Oesophageal varices

What are oesophageal varices?

Variceal haemorrhage occurs from dilated veins (varices) at the junction between the portal and systemic venous systems. Varices tend to be in the distal oesophagus and/or the proximal stomach but isolated varices may be found in the distal stomach, and the large and small intestine.

The majority of patients with variceal bleeding have chronic liver disease. Variceal bleeding is characteristically severe and may be life-threatening. The size of oesophageal varices and their tendency to bleed are directly related to the portal pressure, which is usually directly related to the severity of underlying liver disease. Large oesophageal varices with red spots are at highest risk of rupture.¹

How common are oesophageal varices? (Epidemiology)^{2 3 4}

• The prevalence of oesophageal varices varies between 40% and 95% in people with cirrhosis.

• The annual incidence of oesophageal varices in people with cirrhosis varies from 3% to 22%.

• Oesophageal varices are one of the two most common causes of upper gastrointestinal bleeding (the other being gastric erosions).

• In Western countries, alcoholic and viral cirrhosis are the leading causes of portal hypertension and oesophageal varices.

• The one-year rate of first variceal bleeding is 5% for small varices, and 15% for large varices.

• It is more common in males than in females.

• The mortality rate is 10-20% in the first six weeks after a bleed.

Causes of oesophageal varices (aetiology)

The causes of oesophageal varices are anything that can cause portal hypertension. Some examples are in the table that follows.

Factors that increase the risk of variceal bleeding⁵

Risk factors for rupture of oesophageal varices include size of varices, severity of liver disease, sepsis, and hepatocellular carcinoma.

Symptoms of oesophageal varices (presentation)

Symptoms

• Haematemesis (most commonly), melaena.

• Abdominal pain.

• Features of liver disease and specific underlying condition.

• Dysphagia/odynophagia (pain on swallowing; uncommon).

• Confusion secondary to encephalopathy (even coma).

Signs

• Peripherally shut down.

• Pallor.

• Hypotension and tachycardia (ie shock).

• Reduced urine output.

• Melaena.

• Signs of chronic liver disease.

• Reduced Glasgow Coma Scale.

• Signs of sepsis may also commonly be present.

Diagnosing oesophageal varices (investigations)⁴

Endoscopy is required at an early stage.^{6 7}

• FBC - haemoglobin may be low; MCV may be high, normal or low; platelets may also be low; WCC may be raised. Thrombocytopenia may suggest portal hypertension and/or large oesophageal varices.

• Clotting including INR.

• Renal function.

• LFTs.

• BUN (blood urea nitrogen) may be elevated if there has been a bleed.

• Group and cross-match.

• Hepatic serology.

• CXR - patients may have aspirated or have chest infection.

• Ascitic tap may be needed if bacterial peritonitis is suspected.

• Investigations as indication for the underlying cause of portal hypertension (see the separate Portal Hypertension article).

Imaging⁴

Various imaging techniques are available to assist in diagnosis, identification of underlying cause and risk factors, and response to treatment. These include:

• Transient elastography for identifying chronic liver disease patients at risk of developing clinically significant portal hypertension.

• Hepatic vein pressure gradient to diagnose clinically significant portal hypertension.

• Video capsule endoscopy screening as an alternative to traditional endoscopy.

• Doppler sonography.

• CT or MRI-angiography.

• Ultrasound of the abdomen may reveal biliary obstruction (eg, cancer).

Differential diagnosis

Other causes of UGIB, as listed in the separate Upper Gastrointestinal Bleeding article.

Variceal bleeding management^{1 8 8}

See also the separate Upper Gastrointestinal Bleeding article.

Management for acute variceal haemorrhage consists of vasoactive drugs, endoscopic band ligation and antibiotics prophylaxis. Transjugular intrahepatic portosystemic shunt (TIPS) is reserved for those who do not respond or are unlikely to respond to initial standard management.⁹

National Institute for Health and Care Excellence (NICE) guidance

Preventing bleeding from medium or large oesophageal varices:¹⁰

• Offer carvedilol or propranolol, or

• Endoscopic variceal band ligation, if either carvedilol or propranolol are not tolerated or contraindicated, or the person cannot take tablets regularly because of their circumstances.

Upper gastrointestinal haemorrhage:¹¹

• Terlipressin should be offered to patients with suspected variceal bleeding at presentation. Treatment should be stopped after definitive haemostasis has been achieved, or after five days, unless there is another indication for its use.

• Prophylactic antibiotic therapy should be offered at presentation to patients with suspected or confirmed variceal bleeding. Antibiotic use significantly reduces the mortality of patients who develop acute UGIB in association with chronic liver disease.

• Oesophageal varices:
  

  • Band ligation should be used for patients with UGIB from oesophageal varices.

  • TIPS should be considered if bleeding from oesophageal varices is not controlled by band ligation.

  • NICE recommends that there is sufficient evidence to show that stent insertion is effective for selected patients with oesophageal varices in whom other methods of treatment have failed to control bleeding.¹²

• Gastric varices:
  

  • Endoscopic injection of N-butyl-2-cyanoacrylate should be offered to patients with UGIB from gastric varices.

  • TIPS should be offered if bleeding from gastric varices is not controlled by endoscopic injection of N-butyl-2-cyanoacrylate.

Resuscitation

• Assess airway - can easily be compromised, especially if reduced Glasgow Coma Scale.

• In the community, call an ambulance urgently - assess level of shock, lay the patient down and raise their legs (but, if actively vomiting then there is risk of aspiration, so the recovery position is more appropriate); provide oxygen and gain intravenous access if possible.

• Wide-bore access is needed, with a minimum of two cannulae (central access may also be required).

• Provide 40% oxygen if tachypnoeic or confused.

• Begin fluid resuscitation with rapid infusion of crystalloid and colloid solution.¹³

• Give blood (ideally cross-matched) as soon as possible - if a delay is likely then group O rhesus negative blood may need to be given. The initial aim is to correct hypovolaemia. Whilst a large volume of blood may be required, bear in mind that there are risks associated with over-transfusion (raised portal pressure increases risk of re-bleeding).

• Patients with oesophageal varices should be monitored with a cardiac monitor, blood pressure, pulse rate and urine output (catheterise until the patient is stabilised).

• Correct anaemia and coagulopathy. . Many of the patients will have a coagulopathy, and so give intravenous vitamin K immediately. If INR is prolonged, also give fresh frozen plasma. Platelet transfusion may be required.¹⁴

• There is some concern that saline infusions may worsen ascites but the nature of the emergency warrants their use.

Consider inserting a central venous line/pulmonary artery catheter in haemodynamically unstable or elderly patients, or those with cardiac or pulmonary disease, to monitor fluid balance (overuse can produce oedema, ascites and hyponatraemia).

Endoscopy

• Urgent endoscopy is necessary for variceal haemorrhage. Emergency fibre-optic endoscopy confirms the diagnosis and source of bleeding.

• Urgent endoscopy in unwell patients is not without its risks; adequate staffing and the presence of resuscitation facilities are required.

• Endoscopy allows the bleeding point to be visualised and treated:
  

  • Band ligation is the first choice of treatment.

  • Emergency sclerotherapy is still widely used as a first-line therapy for variceal bleeding in patients with cirrhosis, especially when band ligation is not available. However, drug treatment may stop bleeding in the majority of these patients. There is no convincing evidence to support the use of emergency sclerotherapy for variceal bleeding in cirrhosis as the initial single treatment when compared with vasoactive drugs¹⁵ .

Vasoactive drugs

• The use of vasoactive agents (terlipressin, octreotide or somatostatin) is associated with a significantly lower risk of acute all-cause mortality and transfusion requirements and improved control of bleeding and shorter hospital stay.¹⁶

• Terlipressin is an analogue of vasopressin and studies have shown it to be superior to placebo in variceal haemorrhage.¹³ Terlipressin is considered the vasoactive agent of choice in acute variceal bleeding.¹⁷ It should be given to all patients presenting with suspected variceal bleeding prior to endoscopy and continued until haemostasis is achieved.¹

• Vasopressin and terlipressin should not be used in severe hypovolaemic shock and patients with severe cardiac disease.

Variceal obturation with glue

• This involves embolisation of varices with a glue-like substance (N-butyl-2-cyanoacrylate).

• It is particularly good for gastric or gastro-oesophageal variceal bleeding.

• However, there is a risk of embolisation to the lung, spleen or brain.

Balloon tube tamponade (Sengstaken-Blakemore tube)¹⁸

• Balloon tamponade should be considered as a temporary salvage treatment for uncontrolled variceal haemorrhage.¹

• The Sengstaken-Blakemore tube (preferably kept in the fridge to stiffen rubber and make passage easier) is inserted through the mouth and into the stomach.

• The gastric balloon is inflated with air and the gastric balloon is then pulled up against the oesophagogastric junction, compressing submucosal varices.

• The Sengstaken-Blakemore tube also contains an oesophageal balloon which is only rarely required when the gastric balloon does not work.

• If bleeding continues, it may be that the tube is wrongly positioned or bleeding is from another source.

Transjugular intrahepatic portosystemic shunt¹¹

• Transjugular intrahepatic portosystemic stent shunting is recommended as the treatment of choice for uncontrolled variceal haemorrhage .

• The hepatic vein is cannulated percutaneously via the internal jugular vein, using a needle under ultrasound or fluoroscopic guidance.

• A tract is created through the liver from the hepatic to the portal vein - thus reducing portal pressure. This is dilated and an expandable metal stent inserted to create a shunt.

• This has a high success rate but encephalopathy is found in 25% of cases (as portal blood diverted from the liver) and shunt occludes within one year in up to 50% of cases.¹³

Surgery¹

• Oesophageal transection and gastric devascularisation are rare procedures but may have a role for patients with portal and splenic vein thrombosis who are not suitable candidates for shunt procedures and who continue to have variceal bleeding despite endoscopic and pharmacological treatment.¹⁹

• Liver transplantation is the treatment of choice for patients with advanced liver disease.

Other aspects of management of variceal haemorrhage

• Avoid sedatives if possible.

• Patients are best managed on ITU/HDU.

• Antibiotic prophylaxis - infection occurs in up to 50% of patients and is associated with a worse outcome. It is thought that bacteria release endotoxins that enhance portal pressure and impair coagulation.²⁰ Antibiotics are therefore given early - eg, ciprofloxacin.

• Treat hepatic encephalopathy if this is also present.

Prevention of oesophageal varices⁹

• No specific treatment has been shown to prevent the formation of oesophageal varices.

• Prevention of first variceal haemorrhage depends on the size/characteristics of varices. In patients with small oesophageal varices and high risk of bleeding, non-selective beta-blockers are recommended, while patients with medium/large varices can be treated with either beta-blockers or oesophageal band ligation.

• Prevention of recurrent variceal haemorrhage consists of the combination of beta-blockers and endoscopic band ligation.

Endoscopic screening

• All patients with newly diagnosed cirrhosis should have screening endoscopy, looking for oesophageal varices.

• Presence of moderate or large varices requires beta-blockers in the first instance (indefinite treatment).

• If there are contra-indications to beta-blockers, the varices should be banded or sclerosed.²¹

• In the long term, repeated endoscopic screening is usually required - eg, 2- to 3-yearly in cases of small varices.

• Patients who have survived an oesophageal variceal bleed should receive beta-blockers, ± nitrates and endoscopic screening and treatment.

The use of measures of hepatic vein pressure gradient with an aim to reduce it under 12 mm Hg is associated with a significant reduction in mortality.^{22 23} However, pharmacological options employing this effect have yet to be developed for use in routine medical practice.¹

Variceal bleeding prognosis

• For patients with cirrhosis, one-year survival is 50% for those surviving two weeks following a variceal bleed.

• Prognosis in non-cirrhotic portal fibrosis is better than for cirrhotics.

• Associated renal, respiratory, cardiovascular and immune disorders account for 20-65% of mortality in patients with oesophageal varices.²⁴