Oesophageal Varices

Oesophageal varices are dilatated of oesophageal veins secondary to portal hypertension. They are venous collaterals formed by the increased pressure in portal venous system which occur in areas where there are anastomoses between the portal and systemic venous systems. Veins around the umbilicus (causing caput medusae) and in the rectum (haemorrhoids) are other sites of such anastomoses - but the oesophageal varices are most important as they have an increased tendency to bleed. The commonest cause of portal hypertension is cirrhosis.

Responsible for 5% of episodes of GI bleeding in the UK.

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

These are also the same factors that increase the risk of portal hypertension.

Symptoms

• Haematemesis most commonly
• Abdominal pain
• Dysphagia/odynophagia (pain on swallowing; uncommon)
• Confusion secondary to encephalopathy (may even be obtunded)

Signs

• Pale
• Peripherally shut down
• Pallor
• Hypotension and tachycardia (i.e. shock)
• Reduced urine output
• Melaena
• Signs of chronic liver disease
• Reduced Glasgow Coma Scale
• Signs of sepsis may also commonly be present

• FBC - haemoglobin may be low, MCV may be high, normal or low, platelets may also be low, WCC may be raised
• Clotting including INR
• Renal function
• Liver function tests
• Group and cross-match
• CXR - patients may have aspirated or have chest sepsis
• Ascitic tap may be needed if bacterial peritonitis suspected

Resuscitation

• Assess airway - can easily be compromised, especially if reduced Glasgow Coma Scale.
• In the community, call ambulance urgently - assess level of shock, lie patient down and raise legs (but if actively vomiting then risk of aspiration, so recovery position more appropriate); provide oxygen and gain intravenous access if possible.
• Need wide bore access 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.¹
• Give blood (ideally cross-matched) as soon as possible - if a delay is likely then may need to give group O rhesus negative blood.
• The initial aim is to correct hypovolaemia - this may require several litres.²
• Patients should be monitored with a cardiac monitor, blood pressure, pulse rate and urine output (catheterise until patient stabilised).
• There is some concern that saline infusions may worsen ascites but the nature of the emergency warrants their use.

Consider inserting 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).

Correct anaemia and coagulopathy

• Blood transfusion will be necessary
• Many of the patients will have a coagulopathy, and thus give intravenous vitamin K immediately
• If INR is prolonged also give FFP
• Platelet transfusion may all be required

Vasopressin and its analogues

• Vasopressin acts as a splanchnic vasoconstrictor and thus reduces variceal pressure and azygous blood flow.
• This can reduce the haemorrhage until more definitive treatment is given.
• Terlipressin (Glypressin®) is an analogue of vasopressin and studies have shown it to be superior to placebo in variceal haemorrhage.¹ It should be given to all patients presenting with suspected variceal bleeding prior to endoscopy and following confirmation.²
• Vasopressin and terlipressin should not be used in severe hypovolaemic shock and patients with severe cardiac disease.

Somatostatin and its analogues

• Octreotide is an analogue of somatostatin and reduces the hepatic venous pressure gradient.
• It requires administration by continuous infusion and its effects are short-lived.
• A recent study has not confirmed earlier reports that terlipressin is more effective than octreotide, despite terlipressin being associated with a shorter duration of inpatient stay.^1,3

Balloon tube tamponade (Sengstaken-Blakemore tube)

• Urgent endoscopy is necessary for variceal haemorrhage.
• A Sengstaken tube can be used to control bleeding whilst an emergency endoscopy is arranged.
  • Protect the airway - patients may need to be intubated.
  • The Sengstaken tube (preferably kept in 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 in then pulled up against the oesophagogastric junction compressing submucosal varices.
  • The tube is secured at the mouth to maintain tension.
  • The Sengstaken 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.
• Remove tube within 12 hours, if necessary repeating endoscopic treatment.

Endoscopy

• Emergency fibre optic endoscopy confirms the diagnosis and source of bleeding.
• Urgent endoscopy in unwell patients is not without its risks, and adequate staffing and the presence of resuscitation facilities are required.
• Endoscopy allows the bleeding point to be visualised, and for varices three treatments can be employed:¹
  1. Band ligation
     • This is the first choice of treatment.
     • An elastic banding device is attached to the tip of the endoscope.
     • The varix is sucked into the banding chamber which applies the rubber band.
     • Thrombosis is produced by 1-3 bands to each varix (maximum 5-8 bands).
     • Eliminates varices with fewer treatments and complications than with sclerotherapy.
     • The procedure may be painful and repeat treatments at 2-3 week intervals may be required to obliterate the varix completely.⁴
     • A recent trial suggests banding is superior to beta blockers as primary prevention of bleeding from high-risk varices.⁵
  2. Sclerotherapy
     • In this therapy the varices are sclerosed.
     • Various sclerosants can be used, e.g. ethanolamine oleate or sodium tetradecyl sulphate (sclerosant solution).
     • The sclerosants lead to thrombosis which stops the haemorrhage.
     • Alternatively, inject into overlying submucosa causing inflammation followed by fibrosis.
     • In 80% of cases, first injection produces control of bleeding and repeat sclerotherapy may be needed. Complications include transient fever, dysphagia, chest pain, ulceration, stricture and, very infrequently, perforation.⁶
  3. Variceal obturation with glue
     • This involves embolisation of varices with a glue-like substance (N-butyl-2-cyanoacrylate).
     • Particularly good for gastric or gastro-oesophageal variceal bleeding.
     • However, there is a risk of embolisation to the lung, spleen or brain.

• Transjugular intrahepatic portosystemic shunt (TIPS) procedure is used in cases of portal hypertension of hepatic origin where bleeding is not controlled by endoscopy.
• 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.
• High success rate but encephalopathy found in 25% cases (as portal blood diverted from the liver) and shunt occludes within 1 year in up to 50% cases.¹

• This is required when endoscopy fails or is not available.
• Procedures usually involve formation of surgical shunts but this requires surgical expertise; however, in good hands, results can be as good as TIPS.⁷
• Also major surgery may further worsen liver function.
• Oesophageal transection and gastric devascularisation are rare procedures reserved for those unsuitable for shunts, with significant bleeding despite other treatments.

• 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.⁸
• Thus, antibiotics are given early, e.g. ciprofloxacin.
• Treat hepatic encephalopathy if also present.

This can be primary or secondary prophylaxis (following a bleed). Two groups of drugs are used along with endoscopic screening:^1,4

Beta blockers

• These lower portal blood pressure and risk of further bleeding by reducing portal blood flow.
• Non-selective beta blockers are better at reducing the hepatic venous pressure gradient, e.g. propranolol.
• All at-risk patients should be prescribed these unless contra-indicated.
• Used in both primary and secondary prophylaxis.

Nitrates

• The effects of nitrates on portal blood flow are incompletely understood.
• However, it can lead to systemic hypotension.
• Nitrates are not recommended in primary prophylaxis - thus, just for secondary prophylaxis.
• Nitrates can also be used in the acute variceal haemorrhage with vasopressin and terlipressin.

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 contra-indications to beta blockers, the varices should be banded or sclerosed.⁹
• In the long-term, repeated endoscopic screening is usually required, e.g. 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 mmHg is associated with a significant reduction in mortality.^10,11

About 90% of patients with cirrhosis develop varices, but only about 30% of these will suffer bleeding in their lifetime. Mortality following bleeding is in the order of 30%-50%.⁴ The risk of re-bleeding is roughly 70% with about 30% in-hospital mortality.¹² Another study in alcoholic cirrhosis reported a 5-year cumulative survival of 26% despite successful repeated sclerotherapy - the cause of death being liver failure in most.¹³