Clinical Guides
Oesophageal Varices
A clinically focused guide to oesophageal-varix screening, primary and secondary prevention, acute haemorrhage, endoscopic ligation and escalation to TIPS in Indian clinical practice.
MedNext Academy | 14 min read
Oesophageal Varices
A clinically focused guide to oesophageal-varix screening, primary and secondary prevention, acute haemorrhage, endoscopic ligation and escalation to TIPS in Indian clinical practice.
Summary
Oesophageal varices are dilated submucosal veins created when portal blood is diverted through the gastro-oesophageal collateral circulation. They most often accompany cirrhosis, but may also arise from extrahepatic portal venous obstruction, portal-vein thrombosis or other non-cirrhotic portal-hypertensive disorders. The clinical danger is rupture: acute variceal haemorrhage can cause rapid blood loss, aspiration, shock, infection, kidney injury and hepatic decompensation. Varices themselves are commonly asymptomatic until endoscopy or bleeding. Dysphagia is therefore not a reliable screening symptom, and a patient with cirrhosis must not wait for pain or swallowing difficulty before risk assessment.
Prevention starts by identifying clinically significant portal hypertension and deciding who needs an NSBB, upper gastrointestinal endoscopy or both. In suitable compensated cirrhosis, carvedilol may prevent decompensation as well as a first bleed. Where an NSBB is contraindicated or not tolerated, endoscopic variceal ligation (EVL) is used for high-risk oesophageal varices. EVL eradicates visible columns but does not lower portal pressure, so recurrence surveillance and treatment of the underlying liver disease remain necessary. Gastric varices need separate anatomical classification because cardiofundal bleeding is generally treated with tissue adhesive or an endovascular strategy, not assumed to follow the oesophageal banding pathway.
Suspected acute variceal bleeding is treated before endoscopic confirmation: protect the airway when indicated, restore perfusion without over-transfusion, begin a vasoactive drug and antibacterial prophylaxis, then perform endoscopy within twelve hours after initial resuscitation. EVL is first-line endoscopic haemostasis for oesophageal varices. Selected high-risk patients should be discussed for pre-emptive TIPS within 72 hours, preferably within 24 hours; uncontrolled or early recurrent bleeding requires rescue decompression. After survival, combination secondary prophylaxis with an NSBB and serial EVL is standard unless a contraindication changes the plan.
How Common Is It?
Varices are a frequent consequence of cirrhosis, but reported prevalence varies with whether the population is compensated or decompensated, the cause of liver disease, endoscopy policy and the definition of small versus large varices. A person may have clinically significant portal hypertension before varices are visible, and small varices can enlarge as hepatic dysfunction progresses. Bleeding incidence is concentrated in high-risk lesions: large calibre, red wale or other red signs, and advanced Child-Pugh class confer more risk than the mere presence of a small smooth column. The absence of varices at one endoscopy is not lifelong protection when liver injury remains active.
In India, the denominator is uncertain because no unified national endoscopy registry captures compensated cirrhosis, extrahepatic portal venous obstruction, treatment and follow-up. Tertiary centres see a selected population enriched for haemorrhage, severe cirrhosis and repeat banding. Rural under-diagnosis moves the first recorded encounter toward emergency bleeding, while metropolitan surveillance identifies more asymptomatic disease. Children and younger adults with extrahepatic portal venous obstruction can have large varices despite relatively well-preserved liver biochemistry, a pattern that differs from decompensated cirrhosis.
Public-health burden is better reflected by preventable first bleeds, rebleeding, emergency transfusion, intensive-care need and access to definitive therapy than by a borrowed prevalence percentage. Service measures should include the proportion of eligible patients receiving validated non-invasive stratification or timely endoscopy, documented primary prophylaxis, acute vasoactive treatment and antibiotics before endoscopy, endoscopic haemostasis within the recommended interval, complete eradication sessions, secondary NSBB use and TIPS referral. Screening figures must distinguish those appropriately managed with an NSBB without endoscopy from those simply lost to care. Published international estimates help planning but cannot substitute for transparent Indian service data.
Risk Factors
The prerequisite is portal hypertension, but varix formation and rupture are separate steps. Cirrhosis caused by alcohol, hepatitis B or C, metabolic steatotic disease, autoimmune hepatitis or cholestatic disease increases resistance and collateral flow. Portal-vein thrombosis, extrahepatic portal venous obstruction and porto-sinusoidal vascular disease are important non-cirrhotic routes. Continuing liver injury, rising liver stiffness, falling platelets, ascites and declining synthetic function signal progression. Aetiological treatment can reduce risk but does not instantly remove established collaterals, so prophylaxis cannot be stopped solely because aminotransferases improve.
Endoscopic predictors of a first haemorrhage include varices at least 5 mm, red wale markings and severe liver dysfunction, commonly represented by Child-Pugh C. Pressure, wall tension and varix radius interact; a larger thin-walled vessel under higher pressure is more vulnerable. Infection, acute alcohol-related hepatitis, kidney injury and rapid clinical decompensation may destabilize a patient. Gastric extension changes both risk and treatment. A prior bleed is the strongest practical marker for recurrence, which is why secondary prophylaxis uses combined pharmacological and endoscopic treatment.
Iatrogenic and access risks deserve equal attention. NSAIDs, uncoordinated antithrombotic treatment, excessive transfusion and failure to prescribe infection prophylaxis can worsen an acute episode. Missing repeat EVL before eradication, prescribing an NSBB without blood-pressure monitoring, or stopping treatment because a single endoscopy appears improved exposes patients to recurrence. Anticoagulation is not universally forbidden; portal-vein thrombosis or another thrombotic indication may justify it after risk assessment and appropriate bleeding prophylaxis. In India, travel distance, out-of-pocket cost, unavailable emergency endoscopy and delayed referral to a TIPS-capable centre are system-level risk factors that should be anticipated in the care plan.
Diagnosis
History
For screening, establish the liver or vascular diagnosis, previous decompensation, endoscopy dates, varix size, red signs, banding sessions and tolerance of NSBB therapy. Ask about melaena, haematemesis, presyncope, fatigue, abdominal distension, jaundice, confusion and infection. Document alcohol exposure, viral status, portal-vein thrombosis, pancreatitis, abdominal surgery and childhood bleeding. Reconcile propranolol or carvedilol dose, adherence, asthma, bradycardia, hypotension, anticoagulants, antiplatelets and NSAIDs. During active bleeding, obtain only the history that informs resuscitation and contraindications; do not delay treatment for a complete questionnaire.
Examination
In haemorrhage, assess airway contamination, consciousness, respiratory effort, pulse, blood pressure, capillary refill and peripheral temperature. Look for shock even when tachycardia is blunted by beta blockade. Jaundice, ascites, oedema, splenomegaly, abdominal collaterals, sarcopenia and asterixis establish disease context and prognosis. Fever or abdominal tenderness suggests infection. A normal abdominal examination cannot exclude large varices. Melaena supports an upper source, but fresh rectal blood can occur with brisk upper gastrointestinal bleeding.
Investigations
Send full blood count, group and cross-match, liver and renal panels, electrolytes, glucose, INR and fibrinogen according to the major-haemorrhage protocol. Serial haemoglobin is more informative than the initial value, which may not yet reflect blood loss. Upper gastrointestinal endoscopy confirms the source, records size and red signs, identifies active spurting or stigmata, classifies gastric extension and permits treatment. Perform it within twelve hours after resuscitation in suspected variceal bleeding. Ultrasound-Doppler and contrast imaging assess liver, spleen, portal-vein patency and collateral anatomy; CT angiographic planning may be needed before TIPS or obliteration. Transient elastography and platelet count guide whether screening endoscopy can be avoided in selected compensated disease but do not diagnose an acute bleeding source.
Differential Diagnosis
Peptic ulcer disease remains a common alternative cause of haematemesis or melaena in a person with cirrhosis. Other possibilities include erosive gastritis or duodenitis, reflux oesophagitis, malignancy, Mallory-Weiss tear, Dieulafoy lesion and angiodysplasia. Initial treatment can appropriately assume variceal bleeding when portal hypertension is likely, because vasoactive and antibiotic delays are harmful; endoscopy then establishes whether the lesion is variceal, non-variceal or mixed. Continuing a variceal label after a documented ulcer can lead to the wrong secondary-prevention plan.
Gastric varices must be distinguished from oesophageal columns. Gastro-oesophageal varices type 1 extend along the lesser curvature and may sometimes be managed with EVL when actively bleeding, whereas cardiofundal GOV2 or isolated fundal IGV1 usually require endoscopic cyanoacrylate where expertise exists or an interventional-radiology approach. Ectopic varices may occur in the duodenum, jejunum, colon, rectum or around a stoma. Portal hypertensive gastropathy produces a mosaic or snake-skin mucosal pattern and diffuse oozing; gastric antral vascular ectasia has a different vascular pattern and is not simply severe portal hypertensive gastropathy.
Pseudo-varices and prominent normal folds can confuse inexperienced endoscopy, while downhill oesophageal varices caused by superior vena-cava obstruction differ from the usual distal uphill varices of portal hypertension. Haemoptysis, swallowed epistaxis and oral bleeding may mimic haematemesis. In a child or young adult with splenomegaly and preserved liver function, extrahepatic portal venous obstruction must not be mistaken for cryptogenic cirrhosis. If the endoscopic field is obscured by blood, a temporary diagnosis remains provisional and repeat evaluation or radiological mapping may be necessary after stabilization.
Management
Primary prevention depends on the whole portal-hypertension pathway. Treat the cause of liver disease, support alcohol abstinence and nutrition, and identify compensated patients with clinically significant portal hypertension. Current consensus favours carvedilol in eligible compensated cirrhosis because it can prevent decompensation. When endoscopy is used, high-risk oesophageal varices—large varices, red signs or varices in Child-Pugh C disease—need prophylaxis. NSBB therapy and EVL are alternatives for preventing a first oesophageal-variceal bleed when the choice is driven by contraindications, patient preference and service access. Combining them routinely for primary prophylaxis is not the standard default.
Acute care is simultaneous. Activate a major upper-gastrointestinal-bleed pathway; protect the airway selectively; use cautious crystalloid and a restrictive red-cell threshold, generally transfusing around haemoglobin 7 g/dL and targeting 7–9 g/dL unless individual cardiovascular or shock considerations alter it. Start terlipressin, somatostatin or octreotide immediately and give antibacterial prophylaxis. Arrange skilled endoscopy within twelve hours after resuscitation. EVL is recommended for active oesophageal-variceal haemorrhage. Avoid sclerotherapy when banding is feasible. If bleeding continues, a removable self-expanding oesophageal stent is often a safer bridge than balloon tamponade, but either requires expert monitoring and rapid definitive TIPS.
Discuss pre-emptive TIPS for Child-Pugh C up to 13 points or Child-Pugh B above 7 with active bleeding at endoscopy despite vasoactive therapy, ideally within 24 hours and no later than 72. Rescue TIPS is indicated when combined drug and endoscopic treatment fails. After haemostasis, eradicate varices with EVL at one- to four-week intervals and use an NSBB for secondary prophylaxis. Rebleeding despite both prompts TIPS. Assess transplantation after decompensation, not only after all local measures fail.
Prescribing Information
Carvedilol, propranolol and nadolol are non-selective beta blockers, but they are not dose-equivalent. Begin low, review pulse, orthostatic symptoms, blood pressure, renal function and sodium, then titrate within the product and specialist protocol. Carvedilol has additional alpha-1 blockade and can lower pressure more markedly. Traditional NSBB titration often uses a resting heart-rate range as one safety marker, but tolerance and perfusion take priority. Asthma with active bronchospasm, advanced conduction block and symptomatic bradycardia may preclude treatment. In ascites, reduce or suspend therapy for persistent systolic pressure below 90 mmHg, mean arterial pressure below 65 mmHg or HRS-AKI.
Begin vasoactive treatment when variceal bleeding is suspected, before endoscopy. Terlipressin regimens vary by protocol and must be adjusted after haemostasis; monitor sodium, ECG, peripheral circulation, chest symptoms and respiratory status. Avoid or seek senior advice in significant ischaemic cardiovascular disease, hypoxia or severe arrhythmia. Octreotide or somatostatin may be used where available. Continue effective vasoactive therapy for two to five days after control rather than stopping immediately after banding. Drug choice is influenced by availability and contraindications, not by claiming that one agent is universally harmless.
Antibacterial prophylaxis begins at admission and usually continues for a maximum of seven days. Ceftriaxone is commonly used in advanced cirrhosis or high quinolone resistance; local resistance, allergy, renal function and recent infection determine selection. Stop empiric proton-pump inhibitor therapy when endoscopy confirms an isolated variceal source unless another indication exists. Do not use tranexamic acid routinely for gastrointestinal bleeding. Plasma should not be infused solely to normalize INR, and over-transfusion can raise portal pressure. Secondary prophylaxis needs adherence review for both NSBB and repeat EVL; neither component should silently disappear at discharge.
When to Refer
Refer a patient with compensated cirrhosis when non-invasive assessment cannot safely exclude clinically significant portal hypertension, when NSBB treatment is contraindicated or poorly tolerated, or when endoscopy is needed to define high-risk varices. Provide liver-disease cause, Child-Pugh and MELD components, platelet trend, elastography technique, Doppler findings and prior endoscopy reports. Portal-vein thrombosis, splenic-vein thrombosis, isolated gastric varices and suspected non-cirrhotic portal hypertension require specialist imaging because their interventions differ from routine oesophageal-varix prophylaxis.
Every suspected acute bleed belongs in a hospital capable of resuscitation and urgent therapeutic endoscopy. If that capability is absent, start the emergency bundle and arrange time-critical transfer; do not wait for further haematemesis. Alert an interventional-radiology centre early when the patient meets pre-emptive-TIPS criteria, has ongoing bleeding, requires a bridge device or rebleeds soon after EVL. Transfer communication should state onset, haemodynamics, transfusion, vasoactive and antibiotic timing, Child-Pugh variables, endoscopic findings and airway status.
After discharge, gastroenterology must oversee repeat EVL until eradication and subsequent surveillance. Recurrent haemorrhage despite NSBB plus EVL is an indication for TIPS evaluation. Cardiac dysfunction, pulmonary hypertension, uncontrolled infection, severe encephalopathy and advanced liver failure affect candidacy but should prompt expert assessment rather than automatic abandonment. The first variceal bleed is hepatic decompensation in cirrhosis and should initiate liver-transplant consideration. Young patients with extrahepatic portal venous obstruction may instead need specialised shunt or vascular reconstruction advice. Referral pathways must include a named clinician responsible for results and recall.
Red Flags
Fresh haematemesis, melaena with collapse, syncope, hypotension, altered consciousness or escalating oxygen requirement requires emergency action. A normal first haemoglobin does not exclude severe acute loss. Beta blockade may mask tachycardia, and a transient response to fluid does not prove haemostasis. Repeated large crystalloid boluses or transfusion far above a safe haemoglobin target can worsen portal pressure and pulmonary status. If active bleeding prevents airway protection or endoscopy, involve anaesthesia early; routine prophylactic intubation is not risk-free and must be individualized.
Failure of endoscopic control, recurrent haemorrhage within hours, or continuing transfusion need despite apparently successful banding requires urgent TIPS-capable review. A Sengstaken-Blakemore or similar balloon is a temporary bridge only, with continuous skilled monitoring and a definitive plan. Chest pain, subcutaneous emphysema, severe odynophagia or sepsis after endoscopic treatment raises perforation or deep injury. Post-banding ulcers can bleed later and should not be assumed to represent unchanged variceal rupture.
Fever, abdominal pain, renal deterioration or worsening encephalopathy may signal bacterial infection and predicts poor bleeding outcomes. Severe hyponatraemia, oliguria or falling arterial pressure demands medication reconciliation, including NSBBs and diuretics. Terlipressin-associated ischaemia, arrhythmia, cyanosis, chest pain or respiratory deterioration requires urgent review. After TIPS, new encephalopathy, heart failure or marked liver-test deterioration is dangerous. Any discharge without antibiotic-course documentation, secondary prophylaxis, a repeat-EVL appointment and emergency instructions represents a systems red flag even if the index haemorrhage has stopped.
Indian Clinical Context
Cirrhosis-related oesophageal varices coexist in India with a meaningful burden of extrahepatic portal venous obstruction and other non-cirrhotic causes. Age, spleen size, portal-vein anatomy and hepatic synthetic function therefore matter. A young person with recurrent bleeding, massive splenomegaly and near-normal albumin should not automatically receive the label of end-stage cirrhosis. Doppler expertise and contrast imaging can reveal chronic thrombosis, cavernoma or splenic-vein disease and direct the patient toward a vascular or surgical centre. At the same time, hepatitis B, hepatitis C, alcohol and metabolic disease need systematic treatment rather than episodic banding alone.
Access is uneven. Some hospitals can resuscitate but lack night endoscopy, anaesthesia or interventional radiology. Each unit should maintain a written escalation map, stock a protocol-selected vasoactive agent and appropriate antibiotic, and use telephonic specialist advice while transfer proceeds. Blood-product scarcity strengthens the case for disciplined restrictive transfusion, not undertreatment of shock. Antimicrobial choice must reflect Indian hospital resistance patterns; copying a quinolone regimen from an older foreign pathway without an antibiogram is unsafe.
EVL is more widely available than TIPS, which can lead to repeated banding even after genuine failure of combined secondary prophylaxis. Early referral is essential because TIPS requires imaging, cardiac assessment, expertise and financial planning. Patients travelling long distances need bundled appointments and a written next-band date. Explain black stools, vomiting blood, fainting and confusion in the preferred language, and warn against NSAIDs and unsupervised dose changes. International trials underpin much practice, while Indian comparative data on non-invasive thresholds, resistant infections, early TIPS implementation and non-cirrhotic disease are less complete. These evidence limits should be stated rather than filled with local-sounding but unverified numbers.
NMC Competency Mapping
Oesophageal-variceal care maps directly to NMC outcomes on upper gastrointestinal bleeding, cirrhosis, portal hypertension and emergency stabilization. Physiology supplies portal circulation and haemodynamic responses to blood loss; pathology explains cirrhotic resistance and collateral formation. General Medicine Topic 5 includes history and examination for liver disease, interpretation of relevant investigations and principles of managing portal hypertension and liver failure. Surgery and emergency-medicine teaching cover shock recognition, access, blood-product use, airway decisions and urgent referral for endoscopic haemostasis.
Pharmacology outcomes apply to NSBBs, vasoactive agents, antibiotics and their contraindications. Learners should connect mechanism to practice: NSBBs reduce splanchnic inflow, carvedilol also reduces intrahepatic resistance, and vasoactive drugs temporarily reduce portal inflow during an acute bleed. Rational prescribing requires monitoring rather than memorizing a maximal dose. Endoscopy learning includes recognizing oesophageal columns and red signs, distinguishing gastric varices and portal hypertensive gastropathy, and understanding band ligation conceptually. Performing EVL independently is not an undergraduate competency.
A suitable clinical assessment asks the student to prioritize resuscitation, start protocol-directed pre-endoscopic therapy under supervision, identify the need for endoscopy, and describe primary versus secondary prophylaxis. Higher-level decisions—pre-emptive TIPS, rescue devices, portal-vein intervention and transplant selection—belong to specialist teams. Communication should include non-stigmatizing alcohol assessment, consent, rebleeding risk and clear discharge warnings. This clinically focused draft supports learning but does not certify competence, replace local haemorrhage protocols or authorize unsupervised drug administration and endoscopy.
Key Exam Pearls for NEET PG
Oesophageal varices are portosystemic collaterals, usually in the distal oesophagus, caused by portal hypertension. Larger diameter, red wale signs and Child-Pugh C status predict greater first-bleed risk. Patients are often asymptomatic before rupture; dysphagia is not a screening criterion. Endoscopy describes size, red signs, active bleeding and gastric extension. Remember that isolated fundal varices suggest splenic-vein thrombosis, while preserved synthetic function with massive splenomegaly raises non-cirrhotic portal hypertension.
For primary prevention, use an NSBB—often carvedilol in eligible compensated cirrhosis—or EVL for high-risk oesophageal varices when NSBBs are unsuitable. EVL does not lower portal pressure. Do not routinely combine NSBB plus EVL for primary prophylaxis. Acute bleeding management is a bundle: stabilize, use restrictive red-cell transfusion, start vasoactive therapy and antibiotics before endoscopy, then perform endoscopy within twelve hours after resuscitation. EVL is the preferred endoscopic treatment for oesophageal-variceal haemorrhage; cardiofundal gastric varices usually need cyanoacrylate or radiological treatment.
Pre-emptive TIPS within 72 hours, preferably 24, is considered for Child-Pugh C up to 13 points or Child-Pugh B above 7 with active bleeding at endoscopy despite vasoactive treatment. Uncontrolled bleeding needs rescue TIPS; a covered oesophageal stent or balloon tamponade is only a bridge. Secondary prophylaxis combines an NSBB with repeat EVL at one- to four-week intervals until eradication. Avoid routine plasma merely to normalize INR and avoid over-transfusion. A first variceal bleed marks decompensation and should prompt transplant assessment in cirrhosis.
Frequently Asked Questions
Can oesophageal varices cause symptoms before they rupture and bleed?
Usually they cause no specific symptom and are found through portal-hypertension assessment or endoscopy. Dysphagia, reflux or pain should not be used to predict their presence. People with cirrhosis or relevant vascular disease need risk-based screening or preventive NSBB treatment before waiting for haematemesis or melaena.
Is band ligation always better than a non-selective beta blocker for preventing a first bleed?
No. Both can prevent first oesophageal-variceal bleeding in appropriate high-risk disease. An NSBB also treats portal-pressure biology and may prevent decompensation, while EVL is useful when NSBBs are contraindicated or not tolerated. Blood pressure, asthma, renal status, endoscopy access and informed preference determine the pathway.
Why are antibiotics given when acute oesophageal-variceal bleeding is not obviously infected?
Bacterial infection is common around acute bleeding in cirrhosis and increases rebleeding and mortality. Short-course prophylaxis begun at admission improves outcomes. The exact drug should reflect allergy, liver severity, renal function, prior exposure and local resistance; ceftriaxone is often chosen when quinolone resistance is substantial.
What follow-up is needed after endoscopic control of an oesophageal-variceal bleed?
Secondary prevention normally combines an NSBB with repeat EVL every one to four weeks until eradication, followed by surveillance. Rebleeding despite both should prompt TIPS evaluation. The team must also treat the liver-disease cause, monitor decompensation and assess transplantation because banding alone does not correct portal hypertension.
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