Management of ascites in cirrhosis

Ascites is one of the earliest and most common complications of patients with cirrhosis. A typical circulatory dysfunction characterized by arterial vasodilation, high cardiac output and stimulation of vasoactive systems is commonly present in these patients and is associated with a poor prognosis. The treatment of ascites has been based on the combination of a low-sodium diet and the administration of diuretics. The reintroduction of paracentesis and the recent introduction of the transjugular intrahepatic portosystemic shunt (TIPS) are the most relevant innovations in the treatment of ascites during the past two decades, although controlled trials in large series of patients are needed to delineate whether TIPS is a safe and useful treatment for these patients.     

Management of ascites in cirrhosis

Ascites is a common complication of liver cirrhosis associated with a poor prognosis. The treatment of ascites requires dietary sodium restriction and the judicious use of distal and loop diuretics, sequential at an earlier stage of ascites, and a combination at a later stage of ascites. The diagnosis of refractory ascites requires the demonstration of diuretic non-responsiveness, despite dietary sodium restriction, or the presence of diuretic-related complications. Patients with refractory ascites require second-line treatments of repeat large-volume paracentesis (LVP) or the insertion of a transjugular intrahepatic portosystemic shunt (TIPS), and assessment for liver transplantation. Careful patient selection is paramount for TIPS to be successful as a treatment for ascites. Patients not suitable for TIPS insertion should receive LVP. The use of albumin as a volume expander is recommended for LVP of >5-6 L to prevent the development of circulatory dysfunction, although the clinical significance of post-paracentesis circulatory dysfunction is still debated. Significant mortality is still being observed in cirrhotic patients with ascites and relatively preserved liver and renal function, as indicated by a lower Model for End-Stage Liver Disease (MELD) score. It is proposed that patients with lower MELD scores and ascites should receive additional points in calculating their priority for liver transplantation. Potential new treatment options for ascites include the use of various vasoconstrictors, vasopressin V(2) receptor antagonists, or the insertion of a peritoneo-vesical shunt, all of which could possibly improve the management of ascites.     

肝硬化难治性腹水的治疗

按国际腹水协会定义 ,难治性腹水 (ｒｅｆｒａｃｔｏｒｙａｓｃｉｔｅｓ)是指药物治疗不能消退或经排放腹水等治疗后用药物不能有效防止近期复发的腹水[1 ] 。包括两种亚型 ,即 (1)利尿剂抵抗性腹水 (ｄｉｕｒｅｔｉｃ ｒｅｓｉｓｔａｎｔａｓｃｉｔｅｓ) ,对限钠 (<5 0ｍｍｏｌ/ｄ)和大量利尿剂治疗 (用至最高剂量 ,螺内酯 40 0ｍｇ/ｄ加呋塞米 160ｍｇ/ｄ持续 4ｄ)缺乏反应 (体重减轻甚微 <2 0 0 ｇ/ｄ ,尿钠排泄 <5 0ｍｍｏｌ/ｄ) ,而不能消退的或不能防止近期内 (4周 )复发的腹水。 (2 )利尿剂难治性腹水 (ｄｉｕｒｅｔｉｃ ｉｎ ｔｒａ…     

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??Abstract??Refractory ascites is a common complication of liver cirrhosis associated with a poor prognosis.The current medical managements of refractory ascites include sodium restriction??a combination of albumin and diuretic??large-volume paracentesis??transjugular intrahepatic portosystemic shunt??and ascites concentration-reinfusion.Potential new treatment options for refractory ascites include the use of terlipressin??vasopressin type 2 receptor antagonists??midodrine??and nonselective b-blocker??all of which could possibly improve the management of ascites.This paper makes an introduction of current management and novel therapeutic strategies for refractory ascites.     

成人肝硬化腹水的诊断与治疗

腹水是肝硬化最常见的并发症之一 ,5 0 %的代偿性肝硬化患者 10年内会并发腹水 ,张力性腹水患者 2年死亡率高达5 0 %。为此 ,2 0 0 3年 10月美国肝病年会就成人肝硬化腹水的处理展开充分讨论并在诊治方面形成共识 ,本文就此作一简介。一、诊断策略(一 )病史　美国成人腹水 85 %左右为肝硬化所致 ,为此对腹水患者应询问肝病相关危险因素 ,包括肥胖和非酒精性脂肪性肝炎、肿瘤史 (乳房、结肠、胃、胰腺 )、心衰史 ,结核史有助于非肝性腹水的诊断。嗜血细胞综合征与肝硬化腹水表现相似 ,但前者通常有发热、肝脾淋巴结肿大、肺炎、皮疹 ,且常见…     

Spontaneous chylous ascites of cirrhosis

The spontaneous development of chylous ascites in patients with cirrhosis is documented, but its clinical features are not well defined. The incidence of this complication of chronic liver disease was 0.5% in ascitic patients in our liver unit. These patients were older than a control group with nonchylous cirrhotic ascites and, despite better liver tests, appeared to have a higher diuretic requirement. Several had disabling, recurrent spontaneous encephalopathy. The mechanism of chylous ascites in cirrhosis is probably portal hypertension causing lymphatic rupture; however, the fact that serum-to-ascites albumin gradients were similar in the two groups, indicating similar degrees of portal hypertension, suggests that other factors also play a role. Spontaneous transformation of previously clear ascites appeared to be associated with a poor prognosis. In contrast, the appearance of chylous ascites de novo in a cirrhotic patient appeared to have a more favorable outcome. Conservative management is recommended for most patients, as the degree of their liver disease appears to be the most important factor determining prognosis.     

Resistant ascites in alcoholic liver cirrhosis

A group of 29 patients with decompensated cirrhosis of the liver who retained a large amount of ascites under a hospital regimen during two months or longer was identified. The prognosis for this selected group of patients, while grave [during continuous hospitalization 11 out of 29 patients (=38%) died], is not without hope: 18 patients (62%) improved and could be discharged from the hospital. Their further course was influenced by resumption of alcohol usage. Five of 11 (45.4%) who resumed drinking died due to hepatic causes within 10 months. Of the remaining six only one lost his ascites. Those who abstained (7 patients) remained alive for an average follow-up of 33 months and all lost their ascites. Alcohol resumption significantly decreased both survival (P<0.05) and ascites resorption (P<0.0015). Continued abstinence from alcohol may thus obviate the need for surgical measures to relieve ascites in these patients.     

Hydrothorax without ascites in liver cirrhosis

Pleural effusion in patients with liver cirrhosis and intractable ascites is well known, but hepatic hydrothorax in the absence of ascites is a rare complication. We present the case of a 43-year old male, with a medical history of liver cirrhosis due to hepatitis C virus, who was admitted to the Pneumology Clinic for dyspnoea, worsening of general status and chronic asthenia. The pleural effusion, revealed on physical and laboratory examinations, persisted despite the therapy with diuretics and the frequent thoracocentesis. The thoracostomy followed by pleurodesis also failed. The pecularity of this case was the presence of refractory hydrothorax in the absence of ascites.     

美国肝病学会成人肝硬化腹水诊疗指南(2009版)

评估与诊断 1.首次发生腹水患者无论门诊或住院均应进行腹腔穿剌以明确腹水性质.(Ⅰ,C) 2.因腹腔穿刺时出血非常罕见,腹腔穿剌前不推荐常规预防性应用新鲜冰冻血浆或单采血小板.(Ⅲ,C)     

Pathophysiology and treatment of ascites in cirrhosis

Ascites is the most frequent complication in patients with cirrhosis of the liver. In these patients, the onset of ascites indicates a profound impairment of hepatic and renal function and splanchnic and systemic hemodynamics and is therefore associated with a poor prognosis, the probability of survival at one and five years being of about 50 and 20 per cent, respectively. In patients with cirrhosis and ascites, parameters estimating splanchnic and systemic hemodynamics and renal function are better prognostic indicators than those currently used to evaluate liver function.     

肝硬化腹水发病机制研究现状

腹水是肝硬化常见的并发症,也是临床上腹水的常见原因[1,2]。新发肝硬化患者10年内腹水的发生率高达50%～70%,腹水的出现被视为肝硬化病程的一个重要转折点,是肝硬化疾病进展和肝功能失代偿的重要表现。肝硬化患者腹水的发生不但会导致患者生活质量的下降[3],而且与肝硬化的其他并发症如自发性细菌性腹膜炎、肝肾综合征等密切相关。肝硬化腹水还与不良预后相关,1a病死率约为15%,5a病死率则高达44%[4]。对肝硬化腹水发病机制的研究以及新的治疗方法的探索有助于改善患者的生活质量和预后。然而,目前肝硬化腹水发病机制仍未完全阐明。     

肝硬化腹水形成机制的研究现状

目前,世界范围内肝硬化发病率保持在较高水平,对人类生命健康具有较大的威胁.在我国,病毒性肝炎是导致肝硬化的主要致病因素,尤其以乙型病毒性肝炎性肝硬化最常见.肝硬化腹水的形成是门静脉高压和肝功能减退共同作用的结果,而腹水的形成是肝硬化发展为肝功能失代偿期最突出的临床表现.对腹水形成机制的研究有助于指导临床更为准确的用药,以减轻患者的精神及经济压力.