Band ligation of oesophageal and gastric varices is a key endoscopic procedure used to treat and prevent life-threatening bleeding from enlarged veins in the oesophagus and stomach. These varices develop as a consequence of portal hypertension, most commonly caused by liver cirrhosis. Without treatment, rupture carries a significant risk of death. This article explains how band ligation works, what patients can expect during and after the procedure, the associated risks, and how ongoing care — including pharmacological prophylaxis and surveillance endoscopy — is managed within the NHS, in line with NICE and British Society of Gastroenterology guidance.

What Are Oesophageal and Gastric Varices?

Oesophageal and gastric varices are enlarged collateral veins caused by portal hypertension, most commonly from liver cirrhosis; rupture carries approximately 15–20% six-week mortality even with optimal treatment.

Oesophageal and gastric varices are abnormally enlarged veins that develop in the lower oesophagus and stomach wall. They arise as a direct consequence of portal hypertension — a condition in which blood pressure within the portal venous system becomes significantly elevated, most commonly due to liver cirrhosis. When the liver's architecture is disrupted by scarring, blood cannot flow through it freely, causing it to back up and divert through smaller, more fragile collateral vessels.

These collateral veins are not designed to carry high-pressure blood flow. Over time, they dilate and become tortuous, forming varices that are prone to rupture. Oesophageal varices are more common and clinically significant than gastric varices, though both carry a serious risk of life-threatening haemorrhage. Gastric varices, particularly those at the gastro-oesophageal junction or fundus, can be more difficult to treat and may bleed more severely.

The principal causes of portal hypertension in the UK include:

• Alcohol-related liver disease — the most prevalent cause

• Non-alcoholic fatty liver disease (NAFLD), increasingly referred to as metabolic dysfunction-associated steatotic liver disease (MASLD)

• Viral hepatitis (hepatitis B and C)

• Primary biliary cholangitis and other autoimmune liver conditions

The risk of variceal bleeding depends on variceal size and the degree of liver decompensation. For patients with large oesophageal varices, the annual bleeding risk is approximately 10–15%; overall lifetime risk varies considerably by disease severity. When bleeding does occur, 6-week mortality remains approximately 15–20% even with optimal modern therapy, reflecting the seriousness of this complication. Patients with known cirrhosis are routinely screened for varices via upper gastrointestinal endoscopy, in line with NICE guideline NG50 (Cirrhosis in over 16s: assessment and management). In some centres, non-invasive risk stratification tools may reduce the need for endoscopy in lower-risk individuals, subject to local protocol.

How Band Ligation Works to Treat Varices

Endoscopic band ligation applies elastic rubber bands to varices, causing ischaemic necrosis and fibrotic obliteration; it is the gold-standard treatment for oesophageal varices but not routinely used for fundal gastric varices.

Endoscopic band ligation (EBL), sometimes referred to as variceal band ligation (VBL), is the gold-standard endoscopic treatment for oesophageal varices. The procedure works by mechanically interrupting blood flow through the variceal vessels, causing them to thrombose and eventually slough away, leaving behind scar tissue that obliterates the vein.

During the procedure, a flexible endoscope fitted with a multi-band ligator device is passed through the mouth into the oesophagus. The varix is suctioned into the ligator cap, and a small elastic rubber band is deployed around its base. This strangulates the vessel, cutting off its blood supply. Multiple bands — typically four to ten — are applied per session, targeting the most prominent varices, usually beginning at the gastro-oesophageal junction and working upwards.

The banded tissue undergoes ischaemic necrosis over the following days. Within one to two weeks, the necrotic tissue sloughs off, leaving a superficial ulcer that heals with fibrosis. This process progressively reduces the size and number of varices with each treatment session.

For gastric varices , band ligation is generally not appropriate except for selected varices at the gastro-oesophageal junction (GOV1 type). For bleeding gastric varices at the fundus or isolated gastric varices (GOV2, IGV1), endoscopic injection of tissue adhesive (N-butyl-2-cyanoacrylate glue) is recommended as first-line endoscopic therapy in UK practice. Where available, specialised techniques such as EUS-guided coil embolisation combined with tissue adhesive, or thrombin injection, may be offered. Transjugular intrahepatic portosystemic shunt (TIPS) is an important alternative for gastric varices not amenable to endoscopic control. NICE guideline CG141, NICE NG50, and British Society of Gastroenterology (BSG) guidance inform the choice of intervention based on variceal location, size, and the patient's overall liver function.

What to Expect During and After the Procedure

Band ligation takes 15–30 minutes under conscious sedation; patients commonly experience mild chest discomfort and dysphagia for a few days, and should follow a soft diet for 24–48 hours post-procedure.

Band ligation is typically performed as an inpatient or day-case procedure in a hospital endoscopy unit. Patients are usually asked to fast for at least six hours for solid food and two hours for clear fluids beforehand, though patients should follow the specific instructions given by their clinical team. The procedure is carried out under conscious sedation (commonly using midazolam and fentanyl) or, in some centres, with the patient under general anaesthesia, particularly if there is active bleeding or significant patient distress.

The procedure itself generally takes 15 to 30 minutes. Patients may experience mild discomfort, a sensation of pressure in the chest, or difficulty swallowing during the process. After the procedure, it is normal to experience:

• Mild chest discomfort or retrosternal pain for a few days

• Difficulty swallowing (dysphagia) as banded tissue swells

• Low-grade fever in the first 24–48 hours — any fever persisting beyond this period, or a high fever at any point, should prompt medical review as it may indicate infection

• Mild nausea

Patients are usually advised to follow a soft or liquid diet for 24–48 hours post-procedure to reduce irritation to the treated areas. Pain relief with simple analgesics such as paracetamol (within recommended dosing limits) is generally sufficient. Non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided due to their ulcerogenic and antiplatelet effects, and because they carry additional risks of renal impairment and worsening ascites in patients with cirrhosis. A short course of a proton pump inhibitor (PPI) may be prescribed after banding at some centres to help protect the healing ulcers; patients should follow their clinical team's advice on this.

If conscious sedation has been used, patients must not drive, operate machinery, drink alcohol, or sign any legal documents for 24 hours after the procedure. A responsible adult should escort the patient home and remain with them.

Most patients are discharged within 24 hours if there is no active bleeding. Those treated during an acute variceal haemorrhage will require a longer inpatient stay for monitoring, fluid resuscitation, and management of any underlying liver decompensation. A follow-up endoscopy is typically arranged four to six weeks after the initial session to assess healing and determine whether further banding is required.

Risks, Complications, and When to Seek Help

Serious complications include post-banding ulcer haemorrhage (5–14 days post-procedure), oesophageal stricture, and aspiration; patients should call 999 immediately if they vomit blood or pass black tarry stools after discharge.

Band ligation is considered a safe and well-tolerated procedure, but like all endoscopic interventions, it carries a defined risk profile that patients should be aware of before consenting to treatment.

Common and expected side effects include transient chest pain, dysphagia, and mild odynophagia (painful swallowing), which typically resolve within a week. These are related to the local inflammatory response as banded tissue undergoes necrosis.

More serious complications include:

• Post-banding ulcer haemorrhage — shallow ulcers left after band sloughing can bleed in a small proportion of cases, usually occurring 5–14 days post-procedure; your clinical team can provide further information on the likelihood of this based on your individual circumstances

• Oesophageal stricture — repeated banding sessions may rarely lead to fibrotic narrowing of the oesophagus

• Bacteraemia — transient bacterial translocation can occur; antibiotic prophylaxis is not routinely recommended in elective cases but may be considered in high-risk patients

• Sedation-related effects — conscious sedation carries a small risk of respiratory depression, low blood pressure, or reduced oxygen levels; patients are monitored throughout the procedure and during recovery

• Aspiration — particularly in patients with active bleeding or impaired consciousness

• Perforation — rare but serious

If you experience any suspected side effects from medicines used during or after your procedure, these can be reported to the MHRA Yellow Card scheme at yellowcard.mhra.gov.uk or via the Yellow Card app.

Patients and carers should be clearly advised to call 999 or attend the nearest emergency department immediately if any of the following occur after discharge:

• Vomiting blood (haematemesis) or passing black, tarry stools (melaena)

• Severe or worsening chest or abdominal pain

• High fever or signs of infection

• Sudden dizziness, collapse, or loss of consciousness

These symptoms may indicate post-banding haemorrhage or another serious complication requiring emergency endoscopy or surgical intervention. Patients should be provided with clear written information and emergency contact details prior to discharge, in line with NICE CG141 (Acute upper gastrointestinal bleeding in over 16s: management).

Follow-Up Care and Preventing Variceal Rebleeding

Variceal eradication requires two to four banding sessions, followed by surveillance endoscopy; non-selective beta-blockers combined with band ligation are recommended for secondary prophylaxis per NICE NG50 and BSG guidance.

Successful obliteration of varices typically requires two to four endoscopic sessions, spaced four to six weeks apart. Once variceal eradication is confirmed endoscopically — defined as the absence of varices or reduction to small, non-bleeding varices — surveillance endoscopy is recommended to detect recurrence, as varices can reform due to ongoing portal hypertension. Surveillance intervals vary by centre and clinical risk; a common approach is endoscopy at three to six months after eradication, then every six to twelve months thereafter, in line with NICE NG50 and local protocol.

Non-selective beta-blockers (NSBBs) are a cornerstone of pharmacological secondary prophylaxis. Propranolol reduces portal pressure by decreasing cardiac output (via beta-1 blockade) and causing splanchnic vasoconstriction (via beta-2 blockade). Carvedilol has additional alpha-1 adrenoceptor blockade, which reduces intrahepatic vascular resistance and often produces a greater reduction in portal pressure than propranolol alone. Both agents are used in UK practice; dosing and titration should be guided by a clinician with reference to the British National Formulary (BNF).

NSBBs are contraindicated or require caution in certain patients, including those with asthma or significant bronchospasm, marked bradycardia, hypotension, or acute kidney injury. Their use in patients with refractory ascites requires specialist assessment. NICE guidance and BSG guidelines support the combined use of band ligation and NSBBs for secondary prevention following a variceal bleed, as the combination is more effective than either treatment alone.

Beyond endoscopic and pharmacological management, addressing the underlying liver disease is essential. This includes:

• Complete alcohol abstinence in alcohol-related liver disease

• Antiviral therapy for hepatitis B or C

• Weight management and metabolic control in NAFLD/MASLD

• Nutritional support, as malnutrition is common in cirrhosis

In patients with high-risk acute variceal bleeds (for example, Child-Pugh class C or class B with active bleeding at endoscopy), early or pre-emptive TIPS (transjugular intrahepatic portosystemic shunt) within 72 hours may be considered to decompress the portal system, as recommended by BSG guidance. For patients with refractory or recurrent variceal bleeding despite endoscopic and pharmacological treatment, TIPS remains an important option. Liver transplantation is the definitive treatment for end-stage liver disease and eliminates the risk of variceal haemorrhage by correcting the underlying portal hypertension.

NHS Referral and NICE Guidance on Variceal Management

NICE NG50 and CG141 guide variceal screening, prophylaxis, and acute management in the UK; patients with suspected variceal bleeding should be referred immediately via 999 to the emergency department.

In the UK, the management of oesophageal and gastric varices is guided primarily by:

• NICE guideline NG50 — Cirrhosis in over 16s: assessment and management — covering variceal screening, primary and secondary prophylaxis, and surveillance

• NICE guideline CG141 — Acute upper gastrointestinal bleeding in over 16s: management — defining acute management pathways

• NICE quality standard QS152 — Cirrhosis in adults — setting quality standards for identification, referral, and monitoring

• British Society of Gastroenterology (BSG) guidelines on the management of variceal haemorrhage (2015; updated 2020)

NICE NG50 recommends that all patients with confirmed cirrhosis undergo upper gastrointestinal endoscopy at diagnosis to screen for varices. Those found to have medium or large oesophageal varices should be offered either band ligation or NSBB therapy for primary prophylaxis — i.e., to prevent a first bleed. Band ligation is generally preferred when NSBBs are contraindicated or not tolerated.

For acute variceal haemorrhage, NICE CG141 and BSG guidance recommend:

• Prompt resuscitation and airway protection

• Terlipressin (a vasopressin analogue) to reduce portal pressure, administered as soon as variceal bleeding is suspected, in the absence of contraindications

• Prophylactic antibiotics (e.g., intravenous ceftriaxone) to reduce the risk of bacterial infection and improve outcomes

• Emergency endoscopy after resuscitation — immediately for haemodynamically unstable patients, and within 24 hours for all patients with suspected variceal bleeding; earlier endoscopy is recommended for suspected variceal bleeding where service capacity allows, per BSG guidance

• Band ligation as the primary haemostatic intervention for oesophageal varices; tissue adhesive injection as first-line endoscopic therapy for bleeding gastric varices

GPs play a vital role in identifying patients at risk and facilitating timely referral to hepatology or gastroenterology services. Any patient with known or suspected cirrhosis presenting with haematemesis or melaena should be referred immediately via 999 to the emergency department. Patients with stable cirrhosis and newly identified varices on screening should be referred urgently to a specialist team for risk stratification and prophylactic treatment planning. Early, coordinated care between primary and secondary care significantly improves outcomes in this high-risk patient group.

Suspected adverse reactions to any medicines used in the management of varices — including terlipressin, propranolol, carvedilol, or sedation agents — should be reported to the MHRA Yellow Card scheme at yellowcard.mhra.gov.uk.

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