Oesophageal varices

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Portal pressure rises when resistance to portal flow increases and splanchnic vasodilatation expands inflow. Collaterals develop at the gastro-oesophageal junction and can enlarge into varices. Risk of first bleeding relates to varix size, red wale markings and severity of liver disease, but a patient-level decision also considers ascites, blood pressure, kidney function, aetiology, transplant trajectory and ability to tolerate preventive therapy. Endoscopy remains important, while non-invasive assessment of clinically significant portal hypertension increasingly informs modern hepatology pathways.

Acute haemorrhage is both a bleeding and liver-decompensation event. Hypovolaemia can precipitate kidney injury, encephalopathy and shock, while indiscriminate fluid or transfusion can worsen portal pressure. Cirrhosis produces a rebalanced haemostatic state in which INR alone does not measure bleeding tendency, so routine attempts to normalise it can be harmful. The immediate package is simultaneous: ABC stabilisation, vasoactive treatment, prophylactic antibiotics, risk-directed blood support and urgent therapeutic endoscopy with anaesthetic planning.

Control of the visible varix is only the first phase. Rebleeding risk remains high without portal-pressure treatment. A non-selective beta-blocker plus scheduled repeat band ligation is the established secondary-prevention approach for many patients; early or rescue TIPS is considered when bleeding risk or failure warrants it. Every presentation should trigger treatment of alcohol dependence where present, viral or metabolic aetiology management, nutrition and sarcopenia review, ascites and encephalopathy care, hepatocellular carcinoma surveillance, and transplant consideration. The 2015 BSG guideline remains endorsed for acute and secondary management, while the society explicitly notes that primary prophylaxis guidance is under update, so current local hepatology governance matters.

Key points

Oesophageal varices are portosystemic collaterals caused by portal hypertension, most commonly from cirrhosis but also portal or splenic venous obstruction and other vascular disease.
Bleeding can be massive because elevated portal pressure, fragile variceal walls, infection and cirrhosis-associated haemostatic disturbance act together.
Haematemesis or melaena in a person with cirrhosis is treated as variceal until urgent endoscopy establishes another source.
Resuscitation targets perfusion and oxygen delivery while avoiding unnecessary volume or red-cell excess that can raise portal pressure and promote rebleeding.
Give terlipressin at presentation for suspected variceal bleeding unless contraindicated, with blood pressure, cardiac rhythm, oxygen, electrolytes and fluid monitoring.
Give prophylactic antibacterial therapy at presentation because bacterial infection and rebleeding risk are linked in cirrhosis.
Endoscopic band ligation is first-line definitive haemostasis for bleeding oesophageal varices; gastric or ectopic varices require a different expert pathway.
If banding fails, early specialist portal-decompression planning is essential; balloon tamponade is a temporary bridge with major aspiration and tissue-injury risks.
After survival, combined non-selective beta-blockade and repeat banding is commonly used for secondary prophylaxis, subject to haemodynamics and specialist review.
Primary prevention recommendations are evolving: use current NICE, BSG/BASL position statements and local hepatology policy rather than relying on an old isolated threshold.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Cirrhotic portal hypertension

Architectural distortion and intrahepatic resistance in cirrhosis raise portal pressure and create most oesophageal varices encountered in UK practice.

Portal venous obstruction

Portal-vein thrombosis and other prehepatic disorders can form varices with relatively preserved liver synthesis and different treatment implications.

Segmental venous obstruction

Splenic-vein thrombosis produces predominantly gastric collateral patterns, while posthepatic congestion can also transmit pressure back through the portal system.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Raised portal resistance
Obstructed portal flow combines with splanchnic vasodilatation and increased inflow to sustain a high-pressure venous circuit.
2
Portosystemic collateralisation
Blood is diverted through submucosal veins at the distal oesophagus into systemic azygos channels, progressively enlarging the vessels.
3
Wall tension and rupture
Increasing size, portal pressure and thin mucosal covering raise wall tension until a varix ruptures into the lumen.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Acute variceal haemorrhageRed flag

Large-volume fresh haematemesis, melaena, syncope or shock occurs in a person with cirrhosis, portal hypertension, prior varices or portal venous thrombosis.

Airway-threatened bleedRed flag

Ongoing vomiting of blood, agitation, severe encephalopathy, reduced consciousness or hypoxia predicts aspiration and requires early anaesthetic-led airway planning.

Portal-hypertension phenotype

Splenomegaly, thrombocytopenia, ascites, caput medusae, jaundice and previous decompensation support clinically important portal hypertension but absence does not exclude varices.

Septic decompensationRed flag

Fever, confusion, hypotension, kidney injury or rising lactate may represent infection alongside bleeding and increases mortality, supporting immediate prophylactic antibiotics and infection assessment.

Early rebleedingRed flag

Renewed haematemesis, melaena with haemodynamic change, falling haemoglobin or increasing transfusion need after banding suggests haemostatic failure and prompts rescue escalation.

Terlipressin toxicityRed flag

New chest or abdominal pain, pallor or cyanosis, bradyarrhythmia, hypoxia, pulmonary congestion, hyponatraemia or reduced peripheral perfusion requires urgent medicine review.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Continuous haemodynamic and airway assessmentFirst step
Why
Recognise shock, aspiration risk and response to blood support.
Interpretation and limitations
Trend pulse, blood pressure, respiratory state, mental status and urine output. Compensated shock can precede hypotension, and encephalopathy can make urgent intubation safer than repeated unprotected haematemesis.
02
Full blood count, group-and-screen and coagulation profile
Why
Prepare blood support and quantify anaemia and thrombocytopenia.
Interpretation and limitations
Initial haemoglobin may underestimate acute loss. Platelets and fibrinogen inform major-haemorrhage discussion, while INR in cirrhosis does not alone justify plasma or predict haemostasis.
03
Renal, liver and metabolic profile
Why
Stage decompensation and medicine risk during acute bleeding.
Interpretation and limitations
Creatinine, sodium, potassium, bilirubin, albumin, glucose and lactate influence prognosis, fluid care, terlipressin safety and transplant discussion; calculate a validated liver score after immediate stabilisation.
04
Blood cultures and infection screen
Why
Identify infection accompanying a decompensating variceal bleed.
Interpretation and limitations
Obtain cultures without delaying prophylactic antibacterial therapy. Examine urine, chest and ascitic fluid where indicated, then narrow or extend treatment from results and microbiology advice.
05
Urgent upper gastrointestinal endoscopy
Why
Identify the source and deliver variceal band ligation.
Interpretation and limitations
Active variceal bleeding, a white nipple or varices without another source support the diagnosis. Distinguish oesophageal from gastric varices because glue, radiological and shunt strategies differ.
06
Doppler ultrasonography or portal-phase CT
Why
Define portal and hepatic vascular anatomy after stabilisation or before TIPS.
Interpretation and limitations
Assess portal-vein patency, thrombosis, collaterals, ascites and focal liver lesions. Cross-sectional imaging must not delay first-line resuscitation, vasoactive therapy or endoscopy.
07
Echocardiography and TIPS work-up
Why
Evaluate cardiopulmonary and anatomical suitability for portal decompression.
Interpretation and limitations
Right-sided heart failure, severe pulmonary hypertension, uncontrolled infection or advanced encephalopathy may alter candidacy; the interventional radiology and hepatology team balances urgency against contraindications.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Peptic ulcer bleeding

Ulceration is a frequent alternative source of haematemesis and is distinguished by urgent endoscopy; cirrhosis alone does not establish variceal bleeding.

Portal hypertensive gastropathy

Diffuse congestive gastric oozing has a mosaic mucosal pattern rather than discrete oesophageal collaterals and responds differently to local haemostasis.

Mallory-Weiss tear

A junctional mucosal laceration after retching causes fresh bleeding but lacks the serpiginous venous columns of varices.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01At presentationDeliver the variceal bleed bundle in parallelFirst stepA person with known or possible portal hypertension presents with haematemesis or significant melaena.

1Activate senior gastroenterology, anaesthetic and critical-care support, protect the airway where bleeding or consciousness requires it, and obtain large-bore IV access with continuous observation.
2Send urgent bloods, group-and-screen and cultures, resuscitate to clinical perfusion and use restrictive, individualised red-cell support rather than routine over-transfusion.
3Administer terlipressin and prophylactic antibacterial therapy immediately under NICE and the local cirrhosis bundle, after checking contraindications and beginning required monitoring.
4Arrange urgent therapeutic endoscopy once initial stabilisation and airway planning are adequate, without waiting for correction of an isolated cirrhotic INR.

02Endoscopic haemostasisBand oesophageal varices safelyEndoscopy identifies active or recent oesophageal variceal bleeding.

1Clear the oesophagus carefully with anaesthetic support and identify whether the source is oesophageal, gastric, peptic or another lesion.
2Apply endoscopic band ligation to the bleeding oesophageal varix and additional high-risk columns according to the expert endoscopist's field and stability.
3Continue the defined short vasoactive course and antibiotic regimen, avoiding unnecessary nasogastric trauma immediately after banding unless the treating team requires access.
4Monitor for rebleeding, aspiration, ulceration, perforation and worsening liver failure and plan the next eradication session before discharge.

03Uncontrolled bleedingBridge promptly to portal decompressionHaemorrhage persists or recurs despite vasoactive therapy and adequate endoscopic banding.

1Call interventional radiology, hepatology, anaesthesia and surgery immediately and review whether early or rescue TIPS is indicated and technically feasible.
2DefinitiveIf exsanguinating, use a self-expanding dedicated oesophageal stent where commissioned or balloon tamponade by experienced staff as a temporary bridge, with definitive airway protection and time-limited pressure monitoring.
3Correct major physiological derangement with targeted blood components and calcium or temperature management through the haemorrhage protocol, not routine INR normalisation.
4AlternativeProceed to TIPS when appropriate or an alternative specialist radiological or surgical strategy, then monitor closely for encephalopathy, heart failure and hepatic deterioration.

04After survivalPrevent rebleeding and treat portal diseaseAcute oesophageal variceal haemostasis has been secured.

1Start or reinstate a tolerated non-selective beta-blocker after haemodynamic and renal recovery and arrange serial band ligation until eradication under the hepatology protocol.
2Review early-TIPS eligibility, portal-vein anatomy and any contraindication, especially after a high-risk bleed or difficult haemostasis.
3Address alcohol, viral hepatitis, metabolic disease, nutrition, ascites, encephalopathy, infection prevention, hepatocellular carcinoma surveillance and transplant referral.
4Provide a written recurrence plan covering fresh blood, melaena, fainting and confusion, and ensure primary-care and specialist ownership of medicines and follow-up is explicit.

05Primary preventionUse current specialist risk stratificationVarices or clinically significant portal hypertension are found before any bleed.

1Assess varix size and stigmata, liver stage, blood pressure, kidney function, ascites, asthma, conduction disease and patient preference in a hepatology service.
2Use the current NICE cirrhosis recommendations, the latest BSG/BASL position and local policy to choose a non-selective beta-blocker or endoscopic strategy where indicated.
3Titrate beta-blockade by safety and the local portal-hypertension endpoint, pausing or reviewing during hypotension, acute kidney injury, sepsis or severe decompensation.
4Continue disease-modifying liver care and scheduled reassessment because portal pressure and candidacy for prevention change over time.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces portal inflow and is given at presentation for suspected variceal haemorrhage as an adjunct to urgent endoscopic haemostasis.

Terlipressin acetate for acute variceal bleeding

For Glypressin 1 mg, give 2 mg by intravenous injection every 4 hours initially; after the initial dose reduce to 1 mg every 4 hours if body weight is below 50 kg or adverse effects occur. Continue until bleeding has been controlled for 24 hours, but for no longer than 48 hours. NICE advises stopping terlipressin after definitive haemostasis or by 5 days; this pathway ceiling does not permit a named product to exceed its shorter current SmPC maximum.

Use under specialist monitoring of blood pressure, ECG or heart rate, oxygen saturation, sodium, potassium and fluid balance. It is contraindicated in pregnancy in this SmPC; review cardiovascular or pulmonary disease, hypertension, low-output septic shock, ischaemia, bradycardia, QT-prolonging medicines and skin necrosis risk.

Reduces infection-related complications and rebleeding in suspected or confirmed variceal haemorrhage and is recommended by NICE alongside vasoactive therapy.

Prophylactic antibacterial therapy

Give the locally recommended intravenous antibacterial at presentation, using the current cirrhosis or upper-GI bleed regimen and adjusting for allergy, kidney function, prior resistant organisms and local microbiology; define and review the short course.

Take cultures when clinically indicated but do not delay the first dose in an unstable bleed. Review Clostridioides difficile risk, QT or renal effects and narrow to culture results; persistent sepsis requires a source search rather than prolonged blind prophylaxis.

Lowers portal pressure for selected primary prophylaxis and, combined with repeat banding in many patients, reduces recurrent oesophageal variceal bleeding.

Carvedilol or another non-selective beta-blocker

When the current hepatology pathway selects carvedilol, the BNF primary-prevention start is 6.25 mg once daily with specialist titration; secondary prevention, alternative propranolol regimens and targets follow the current NICE, BSG/BASL and local protocol.

Do not initiate during uncontrolled haemorrhage, shock or acute kidney injury. Monitor blood pressure, pulse, renal function and ascites; review asthma, heart block, severe peripheral vascular disease and interacting rate-limiting medicines, and avoid abrupt unsupervised withdrawal.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Massive haemorrhage

Variceal rupture can rapidly cause shock, aspiration, myocardial strain and death, requiring immediate vasoactive, antibacterial and endoscopic care.

Hepatic decompensation

Blood loss, infection and absorbed blood products precipitate encephalopathy, acute kidney injury and worsening ascites in limited hepatic reserve.

Early and late rebleeding

Failure of portal-pressure control or eradication leaves substantial recurrence risk, making secondary prophylaxis and shunt assessment essential.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During active bleeding continuously track haemodynamics, consciousness, oxygenation, urine output and visible blood loss, with repeated senior review of airway and transfusion needs.
While giving terlipressin monitor blood pressure, ECG or heart rate, oxygen saturation, sodium, potassium, fluid balance and symptoms or signs of myocardial, mesenteric, peripheral or skin ischaemia.
Trend haemoglobin, platelets, fibrinogen, kidney and liver function and lactate at clinically determined intervals, avoiding treatment decisions from INR alone.
After banding observe for recurrent haematemesis or melaena, post-banding ulcer bleeding, dysphagia, severe pain, aspiration and evolving encephalopathy.
For beta-blockade record sitting blood pressure, pulse, renal function, sodium, ascites control, falls and exercise tolerance at each titration or decompensation review.
Ensure repeat endoscopy, eradication, HCC surveillance and hepatology or transplant follow-up are booked, with non-attendance actively tracked after a life-threatening bleed.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Treat before proof

In a cirrhotic patient with major upper-GI bleeding, terlipressin and prophylactic antibiotics start at presentation because waiting for endoscopic confirmation loses benefit.

INR is not the whole haemostasis

Cirrhosis reduces procoagulant and anticoagulant factors together; routine plasma to normalise INR can add volume without reliably improving clot formation.

The airway is part of haemostasis

Massive haematemesis or encephalopathy can make aspiration and unsafe endoscopy the immediate threat, so early anaesthetic planning is decisive.

A balloon buys time only

Tamponade can arrest exsanguination temporarily but causes aspiration, ulceration and necrosis; it requires an airway, expert placement and a defined destination such as TIPS.

Primary guidance is moving

BSG still endorses its acute and secondary sections while signalling evolution in first-bleed prevention, making current hepatology policy essential in 2026.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for endoscopy before starting terlipressin and prophylactic antibiotics in a credible suspected variceal bleed.
02
Over-transfusing a stable cirrhotic patient to a normal haemoglobin target and potentially increasing portal pressure.
03
Trying to normalise INR routinely with plasma while delaying definitive haemostasis and adding intravascular volume.
04
Attempting band ligation during uncontrolled massive haematemesis without appropriate anaesthetic airway support.
05
Leaving balloon tamponade in place without pressure, time, airway monitoring and a definitive rescue procedure.
06
Discharging after successful banding without beta-blocker review, repeat eradication, liver aetiology treatment and transplant consideration.