Oesophageal Varices

Complications of portal hypertension¹

• Bleeding of oesophageal varices
• Spontaneous bacterial peritonitis
• Hepatorenal syndrome secondary to ascites

This article will review oesophageal varices and the management of bleeding varices.

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

The causes of oesophageal varices is anything that can increase the 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 shutdown
• 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 be commonly present

• FBC - haemoglobin may be low, MCV may be high, normal or low, platelets may also be low
• Clotting including INR
• Renal function
• Liver function tests
• Group & 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 may be better); 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.
• 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 International Normalised Ratio 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 given
• Terlipressin (Glypressin®) is an analogue of vasopressin and studies have shown it to be superior to placebo in variceal haemorrhage (unlike octreotide)¹
• 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 reduces the hepatic venous pressure gradient
• It requires administration by continuous infusion and its affects are short-lived
• Terlipressin is as effective as octreotide¹

Balloon tube tamponade (Sengstaken-Blakemore tube)

• Urgent endoscopy is necessary for variceal haemorrhage
• There may be a few hours delay before this can occur
• In these cases a Sengstaken tube can be used
• However, the airway must be protected and patients 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 with out 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
  2. Sclerotherapy
  3. Variceal obturation with glue

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 completely obliterate the varix²
• A recent trial suggests banding is superior to beta-blockers as primary prevention of bleeding from high-risk varices³

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% cases, first injection produced control of bleeding and repeat sclerotherapy may be needed. Complications include transient fever, dysphagia, chest pain, ulceration, stricture and very infrequently perforation⁴

Variceal occlusion with glue

• This involves embolisation of varices with a glue like substance (N-butyl-2-cyanoacrylate)
• Particularly good for gastric or gastrooesophageal variceal bleeding
• But there is a risk of embolization to the lung, spleen or brain

• 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% cases¹

• 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 TIPS⁵
• Also major surgery may further worsen liver function
• Oesophageal transection and gastric devascularization 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.⁶
• 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.^1,2:

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 contraindicated.
• 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 contraindications to beta blockers the varices should be banded or sclerosed⁷
• In the long-term repeated endoscopic screening is usually required e.g. 2-3 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.^8,9

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%.² The risk of re-bleeding is roughly 70% with about 30% in-hospital mortality.¹⁰ 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.¹¹