Written by Aw Pei Ying Amanda Aw
Last Reviewed: August 2019
Review Due: August 2020
‘submucosal venous dilatations secondary to raised portal pressures, commonly occurring at the gastro-oesophageal junction and usually associated with cirrhosis, with bleeding risk depending on the severity of underlying cirrhosis’
The cause of oesophageal varices is portal hypertension, which can be classified depending on the site of the pathology.
Portal vein thrombosis
Primary biliary cholangitis
Right heart failure
History of alcohol abuse
Hepatitis B or C infection
SIGNS AND SYMPTOMS1
Acute bleeding resulting in altered mental state, tachycardia, hypotension, syncope or shock
Stigmata of chronic liver disease (e.g. ascites, spider angioma, caput medusa, jaundice etc.)
Acute upper GI bleeding resulting in haematemesis and/or melaena
Many patients may initially be asymptomatic
Normal portal pressure lies at 5- 8 mmHg. When portal pressure rises above 10 – 12 mmHg, dilatation and opening of venous collaterals at regions of porto-systemic anastomosis occurs. Specifically, submucosal venous collaterals at the gastro-oesophageal junction are superficial in location, hence being prone to rupture and bleeding.
Portal hypertension in liver cirrhosis occurs due to increased parenchymal resistance to blood flow as a result of increased fibrogenesis. This is also compounded by the presence of a hyperdynamic circulation due to the release of vascular mediators such as nitric oxide and glucagon, as well as sodium retention that contributes to abnormal blood flow patterns.
TO ESTABLISH DIAGNOSIS
The gold standard method for diagnosing oesophageal varices is an oesophago- gastro-duodenoscopy (OGD), also known as an upper GI endoscopy.
Further investigations to establish the underlying cause may include;
Liver Function Tests
in an acute bleed
FBC: Reduced Hb (secondary to acute bleed) and/or thrombocytopenia (secondary to chronic liver disease)
Coagulation (INR/PT): To assess/monitor liver synthetic function
U&Es: To assess renal function and obtain urea for acute bleed risk stratification (e.g. using Glasgow-Blatchford score)
Lactate: To assess organ perfusion following acute bleed
Group and Save/Crossmatch
It is likely that blood products will be required in an acute bleed, so these samples should be taken as soon as possible
May be of diagnostic benefit in patients presenting for the first time, however may also be used therapeutically
The management of oesophageal varices can be categorised as;
Managing an acute bleed
Preventing oesophageal varices
acute variceal bleed
Urgent resuscitation with an ABCDE approach is needed. An acute variceal bleed carries a 10-20% mortality.
15l oxygen through a non-rebreathing mask (trauma mask)
2 large bore IV cannulae plus fluid resuscitation
Reversal of anti-coagulants (if appropriate)
Consideration of HDU care
IV Terlipressin - a vasoconstrictor that has been shown to reduce mortality
IV Co-Amoxiclav - early broad-spectrum antibiotics reduce bacteraemia and improve outcomes
Urgent endoscopy in patients with suspected or confirmed variceal bleeding is vital. Endoscopic variceal ligation (EVL/banding) can stop bleeding vessels.
A Sengstaken tube is an inflatable tube that can be inserted into the oesophagus and used to tamponade the bleeding vessels. It should only be used for a short time as a bridge to definitive treatment, where there may be a delay to endoscopy and the patient requires urgent support.
There is a 60% chance of re-bleeding within the first year following a variceal bleed.
Treatment with a non-selective beta-blocker (e.g. Propranol) decreases cardiac output and causes splanchnic vasoconstriction which reduces the hyperdynamic circulation and portal pressures.
Variceal Eradication Programme
Repeated endoscopic banding at 2-3 weekly intervals helps eradicate varices, while subsequent endoscopic surveillance helps detect recurrence.
Transjugular Intrahepatic Portosystemic Shunt
The TIPS procedure is carried out by interventional radiology and involves the creation of an artificial shunt between the portal vein and hepatic vein, to reduce portal hypertension.
The choice of primary preventative treatment depends on risk stratification, and may include endoscopic surveillance, drug treatment with non-selective beta-blockers or endoscopic banding.
Approximately 90% of patients with cirrhosis develop varices over a 10-year period, of which 1/3 will have a bleeding episode
Acute variceal bleeds are associated with a 6-week mortality of 10%
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Kumar P, Clark M. Kumar & Clark clinical medicine. Edinburgh: Elsevier Saunders; 2009.
D'Amico G, Malizia G. Oesophageal varices. BMJ Best Practice. 2019.
GGC Medicines - Adult Therapeutics Handbook 2019