Epidemiology
The estimated global prevalence of cirrhosis and other chronic liver disease was above 1.69 billion in 2019.[11] In 2019, an estimated 1.47 million people died from cirrhosis worldwide, a 10% increase from 2010.[12] The age-standardised cirrhosis mortality rate decreased by 22%, largely due to the decreasing cirrhosis mortality rates in China, the US, and countries in Western Europe.[13]
In Europe, a decline in mortality from cirrhosis in the first half of the 1980s was related to a decrease in per capita alcohol consumption.[14] However, in the 1990s, the UK saw a steep rise in cirrhosis mortality related to increasing alcohol consumption, and over the past 20 years, the number of premature deaths has risen by 62.5% in males and 65.4% in females.[15] Between 2011 and 2020, average mortality per year in Scotland was 30.6 per 100,000, one of the highest compared with other European countries. Mortality rates in England are also increasing, with 20.6 per 100,000 reported in 2020-2021.[16]
Gastro-oesophageal varices are present in almost half of patients at the time of the diagnosis of cirrhosis.[17][18] One third of all patients with oesophageal varices will experience bleeding at some point.[17] The 1-year incidence of bleeding is 5% with small varices, and 15% with large varices.[4] Development of varices and their progression from small to large occur at a rate of approximately 7% to 8% per year.[4][9] One clinical audit in the UK suggested that variceal haemorrhage is associated with overall 30-day mortality of 15%.[19] A systematic review of cohort studies (that assessed acute variceal haemorrhage outcomes) reported a 6-week mortality rate of 18%.[20] Without additional therapy, late rebleeding occurs in approximately 60% of patients within 1 to 2 years of the index event.[4][21]
Risk factors
Portal hypertension leading to the formation of porto-systemic collaterals is the underlying cause of oesophageal varices. Although a small proportion of patients may have varices when the hepatic venous pressure gradient (HVPG) is >5 mmHg and <10 mmHg (mild portal hypertension), varices mostly develop when the HVPG is >10 mmHg.[24] HVPG ≥10 mmHg has been defined as the threshold for clinically significant portal hypertension.[6]
In the majority of patients this is due to chronic liver disease (of any aetiology) resulting in cirrhosis. In Western countries alcoholic liver disease is the most common cause of cirrhosis. However, non-alcoholic fatty liver disease is an increasingly common cause of cirrhosis, and chronic viral hepatitis (B and C) is also relevant.[25][26] Direct antiviral agents are expected to reduce the burden of chronic hepatitis C.[27]
Autoimmune liver disease, haemochromatosis, and Wilson's disease may also result in cirrhosis. Less commonly, other recognised causes of portal hypertension, such as Budd-Chiari syndrome, myeloproliferative disorders, and sarcoidosis, may also lead to oesophageal variceal development.
Decompensated cirrhosis (Child-Pugh class B/C) has been shown to predict increased risk of variceal bleeding.[3]
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