Villanueva Cándid, Balanzó Joaquim
Gastrointestinal Bleeding Unit, Department of Gastroenterology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
Drugs. 2008;68(16):2303-24. doi: 10.2165/0003495-200868160-00004.
Oesophageal varices and ascites may develop when the hepatic venous pressure gradient (HVPG) increases above 10 mmHg, and variceal bleeding may occur when the HVPG rises above 12 mmHg. Pharmacological therapy of portal hypertension may prevent bleeding by reducing the HVPG below 12 mmHg. Even if this threshold level is not reached, the risk of bleeding decreases markedly with reductions in HVPG that are >20% from baseline.Endoscopic therapy is a local treatment that prevents bleeding by obliterating the varices, and has no effect on the pathophysiological mechanisms that lead to portal hypertension and variceal rupture. When used together, both pharmacological and endoscopic therapies may have an additive effect, which has been demonstrated in different clinical settings. In acute oesophageal variceal bleeding, vasoactive drugs (either terlipressin or somatostatin) should be started as soon as possible (before diagnostic endoscopy) and maintained for 2-5 days. The efficacy of pharmacotherapy is improved with the addition of emergency endoscopic therapy. Adding endoscopic variceal ligation (EVL) improves the efficacy and safety achieved with the combination of emergency sclerotherapy and vasoactive drugs. Antibacterial prophylaxis should be an integral part of therapy in acute bleeding.To prevent rebleeding, both EVL and the combination of beta-adrenoceptor antagonists (beta-blockers) and isosorbide mononitrate (ISMN) may be a valid first-line choice. Adding beta-blockers improves the efficacy of EVL alone. Haemodynamic responders to beta-blockers with or without ISMN (i.e. those with a decrease in HVPG to <12 mmHg or by >20% of baseline) have a reduction in the risk of haemorrhage to below 10% of patients and, consequently, will not need further treatment, while rescue therapies should be provided to nonresponders. Transjugular intrahepatic portosystemic shunts are the recommended rescue therapy when EVL and/or beta-blockers with or without ISMN fail. beta-Blockers significantly reduce the risk of a first haemorrhage in patients with large varices and improve survival. Compared with beta-blockers, EVL reduces the risk of first bleeding without any differences in mortality and should be offered to patients with large varices who have contraindications or an intolerance to beta-blockers.
当肝静脉压力梯度（HVPG）升高超过10 mmHg时，可能会出现食管静脉曲张和腹水，而当HVPG升高超过12 mmHg时，可能会发生曲张静脉出血。门静脉高压的药物治疗可通过将HVPG降低至12 mmHg以下来预防出血。即使未达到该阈值水平，随着HVPG较基线水平降低>20%，出血风险也会显著降低。内镜治疗是一种局部治疗方法，通过消除曲张静脉来预防出血，对导致门静脉高压和曲张静脉破裂的病理生理机制没有影响。联合使用时，药物治疗和内镜治疗可能具有相加作用，这已在不同临床环境中得到证实。在急性食管曲张静脉出血时，血管活性药物（特利加压素或生长抑素）应尽快开始使用（在诊断性内镜检查之前）并维持2 - 5天。紧急内镜治疗可提高药物治疗的疗效。添加内镜下曲张静脉套扎术（EVL）可提高紧急硬化治疗与血管活性药物联合使用的疗效和安全性。抗菌预防应是急性出血治疗的一个组成部分。为预防再出血，EVL以及β肾上腺素能受体拮抗剂（β受体阻滞剂）与单硝酸异山梨酯（ISMN）联合使用可能是有效的一线选择。添加β受体阻滞剂可提高单独使用EVL的疗效。对β受体阻滞剂（无论是否联合ISMN）有血流动力学反应者（即HVPG降低至<12 mmHg或较基线降低>20%者）出血风险降至低于10%的患者，因此无需进一步治疗，而对无反应者应提供挽救治疗。当EVL和/或β受体阻滞剂（无论是否联合ISMN）无效时，经颈静脉肝内门体分流术是推荐的挽救治疗方法。β受体阻滞剂可显著降低大曲张静脉患者首次出血的风险并提高生存率。与β受体阻滞剂相比，EVL可降低首次出血风险，在死亡率方面无差异，应提供给有β受体阻滞剂禁忌证或不耐受的大曲张静脉患者。
