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    Study MaterialMedicineUpper GI Bleed Management for NEET PG — Complete Guide 2026
    10 February 2026
    medicine
    gastroenterology
    neet pg 2026

    Upper GI Bleed Management for NEET PG — Complete Guide 2026

    Master upper GI bleed for NEET PG 2026: variceal vs non-variceal causes, Glasgow-Blatchford and Rockall scoring, Forrest classification, endoscopic therapy, TIPS indications, octreotide, PPI, and H. pylori eradication.

    NEETPGAI EditorialPublished 10 Feb 202618 min read
    Upper GI Bleed Management for NEET PG — Complete Guide 2026
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    This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.

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    NEET PG 2026 Myth Busters: 18 Common Prep Misconceptions Debunked with Evidence

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    Version 1.0 — Published February 2026

    Quick Answer

    Upper GI bleed contributes 2–3 NEET PG questions per paper. Master these 10 high-yield anchors:

    1. Definition — bleeding proximal to ligament of Treitz; hematemesis, coffee-ground vomitus, melena (upper), occasionally hematochezia if brisk
    2. Causes — non-variceal: peptic ulcer (most common, ~50%), Mallory-Weiss, erosive gastritis/esophagitis, malignancy, Dieulafoy, angiodysplasia; variceal: esophageal > gastric varices (cirrhosis)
    3. Resuscitation — 2 large-bore IVs, crystalloid, restrictive transfusion Hb 7–9 g/dL (Villanueva NEJM 2013), type and cross-match, NPO, HDU monitoring
    4. Pharmacology — IV PPI (pantoprazole 80 mg bolus → 8 mg/h) for suspected non-variceal; IV octreotide/terlipressin + ceftriaxone for suspected variceal, started before endoscopy
    5. Risk stratification — Glasgow-Blatchford (pre-endoscopy; 0 = outpatient) and Rockall (clinical + post-endoscopy)
    6. Endoscopy timing — within 24 h non-variceal; within 12 h variceal or unstable
    7. Forrest classification — Ia spurting, Ib oozing, IIa visible vessel, IIb adherent clot (all high-risk → endoscopic therapy + IV PPI); IIc pigmented spot, III clean base (low-risk)
    8. Endoscopic therapy — combination (injection + thermal or clip) for non-variceal; band ligation preferred for esophageal varices; cyanoacrylate glue for gastric varices
    9. TIPS — rescue after failed EBL; early TIPS within 72 h for Child B active-bleeding or Child C (Baveno VII)
    10. Secondary prevention — H. pylori test-and-treat (bismuth quadruple first-line in India), stop NSAIDs, beta-blocker ± EBL for variceal

    Upper GI bleed is a common NEET PG vignette — the alcoholic with hematemesis, the elderly patient on NSAIDs with melena, the cirrhotic with massive variceal bleed — and the correct first move (octreotide vs PPI, EBL vs clip, FFP vs platelets) separates marks. This guide covers initial resuscitation, risk scoring, endoscopic therapy, TIPS decision-making, and H. pylori eradication. Pair with the medicine subject hub, the medicine high-yield topics overview, and the COPD exacerbation clinical case for critical-care integration.

    Definition and epidemiology

    Upper GI bleed (UGIB) is bleeding originating proximal to the ligament of Treitz — from the esophagus, stomach, or duodenum — presenting with hematemesis, coffee-ground vomitus, melena, or (if brisk) hematochezia.

    Epidemiology (Indian and global):

    • Incidence: 50–150 per 100,000 adults per year
    • Male-to-female ratio 2:1
    • Peptic ulcer disease remains the single most common cause globally (~50%)
    • Variceal bleed accounts for ~10–30% in centres caring for cirrhosis-heavy populations (high in India due to alcohol and chronic hepatitis B/C)
    • Mortality: 2–10% non-variceal; up to 20–30% variceal
    • NSAID use, H. pylori, alcohol, and cirrhosis are the dominant risk factors

    Clinical presentation:

    • Hematemesis — fresh blood (brisk, usually proximal) or coffee-ground vomitus (oxidised haem, slower bleed)
    • Melena — black, tarry, foul-smelling stool; requires ~50–100 mL blood in stomach for >=4 h
    • Hematochezia — bright red rectal blood; in UGIB implies brisk bleed (>1000 mL) or rapid transit
    • Haemodynamic features — tachycardia (early), hypotension, syncope, shock
    • Chronic bleed — iron-deficiency anaemia, fatigue, occult melena

    Causes — variceal vs non-variceal

    Upper GI bleed causes split into two decision-changing buckets: non-variceal (most common) and variceal (cirrhosis-related) — because initial pharmacological therapy differs.

    Non-variceal causes:

    CauseFrequencyKey features
    Peptic ulcer disease~50%Duodenal > gastric; NSAIDs, H. pylori, steroids, stress
    Erosive gastritis / esophagitis10–15%Alcohol, NSAIDs, stress (ICU — Curling, Cushing)
    Mallory-Weiss tear5–15%Retching/vomiting; alcoholic, bulimia, hyperemesis gravidarum
    Gastric / esophageal malignancy3–5%Weight loss, dysphagia, anaemia; biopsy at index endoscopy
    Dieulafoy lesion1–2%Aberrant submucosal artery; proximal stomach; massive bleed with normal-looking mucosa
    Angiodysplasia (AVM)1–2%Older adults, CKD, aortic stenosis (Heyde syndrome)
    Aorto-enteric fistulaRarePrior AAA repair; "herald bleed" then exsanguination
    Hemobilia / hemosuccus pancreaticusRarePost-ERCP, hepatobiliary trauma, pseudoaneurysm

    Variceal causes:

    • Esophageal varices — most common variceal source; portal hypertension from cirrhosis
    • Gastric varices — Sarin classification (GOV1, GOV2, IGV1, IGV2); IGV1 carries the highest rebleeding risk
    • Portal hypertensive gastropathy — diffuse mucosal mosaic/cherry-red spots; chronic oozing bleed

    Peptic ulcer disease — a closer look:

    • Duodenal ulcer — posterior wall bulb most common (gastroduodenal artery — classic "spurter"); hunger pain, relieved by food
    • Gastric ulcer — lesser curvature (left gastric artery); pain worse with food; always biopsy to exclude malignancy
    • Risk factors: H. pylori (70–90% duodenal, 70% gastric), NSAIDs, smoking, steroids, physiological stress
    • Zollinger-Ellison syndrome — multiple/refractory/atypical ulcers, diarrhea, elevated fasting gastrin >1000 pg/mL with low gastric pH

    Initial resuscitation and empirical drug therapy

    Initial management of upper GI bleed prioritises airway, fluid resuscitation, transfusion, and early empirical pharmacotherapy — before endoscopy confirms the source.

    Step-by-step resuscitation:

    1. Airway — intubate if altered sensorium, massive hematemesis with aspiration risk, or active variceal bleed with anticipated EUGD
    2. Breathing — supplemental O2; monitor SpO2
    3. Circulation — two large-bore IVs (16–18 G); crystalloid bolus 500–1000 mL; recheck
    4. Labs — CBC, urea, creatinine, LFT, coagulation, type and cross-match 2–4 units PRBC, ABG, lactate
    5. NPO, nasogastric tube (NOT contraindicated in varices as once taught — may clear stomach for endoscopy)
    6. Monitoring — HDU / ICU, continuous ECG, SpO2, urine output, mental status

    Transfusion strategy (key NEET PG point):

    • Restrictive: target Hb 7–9 g/dL (Villanueva et al., NEJM 2013 — showed better 6-week survival and lower rebleeding than liberal)
    • Exceptions: ongoing massive bleed, ischemic heart disease, severe haemodynamic instability — target higher
    • Platelets if <50 × 10^9/L with active bleed
    • FFP if INR >1.5 (in cirrhosis, routine FFP correction is no longer recommended)
    • Prothrombin complex concentrate (PCC) in warfarin-associated bleed with life-threatening haemorrhage

    Empirical pharmacotherapy:

    DrugSuspected non-varicealSuspected variceal
    IV PPIPantoprazole 80 mg bolus → 8 mg/h infusion × 72 hAlso started (suspect dual pathology)
    IV octreotideNot indicated50 mcg bolus → 50 mcg/h × 3–5 d
    IV terlipressinNot indicated2 mg every 4 h × 48 h → 1 mg every 4 h × 3 d (only vasoactive drug with mortality benefit)
    Prophylactic antibioticNot routineCeftriaxone 1 g IV daily × 5–7 d (reduces SBP, mortality)
    ProkineticOptional (erythromycin 250 mg IV 30–90 min pre-EGD) clears stomachSame
    Vitamin KIf warfarin / INR elevationIf INR elevated in cirrhosis

    In cirrhotic patients with suspected variceal bleed, start octreotide and ceftriaxone BEFORE endoscopy. Do not wait.

    IV PPI rationale (non-variceal):

    • Sustained gastric pH >6 stabilises clot
    • High-dose IV PPI before endoscopy downstages lesions and reduces need for endoscopic therapy (Lau NEJM 2007)
    • Post-endoscopy in high-risk ulcers (Forrest Ia-IIb), continue infusion × 72 h then oral

    Risk stratification — Glasgow-Blatchford and Rockall

    Risk stratification triages patients to outpatient management, ward admission, or HDU — and predicts rebleeding and mortality.

    Glasgow-Blatchford score (GBS) — pre-endoscopy:

    VariableValues and points
    Blood urea (mmol/L)6.5–8.0: 2; 8.0–10.0: 3; 10.0–25.0: 4; >=25: 6
    Hemoglobin — men (g/dL)12.0–12.9: 1; 10.0–11.9: 3; <10: 6
    Hemoglobin — women (g/dL)10.0–11.9: 1; <10: 6
    Systolic BP (mmHg)100–109: 1; 90–99: 2; <90: 3
    Pulse >=1001
    Melena1
    Syncope2
    Hepatic disease2
    Cardiac failure2
    • Score 0 → outpatient management possible (NICE 2012)
    • Score >=1 → admit and endoscopy
    • Validated for early discharge of low-risk patients (Stanley Lancet 2009)

    Clinical (pre-endoscopy) Rockall score — 0–7:

    Variable0123
    Age<6060–79>=80—
    ShockNoneHR >=100, SBP >=100SBP <100—
    ComorbidityNone—CHF, IHDRenal/hepatic failure, malignancy

    Complete (post-endoscopy) Rockall score — 0–11: adds diagnosis (0 Mallory-Weiss / no lesion → 2 malignancy) and stigmata (0 clean base → 2 spurting / visible vessel / adherent clot).

    • Total <=2 → low risk, <5% rebleed, <1% mortality
    • Total >=8 → >40% mortality

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    Endoscopy timing and endoscopic therapies

    Endoscopy is the diagnostic and therapeutic cornerstone of upper GI bleed — timing depends on variceal suspicion and haemodynamic stability.

    Timing:

    • Within 24 h: all non-variceal UGIB after resuscitation
    • Within 12 h: suspected variceal bleed, ongoing active bleed, haemodynamic instability, cirrhosis with decompensation
    • Urgent (<6 h): not routinely superior unless exsanguinating
    • Endoscopy too early (<6 h) in stable patients does NOT improve outcomes (Lau NEJM 2020)

    Endoscopic therapies — non-variceal peptic ulcer:

    ModalityMechanismNotes
    InjectionAdrenaline 1:10,000 in 4 quadrants; tamponade + vasoconstrictionNever alone — must combine with 2nd modality
    ThermalBipolar coagulation, heater probe, argon plasma coagulationCoagulates vessel
    Mechanical (clip)Hemoclip (TriClip, Resolution) or over-the-scope clip (OTSC)Best for visible vessel, large ulcers
    Hemostatic powderTC-325 (Hemospray)Rescue / diffuse bleed

    Combination (injection + thermal/clip) is superior to injection alone — reduces rebleeding.

    Endoscopic therapies — variceal:

    ModalityIndicationNotes
    Endoscopic band ligation (EBL)Esophageal varices (primary and secondary prophylaxis, acute bleed)Preferred over sclerotherapy; lower rebleed and complications
    Endoscopic sclerotherapyAcute esophageal varices when EBL unavailableAgents: ethanolamine oleate, sodium tetradecyl sulphate; complications include ulcer, stricture, perforation
    Cyanoacrylate glue (N-butyl-cyanoacrylate)Gastric varices (IGV1, GOV2)Polymerises on contact with blood
    Sengstaken-Blakemore tubeRescue bridge in uncontrolled variceal bleed24 h max; complications — aspiration, esophageal necrosis; inflate gastric balloon first, then esophageal at 30–45 mmHg
    Self-expanding metallic stent (Danis stent)Rescue bridge, better than balloon tamponadeUp to 7 d

    Forrest classification and rebleeding prediction

    Forrest classification describes endoscopic appearance of a peptic ulcer and predicts 30-day rebleeding risk — it guides endoscopic therapy and duration of PPI infusion.

    Forrest classDescriptionRebleed riskManagement
    IaSpurting arterial bleed~55%Endoscopic therapy + IV PPI × 72 h
    IbOozing bleed~55%Endoscopic therapy + IV PPI × 72 h
    IIaNon-bleeding visible vessel (NBVV)~43%Endoscopic therapy + IV PPI × 72 h
    IIbAdherent clot~22%Clot removal and assess; therapy if stigmata; IV PPI × 72 h
    IIcFlat pigmented spot~10%No therapy; oral PPI; early feeding
    IIIClean ulcer base<5%No therapy; oral PPI; discharge

    Forrest I–IIb = high-risk → endoscopic therapy + admission + IV PPI 72 h. Forrest IIc–III = low-risk → oral PPI, early refeeding, consider early discharge.

    Post-endoscopy disposition:

    • High-risk → HDU 24 h; clear fluids after 6 h; step down to oral PPI after 72 h
    • Low-risk (Forrest III + Rockall <=2 + GBS 0–1) → discharge-ready
    • Rebleed (recurrent hematemesis, drop in Hb >=2 g/dL, haemodynamic instability) → repeat endoscopy; if fails → interventional radiology embolisation or surgery (oversewing, pyloroplasty)

    TIPS and secondary prevention of variceal bleed

    TIPS (Transjugular Intrahepatic Portosystemic Shunt) reduces portal pressure by creating a communication between a hepatic vein and a portal vein branch through a stent — it is used as rescue after failed EBL and as early pre-emptive therapy in high-risk variceal bleed.

    TIPS indications (Baveno VII 2022):

    • Rescue TIPS — failure to control bleed despite optimal EBL + vasoactive drugs (persistent bleed at 24 h or rebleed within 5 days)
    • Pre-emptive (early) TIPS within 72 h — high-risk variceal bleed: Child-Pugh C (10–13) OR Child-Pugh B with active bleeding on endoscopy
    • Refractory ascites (not responding to diuretics + paracentesis)
    • Hepatic hydrothorax refractory to medical management

    TIPS contraindications:

    • Absolute: right heart failure, severe pulmonary hypertension, polycystic liver disease, biliary obstruction
    • Relative: Child-Pugh >13 with MELD >30 (no survival benefit), severe hepatic encephalopathy, hepatocellular carcinoma in TIPS track

    Complications: hepatic encephalopathy (25–35%), shunt dysfunction (stenosis, thrombosis — reduced with PTFE-covered stents), haemolysis.

    Secondary prophylaxis after variceal bleed:

    ComponentDetail
    Non-selective beta-blocker (NSBB)Propranolol titrated to max tolerated dose or HR 55–60; or carvedilol 6.25–12.5 mg/day (preferred — added alpha-1 effect); nadolol alternative
    Endoscopic band ligationEvery 2–4 weeks until obliteration, then surveillance
    CombinationNSBB + EBL superior to either alone for secondary prophylaxis
    TIPSRefractory rebleed despite NSBB + EBL
    Liver transplantationDecompensated cirrhosis, MELD >=15

    Primary prophylaxis (no prior bleed, varices on screening endoscopy):

    • Small varices (<5 mm) with red wale signs OR Child C → NSBB
    • Medium/large varices (>5 mm) → NSBB OR EBL (equivalent; NSBB preferred for lower cost/availability)
    • Carvedilol preferred NSBB — also effective in compensated cirrhosis with clinically significant portal hypertension (HVPG >=10)

    H. pylori eradication for PUD

    H. pylori is the primary reversible cause of peptic ulcer disease — eradication after a bleeding ulcer reduces 1-year recurrence from 20–40% to <5%.

    Testing:

    • Rapid urease test / histology / culture at index endoscopy (PPI must be stopped 2 weeks prior for accuracy — in acute bleed, test even on PPI and confirm later with UBT)
    • Urea breath test (UBT) and stool antigen test (SAT) are non-invasive — best for confirming eradication ≥4 weeks after therapy and ≥2 weeks off PPI
    • Serology has poor specificity (can't distinguish active from past infection); not used for diagnosis or eradication confirmation

    First-line regimens (14 days):

    RegimenCompositionUse
    Bismuth quadruplePPI BD + bismuth subsalicylate 525 mg QID + tetracycline 500 mg QID + metronidazole 500 mg TIDPreferred in India (high clarithromycin resistance)
    ConcomitantPPI BD + amoxicillin 1 g BD + clarithromycin 500 mg BD + metronidazole 500 mg BDAlternative
    Clarithromycin triplePPI BD + amoxicillin 1 g BD + clarithromycin 500 mg BDOnly if clarithromycin resistance <15% locally — uncommon in India

    Post-bleed specifics:

    • Start eradication regimen once oral intake tolerated
    • Continue PPI × 4–8 weeks beyond eradication to heal ulcer
    • Confirm eradication 4 weeks after regimen and 2 weeks off PPI (UBT or SAT)
    • Discontinue NSAIDs permanently if possible; if needed, add maintenance PPI and/or switch to COX-2 selective (celecoxib)

    Special situations:

    • Gastric ulcer — always repeat endoscopy at 8–12 weeks to confirm healing and exclude malignancy
    • NSAID-associated ulcer — stop NSAID; H. pylori test-and-treat; PPI continued
    • Refractory ulcer (unhealed at 12 weeks) — compliance, persistent H. pylori, occult NSAID use, Zollinger-Ellison, malignancy

    Sources and references

    1. Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo, Fauci, Kasper, Hauser, Longo, Jameson, Eds., 2022) — Chapter on Gastrointestinal Bleeding.
    2. Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th Edition (Feldman, Friedman, Brandt, Eds., 2020) — Chapters on upper GI bleeding and portal hypertension.
    3. Laine L, Barkun AN, Saltzman JR, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021; 116:899-917.
    4. de Franchis R et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022; 76:959-974.
    5. Villanueva C et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013; 368:11-21.
    6. Lau JYW et al. Omeprazole before endoscopy in patients with gastrointestinal bleeding. N Engl J Med 2007; 356:1631-1640.

    Frequently asked questions

    How many upper GI bleed questions appear in NEET PG?

    Upper GI bleed and its management contribute 2-3 direct questions per NEET PG paper across medicine, gastroenterology and surgery papers. The most tested subtopics are Forrest classification, Glasgow-Blatchford score cutoffs, variceal vs non-variceal initial management, TIPS indications, and Mallory-Weiss tear features based on 2019-2025 pattern analysis.

    What is the initial resuscitation for upper GI bleed?

    Initial resuscitation follows the ABC approach. Two large-bore IV cannulae (16-18 G), crystalloid bolus (1 L Ringer lactate), type and cross-match 2 units PRBC, target hemoglobin 7-9 g/dL (restrictive transfusion — Villanueva NEJM 2013). Start IV PPI (pantoprazole 80 mg bolus then 8 mg/h infusion) in suspected non-variceal; add IV octreotide 50 mcg bolus then 50 mcg/h or terlipressin 2 mg every 4 h plus prophylactic ceftriaxone 1 g in suspected variceal bleed. NPO, monitor in HDU. Urgent endoscopy within 24 h (within 12 h for variceal).

    What is the Forrest classification?

    Forrest classification describes endoscopic appearance of peptic ulcers and predicts rebleeding risk. Forrest Ia active spurting bleed — 55 percent rebleed, high mortality. Forrest Ib active oozing — 55 percent rebleed. Forrest IIa non-bleeding visible vessel — 43 percent rebleed. Forrest IIb adherent clot — 22 percent rebleed. Forrest IIc flat pigmented spot — 10 percent rebleed. Forrest III clean ulcer base — less than 5 percent rebleed. Forrest Ia, Ib, IIa, IIb are high risk and require endoscopic therapy plus IV PPI; Forrest IIc and III are low risk and discharge-ready.

    What is the Glasgow-Blatchford score?

    Glasgow-Blatchford score (GBS) is a pre-endoscopy risk score using blood urea, hemoglobin, systolic BP, heart rate, melena, syncope, hepatic disease, cardiac failure. Score 0 identifies very low-risk patients eligible for outpatient management. Score greater than or equal to 1 typically warrants admission and endoscopy. Unlike Rockall, it does NOT require endoscopy findings. Validated in NEJM 2000 (Blatchford) and now preferred over clinical Rockall for triage.

    What is the Rockall score?

    Rockall score has two versions. Clinical (pre-endoscopy) Rockall uses age, shock (HR, SBP), comorbidity — score 0-7. Complete (post-endoscopy) Rockall adds diagnosis and stigmata of recent hemorrhage — score 0-11. Score less than or equal to 2 is low-risk (less than 5 percent rebleed, less than 1 percent mortality). Score greater than or equal to 8 is high-risk (more than 40 percent mortality). Guides decisions on admission level, endoscopy timing, and discharge.

    When is TIPS indicated in variceal bleed?

    TIPS (Transjugular Intrahepatic Portosystemic Shunt) is indicated as rescue therapy when endoscopic band ligation fails to control variceal bleed, or for refractory/recurrent bleed. Baveno VII consensus recommends early (pre-emptive) TIPS within 72 h in high-risk variceal bleed (Child-Pugh B with active bleeding on endoscopy, or Child-Pugh C up to 13). Contraindications include Child-Pugh greater than 13 with MELD greater than 30 (no survival benefit), severe hepatic encephalopathy, heart failure, pulmonary hypertension. Child-Turcotte-Pugh C with MELD greater than or equal to 19 may still benefit from TIPS as a bridge to transplant.

    What is the role of octreotide in variceal bleed?

    Octreotide is a somatostatin analogue that reduces splanchnic blood flow and portal pressure. Dose is 50 mcg IV bolus followed by 50 mcg/h infusion for 3-5 days. Equally effective as terlipressin and vasopressin plus nitroglycerin but better safety profile. Start as soon as variceal bleed is suspected — before endoscopic diagnosis. Reduces rebleeding but modest mortality benefit. Terlipressin is the only vasoactive drug shown to reduce mortality in variceal bleed (meta-analysis) and is preferred where available.

    How is H. pylori treated after a bleeding peptic ulcer?

    H. pylori eradication after a bleeding peptic ulcer reduces recurrence from 20-40 percent at 1 year to less than 5 percent. Standard triple therapy is PPI plus clarithromycin 500 mg BD plus amoxicillin 1 g BD for 14 days (avoid in areas with clarithromycin resistance greater than 15 percent). Bismuth-based quadruple therapy (PPI plus bismuth plus tetracycline plus metronidazole for 14 days) is preferred first-line in India given high clarithromycin resistance. Test for eradication with urea breath test or stool antigen at least 4 weeks after therapy completion.

    What is the difference between variceal and non-variceal bleed management?

    Variceal bleed requires IV octreotide/terlipressin plus prophylactic ceftriaxone plus endoscopic band ligation (EBL, preferred over sclerotherapy) within 12 h. Beta-blocker (propranolol/carvedilol/nadolol) is started after bleed control for secondary prophylaxis. Non-variceal bleed (usually PUD) requires high-dose IV PPI plus endoscopic therapy (injection plus thermal/clip — combination is superior to single modality) within 24 h. Test and treat H. pylori. Discontinue NSAIDs. Restrictive transfusion strategy (Hb 7-9 g/dL) applies to both.

    What is the Mallory-Weiss tear?

    Mallory-Weiss tear is a longitudinal mucosal laceration at the gastroesophageal junction caused by forceful retching or vomiting. Classic history is repeated vomiting followed by hematemesis in an alcoholic or pregnant patient with hyperemesis gravidarum. Most heal spontaneously within 48-72 h with conservative management (PPI, antiemetics). Endoscopic therapy (injection, clip, band) is indicated for active bleeding. Boerhaave syndrome is the feared differential — full-thickness esophageal rupture with pneumomediastinum and surgical emergency.

    Want more high-yield medicine revision? Revise the medicine high-yield topics overview, walk through the COPD exacerbation clinical case, and use the AI tutor to drill variceal vs non-variceal decision points on demand.

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    This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.


    Written by: NEETPGAI Editorial Team Reviewed by: Pending SME Review Last reviewed: February 2026

    This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.