中西医诊治肝硬化腹水进展

腹水是肝硬化最常见的并发症。肝硬化腹水形成的机制尚未完全阐明,目前认为门静脉高压是形成腹水的主要原因。腹水的诊断可依据病史、查体和腹水常规检查。对于肝硬化腹水患者,采取及时有效的药物治疗可以提高患者的生活质量和生存率。一旦出现肝硬化晚期并发症,最终需要进行肝脏移植,故腹水的治疗越早越好。西医治疗腹水主要为限钠饮食、应用利尿剂、普坦类药物和白蛋白。顽固性腹水可以采用腹穿大量放液术、经颈静脉肝内门体支架分流术、腹腔静脉分流术等手术治疗。国内外越来越多的文献报道中医药联合利尿剂治疗肝硬化腹水取得较好的疗效。但目前中医辨证理论和疗效评价体系尚不统一,可重复性差。因此,拟定一套规范化和可重复性强的综合治疗方案,对于提高肝硬化腹水的临床疗效具有重要的现实意义。本文将重点介绍肝硬化腹水的诊断及治疗管理进展。     

肝硬化难治性腹水的治疗现状

腹水是肝硬化患者常见的并发症,预示患者生存率降低.绝大部分腹水患者对于低盐饮食和利尿剂治疗有良好反应,少部分患者则需要反复腹腔大量穿刺放液、经颈静脉肝内门体分流术等处理.目前肝脏移植是唯一被证实可以提高患者远期生存率的方法,新治疗方法的目的 在于纠正血流动力学紊乱及神经-内分泌系统过度兴奋状态.     

醋酸奥曲肽治疗肝硬化顽固性腹水26例观察

肝硬化顽固性腹水是指经限钠、限水和利尿剂(螺内酯400mg/d和呋塞米160mg/d)治疗无效,或一度有效但随之利尿作用丧失的状态。大量利尿剂长期应用可以出现肝性脑病,肾功能损害,低钠血症,低钾或者高钾血症等不良反应,而且对于顽固性腹水疗效有限。患者常常反复入院,病死率高。临床治疗除了利尿剂外,还有重复腹水回输或者多次的大剂量放腹水,经颈静脉肝内门体分流术TIPS,腹腔静脉分流术(PVS),甚至肝移植。目前研究性药物主要针对于改善肾脏供血以及选择性血管加压素受体拮抗剂[1-3],而针对顽固性腹水成     

肝硬化难治性腹水的诊治进展

内脏血管舒张、门静脉高压激活肾素-血管紧张素-醛固酮系统(RAAS系统)是引起肝硬化患者出现水钠潴留的关键因素。当患者严格限钠饮食且使用最大剂量利尿剂(400 mg/d螺内酯联合160 mg/d呋塞米)1周后仍无应答，或患者因服用利尿剂后会出现并发症，而不能使用有效剂量的利尿剂导致腹水时，可被诊断为难治性腹水。目前，腹腔穿刺大量放液联合白蛋白、经颈静脉肝内门体静脉分流术及肝脏移植是治疗难治性腹水的有效方法。随着对难治性腹水的进一步研究，血管收缩剂、高选择性血管加压素V2受体拮抗剂、自动低流量腹水泵等新的治疗方式也逐渐应用于临床。这些新的治疗方式的应用，有望进一步提高难治性腹水的治疗效果。     

肝硬化腹水治疗的新进展

腹水是肝硬化最常见并发症之一,预防和控制腹水的发生和发展是改善肝硬化患者预后的关键。就近几年腹水治疗的新进展进行总结与讨论,主要包括病因治疗、限钠摄入、利尿剂治疗等一线治疗方法的更新,以及对于顽固性腹水治疗的新探索。     

肝硬化腹水诊治争议问题

腹水是肝硬化预后不良的重要指标。近年来尽管出台了很多有关肝硬化腹水的指南和共识,但其处理中仍存在一些争议。回顾了目前肝硬化腹水处置中的难点及争议问题,如补钠和限钠的时机、利尿剂的选择、利水剂的应用价值、大量放腹水后补充白蛋白的方案、经颈静脉肝内门体分流术的指征和疗效等;并指出运用循证医学手段解决上述争议性问题,有助于提高肝硬化腹水的诊疗水平,改善患者预后。     

肝硬化腹水治疗的研究现状与展望

腹水是肝硬化最常见的并发症,并与发生感染、稀释性低钠血症、肾功能衰竭和病死率增加密切相关。无并发症的少量腹水患者早期处理原则是,休息加上低钠饮食。中等量腹水患者,一般选择低剂量利尿剂就能达到利尿效果。大量腹水患者,可大量放腹水＋静点白蛋白（8g/每放腹水1000ml）。顽固性腹水患者,可用重复多次大量放腹水＋血浆扩容治疗或用经颈静脉肝内门体分流术（TIPS）治疗。新药（如V2受拮抗剂和血管收缩剂等）对肝硬化腹水的治疗可能带来希望。     

肝硬化为何应用腹腔静脉分流术治疗

临床试验证实,用腹水或血浆间断扩充血浆容量,虽能防止由肝硬化腹水引起的急性肾衰竭发生,但不能降低肾衰竭死亡率。只有连续扩充血浆容量才能维持肾功能。给腹水狗施行腹腔静脉分流术,腹水即可消失。即使再给予高钠饮食,腹水也不会重新出现,但会出现外周水肿。分流后,一般不需再用利尿剂,除非病员同时有轻度心衰引起的外周水肿。腹水来自血液,亦应返流回血液,因此腹腔静脉分流术是治疗肝硬化腹水的生理性疗法。利尿剂治疗重度腹水,外周水肿首先消失。但一旦腹水排出时,肾功能也开始受损,表现为血清尿素氮或肌酐值增高。腹水消失与血浆容量降低有密切关系,减     

特利加压素治疗失代偿期肝硬化疗效观察

目的观察特利加压素和托拉塞米治疗失代偿期肝硬化和非顽固性肝硬化腹水的疗效。方法选择2011年2月到6月于我院住院的失代偿期肝硬化患者36例,按2000年中华医学会传染病与寄生虫病学分会和肝病学分会联合修订的标准诊断,18例非顽固性肝硬化腹水患者给予特利加压素治疗,另18例患者接受托拉塞米治疗,通过测量腹围、腹水深径及尿量观察疗效。结果特利加压素治疗的患者在腹围、腹水深径及尿量变化方面,好于托拉塞米治疗,且在用药安全性方面无明显差异。结论特利加压素治疗非顽固性肝硬化腹水的临床疗效优于单纯利尿剂治疗,可以作为失代偿期肝硬化患者治疗非顽固性腹水新的选择方案。     

肝硬化难治性腹水

肝硬化患者可发生严重的水、电解质平衡失调，其主要表现为腹水和水肿。晚期肝硬化和严重的尿钠潴留可进展为难治性腹水（refractory ascites，RA）。RA是指对肝硬化腹水利尿剂无治疗反应或因利尿剂的严重副作用而妨碍了它的应用者。近20年来，无论在RA的发病机制和治疗方面均取得了重要进展。上世纪80年代重新受到青睐的腹腔穿刺放腹水加输注白蛋白的治疗方法堪称RA治疗的里程碑。经颈静脉肝内门-体分流术（transjugular intrahepatic portosystemic shunts，TIPS）治疗RA的合理性和有效性也已得到确认。     

Refractory Ascites: How to Establish the Diagnosis and What Can Be Done?

Refractory ascites accounts for 5-10 % of all ascites and portends a very poor prognosis. Refractory ascites can be diuretic-resistant (unresponsive to maximal dose of diuretics) or diuretic-intractable (inability to use an effective dose of diuretics due to development of complications). Management is challenging as therapeutic options are limited. Available options include serial large volume paracentesis or placement of transjugular intrahepatic portosystemic shunt. A novel device involving an automated low flow ascites pump and a peritoneo-vesical shunt has been recently developed but long term safety and efficacy data are awaited. Liver transplantation is the only modality proven to improve long-term survival.     

Treatment for cirrhotic ascites

Common complications of decompensated liver cirrhosis are esophageal varices, hepatic encephalopathy and ascites. After the onset of complications, the prognosis worsens. In patients with ascites, the 5‐year mortality rate is 44%. Furthermore, hyponatremia, spontaneous bacterial translocation and hepatorenal syndrome also greatly worsen the prognosis. Effective treatment of cirrhotic ascites improves the quality of life and survival rate. Recently, the newly produced diuretic, tolvaptan (vasopressin V2 receptor antagonist), was reported to be effective in the treatment of refractory ascites in liver cirrhosis; however, there has not been an associated positive effect on the prognosis. There are various types of treatment for ascites, such as large‐volume paracenteses, a cell‐free and concentrated ascites reinfusion therapy, a transjugular intrahepatic portosystemic shunt, and a peritoneo‐venous shunt. Although they improve the prognosis, liver transplantation remains the ultimate form of treatment. The present article discusses the therapeutic management of cirrhotic ascites.     

The management of ascites in cirrhosis: report on the consensus conference of the International Ascites Club

Ascites is a common complication of cirrhosis, and heralds a new phase of hepatic decompensation in the progression of the cirrhotic process. The development of ascites carries a significant worsening of the prognosis. It is important to diagnose noncirrhotic causes of ascites such as malignancy, tuberculosis, and pancreatic ascites since these occur with increased frequency in patients with liver disease. The International Ascites Club, representing the spectrum of clinical practice from North America to Europe, have developed guidelines by consensus in the management of cirrhotic ascites from the early ascitic stage to the stage of refractory ascites. Mild to moderate ascites should be managed by modest salt restriction and diuretic therapy with spironolactone or an equivalent in the first instance. Diuretics should be added in a stepwise fashion while maintaining sodium restriction. Gross ascites should be treated with therapeutic paracentesis followed by colloid volume expansion, and diuretic therapy. Refractory ascites is managed by repeated large volume paracentesis or insertion of a transjugular intrahepatic portosystemic stent shunt (TIPS). Successful placement of TIPS results in improved renal function, sodium excretion, and general well-being of the patient but without proven survival benefits. Clinicians caring for these patients should be aware of the potential complications of each treatment modality and be prepared to discontinue diuretics or not proceed with TIPS placement should complications or contraindications develop. Liver transplantation should be considered for all ascitic patients, and this should preferably be performed prior to the development of renal dysfunction to prevent further compromise of their prognosis.     

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.     

Treatment of ascites in cirrhosis. Diuretics, peritoneovenous shunt, and large-volume paracentesis.

The medical treatment of ascites in cirrhosis is based on sodium restriction and the administration of diuretics. Because the natriuretic potency of spironolactone is greater than that of loop diuretics (i.e., furosemide) in patients with marked sodium retention, spironolactone is the basic drug for the treatment of ascites. The simultaneous administration of spironolactone and furosemide increases the natriuretic effect of each drug and diminishes their effects on potassium metabolism. Recent studies indicate that large-volume paracentesis associated with intravenous albumin infusion is more effective than diuretic therapy in eliminating the ascitic fluid; is associated with a lower incidence of complications (hepatic encephalopathy, renal impairment, and hyponatremia); and considerably reduces the duration of hospital stay. Therapeutic paracentesis associated with intravenous albumin infusion is therefore the treatment of choice for cirrhotic patients with tense ascites. The mobilization of the ascitic fluid by paracentesis without plasma volume expansion is constantly associated with a deterioration of effective circulating blood volume and may induce renal impairment and severe hyponatremia. Dextran 70 and polygeline appear as effective as albumin in preventing these abnormalities. Cirrhotic patients treated with paracentesis require the administration of diuretics to avoid reaccumulation of ascites. Peritoneovenous shunt, a prosthesis capable to correct most abnormalities involved in the accumulation of fluid in the abdominal cavity, is an effective treatment of ascites in cirrhosis. It is especially indicated in patients who do not respond to diuretics and develop repeated episodes of ascites despite adequate treatment. The use of peritoneovenous shunting is limited by the high incidence of complications induced by the procedure, however. In addition, approximately 40% of patients develop an obstruction of the prosthesis within the first postoperative year.     

Transjugular intrahepatic portosystemic shunt: current status

The transjugular intrahepatic portosystemic shunt (TIPS) was developed in the 1980s for treatment of complications of portal hypertension. Once it was shown that the shunt could be placed with relative ease, TIPS was rapidly applied to the treatment of many of the complications of portal hypertension. These complications include actively bleeding gastroesophageal varices, prevention of rebleeding from varices, control of refractory cirrhotic ascites and hepatic hydrothorax, and treatment of hepatorenal failure and hepatopulmonary syndrome. TIPS has also been used as therapy for Budd-Chiari syndrome and veno-occlusive disease. Despite these broad applications, TIPS has been compared with other forms of therapy in only 2 situations: prevention of rebleeding from varices and control of refractory cirrhotic ascites. In the trials, TIPS was shown to provide better control of these 2 complications of portal hypertension than standard forms of therapy. However, there was no improvement in survival and the incidence of encephalopathy was greater for patients receiving a TIPS. Thus, the use of TIPS for the control of ascites and prevention of rebleeding from varices should be limited to a select group of patients. There have been no controlled trials for the other indications listed. Despite the apparent efficacy of TIPS in many of these situations, its use should be limited to salvage therapy pending the publication of controlled trials showing it is a better treatment than other forms of therapy.     

Management of ascites

The evaluation of ascites includes a directed history, focused physical examination, and diagnostic paracentesis with ascitic fluid analysis. Dietary sodium restriction and oral diuretics are the mainstay of therapy for the majority of patients with cirrhotic ascites. Transjugular intrahepatic portocaval shunt has emerged as the treatment of choice for selected patients with refractory ascites, although serial large-volume paracenteses should be attempted first. Early diagnosis, broad-spectrum antibiotics, and albumin infusion contribute to the successful management of spontaneous bacterial peritonitis (SBP). Referral for liver transplant evaluation should be considered at the first sign of decompensation and should not be delayed until development of ominous clinical features, such as refractory ascites and SBP.     

Cirrhotic ascites review: Pathophysiology, diagnosis and management

Ascites is a pathologic accumulation of peritoneal fluidcommonly observed in decompensated cirrhotic states. Its causes are multi-factorial, but principally involve significant volume and hormonal dysregulation in the setting of portal hypertension. The diagnosis of ascites is considered in cirrhotic patients given a constellation of clinical and laboratory findings, and ultimately confirmed, with insight into etiology, by imaging and paracentesis procedures. Treatment for ascites is multimodal including dietary sodium restriction, pharmacologic therapies, diagnostic and therapeutic paracentesis, and in certain cases transjugular intra-hepatic portosystemic shunt. Ascites is associated with numerous complications including spontaneous bacterial peritonitis, hepato-hydrothorax and hepatorenal syndrome. Given the complex nature of ascites and associatedcomplications, it is not surprising that it heralds increased morbidity and mortality in cirrhotic patients and increased cost-utilization upon the health-care system. This review will detail the pathophysiology of cirrhotic ascites, common complications derived from it, and pertinent treatment modalities.     

Diastolic dysfunction in cirrhosis

Development of esophageal varices, ascites, and hepatic nephropathy is among the major complications of cirrhosis. The presence of cirrhotic cardiomyopathy, which includes a left ventricular diastolic dysfunction (DD), seems to deteriorate the course of the disease and the prognosis. Increased stiffness of the cirrhotic heart may decrease the compliance and result in DD. The prevalence of DD in cirrhotic patients averages about 50 %. It can be evaluated by transmitral Doppler echocardiography, tissue Doppler echocardiography, and cardiac magnetic resonance imaging. There seems to be a relation between DD and the severity of liver dysfunction and the presence of ascites. After liver transplantation, DD worsens the prognosis and increases the risk of graft rejection, but DD improves after few months. Insertion of a transjugular intrahepatic portosystemic shunt increases left ventricular diastolic volumes, and DD is a predictor of poorer survival in these patients. Future studies should aim at disclosing pathophysiological mechanisms behind the developing of DD in cirrhosis in relation to patient characteristics, development of complications, treatment, and risk associated with interventional procedures.