Oesophageal varices are a direct consequence of portal hypertension as a progressive complication of cirrhosis.
The development of bleeding carries significant morbidity and mortality.
Non-selective beta-blockers and/or endoscopic ligation can prevent the development of variceal bleeding.
Acute haemorrhage can be managed with resuscitation, terlipressin or a somatostatin analogue (e.g., octreotide), and endoscopic band ligation. Additional management includes prophylactic antibiotics and in some patients trans-jugular intrahepatic shunt therapy.
Diagnosis and surveillance by endoscopy is an important aspect of management.
Oesophageal varices are dilated collateral blood vessels that develop as a complication of portal hypertension, usually in the setting of cirrhosis. They can be seen on endoscopy. In the US and Europe the major cause of cirrhosis is alcoholic liver disease. Worldwide, hepatitis B virus infection and hepatitis C virus infection are the major causes of cirrhosis. Once cirrhosis has developed, increasing hepatic vein pressure gradient and deteriorating liver function may result in the formation of oesophageal varices.
Rupture of oesophageal varices can cause life-threatening bleeding. The most important predictor of variceal haemorrhage is the size of varices, with the highest risk of first haemorrhage occurring in patients with large varices (15% per year). Other important predictors of haemorrhage are decompensated cirrhosis (Child-Pugh B/C) and the endoscopic finding of red wale marks.
This topic covers oesophageal varices in adults.
History and exam
Key diagnostic factors
- presence of risk factors for variceal bleeding
- severe liver disease
- alcohol misuse
- intravenous drug use
- hepatitis B or hepatitis C infection
- spider angioma
- caput medusa
- HIV co-infection
Other diagnostic factors
- portal hypertension
- large varices
- red wale marks
- decompensated cirrhosis
1st investigations to order
- full blood count
- serum LFTs
- serum urea and creatinine
- coagulation profile (INR/prothrombin time)
- blood typing/cross-matching
- hepatitis B surface antigen (HBsAg)
- anti-hepatitis C virus IgG (anti-HCV IgG)
Investigations to consider
- capsule endoscopy
- liver ultrasound
acute variceal bleeding
no acute variceal bleeding: medium to large varices
no acute variceal bleeding: small varices
previous variceal bleed
Joe Geraghty, BSC (Hons), MB BS (Dist), MRCP, PhD
Department of Gastroenterology
Manchester Royal Infirmary
Central Manchester University Hospitals NHS Foundation Trust
JG declares that he has no competing interests.
BMJ Best Practice would like to gratefully acknowledge the previous expert contributor, whose work has been retained in parts of the content:
Grace E. Dolman, PhD, MA (Cantab), MRCP
Clinical Research Fellow
Barts Liver Centre
Barts and the London School of Medicine and Dentistry
Andrew Austin, PhD, FRCP
Lead Clinician in Gastroenterology
Royal Derby Hospital
AA declares that he has no competing interests.
Section Editor, BMJ Best Practice
HDC declares that she has no competing interests.
Lead Section Editor, BMJ Best Practice
TAO declares that she has no competing interests.
Comorbidities Editor, BMJ Best Practice
AS declares that she has no competing interests.
Drug Editor, BMJ Best Practice
AM declares that he has no competing interests.
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