Inferior meso-caval shunt for portal hypertension with bleeding esophageal varices.

We report a 12-year-old boy with cavernomatous malformation of the portal vein who presented with repeated hematemesis. Inferior meso-caval shunt was performed to decompress the portal hypertension. There was minimal dissection and disturbance of periportal collateral channels in comparison to using the superior mesenteric vein. One year later, esophagoscopy showed no varices, and he has had no further episode of bleed.     

Pharmacologic therapy for portal hypertension

Pharmacologic therapy for portal hypertension is effective in the treatment and prevention of hemorrhage from esophagogastric varices. Acute hemorrhage from varices can be treated with intravenous agents such as somatostatin or terlipressin, either alone or in combination with endoscopic sclerotherapy or band ligation. Intravenous octreotide has not shown effectiveness as monotherapy, but it appears to be beneficial when combined with endoscopic treatment. The prevention of rebleeding after initial hemorrhage is best accomplished with non-selective beta blockers, endoscopic band ligation of varices, or a combination of endoscopic and pharmacologic therapies. The addition of oral nitrates may further decrease rebleeding rates, but more data from randomized trials are needed. Beta blockers are currently the only agents recommended for the primary prevention of variceal hemorrhage.     

Drug therapy of esophageal varices hemorrhage in portal hypertension

The author discusses the etiopathogenesis of portal hypertension and possibilities how to influence it during treatment of acute haemorrhage from varicosities and how to implement primary and secondary prevention. In treatment of acute haemorrhage the author recommends terlipresin, 1 mg every 4 hours. In primary and in particular in secondary prevention he emphasizes the necessity of early administration of beta-blockers.     

Duodenal varices as an unusual cause of gastrointestinal bleeding due to portal hypertension: a case report.

Duodenal varices that develop in patients with portal hypertension rarely cause hemorrhage, but varix rupture is a serious and often fatal event. We report the case of a 38-year-old man with hepatic vein occlusion who was referred to our hospital for gastrointestinal hemorrhage of unknown origin. Upper gastrointestinal endoscopy revealed varices in the distal third of the duodenum. These varices were identified as the source of the bleeding. The patient was treated with endoscopic band ligation, and with coil embolization of a shunt between the superior mesenteric vein and the left renal vein.     

断流术治疗门脉高压症上消化道出血疗效分析

目的 探讨采用贲门周围血管断流术治疗肝硬化门脉高压并食管胃底静脉曲张破裂出血的效果及预后.方法 对我院3年间行经腹贲门周围门奇血管断流术治疗门脉高压症并发上消化道出血47例及20例保守治疗患者近、远期疗效进行对比分析.结果 手术组除1例近期死亡外,总体效果满意.近期出血5例,远期出血2例,再出血率14.9%,全组无肝性脑病发生.保守治疗组死亡2例,近期出血4例,远期出血6例,1例发生肝性脑病,再出血率50%.结论 规范而彻底的贲门周围血管断流术治疗门脉高压并上消化道出血创伤小,止血率高,肝性脑病等并发症发生率低,便于开展与推广.     

Pharmacologic therapy of portal hypertension

Portal hypertension is a progressively debilitating complication of cirrhosis and a principal cause of mortality in patients who have hepatic decompensation. During the last few decades, significant clinical advances in the prevention of initial variceal hemorrhage, the management of acute variceal hemorrhage, and the prevention of recurrent variceal hemorrhage have reduced the morbidity and mortality of this lethal complication of cirrhosis. This article discusses the pharmacologic treatment of portal hypertension, including preprimary prophylaxis, prevention of a first variceal hemorrhage, treatment of acute variceal hemorrhage, and secondary prophylaxis of a variceal hemorrhage.     

Hyponatremia in patients treated with terlipressin for severe gastrointestinal bleeding due to portal hypertension

Terlipressin is frequently used in acute variceal bleeding due to its powerful effect on vasopressin V1 receptors. Although terlipressin is also a partial agonist of renal vasopressin V2 receptors, its effects on serum sodium concentration have not been specifically investigated. To examine the effects of terlipressin on serum sodium concentration in patients with acute portal-hypertensive bleeding, 58 consecutive patients with severe portal-hypertensive bleeding treated with terlipressin were investigated. In the whole population, serum sodium decreased from 134.9 ± 6.6 mEq/L to 130.5 ± 7.7 mEq/L (P = 0.002). Thirty-nine patients (67%) had a decrease in serum sodium ≥ 5 mEq/L during treatment: in 18 patients (31%), between 5 and 10 mEq/L and in 21 patients (36%), greater than 10 mEq/L. In this latter group, serum sodium decreased from 137.2 ± 5 to 120.5 ± 5 mEq/L (P < 0.001). In multivariate analysis, the reduction in serum sodium was related to baseline serum sodium and Model for End-Stage Liver Disease (MELD) score; patients with low MELD and normal or near-normal baseline serum sodium had the highest risk of hyponatremia. Serum sodium returned to baseline values in most patients shortly after cessation of therapy. Three of the 21 patients with marked reduction in serum sodium developed neurological manifestations, including osmotic demyelination syndrome in one patient due to a rapid recovery of serum sodium (serum sodium in these three patients decreased from 135, 130, and 136 to 117, 114, and 109 mEq/L, respectively). CONCLUSION: An acute reduction in serum sodium concentration is common during treatment with terlipressin for severe portal-hypertensive bleeding. It develops rapidly after start of therapy, may be severe in some patients and is associated with neurological complications, and is usually reversible after terlipressin withdrawal.     

Endoscopic sclerotherapy for bleeding esophageal varices secondary to extrahepatic portal vein obstruction

Portal hypertension and variceal bleeding secondary to extrahepatic portal vein obstruction continue to present a therapeutic challenge. We performed endoscopic injection sclerotherapy in eight patients with extrahepatic portal vein obstruction and bleeding esophageal varices. In contrast to other reported series, all but one of our patients were adults at the time sclerotherapy was initiated. Six had episodes of continued bleeding after a variety of surgical procedures. After sclerotherapy, five had no further bleeding with a mean follow-up of 26 months. Three patients had episodes of bleeding prior to variceal obliteration; two of these patients underwent surgical intervention after emergency sclerosis to stabilize their condition. Transfusion requirements were less after sclerosis (p = 0.035), although the follow-up has been relatively short (mean, 24 months) compared to the duration of bleeding. Our results suggest that endoscopic sclerotherapy is an effective therapeutic alternative, and perhaps the initial treatment of choice, in patients with extrahepatic portal vein obstruction and bleeding esophageal varices.     

肝硬化门静脉高压症合并食管胃底静脉曲张破裂出血的急救处理

目的：探讨肝硬化门静脉高压症合并食管胃底静脉曲张破裂出血急诊抢救治疗的临床经验并评估其疗效。方法回顾性分析2005年1月至2012年12月浙江省湖州市南浔区人民医院收治的11例肝硬化门静脉高压症合并食管胃底静脉曲张破裂出血患者的临床资料。结果11例患者上消化道出血24 h内止血比例为9／11,全部11例患者上消化道出血72 h内出血停止。但其中1例患者于治疗后第7天再出血,因拒绝再次三腔二囊管止血而死亡;1例患者上消化道出血后13 d死于肝功能衰竭。治疗总有效率为82％（9／11）,死亡率为18％（2／11）。结论采取内科措施控制出血,将紧急手术转为择期手术,可提高肝硬化门静脉高压症合并食管胃底静脉曲张破裂出血急诊抢救治疗的成功率。     

评分法对门静脉高压症上消化道出血手术方式选择的指导

目的:建立评分系统指导门静脉高压并发上消化道出血的手术方式的选择.方法:2004-06/2007-10本组收治门静脉高压症患者178例,将患者病因、年龄、肝功能状态、临床特征、手术史等进行评分,根据评分值选择适宜手术方式治疗门静脉高压并发上消化道出血,术后随访患者.结果:根据评分,行贲门周围血管离断术术89例,加食管下段横断吻合术22例,经胸食管横断吻合2例,近端脾肾分流术39例,肠腔限制分流术21例,门腔侧侧分流术5例.围手术期可逆性腹水41例,中量胸水8例,食管吻合口漏1例,食管吻合口狭窄1例.术后随访99例,偶发黑便16例,再发呕血并死亡1例,1级肝性脑病2例.切口疝1例.结论:针对门静脉高压并发上消化道出血的不同病理生理特征建立评分系统,根据评分选择合适的手术方式可改善该疾病的治疗效果.     

Pharmacologic therapy of portal hypertension and variceal hemorrhage

Patients with large esophageal varices who are deemed compliant and have no contraindications to beta-blocker therapy should be started on nonselective beta-adrenergic blockers (Fig. 5). The dose should be titrated to a 25% decrease in resting heart rate, a resting heart rate of 55 to 60 beats per minute, or development of symptoms, in which case the dose should be decreased until the patient's symptoms abate. If available, measurements of the HVPG at baseline and 3 months can be very helpful in ascertaining the response to treatment and in making the appropriate adjustments (e.g., adding a second drug). Sclerotherapy or endoscopic variceal ligation are the preferred therapies for treatment of acute esophageal variceal bleeding. Concomitant use of vasoactive drugs can supplement endoscopic treatment. They offer the advantage of early administration as soon as the diagnosis is suspected while awaiting endoscopy. Unlike endoscopic treatment, they decrease portal pressure and are the only established treatment for nonvariceal sources of bleeding related to portal hypertension. Once the index bleed is controlled, the patient should be started on treatment to reduce the high risk of recurrent variceal hemorrhage (Fig. 6). For patients with well-compensated cirrhosis, pharmacologic therapy may be desirable. For less compliant patients or patients with decompensated cirrhosis, an endoscopic technique, such as variceal ligation, may be preferable. Combinations of pharmacologic agents or pharmacologic agents and endoscopic procedures may offer hope for better control, but their efficacy needs to be demonstrated in RCTs. For patients who rebleed despite maximal pharmacologic or endoscopic therapy, a TIPS procedure, surgically created shunt, or liver transplantation should be considered, with the decision based on the patient's condition and the local availability of these options.     

Risk stratification for secondary prophylaxis of gastric varices due to portal hypertension

BackgroundGastroesophageal variceal hemorrhage is a common complication associated with portal hypertension. Current guidelines provide well-established recommendations for esophageal varices, while that of gastric varices remain scarce and lack evidential strength. The aim of the study is to identify a feasible risk stratification method based on imaging findings to evaluate patient response to cyanoacrylate injection for the treatment of gastric varices.MethodsA prospective cohort study including patients diagnosed with gastric varices admitted for initial secondary prophylactic treatment for GV was conducted. Routine endoscopic examination and endoscopic ultrasound (EUS) were performed on all subjects to evaluate extraluminal collaterals. All patients with gastric varices were treated uniformly with cyanoacrylate injection. Patients were prospectively followed for at least 12 months and any occurrence of variceal rebleed was recorded.Results102 subjects were enrolled in the study, 66.7% had GOV Type 2, 27.5% had GOV Type 1 and 5.9% had IGV Type 1. During the 12 months follow-up, 33.3% patients experienced variceal rebleed. A risk assessment scoring system was proposed based on endoscopic and EUS findings. A Cox regression analysis demonstrated a significant association between the merited risk score and incidence of variceal rebleed (P < 0.001).ConclusionsPresence of red wales sign, size of varix, and presence of para-gastric vein were all independent risk factors for variceal rebleed after endoscopic therapy for the treatment of gastric varices. Early identification of this subgroup, especially those with higher risk scores, necessitates a change in course of treatment, which can improve prognosis and overall patient outcome.     

Endoprosthetics for bleeding esophageal varices

Refractory esophageal hemorrhage and early rebleeding following endoscopic therapy remain challenging conditions to treat and are associated with a high mortality. Techniques such as balloon tamponade (BT) and transjugular intrahepatic portosystemic shunt (TIPS) are highly effective at controlling refractory bleeding, but they can be associated with a high rate of complications and, in the case of TIPS, may not be immediately available outside specialist centers. Recently, removable self-expanding metal stents (SEMSs) have been introduced in clinical practice for the management of esophageal variceal bleeding. SEMSs control bleeding by tamponade of varices in the distal esophagus and can remain in situ for a number of days, thus preventing early rebleeding. The use of SEMSs does not require the transfer of the patient to a specialist center, and unlike TIPS, it is not associated with deterioration in liver function. The use of SEMSs has been described in small series of patients with refractory bleeding. These series report high rates of hemostasis with low complication rates, suggesting that SEMSs may have an important role in the management of refractory bleeding either as an alternative to BT or where TIPS is contraindicated. SEMSs may also have a role in treating complications of therapy for bleeding esophageal varices, such as postbanding ulceration and BT-induced esophageal tears. The aim of this review is to summarize the published data on the efficacy of SEMSs and suggest future studies that may clarify its role in the management of esophageal variceal hemorrhage.