肝硬化的自然病程是指肝硬化作为一种疾病发生发展过程中没有受任何人为干扰，也即未经任何治疗而完全处于一种自然状况。 当肝硬化被诊断的时候，大约有30-40%的病人有静脉曲张，60%病人有腹水【1】。没有食道静脉曲张的肝硬化病人每年新发生食道静脉曲张的几率为5-10%【2】。一旦被诊断静脉曲张，2年内发生静脉曲张出血大约在25%。从轻度的静脉曲张到重度的静脉曲张进展率是不一样的，5%~30%/年【2】。在随访中持续与静脉曲张进展最为相关的因素是基于Child-Pugh或其恶化【2，4】。肝静脉压力梯度（HVPG）超过10mmHg（正常＜5mmHg）是静脉曲张最强的预测因素【3】。静脉曲张出血是肝硬化最常见和最严重的并发症之一。即使是目前最好的治疗，静脉曲张破裂出血的死亡率仍然在20%左右。 The incidence, prevalence and outcome of varicesGastroesophageal varices are present in about 50% of all patients with cirrhosis and a good predictor of their presence is the severity of liver disease. Cumulative incidence of varices over 10 years is 44% as calculated using a competing risk model [18]. For example, 85% of Child C cirrhotic patients have varices compared to 40% of Child A patients [19]. In cirrhotic patients without varices, the rate of developing them is 8% per year and the main risk factor and predictor of developing varices is a HVPG is >10 mmHg [20]. Patients with small varices go on to develop large varices at an annual rate of 8% as well. The main risk factors for developing large varices are: decompensated disease, alcoholic cirrhosis and the presence of red whale marks at initial endoscopy [21]. The rate of variceal haemorrhage is 5–15% per year and the risk of bleeding increases in patients with larger varices, the presence of red-signs and more advanced liver disease in particular Child’s B and C cirrhosis [22]. The wall tension of the varix is one of the main factors that predicts rupture and wall tension is directly related to vessel diameter. For any given equal pressure, a large-diameter vessel is more likely to rupture than a small-diameter vessel [23]. The other major factor that influences wall tension is the pressure within the varix and this is related to the HVPG. Hence, decreasing the HVPG can reduce the risk of variceal rupture and haemorrhage. In the context of secondary prophylaxis, the risk of variceal haemorrhage is very low when the HVPG is < 12 mmHg [24,25]. Reductions in HVPG of more than 20% from baseline or to an absolute value below 12 mmHg is associated with reduced rates of recurrent bleeding, ascites, SBP and death [26–28].
The mortality from an index variceal bleed is 20% at 6 weeks [29–31]. An important cut-off for HVPG is 20 mmHg; in patients where the HVPG is > 20 mmHg within 24 hours of a variceal bleed, there is a higher risk of recurrent bleeding within 1 week and higher risk of failure to control bleeding (83% vs 29%) as well as a higher 12-month mortality (64% vs 20%) [32,33].
Gastric varices
The management of bleeding gastric varices continues to present a significant clinical challenge. In general, gastric varices are less prevalent than oesophageal varices. In addition, gastric varices are about 50% less likely to bleed than oesophageal varices. However, once gastric varices rupture, transfusion requirements and mortality are higher than bleeding oesophageal varices [34,35]. The overall incidence of gastric varices in cirrhotic patients who have not previously bled is 4%. At screening endoscopy, 25% of patients had gastric varices and 18% had both gastric and oesophageal varices [36]. The reported incidence of bleeding from gastric varices is about 25% in 2 years, with a higher bleeding rate for fundal varices (IGV1—see below). The main risk factors identified for gastric variceal haemorrhage are:
size of varix, with the greatest risk of bleeding occurring in large (>10 mm) > medium (5–10 mm) > small (<5 mm);
cirrhosis severity—Child C > B > A;
endoscopic appearance of red spots [35,36].
Gastric varices are classified based on their relationship with oesophageal varices as well as their location in the stomach [34]. Gastro-oesophageal varices (GOV) are where the gastric varices are associated with oesophageal varices. This association can be along the lesser curve (GOV1) or along the fundus (GOV2). Isolated gastric varices (IGV) are isolated varices that form in the fundus (IGV1) or ectopically in the stomach or duodenum (IGV2). The commonest type of gastric varices are GOV 1 (about 70% of all gastric varices) followed by fundal varices GOV2 (21%) and IGV1 (7%); only about 2% of gastric varices are IGV2. IGV1 has the highest incidence of bleeding at 78%, with GOV2 the second most likely to bleed with an incidence of 55%. The incidence of bleeding from GOV1 and IGV2 is 10% [37].
Gastroenterol Rep (Oxf). 2017 May; 5(2): 113–126.
Published online 2017 Apr 7. doi: 10.1093/gastro/gox007
PMCID: PMC5421505
Recent advances in the management of variceal bleeding
******************************************************************************************************8 1. G. D'Amico Esophageal varices: from appearance to rupture; natural history and prognostic indicators. R.J. Groszmann, J. Bosch (Eds.), Portal hypertension in the 21st century, Kluwer Academic Publishers, Dordrecht (2004), pp. 147–154 2. Merli M, Nicolini G, Angeloni S, Rinaldi V, De Santis A, Merkel C, Attili AF, Riggio O. Incidence and natural history of small esophageal varices in cirrhotic patients. J Hepatol. 2003 Mar;38(3):266-72. 3. Groszmann RJ, Wongcharatrawee S. The hepatic venous pressure gradient: anything worth doing should be done right. Hepatology. 2004 Feb;39(2):280-2. 4. M. Zoli, C. Merkel, D. Magalotti, C. Gueli, M. Grimaldi, A. Gatta. Natural history of cirrhotic patients with small esophageal varices: a prospective study. Am J Gastroenterol, 95 (2) (2000 Feb), pp. 503–508 |