Bleeding oesophageal varices
Oesophageal varices are dilated vessels at the junction between the oesophagus and the stomach and occur in portal hypertension. They may rupture and cause an acute and severe upper gastrointestinal bleed.
30–50% of patients with portal hypertension will bleed from varices.
Varices result from portal hypertension, the most common cause of which is cirrhosis. Factors predicting bleeding in varices include pressure within the varix, variceal size and severity of the underlying liver disease.
Patients with acute upper gastrointestinal bleeding present with haematemesis, which is usually a large volume of fresh blood. Melaena may also be present. Severe blood loss results in hypovolaemic shock. Signs of chronic liver disease may be present (jaundice, pallor spider naevi, liver palms, opaque nails, clubbing). Other features of portal hypertension may be seen.
The diagnostic investigation is endoscopy, which may also be therapeutic during an acute bleed. The varices must be confirmed to be the source of bleeding, because up to 20% of patients with varices also have peptic ulcers and/or gastritis. The varices are seen as tortuous columns in the lower third of the oesophagus. They usually bleed
from the lowest point of the oesophagus. Urgent blood samples should be sent for full blood count, group and crossmatch for at least 6 units, U&Es, glucose, liver function tests and clotting profile.
At least two large bore peripheral cannulae should be sited for fluid resuscitation. Packed red blood cells
should be given as soon as possible, O −ve blood may be required before cross-matched blood is available.
Any abnormalities in prothrombin time or platelet count should be corrected.
Careful fluid balance assessment is essential and may require urinary catheterisation and central venous pressure measurements.
Elective intubation may be required in severe uncontrolled variceal bleeding, severe encephalopathy, in patients unable to maintain oxygen saturation above 90%, or in patients with evidence of an aspiration
An upper gastrointestinal endoscopy should be performed as soon as the patient is haemodynamically stable. Variceal band ligation is the treatment of choice. If banding is not possible, the varices should be injected with a sclerosant.
If endoscopy is unavailable, vasoconstrictors, such as octreotide or glypressin, or a Sengstaken tube may be used while more definitive therapy is arranged.
In case of bleeding that is difficult to control, a Sengstaken tube should be inserted until further endoscopic treatment, transjugular intrahepatic portosystemic shunting (TIPSS) or surgical treatment is performed.
Infection may occur following a variceal haemorrhage in cirrhotic patients resulting in significant morbidity and mortality. All patients should receive a course of broadspectrum antibiotics as prophylaxis.
Secondary prophylaxis following a variceal bleed in cirrhosis:
Following control of active bleeding the varices should be eradicated using endoscopic band ligation (sclerotherapy if banding unavailable). Following successful eradication of the varices repeated upper gastrointestinal endoscopy is required to screen for recurrence.
β-blockers may be used as secondary prophylaxis either in combination with endoscopic therapies or alone. If they are used alone, it is recommended that hepatic venous pressure gradient is measured to confirm the success of treatment.
TIPSS is more effective than endoscopic treatment in reducing variceal rebleeding but does not improve survival and is associated with more encephalopathy.
There is a 50% mortality in patients presenting for the first time with bleeding oesophageal varices. Prognosis is worse in patients with high Child–Pugh grading. Without treatment to prevent recurrence two thirds of patients rebleed whilst in hospital and 90% rebleed within a year.