Acute variceal haemorrhage

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

Varices rupture when wall tension, portal pressure and vessel size exceed local tissue support. Cirrhosis also creates circulatory vasodilatation, renal vulnerability, immune dysfunction and a fragile but rebalanced coagulation state. Bleeding can therefore trigger infection, encephalopathy and organ failure even after the visible vessel is controlled. A structured upper-GI bleed bundle reduces omissions by addressing recognition, resuscitation, risk, treatment, referral and review in parallel.

The first goal is oxygen delivery and safe endoscopy, not a normal blood pressure or laboratory panel. Two large IV cannulas, group-and-screen or crossmatch, serial observations, urine output and balanced blood-component decisions are central. Stable patients usually follow a restrictive red-cell strategy, but active exsanguination, acute coronary disease and delayed laboratory change require individual major-haemorrhage judgement. Platelets, fibrinogen and viscoelastic testing where available can inform targeted support; INR alone should not trigger reflex plasma.

Drug and endoscopic therapy are complementary. Terlipressin lowers splanchnic inflow, antibacterial prophylaxis reduces infectious amplification and urgent endoscopy applies oesophageal bands. Failure activates a predefined rescue route: temporary compression or covered stent under airway control, urgent interventional radiology assessment and TIPS where appropriate. After haemostasis the clinical team must prevent recurrence, diagnose the cause and stage of liver disease, address alcohol or viral drivers, manage nutrition and consider transplantation after this life-changing decompensation.

Key points

Haematemesis or melaena in cirrhosis is managed as portal hypertensive bleeding until endoscopy identifies a different lesion.
Resuscitation restores perfusion while avoiding excessive crystalloid and red-cell replacement that can raise portal pressure and provoke further haemorrhage.
A normal first haemoglobin does not exclude major acute loss because plasma equilibration has not yet occurred.
Terlipressin should begin when variceal bleeding is suspected, before endoscopic proof, unless a product-specific contraindication makes risk unacceptable.
Prophylactic antibiotics are part of haemostasis because bacterial infection increases failure, rebleeding and mortality in cirrhosis.
Endoscopic variceal band ligation is first-line control for oesophageal varices; gastric fundal varices need a glue, radiological or shunt pathway.
INR in cirrhosis does not measure the whole rebalanced haemostatic system, and routine plasma normalisation adds volume without reliable benefit.
Balloon tamponade or a dedicated self-expanding oesophageal stent is a short bridge for uncontrolled oesophageal bleeding, never destination therapy.
Early or pre-emptive TIPS benefits selected high-risk patients, but the current BSG position adds UK caveats and requires rapid multidisciplinary selection.
After control, secondary prevention generally combines a tolerated non-selective beta-blocker with repeat banding and a complete liver-transplant and aetiology review.

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

Cirrhotic portal hypertension

Cirrhosis raises intrahepatic resistance and portal pressure, producing fragile oesophagogastric collaterals that account for most variceal haemorrhage.

Non-cirrhotic portal obstruction

Portal or splenic venous thrombosis and other prehepatic or vascular disorders can generate varices despite preserved hepatic synthetic function.

Pressure and inflammatory triggers

Large varices, advanced liver disease, infection and increased portal pressure increase bleeding likelihood; haemorrhage may occur without a discrete precipitating event.

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

1
Collateral formation
Sustained portal hypertension diverts blood through submucosal veins at the distal oesophagus and proximal stomach, progressively dilating their thin walls.
2
Variceal rupture
Wall tension and mucosal injury overcome vessel integrity, releasing high-flow portal blood into the gastrointestinal lumen.
3
Circulatory and hepatic deterioration
Acute blood loss reduces perfusion while excessive volume replacement can raise portal pressure; absorbed blood and infection can precipitate encephalopathy and rebleeding.

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

Major portal bleedRed flag

Large fresh haematemesis, melaena, syncope, cool peripheries, oliguria or confusion occurs in a person with cirrhosis, splenomegaly or known varices.

Threatened airwayRed flag

Repeated blood-filled vomiting, reduced consciousness, agitation, severe encephalopathy or hypoxia makes aspiration prevention and anaesthetic control an immediate priority.

Occult compensated shockRed flag

Tachycardia, narrow pulse pressure, delayed capillary refill or rising lactate can precede hypotension and a fall in measured haemoglobin.

Gastric variceal sourceRed flag

Endoscopy shows fundal or cardiofundal varices with active bleeding, requiring anatomy-directed glue, radiological obliteration or TIPS expertise rather than routine oesophageal bands.

Early haemostatic failureRed flag

Continued haematemesis, persistent transfusion need, shock or recurrent bleeding shortly after treatment prompts rescue escalation and portal decompression review.

Terlipressin adverse effectRed flag

Chest or abdominal pain, bradycardia, hypoxia, pulmonary oedema, cyanosis, skin change or hyponatraemia suggests clinically important vasoconstrictive toxicity.

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 ABC and perfusion observationsFirst step
Why
Identify airway threat, haemorrhagic shock and response to resuscitation.
Interpretation and limitations
Trend mental state, respiratory effort, oxygen, pulse, pressure, capillary refill, urine output and ongoing blood. A single normal observation cannot overrule an actively changing bleed.
02
Full blood count and crossmatch
Why
Prepare blood support and quantify anaemia and thrombocytopenia serially.
Interpretation and limitations
Early haemoglobin may remain deceptively normal. Platelet count adds procedural context but is not the only determinant of cirrhotic clot formation.
03
Coagulation, fibrinogen and metabolic profile
Why
Assess severe haemostatic derangement, kidney injury, sodium and tissue perfusion.
Interpretation and limitations
INR reflects reduced procoagulants but not counterbalancing anticoagulants; use fibrinogen and clinical bleeding, with viscoelastic testing where governed locally, to avoid indiscriminate components.
04
Blood cultures and infection assessment
Why
Detect infection precipitating or complicating haemorrhage.
Interpretation and limitations
Culture blood and sample urine, chest or ascites where indicated without postponing prophylactic antibiotics. Fever can be absent in decompensated cirrhosis.
05
Glasgow-Blatchford score
Why
Document pre-endoscopic upper-GI bleeding risk after immediate stabilisation starts.
Interpretation and limitations
The score does not diagnose a varix or override cirrhosis-specific danger. A low value cannot justify discharge from ongoing haematemesis or hepatic decompensation.
06
Urgent upper gastrointestinal endoscopy
Why
Identify the source and deliver definitive oesophageal band haemostasis.
Interpretation and limitations
Active bleeding, a white nipple or varices without another source supports diagnosis. Classify gastric anatomy and record alternative peptic, portal-gastropathy or malignant lesions.
07
Portal-phase CT and TIPS work-up
Why
Map portal patency, collaterals and technical or cardiac constraints for rescue shunting.
Interpretation and limitations
Perform when sufficiently stable and without delaying emergency endoscopy. Portal thrombosis, tumour, right-heart failure or severe pulmonary hypertension changes the rescue plan.

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

Peptic ulcer bleeding

Ulceration is a common alternative upper-GI source and is distinguished at endoscopy; cirrhosis does not prove that every haematemesis is variceal.

Portal hypertensive gastropathy

Diffuse mosaic gastric mucosa causes chronic or acute oozing rather than a focal variceal jet and requires a different haemostatic strategy.

Mallory-Weiss tear

Fresh bleeding after repeated retching with a junctional mucosal laceration supports a tear, although forceful vomiting may also follow any major haemorrhage.

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

01First hourRun resuscitation and variceal treatment togetherFirst stepA patient with possible portal hypertension has significant haematemesis or melaena.

1Call senior gastroenterology, anaesthesia and critical care, assess airway and circulation, obtain large-bore IV access and activate major haemorrhage support when indicated.
2Send crossmatch, blood count, coagulation, fibrinogen, renal, liver, lactate and cultures and resuscitate to organ perfusion with individually targeted blood products.
3Give monitored terlipressin and the local prophylactic antibacterial regimen immediately after checking key contraindications, without waiting for endoscopy.
4Arrange urgent endoscopy after initial stabilisation and use anaesthetic airway protection when active bleeding or encephalopathy makes the procedure unsafe.

02Endoscopic controlIdentify anatomy and secure haemostasisThe patient reaches endoscopy with suspected variceal bleeding.

1Clear clot cautiously, find the active or recent source and distinguish oesophageal columns from gastric varices and non-variceal lesions.
2Apply endoscopic bands to oesophageal varices using an experienced operator and continue short-course vasoactive and antibacterial treatment.
3For gastric varices contact the regional HPB and interventional team for cyanoacrylate, endovascular or TIPS management according to anatomy.
4Observe in a high-acuity setting for early rebleeding, aspiration, encephalopathy, kidney injury and post-banding ulcer complications.

03Failure rescueBridge once and decompress decisivelyBleeding continues or recurs early despite adequate first endoscopic treatment.

1Activate interventional radiology, hepatology and anaesthesia immediately and reassess portal patency, cardiac status and candidacy for early or rescue TIPS.
2Secure the airway and use a commissioned covered oesophageal stent or balloon tamponade by trained staff only as a time-limited bridge.
3Continue targeted haemorrhage correction, temperature and calcium management and drain or treat other sources of instability.
4DefinitiveProceed to TIPS or the chosen definitive radiological or surgical strategy and monitor afterwards for encephalopathy, cardiac failure and hepatic deterioration.

04Secondary preventionPrevent the next bleed before dischargeHaemostasis is secured after an oesophageal variceal event.

1Start or restart a tolerated non-selective beta-blocker once shock, kidney injury and infection have resolved and arrange serial banding to eradication.
2Review pre-emptive TIPS eligibility, portal-vein anatomy and the BSG UK caveats before the high-risk treatment window closes.
3Treat liver aetiology, alcohol use, ascites, infection, encephalopathy and malnutrition and initiate transplant assessment after this decompensation.
4Book banding and hepatology follow-up with a fail-safe system and give written advice for fresh blood, black stool, fainting or confusion.

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

Reduces portal inflow from presentation until definitive endoscopic haemostasis is established and maintained.

Terlipressin acetate, Glypressin

Adult Glypressin regimen: give 2 mg intravenously every 4 hours at first. From the second dose, reduce each dose to 1 mg when body weight is under 50 kg or adverse effects develop. Continue only until haemostasis has been maintained for 24 hours and never beyond the current 48-hour SmPC maximum. NICE's instruction to stop after definitive haemostasis or by day 5 is an outer pathway limit, not permission to exceed the shorter product licence.

Monitor blood pressure, ECG or heart rate, oxygen saturation, sodium, potassium and fluid balance. The product is contraindicated in pregnancy and needs particular caution with cardiac or pulmonary disease, hypertension, low-output septic shock, QT risk and any myocardial, mesenteric, limb or skin ischaemia.

Reduces bacterial infection, treatment failure and rebleeding in suspected or confirmed cirrhotic variceal haemorrhage.

Prophylactic antibacterial treatment

Give the locally recommended intravenous agent at presentation and define the short course using allergy, renal function, previous cultures, community or hospital acquisition and current antimicrobial resistance.

Obtain cultures when clinically indicated without delaying the first dose. Review renal, QT and Clostridioides difficile risks and narrow or redirect therapy when a source or organism is identified.

Restores oxygen delivery and treats selected clinically significant haemostatic deficits during uncontrolled bleeding.

Blood components

Use red cells and targeted platelets, fibrinogen-containing product or plasma through the current major-haemorrhage protocol, guided by active loss, physiology, haemoglobin trajectory, fibrinogen and specialist testing rather than a fixed normal target.

Excess volume can raise portal pressure and cause pulmonary oedema. Cirrhotic INR alone is not an indication for routine plasma; balance transfusion thresholds against coronary ischaemia, ongoing shock and delayed laboratory equilibration.

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

Haemorrhagic shock and aspiration

Rapid blood loss causes tissue hypoperfusion, while massive haematemesis and impaired consciousness threaten airway contamination and respiratory failure.

Encephalopathy and kidney injury

Hypoperfusion, absorbed nitrogenous material, infection and reduced hepatic reserve can precipitate confusion, acute kidney injury and multiorgan decompensation.

Infection and early rebleeding

Bacterial infection is common around variceal bleeding and increases failure of haemostasis, recurrent bleeding and mortality, supporting immediate cause-specific prophylaxis.

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

Continuously observe airway, oxygenation, pulse, pressure, mental state, urine output, temperature and visible bleeding through the unstable and early post-haemostasis phases.
Repeat haemoglobin, platelets, fibrinogen, renal function, sodium, potassium, glucose and lactate at clinically responsive intervals rather than a fixed low-risk schedule.
During terlipressin therapy document cardiovascular rhythm, oxygen, fluid balance and any skin, chest or abdominal ischaemic symptom before each continued dose.
After endoscopy track rebleeding, transfusion requirement, post-banding pain or dysphagia, infection, encephalopathy and acute kidney injury.
If TIPS is placed monitor neurological state, liver tests, cardiac congestion and shunt patency under the interventional radiology pathway.
Before discharge confirm secondary beta-blocker ownership, next banding date, transplant review, alcohol or aetiology treatment and an emergency recurrence plan.

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

Two medicines start before the scope

Vasoactive and antibacterial treatment are indicated on credible suspicion because their early benefit does not depend on first seeing the varix.

Restrictive is not neglectful

Avoiding unnecessary transfusion protects portal pressure, but active shock and myocardial ischaemia still demand individual physiological judgement.

Cirrhotic INR is incomplete

Both clot-forming and anticoagulant proteins fall, so a prolonged result neither predicts bleeding alone nor provides a universal plasma target.

Compression needs a destination

A balloon or covered stent is justified only when an airway, trained team and immediate route to TIPS or other definitive control already exist.

Survival begins secondary prevention

The first bleed is proof of decompensation and should trigger band eradication, portal-pressure therapy, cause treatment and transplant thinking before discharge.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for endoscopic confirmation before giving terlipressin and prophylactic antibiotics in a convincing variceal presentation.
02
Transfusing to a normal haemoglobin in a stable patient and worsening portal pressure through avoidable volume.
03
Giving plasma solely to correct cirrhotic INR while delaying band ligation and adding circulatory load.
04
Attempting repeated unprotected endoscopy during massive haematemesis without anaesthetic airway control.
05
Leaving balloon tamponade as definitive therapy without time limits, pressure checks and urgent TIPS planning.
06
Discharging after haemostasis without combined secondary prevention, liver aetiology treatment and transplant review.