Gastrointestinal Bleeding

Gastrointestinal (GI) bleeding is a high-frequency medical emergency divided by an anatomical landmark — the ligament of Treitz (duodenojejunal flexure) — into upper GI bleed (UGIB) above and lower GI bleed (LGIB) below. This note covers presentation, scoring (Glasgow-Blatchford and Rockall), causes, resuscitation, transfusion thresholds, endoscopy timing, and the drug/endoscopic therapy of choice for each.

Definition & classification

GI bleeding is loss of blood from anywhere along the alimentary tract. The proximal/distal split is clinically critical because cause, presentation, work-up, and therapy differ.

Feature	Upper GI bleed (proximal to Treitz)	Lower GI bleed (distal to Treitz)
Frequency	~4-5× commoner than LGIB	Less common, often self-limiting
Typical presentation	Haematemesis, "coffee-ground" vomitus, melaena	Haematochezia (fresh red blood per rectum)
Blood urea	Raised (digested protein load)	Usually normal
BUN/creatinine ratio	High (>30:1 suggests UGIB)	Normal
Diagnostic test of choice	Upper GI endoscopy (OGD)	Colonoscopy
Aspirate via NG tube	Blood/coffee grounds	Clear/bilious

Key terms

• Haematemesis — vomiting of blood (bright red = brisk; coffee-ground = altered by acid).
• Melaena — black, tarry, foul-smelling stool; needs ≥ 50-100 mL of blood and ~14 h transit. Almost always UGIB, but can be from caecum/right colon or small bowel.
• Haematochezia — fresh/maroon blood per rectum; usually LGIB, but a brisk UGIB (~10-15%) can present this way (with haemodynamic instability).
• Occult bleeding — not visible; detected by faecal occult blood/FIT or iron-deficiency anaemia.
• Obscure GI bleeding — bleeding persisting/recurring after negative OGD and colonoscopy; source usually small bowel (angiodysplasia commonest).

High-yield: Melaena needs only 50 mL of blood; black stool persists for days after bleeding stops. A raised urea with normal creatinine strongly favours an upper source — a classic single-best-answer clue.

Etiology

Upper GI bleed — causes (descending order)

Cause	Approx share	Pearl
Peptic ulcer disease	~50% (commonest)	Duodenal > gastric; H. pylori and NSAIDs are the two big drivers
Oesophageal/gastric varices	10-20%	Portal hypertension; highest mortality
Mallory-Weiss tear	5-15%	Mucosal tear at GO junction after retching/vomiting
Erosive gastritis/oesophagitis	~10-15%	NSAIDs, alcohol, stress
Malignancy	~5%	Gastric carcinoma, GIST
Dieulafoy lesion	rare	Large submucosal artery, proximal stomach; recurrent brisk bleed
Angiodysplasia, aortoenteric fistula	rare	Fistula → prior aortic graft; "herald bleed" then exsanguination

High-yield: Peptic ulcer disease is the single commonest cause of UGIB (~50%). Variceal bleed carries the highest mortality and demands a different drug protocol.

Lower GI bleed — causes by age

The dominant cause shifts with age — a favourite exam axis.

Age group	Commonest causes
Children/young adults	Meckel's diverticulum, IBD, juvenile polyps, intussusception, infective colitis
Adults (< 60 y)	Diverticulosis, IBD, infective colitis, haemorrhoids, anal fissure
Elderly (> 60 y)	Diverticulosis (commonest overall in LGIB) and angiodysplasia (angiectasia)

Other causes: ischaemic colitis, colorectal carcinoma/polyps, radiation proctitis, post-polypectomy bleed, NSAID colopathy.

High-yield: Diverticulosis is the commonest cause of significant LGIB overall; angiodysplasia is the commonest cause of obscure/recurrent LGIB and small-bowel bleeding in the elderly. Diverticular bleeds are typically painless and from the right colon (despite diverticula being commoner on the left).

Associations to remember

• Angiodysplasia ↔ aortic stenosis (Heyde syndrome — acquired von Willebrand from sheared vWF multimers) and chronic kidney disease.
• Aortoenteric fistula ↔ previous abdominal aortic aneurysm graft (3rd/4th part of duodenum).

Pathophysiology of variceal bleeding

Cirrhosis → increased intrahepatic resistance + splanchnic vasodilation → portal hypertension → portosystemic collaterals open (gastro-oesophageal junction, rectum, umbilicus). Varices bleed when the hepatic venous pressure gradient (HVPG) > 12 mmHg; risk rises with large varices, red wale signs, and Child-Pugh C disease.

High-yield cut-offs: Normal HVPG = 1-5 mmHg. Varices form > 10 mmHg; bleeding risk appears > 12 mmHg. Lowering HVPG by ≥ 20% (or below 12) with beta-blockers markedly cuts rebleeding.

Clinical features & severity assessment

• Volume assessment first: tachycardia, postural drop, cool peripheries, oliguria, altered sensorium. Loss > 30% blood volume → frank shock.
• Haemoglobin may be normal early (acute loss is isovolaemic); it falls after fluid shift/resuscitation — never reassure based on a single early Hb.
• Stigmata of chronic liver disease (spider naevi, ascites, splenomegaly, caput medusae) point to a variceal source.
• Epigastric pain/NSAID use → peptic ulcer; preceding vomiting then haematemesis → Mallory-Weiss.

Risk scores

Glasgow-Blatchford Score (GBS) — uses only clinical and lab data (urea, Hb, systolic BP, pulse, melaena, syncope, hepatic/cardiac disease). Done before endoscopy to decide who can go home.

High-yield: GBS = 0 (or ≤1) identifies very-low-risk patients suitable for outpatient management — no need for urgent admission/endoscopy. It is the best score for triage.

Rockall Score — predicts rebleeding and mortality.

• Pre-endoscopy (clinical) Rockall: age, shock, comorbidity.
• Full (complete) Rockall: adds endoscopic diagnosis + stigmata of recent haemorrhage. Score 0-2 = low risk.

AIMS65 — Albumin <3, INR >1.5, altered Mental status, Systolic BP <90, age >65 — predicts in-hospital mortality.

Forrest classification (endoscopic appearance of a peptic ulcer → guides rebleed risk & therapy):

Forrest	Appearance	Rebleed risk	Endoscopic therapy?
Ia	Spurting arterial bleed	Very high (~80-90%)	Yes
Ib	Oozing	High	Yes
IIa	Non-bleeding visible vessel	~50%	Yes
IIb	Adherent clot	~25-30%	Consider (remove clot)
IIc	Flat pigmented spot	~10%	No
III	Clean ulcer base	< 5%	No

High-yield: Forrest Ia, Ib, IIa, IIb warrant endoscopic haemostasis; IIc and III do not (low rebleed risk) and can usually be managed with PPI alone.

Diagnosis & investigation of choice

Initial labs: CBC, blood group & cross-match, urea/creatinine & electrolytes, LFTs, coagulation profile (PT/INR), lactate.

Stepwise diagnostic approach:

1. Resuscitate first (ABC) — diagnosis follows stabilisation.
2. Risk-stratify (GBS for triage).
3. Upper GI endoscopy (OGD) = investigation and treatment of choice for UGIB; ideally within 24 h of presentation.
4. If OGD is negative and bleeding continues → colonoscopy (for suspected LGIB) or CT angiography.
5. Colonoscopy = test of choice for LGIB (both diagnostic and therapeutic) after bowel prep, usually within 24 h in significant bleeds.
6. CT angiography detects active bleeding at rates ≥ 0.3-0.5 mL/min; rapid, non-invasive, localises before catheter angiography.
7. Catheter (mesenteric) angiography — needs ≥ 0.5-1 mL/min; allows therapeutic embolisation.
8. Tagged RBC (Tc-99m) scan — most sensitive, detects slow bleeds ≥ 0.1-0.2 mL/min, but poor localisation.
9. Capsule endoscopy / push or double-balloon enteroscopy — for obscure/small-bowel bleeding after negative OGD and colonoscopy.
10. Meckel's scan (Tc-99m pertechnetate) — for suspected Meckel's in young patients (detects ectopic gastric mucosa).

High-yield (sensitivity ladder): Tagged RBC scan (0.1 mL/min) > CT angiography (0.3-0.5) > catheter angiography (0.5-1). Most sensitive = RBC scan; best for therapy = angiography.

Management

Resuscitation (applies to both UGIB and LGIB)

Stepwise: Secure airway (protect from aspiration in massive haematemesis) → two large-bore (16-18 G) IV cannulae → crystalloid bolus → cross-match & transfuse → correct coagulopathy → definitive endoscopy.

Transfusion thresholds (restrictive strategy):

Situation	Transfuse packed RBCs to keep Hb
Haemodynamically stable, no cardiac disease	Threshold Hb < 7 g/dL, target 7-9 g/dL
Acute coronary syndrome / unstable cardiac	Threshold Hb < 8 g/dL

High-yield: A restrictive transfusion strategy (threshold 7 g/dL) improves survival in acute UGIB compared with liberal transfusion (Villanueva NEJM 2013) — over-transfusion worsens variceal rebleeding by raising portal pressure. Target platelets > 50,000 and reverse warfarin/correct INR; do not delay endoscopy for minor coagulopathy.

Drug of choice

Non-variceal (peptic ulcer) UGIB:

• Proton pump inhibitor (PPI) — high-dose IV (e.g. pantoprazole/esomeprazole 80 mg bolus then 8 mg/h infusion, or high-dose intermittent). Raises gastric pH, stabilises clot. Continue after endoscopic therapy for Forrest Ia-IIb ulcers.
• Prokinetics (IV erythromycin/metoclopramide) ~30-60 min before OGD improves gastric visualisation.

Variceal UGIB (different protocol):

• Vasoactive drug of choice — terlipressin (splanchnic vasoconstrictor; only agent shown to improve survival). Alternatives: octreotide/somatostatin.
• Antibiotic prophylaxis is mandatory — IV ceftriaxone (or norfloxacin) for up to 7 days; reduces infection, rebleeding and mortality.
• Endoscopic band ligation (EVL) = therapy of choice for oesophageal varices (superior to sclerotherapy).
• Gastric (fundal) varices → cyanoacrylate (glue) injection.

Endoscopic therapy

• Peptic ulcer: combination therapy — adrenaline (1:10,000) injection PLUS a second modality (thermal coagulation/heater probe, or mechanical clips). Adrenaline alone is inadequate (high rebleed); always add a second method.
• Varices: band ligation; glue for gastric varices.
• Mallory-Weiss tear: usually self-limiting (~90%); endoscopic clipping/adrenaline if active.

Escalation when endoscopy fails

• Recurrent peptic ulcer bleed → repeat endoscopy → angiographic embolisation → surgery (under-running the vessel) as last resort.
• Refractory variceal bleed → balloon tamponade (Sengstaken-Blakemore tube) as a temporary bridge (≤ 24 h; aspiration risk) → TIPS (transjugular intrahepatic portosystemic shunt) = definitive rescue.

High-yield: TIPS is the rescue for uncontrolled/recurrent variceal bleeding. The major complication of TIPS is worsening hepatic encephalopathy (blood bypasses hepatic detoxification).

Secondary prevention

• Peptic ulcer: eradicate H. pylori (triple therapy), stop NSAIDs, maintenance PPI.
• Varices: non-selective beta-blocker (propranolol/carvedilol) + repeat band ligation programme until obliteration.

LGIB-specific management

• Most diverticular and angiodysplastic bleeds stop spontaneously (~80%).
• Colonoscopic haemostasis (clips, thermal, adrenaline) for active diverticular/angiodysplastic bleeding.
• Ongoing brisk bleed → CT angiography → catheter embolisation; surgery (segmental or subtotal colectomy) if all fail.

Complications

• Hypovolaemic shock, acute kidney injury, myocardial ischaemia.
• Aspiration pneumonia (massive haematemesis, encephalopathy).
• In cirrhotics: hepatic encephalopathy precipitated by blood in the gut (nitrogen load), spontaneous bacterial peritonitis, hepatorenal syndrome.
• Rebleeding (the key prognostic event — drives most mortality).
• Transfusion-related complications and dilutional coagulopathy in massive transfusion.

Key differentials

• Haemoptysis vs haematemesis — haemoptysis is frothy, bright red, alkaline pH, mixed with sputum, follows coughing; haematemesis is acidic, may contain food, follows vomiting.
• Pseudo-melaena — iron, bismuth, liquorice, beetroot, spinach can darken stool without bleeding; occult blood test negative.
• Swallowed blood — epistaxis or haemoptysis swallowed then vomited/passed as melaena.
• Brisk UGIB presenting as haematochezia — always suspect when haematochezia + haemodynamic instability + raised urea; do OGD first.

Recently asked / exam angle

• Commonest cause of UGIB = peptic ulcer disease (~50%) — recurring single-best-answer.
• Drug of choice in variceal bleed = terlipressin; antibiotic prophylaxis (ceftriaxone) is mandatory in cirrhotic GI bleed.
• Restrictive transfusion threshold = Hb 7 g/dL (8 in cardiac disease) — frequently tested NEJM-based fact.
• Glasgow-Blatchford score 0 → safe outpatient management; Rockall predicts rebleeding/mortality.
• Forrest classification — match the picture to rebleed risk and decide need for endoscopic therapy (Ia-IIb treat; IIc/III don't).
• Most sensitive test for slow obscure bleed = tagged RBC scan; CT/catheter angiography need faster bleeding but allow embolisation.
• Heyde syndrome = aortic stenosis + angiodysplasia + acquired von Willebrand disease.
• Commonest cause of massive LGIB = diverticulosis; obscure/small-bowel = angiodysplasia; young child = Meckel's diverticulum (rule of 2s, Meckel scan).
• TIPS rescue → complication is encephalopathy; Sengstaken-Blakemore tube is only a bridge.
• Adrenaline injection alone is insufficient — always add a second endoscopic modality.
• Endoscopy timing: within 24 h for UGIB (within 12 h if unstable variceal bleed after resuscitation).

Mnemonics

• UGIB causes — "VOMITED": Varices, Oesophagitis, Mallory-Weiss, Inflammation/erosions, Tumour, Erosive gastritis, Duodenal/peptic ulcer.
• Meckel's rule of 2s: 2% population, 2 feet from ileocaecal valve, 2 inches long, 2 types of ectopic mucosa (gastric/pancreatic), presents < 2 years, 2:1 male.

Rapid revision

1. Ligament of Treitz divides upper (above) from lower (below) GI bleed.
2. Melaena needs only ~50 mL blood; raised urea with normal creatinine = upper source.
3. Peptic ulcer = commonest cause of UGIB (~50%); H. pylori + NSAIDs are the drivers.
4. Variceal bleed = highest mortality; drug of choice terlipressin + mandatory ceftriaxone.
5. Transfuse at Hb < 7 g/dL (restrictive); < 8 in cardiac disease — over-transfusion worsens variceal bleed.
6. Glasgow-Blatchford = 0 → outpatient; Rockall → rebleed/mortality prediction.
7. Forrest Ia-IIb ulcers need endoscopic therapy; IIc/III do not.
8. Peptic ulcer endoscopy = adrenaline plus a second modality (clip/thermal); never adrenaline alone.
9. OGD = test of choice for UGIB, ideally within 24 h after resuscitation.
10. Diverticulosis = commonest massive LGIB; angiodysplasia = obscure/elderly small-bowel bleed; Meckel's in children.
11. Sensitivity ladder: tagged RBC scan (0.1) > CT angiography (0.3-0.5) > catheter angiography (0.5-1 mL/min).
12. TIPS rescues refractory variceal bleed; main complication = hepatic encephalopathy; Sengstaken-Blakemore tube is only a temporary bridge.