KEEP IN TOUCH
follow us
  • Facebook
  • Twitter
  • Instagram

DASPITE is an educational resource for healthcare professionals in training. DASPITE should not be used for diagnostic purposes. Always consult local guidelines for treatment decisions. Should you have concerns about your health, please visit your doctor. 

By visiting this site, you agree to our terms of use and privacy policy.

DASPITE Limited is a company registered in Scotland (No. SC627155)

DASPITE © 2019

oesophageal varices

Written by Aw Pei Ying Amanda Aw

Last Reviewed: August 2019

Review Due: August 2020

 

DEFINITION1

‘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’

 

AETIOLOGY2

The cause of oesophageal varices is portal hypertension, which can be classified depending on the site of the pathology.

 

Pre-Hepatic 

Portal vein thrombosis 

Hepatic 

Cirrhosis

Schistosomiasis 

Sarcoidosis 

Primary biliary cholangitis 

Post-Hepatic 

Budd-Chiari syndrome 

Constrictive pericarditis 

Restrictive cardiomyopathy 

Right heart failure 

IVC obstruction 

risk factors2

History of alcohol abuse 

Hepatitis B or C infection

SIGNS AND SYMPTOMS1

Signs

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.)

Symptoms

Acute upper GI bleeding resulting in haematemesis and/or melaena

Many patients may initially be asymptomatic

 

PATHOPHYSIOLOGY2,3

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.

 

Investigations1,2,3

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

Abdominal Ultrasound

Abdominal CT

Echocardiography

in an acute bleed

Blood Tests

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

Endoscopy

May be of diagnostic benefit in patients presenting for the first time, however may also be used therapeutically

Other

ECG

Chest X-Ray

 

TREATMENT2,3,4

The management of oesophageal varices can be categorised as;

  1. Managing an acute bleed

  2. Preventing rebleeds

  3. Preventing oesophageal varices

acute variceal bleed

Urgent resuscitation with an ABCDE approach is needed. An acute variceal bleed carries a 10-20% mortality.

Initial Management

15l oxygen through a non-rebreathing mask (trauma mask)

2 large bore IV cannulae plus fluid resuscitation

Reversal of anti-coagulants (if appropriate)

Airway protection

Consideration of HDU care

Drug Therapy

IV Terlipressin - a vasoconstrictor that has been shown to reduce mortality

IV Co-Amoxiclav - early broad-spectrum antibiotics reduce bacteraemia and improve outcomes

Endoscopy

Urgent endoscopy in patients with suspected or confirmed variceal bleeding is vital. Endoscopic variceal ligation (EVL/banding) can stop bleeding vessels.

Sengstaken-Blakemore Tube

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.

secondary prevention

There is a 60% chance of re-bleeding within the first year following a variceal bleed.

Drug Treatment

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.

primary prevention

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.

 
 

EPIDEMIOLOGY2

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%

REFERENCES

  1. Wilkinson I, Raine T, Wiles K, Goodhart A, Hall C, O'Neill H. Oxford handbook of clinical medicine. 10th ed. 2017.

  2. Kumar P, Clark M. Kumar & Clark clinical medicine. Edinburgh: Elsevier Saunders; 2009.

  3. D'Amico G, Malizia G. Oesophageal varices. BMJ Best Practice. 2019.

  4. GGC Medicines - Adult Therapeutics Handbook 2019