the general population have abnormal liver function or liver disease8 and approximately 10-20% of those with one of the three most common chronic liver diseases (non-alcoholic fatty liver disease, alcoholic liver disease, and chronic hepatitis C) develop cirrhosis over a period of 10-20 years. With a rising frequency of alcoholic and non-alcoholic fatty liver disease, a huge increase in the burden of liver disease is expected over the next few years8 with an inevitable increase in the complications of cirrhosis. There have been several changes in the clinical management of cirrhotic ascites over recent years, and the purpose of these guidelines is to promote a consistent clinical practice throughout the UK.
1.0绪论
腹水是肝硬化的一个主要并发症，1随访超过10年的病人中50%发生。2腹水的出现在肝硬化自然史中是一个重要的里程碑，因为其标示着2年间有50%的死亡率，2-5而且意味着需要考虑进行肝移植做为治疗方案。3以腹水为表现的病人大部分(75%)有潜在的肝硬化，其余的可能是恶性肿瘤(10%)、心衰(3%)、结核(2%)、胰腺炎(1%)和其它少见原因。6英国肝硬化真正的流行情况和发生率及其并发症尚不清楚。肝硬化的死亡率已经从1993年的6/10万上升到了2000年的12.7/10万。7普通人群中约4%有肝功能异常或肝病8，患三种最常见的慢性肝病(非酒精性脂肪肝，酒精性脂肪肝和慢性丙型肝炎)之一的病人约10-20%在10-20年间会发展成肝硬化。随着酒精性和非酒精性脂肪肝发生率的上升，在今后的数年间肝病的负担会大幅增加8并且不可避免要伴随着肝硬化并发症增加。在最近的几年间肝硬化腹水的临床处理上已有几个变化，本指南的目的是在全英国倡仪一个一致性的临床实践。
These guidelines are based on a comprehensive literature search, including the results of randomised control trials, systematic reviews, prospective retrospective studies and, in some instances, evidence obtained from expert committee reports. Where possible a judgement is made on the quality of the information used to generate the guidelines, and the specific recommendations have been graded according to the Oxford Centre for Evidence-based Medicine Levels of Evidence (May 2001) (see appendices 1 and 2).9 These guidelines conform to the international guidelines recently published by the International Ascites Club10 and are intended for use by physicians. We hope to revise these guidelines in three years time.
这些指南建立在深入的文献调查基础之上，包括RCT结果，系统综述，前瞻性回顾性研究，在有些情况下，证据是源于专家委员会的报告。如果可能的话，要对产生指南的材料的质量进行判断，并根据剑桥EBM中心的证据水平(2001年5月)(见附录1和2)对详细的建议进行分级。9这些指南符合最近由国际腹水俱乐部10出版的国际指南，也希望为内科医师所用。我们希望在3年的时间内对这些指南进行更新。
2.0 DEFINITIONS
The terms used in this article have been defined by the International Ascites Club.11
Uncomplicated ascites
Ascites that is not infected and which is not associated with the development of the hepatorenal syndrome. Ascites can be graded as follows:
● Grade 1 (mild). Ascites is only detectable by ultrasound examination.
● Grade 2 (moderate). Ascites causing moderate symmetrical distension of the abdomen.
● Grade 3 (large). Ascites causing marked abdominal distension.
Refractory ascites
Ascites that cannot be mobilised or early recurrence of which (that is, after therapeutic paracentesis) cannot be satisfactorily prevented by medical therapy. This includes two different subgroups.
● Diuretic resistant ascites-ascites that is refractory to dietary sodium restriction and intensive diuretic treatment (spironolactone 400 mg/day and frusemide 160 mg/day for at least one week, and a salt restricted diet of less than 90 mmol/day (5.2 g of salt)/day).
● Diuretic intractable ascites-ascites that is refractory to therapy due to the development of diuretic induced complications that preclude the use of an effective diuretic dosage.
2.0定义
本文中所用的词汇已为国际腹水俱乐部所定义。11
简单的(无并发症的)腹水
指没有被感染的腹水，其与肝肾综合征的出现无关。腹水分级如下：
●1级(少量)：腹水为超声检查所检测到。
●2级(中量)：腹水可引起中度对称性的腹部膨胀。
●3级(大量)：腹水可引起明显的腹胀。
难治性腹水
药物治疗不能消除腹水或无法满意阻止早期复发(指治疗性腹水穿刺后)。这包括两个不同的亚群。
●利尿剂抵抗性腹水-限盐饮食和增加利尿治疗(安体舒通400mg/d及速尿160mg/d至少一周，饮食中每日盐少于90mmol/d即5.2g盐)腹水仍难以控制。
●利尿剂难治性腹水-由于利尿导致并发症使得有效的利尿剂的量无法应用。
3.0 PATHOGENESIS OF ASCITES FORMATION
A detailed description of the pathogenesis of ascites formation is beyond the scope of this article but more detailed reviews are available.12-14 There are two key factors involved in the pathogenesis of ascites formation-namely, sodium and water retention, and portal (sinusoidal) hypertension.
3.0腹水形成的病机
对腹水形成的病机进行详细阐述不在本文的范围，不过有许多详细的综述可以参阅。12-14有两个关键因素涉及到腹水形成的病机，即钠水的潴留和门脉(肝窦)高压。
3.1 Role of portal hypertension
Portal hypertension increases the hydrostatic pressure within the hepatic sinusoids and favours transudation of fluid into the peritoneal cavity. However, patients with presinusoidal portal hypertension without cirrhosis rarely develop ascites. Thus patients do not develop ascites with isolated chronic extrahepatic portal venous occlusion or non-cirrhotic causes of portal hypertension such as congenital hepatic fibrosis, except following an insult to liver function such as gastrointestinal haemorrhage. Conversely, acute hepatic vein thrombosis, causing postsinusoidal portal hypertension, is usually associated with ascites. Portal hypertension occurs as a consequence of structural changes within the liver in cirrhosis and increased splanchnic blood flow. Progressive collagen deposition and formation of nodules alter the normal vascular architecture of the liver and increase resistance to portal flow. Sinusoids may become less distensible with the formation of collagen within the space of Disse. While this may give the impression of a static portal system, recent studies have suggested that activated hepatic stellate cells may dynamically regulate sinusoidal tone and thus portal pressure.......（后略) ......
肝硬化腹水处理指南(2006年英国)
K P Moore, G P Aithal
1.0 INTRODUCTION
Ascites is a major complication of cirrhosis,1 occurring in 50% of patients over 10 years of follow up.2 The development of ascites is an important landmark in the natural history of cirrhosis as it is associated with a 50% mortality over two years,2-5 and signifies the need to consider liver transplantation as a therapeutic option.3 The majority (75%) of patients who present with ascites have underlying cirrhosis, with the remainder being due to malignancy (10%), heart failure (3%), tuberculosis (2%), pancreatitis (1%), and other rare causes.6 The true prevalence and incidence of cirrhosis of the liver and its complications in the UK are unknown. Mortality from cirrhosis has increased from 6 per 100 000 population in 1993 to 12.7 per 100 000 population in 2000.7 Approximately 4% of the general population have abnormal liver function or liver disease8 and approximately 10-20% of those with one of the three most common chronic liver diseases (non-alcoholic fatty liver disease, alcoholic liver disease, and chronic hepatitis C) develop cirrhosis over a period of 10-20 years. With a rising frequency of alcoholic and non-alcoholic fatty liver disease, a huge increase in the burden of liver disease is expected over the next few years8 with an inevitable increase in the complications of cirrhosis. There have been several changes in the clinical management of cirrhotic ascites over recent years, and the purpose of these guidelines is to promote a consistent clinical practice throughout the UK.
1.0绪论
腹水是肝硬化的一个主要并发症，1随访超过10年的病人中50%发生。2腹水的出现在肝硬化自然史中是一个重要的里程碑，因为其标示着2年间有50%的死亡率，2-5而且意味着需要考虑进行肝移植做为治疗方案。3以腹水为表现的病人大部分(75%)有潜在的肝硬化，其余的可能是恶性肿瘤(10%)、心衰(3%)、结核(2%)、胰腺炎(1%)和其它少见原因。6英国肝硬化真正的流行情况和发生率及其并发症尚不清楚。肝硬化的死亡率已经从1993年的6/10万上升到了2000年的12.7/10万。7普通人群中约4%有肝功能异常或肝病8，患三种最常见的慢性肝病(非酒精性脂肪肝，酒精性脂肪肝和慢性丙型肝炎)之一的病人约10-20%在10-20年间会发展成肝硬化。随着酒精性和非酒精性脂肪肝发生率的上升，在今后的数年间肝病的负担会大幅增加8并且不可避免要伴随着肝硬化并发症增加。在最近的几年间肝硬化腹水的临床处理上已有几个变化，本指南的目的是在全英国倡仪一个一致性的临床实践。
These guidelines are based on a comprehensive literature search, including the results of randomised control trials, systematic reviews, prospective retrospective studies and, in some instances, evidence obtained from expert committee reports. Where possible a judgement is made on the quality of the information used to generate the guidelines, and the specific recommendations have been graded according to the Oxford Centre for Evidence-based Medicine Levels of Evidence (May 2001) (see appendices 1 and 2).9 These guidelines conform to the international guidelines recently published by the International Ascites Club10 and are intended for use by physicians. We hope to revise these guidelines in three years time.
这些指南建立在深入的文献调查基础之上，包括RCT结果，系统综述，前瞻性回顾性研究，在有些情况下，证据是源于专家委员会的报告。如果可能的话，要对产生指南的材料的质量进行判断，并根据剑桥EBM中心的证据水平(2001年5月)(见附录1和2)对详细的建议进行分级。9这些指南符合最近由国际腹水俱乐部10出版的国际指南，也希望为内科医师所用。我们希望在3年的时间内对这些指南进行更新。
2.0 DEFINITIONS
The terms used in this article have been defined by the International Ascites Club.11
Uncomplicated ascites
Ascites that is not infected and which is not associated with the development of the hepatorenal syndrome. Ascites can be graded as follows:
● Grade 1 (mild). Ascites is only detectable by ultrasound examination.
● Grade 2 (moderate). Ascites causing moderate symmetrical distension of the abdomen.
● Grade 3 (large). Ascites causing marked abdominal distension.
Refractory ascites
Ascites that cannot be mobilised or early recurrence of which (that is, after therapeutic paracentesis) cannot be satisfactorily prevented by medical therapy. This includes two different subgroups.
● Diuretic resistant ascites-ascites that is refractory to dietary sodium restriction and intensive diuretic treatment (spironolactone 400 mg/day and frusemide 160 mg/day for at least one week, and a salt restricted diet of less than 90 mmol/day (5.2 g of salt)/day).
● Diuretic intractable ascites-ascites that is refractory to therapy due to the development of diuretic induced complications that preclude the use of an effective diuretic dosage.
2.0定义
本文中所用的词汇已为国际腹水俱乐部所定义。11
简单的(无并发症的)腹水
指没有被感染的腹水，其与肝肾综合征的出现无关。腹水分级如下：
●1级(少量)：腹水为超声检查所检测到。
●2级(中量)：腹水可引起中度对称性的腹部膨胀。
●3级(大量)：腹水可引起明显的腹胀。
难治性腹水
药物治疗不能消除腹水或无法满意阻止早期复发(指治疗性腹水穿刺后)。这包括两个不同的亚群。
●利尿剂抵抗性腹水-限盐饮食和增加利尿治疗(安体舒通400mg/d及速尿160mg/d至少一周，饮食中每日盐少于90mmol/d即5.2g盐)腹水仍难以控制。
●利尿剂难治性腹水-由于利尿导致并发症使得有效的利尿剂的量无法应用。
3.0 PATHOGENESIS OF ASCITES FORMATION
A detailed description of the pathogenesis of ascites formation is beyond the scope of this article but more detailed reviews are available.12-14 There are two key factors involved in the pathogenesis of ascites formation-namely, sodium and water retention, and portal (sinusoidal) hypertension.
3.0腹水形成的病机
对腹水形成的病机进行详细阐述不在本文的范围，不过有许多详细的综述可以参阅。12-14有两个关键因素涉及到腹水形成的病机，即钠水的潴留和门脉(肝窦)高压。
3.1 Role of portal hypertension
Portal hypertension increases the hydrostatic pressure within the hepatic sinusoids and favours transudation of fluid into the peritoneal cavity. However, patients with presinusoidal portal hypertension without cirrhosis rarely develop ascites. Thus patients do not develop ascites with isolated chronic extrahepatic portal venous occlusion or non-cirrhotic causes of portal hypertension such as congenital hepatic fibrosis, except following an insult to liver function such as gastrointestinal haemorrhage. Conversely, acute hepatic vein thrombosis, causing postsinusoidal portal hypertension, is usually associated with ascites. Portal hypertension occurs as a consequence of structural changes within the liver in cirrhosis and increased splanchnic blood flow. Progressive collagen deposition and formation of nodules alter the normal vascular architecture of the liver and increase resistance to portal flow. Sinusoids may become less distensible with the formation of collagen within the space of Disse. While this may give the impression of a static portal system, recent studies have suggested that activated hepatic stellate cells may dynamically regulate sinusoidal tone and thus portal pressure.......（后略) ......
附件资料：
相关资料1：