de Franchis R, Primignani M
Department of Internal Medicine, University of Milan, Italy.
Clin Liver Dis. 2001 Aug;5(3):645-63. doi: 10.1016/s1089-3261(05)70186-0.
All patients with cirrhosis will eventually develop portal hypertension and esophagogastric varices. Bleeding from ruptured esophagogastric varices is the most severe complication of cirrhosis and is the cause of death in about one third of patients. The rate of development and growth of esophageal varices is poorly defined but in general seem to be related to the degree of liver dysfunction. Once varices have formed, they tend to increase in size and eventually to bleed. In unselected patients, the incidence of variceal bleeding is about 20% to 30% at 2 years. Variceal size is the single most important predictor of a first variceal bleeding episode. Several prognostic indexes based on endoscopic and clinical parameters have been developed to predict the risk of bleeding; however, their degree of accuracy is unsatisfactory. Death caused by uncontrolled bleeding occurs in about 6% to 8% of patients; the 6-week mortality rate after a variceal hemorrhage is 25% to 30%. There are no good prognostic indicators of death caused by uncontrolled bleeding or death within 6 weeks. Untreated patients surviving a variceal hemorrhage have a 1- to 2-year risk of rebleeding of about 60% and a risk of death of about 40% to 50%. The risk of bleeding is greatest in the first days after a bleeding episode and slowly declines thereafter. All patients surviving a variceal hemorrhage must be treated to prevent rebleeding. Varices can also be found in the stomach of cirrhotic patients, alone or in association with esophageal varices. Gastric varices bleed less frequently but more severely than esophageal varices. Portal hypertensive gastropathy is a common feature of cirrhosis, and its prevalence parallels the severity of portal hypertension and liver dysfunction. Portal hypertensive gastropathy can progress from mild to severe and vice-versa or even disappear completely. Acute bleeding from portal hypertensive gastropathy seems to be relatively uncommon, and less severe than bleeding from varices.
所有肝硬化患者最终都会发展为门静脉高压和食管胃静脉曲张。食管胃静脉曲张破裂出血是肝硬化最严重的并发症，约三分之一的患者因此死亡。食管静脉曲张的发生和生长速度尚不清楚，但一般似乎与肝功能障碍的程度有关。一旦静脉曲张形成，它们往往会增大并最终出血。在未经选择的患者中，2年内静脉曲张出血的发生率约为20%至30%。静脉曲张大小是首次静脉曲张出血事件的唯一最重要预测指标。已经开发了几种基于内镜和临床参数的预后指标来预测出血风险；然而，它们的准确性程度并不令人满意。约6%至8%的患者死于无法控制的出血；静脉曲张出血后6周的死亡率为25%至30%。对于因无法控制的出血导致的死亡或6周内的死亡，没有良好的预后指标。静脉曲张出血后存活的未治疗患者1至2年的再出血风险约为60%，死亡风险约为40%至50%。出血风险在出血事件后的头几天最大，此后逐渐下降。所有静脉曲张出血后存活的患者都必须接受治疗以预防再出血。静脉曲张也可单独或与食管静脉曲张一起出现在肝硬化患者的胃中。胃静脉曲张出血的频率低于食管静脉曲张，但比食管静脉曲张更严重。门静脉高压性胃病是肝硬化的常见特征，其患病率与门静脉高压和肝功能障碍的严重程度平行。门静脉高压性胃病可从轻度发展为重度，反之亦然，甚至可完全消失。门静脉高压性胃病引起的急性出血似乎相对少见，且不如静脉曲张出血严重。
