Gastrointestinal Haemorrhage

Gastrointestinal (GI) bleeding is a common surgical and medical emergency, classically divided by the ligament of Treitz into upper (UGIB, proximal to it) and lower (LGIB, distal to it) sources. This topic bridges medicine and surgery and is heavily tested for resuscitation priorities, risk scores, the variceal-vs-non-variceal split, and the endoscopic/surgical decision tree.

Definition & Anatomical Classification

The ligament of Treitz (suspensory muscle of the duodenum, at the duodeno-jejunal flexure) is the anatomical landmark separating upper from lower GI tract.

Type	Source	Hallmark presentation
Upper GI bleed (UGIB)	Proximal to ligament of Treitz (oesophagus, stomach, duodenum)	Haematemesis, coffee-ground vomitus, melaena
Lower GI bleed (LGIB)	Distal to ligament of Treitz (jejunum → anus)	Haematochezia (fresh red blood per rectum), maroon stools
Mid-GI / obscure bleed	Ampulla of Vater to ileocaecal valve (small bowel)	Recurrent bleed with negative OGD + colonoscopy

A newer functional classification uses endoscopic accessibility: upper (reachable by gastroscope), mid (small bowel, needs capsule/enteroscopy), and lower (reachable by colonoscope).

High-yield: UGIB is roughly 4–5 times more common than LGIB. Melaena needs only ~50–100 mL of blood and ~14 hours in the gut to form; black tarry stool implies a source proximal to (or at) the right colon, usually upper GI.

Terminology to nail:

• Haematemesis – vomiting fresh/altered blood → always UGIB.
• Coffee-ground vomitus – blood altered by gastric acid → UGIB, slower/stopped bleed.
• Melaena – black, tarry, foul stool from haemoglobin → globin degradation by gut bacteria → usually UGIB (occasionally right colon/small bowel).
• Haematochezia – bright red blood per rectum → usually LGIB; but a brisk UGIB (~10–15% of haematochezia) can present this way with haemodynamic instability.

Etiology

Upper GI bleed causes

Cause	Notes / NEET pearls
Peptic ulcer disease	Most common overall cause of UGIB (~50%). Duodenal (posterior wall) ulcer eroding gastroduodenal artery = classic massive bleed.
Oesophageal/gastric varices	Portal hypertension; highest mortality per bleed
Mallory–Weiss tear	Mucosal tear at GE junction after retching/vomiting; often self-limiting
Erosive gastritis / oesophagitis	NSAIDs, alcohol, stress
Dieulafoy lesion	Abnormally large submucosal artery, usually lesser curve of stomach; recurrent obscure massive bleed
Gastric/oesophageal malignancy	Older patient, weight loss
Aorto-enteric fistula	Prior aortic graft; "herald bleed" then exsanguination — classic exam trap
Angiodysplasia, GAVE (watermelon stomach)	GAVE associated with cirrhosis & scleroderma

Lower GI bleed causes

Cause	NEET pearls
Diverticulosis	Most common cause of major LGIB in adults; painless, often right-sided diverticula bleed more
Angiodysplasia	Right colon/caecum; associated with aortic stenosis (Heyde syndrome — acquired von Willebrand deficiency) and ESRD
Haemorrhoids / anal fissure	Most common cause of minor bright bleeding (blood coating stool / on paper)
Colorectal carcinoma & polyps	Painless, iron-deficiency anaemia, change in bowel habit
Inflammatory bowel disease	Bloody diarrhoea, especially ulcerative colitis
Ischaemic colitis	Watershed (splenic flexure), elderly, "thumbprinting"
Meckel diverticulum	Commonest cause of significant LGIB in children; ectopic gastric mucosa
Infective colitis, post-polypectomy bleed, radiation proctitis	Context-dependent

High-yield: Diverticulosis is the commonest cause of brisk lower GI bleed; diverticula are more common on the left colon but bleed more often from the right colon. Angiodysplasia is the second commonest and also right-sided.

Pathophysiology

Bleeding occurs when a vessel is breached by ulceration, mechanical tear, raised venous pressure, neovascularisation, or tumour invasion.

• Peptic ulcer: acid–pepsin and H. pylori/NSAID injury erodes through mucosa into a vessel. Posterior duodenal ulcer → gastroduodenal artery; lesser-curve gastric ulcer → left gastric artery.
• Variceal: portal hypertension (portal pressure > hepatic) opens porto-systemic collaterals. Bleeding risk rises sharply once the hepatic venous pressure gradient (HVPG) > 12 mmHg.
• Angiodysplasia: chronic low-grade colonic muscular obstruction of submucosal veins → dilated tortuous ectatic vessels.

Blood loss → reduced preload → compensatory tachycardia, vasoconstriction, then hypotension. In cirrhotics, blood in the gut is a nitrogen load that precipitates hepatic encephalopathy.

Clinical Features & Severity Assessment

Look for: haematemesis/melaena/haematochezia, pallor, tachycardia, postural drop, cool peripheries, oliguria, altered sensorium. Stigmata of chronic liver disease (jaundice, ascites, spider naevi, splenomegaly, caput medusae) point to a variceal source.

Estimating blood loss (clinical):

• Postural hypotension (drop > 10 mmHg / pulse rise > 20) ≈ 15% volume loss.
• Supine hypotension ≈ > 30–40% loss → Class III/IV shock.

High-yield: A raised blood urea with normal creatinine (high urea:creatinine ratio) strongly suggests UGIB — from digested-blood protein absorption plus pre-renal azotaemia.

Diagnosis & Investigation of Choice

Stepwise approach (the "ABC then scope" rule):

Resuscitate (A-B-C, two large-bore IV cannulae) → Risk-stratify (scores) → Localise & treat (endoscopy) → Definitive (rebleed → repeat scope/IR/surgery)

1. Bloods: haemoglobin (may be normal early before haemodilution), platelets, coagulation/INR, urea & creatinine, LFTs, group & crossmatch.
2. UGIB → Upper GI endoscopy (OGD) is the investigation AND treatment of choice, ideally within 24 hours (within 12 h if variceal/unstable).
3. LGIB:
   • Always do digital rectal examination + proctoscopy first (exclude anorectal source).
   • Colonoscopy = investigation of choice for stable LGIB (diagnostic + therapeutic), after bowel prep.
   • CT angiography for active brisk bleed (detects bleeding ≥ 0.3–0.5 mL/min); guides catheter angiography.
   • Catheter (mesenteric) angiography detects ≥ 0.5–1 mL/min and allows embolisation.
   • Tc-99m labelled RBC scan is the most sensitive (detects 0.1–0.4 mL/min) but only localises to a region; good for slow/intermittent bleeds.
4. Obscure/mid-GI bleed: capsule endoscopy (first-line for obscure-overt after negative OGD/colonoscopy), then double-balloon enteroscopy. Meckel scan (Tc-99m pertechnetate) in children.

Modality	Minimum detectable bleed rate	Role
Catheter angiography	0.5–1.0 mL/min	Localise + embolise active bleed
CT angiography	0.3–0.5 mL/min	Rapid localisation, triage
Tagged RBC scan	0.1–0.4 mL/min	Most sensitive; slow/intermittent bleeds
Endoscopy	Any (direct vision)	Diagnostic + therapeutic, first-line

High-yield: Order of sensitivity for detecting bleed: Tagged RBC scan > CT angiography > catheter angiography. But angiography is preferred when you want to treat (embolise) a brisk bleed.

Risk Scores

Rockall score (UGIB)

Predicts rebleeding and mortality. "Full" Rockall uses age, shock (BP/pulse), comorbidity, endoscopic diagnosis, and stigmata of recent haemorrhage (max 11).

Variable	Components
Age	< 60 / 60–79 / ≥ 80
Shock	Pulse > 100; SBP < 100
Comorbidity	Cardiac/major; renal/liver/metastatic
Endoscopic diagnosis	Mallory–Weiss vs malignancy
Stigmata of recent bleed	Active bleed / visible vessel / clot

Glasgow–Blatchford Score (GBS)

Pre-endoscopy score using only clinical + lab data (urea, Hb, SBP, pulse, melaena, syncope, hepatic/cardiac disease). GBS = 0 (or ≤1) identifies very low-risk patients suitable for outpatient management — its key exam use.

High-yield: GBS is for the pre-endoscopy triage / discharge decision; Rockall (full) is post-endoscopy and predicts rebleed & death. Don't confuse them.

Forrest classification (endoscopic stigmata of peptic ulcer)

Predicts rebleed risk and decides whether endoscopic therapy is needed.

Forrest	Finding	Rebleed risk	Therapy
Ia	Spurting arterial bleed	Highest (~90%)	Yes
Ib	Oozing	High	Yes
IIa	Non-bleeding visible vessel	~50%	Yes
IIb	Adherent clot	~25–30%	Consider (clot removal)
IIc	Flat pigmented spot	~10%	No
III	Clean ulcer base	< 5%	No

High-yield: Forrest Ia, Ib, IIa, IIb warrant endoscopic therapy; IIc and III can be managed medically and considered for early discharge.

Management

General resuscitation (applies to all)

• Two large-bore (14–16G) IV cannulae, crystalloid bolus, oxygen, monitor.
• Transfusion: restrictive strategy — transfuse at Hb < 7 g/dL (target 7–9), and < 8 in cardiac disease. Restrictive transfusion improves survival especially in variceal bleeds (over-transfusion raises portal pressure).
• Correct coagulopathy; platelets if < 50,000 and bleeding; reverse warfarin (vitamin K + PCC).
• Catheterise, monitor urine output; NBM; NG tube optional.

Non-variceal UGIB (e.g. peptic ulcer)

1. High-dose IV proton pump inhibitor (PPI) — e.g. pantoprazole/esomeprazole 80 mg bolus then 8 mg/h infusion (or 40 mg BD). Stabilises clot by raising gastric pH > 6.
2. Endoscopic haemostasis — combination therapy is best: adrenaline injection (1:10,000) PLUS a second modality (thermal coagulation / clips / sclerosant). Adrenaline alone is inferior.
3. Test & treat H. pylori; stop NSAIDs.
4. Rebleed → repeat endoscopy once; failing that, angiographic embolisation or surgery (under-running the vessel, e.g. ligation of gastroduodenal artery for duodenal ulcer).

Variceal UGIB

Flow: Resuscitate → vasoactive drug + antibiotic → urgent endoscopic band ligation → balloon tamponade (bridge) → TIPS (rescue)

1. Vasoactive drugs (start before endoscopy): terlipressin (drug of choice; reduces mortality) or octreotide/somatostatin — reduce portal/splanchnic flow.
2. Prophylactic antibiotics (ceftriaxone/norfloxacin) — mandatory, reduce infection, rebleed and mortality.
3. Endoscopic variceal band ligation (EVL) = treatment of choice for oesophageal varices (better than sclerotherapy). Gastric varices → cyanoacrylate (glue) injection.
4. Balloon tamponade (Sengstaken–Blakemore / Minnesota tube) = temporary bridge for uncontrolled bleed (max 24 h).
5. TIPS (transjugular intrahepatic porto-systemic shunt) = rescue for refractory bleeding; risk of encephalopathy.
6. Lactulose to prevent encephalopathy; non-selective beta-blocker (propranolol/carvedilol) + repeat EVL for secondary prophylaxis.

High-yield: Terlipressin = drug of choice for acute variceal bleed; band ligation = procedure of choice for oesophageal varices; cyanoacrylate glue for gastric (fundal) varices; antibiotics are non-negotiable in any cirrhotic with GI bleed.

Lower GI bleed

• ~80% stop spontaneously → resuscitate and observe.
• Colonoscopy: clip/coagulate/inject for diverticular or angiodysplastic bleed.
• Angiographic embolisation for ongoing brisk bleed not amenable to scope.
• Surgery (segmental resection) if localised; subtotal colectomy only if life-threatening bleed with unidentified source.
• Haemorrhoids → band ligation / sclerotherapy / surgery as indicated.

Complications

• Hypovolaemic shock, acute kidney injury, multi-organ failure.
• Rebleeding (highest in first 72 h; Forrest Ia/IIa).
• Aspiration pneumonia (haematemesis + altered sensorium).
• Hepatic encephalopathy and hepatorenal syndrome in cirrhotics.
• Transfusion-related complications; myocardial ischaemia from anaemia.
• Death — variceal bleeds carry the highest mortality (up to 15–20% per episode).

Key Differentials / Mimics

• Pseudo-haematemesis: swallowed blood (epistaxis, haemoptysis, dental).
• Pseudo-melaena: iron tablets, bismuth, liquorice, spinach, beetroot (red urine/stool).
• Haemoptysis vs haematemesis: haemoptysis is frothy, bright red, alkaline, with cough; haematemesis is acidic, has food particles, with nausea/vomiting.
• Brisk UGIB presenting as haematochezia in a shocked patient — always pass a scope upward if upper source suspected.

Mnemonics & Eponyms

• UGIB causes — "GUM BED": Gastritis/varices, Ulcer (peptic), Mallory–Weiss, Bleeding disorders, Erosions/Oesophagitis, Dieulafoy/malignancy.
• Heyde syndrome: Aortic stenosis + colonic angiodysplasia + acquired von Willebrand syndrome.
• Dieulafoy = caliber-persistent submucosal artery; Cameron lesion = erosions within a hiatus hernia causing chronic bleed/anaemia.
• Cullen / Grey-Turner signs (retroperitoneal bleed) — not GI lumen but commonly paired in exams.

Recently asked / exam angle

• Most common cause of UGIB → peptic ulcer disease; most common artery in massive duodenal ulcer bleed → gastroduodenal artery (posterior duodenal ulcer).
• Most common cause of massive lower GI bleed in adults → diverticulosis; in children → Meckel diverticulum.
• Investigation of choice — UGIB → OGD; stable LGIB → colonoscopy; brisk active LGIB → CT/catheter angiography; most sensitive for slow bleed → tagged RBC scan.
• Pre-endoscopy triage / safe discharge score → Glasgow–Blatchford (=0); post-endoscopy mortality/rebleed → Rockall.
• Forrest classes needing endoscopic therapy → Ia, Ib, IIa, IIb.
• Drug of choice in variceal bleed → terlipressin; procedure → band ligation (oesophageal), cyanoacrylate (gastric).
• Transfusion threshold → restrictive, Hb < 7 g/dL.
• Antibiotic in cirrhotic GI bleed → mandatory (ceftriaxone), reduces mortality.
• Heyde syndrome triad and aorto-enteric fistula herald bleed are recurring image/vignette favourites.

Rapid revision

1. Ligament of Treitz divides upper from lower GI bleed; UGIB is 4–5× commoner.
2. Peptic ulcer = commonest UGIB; diverticulosis = commonest major LGIB; Meckel = commonest significant LGIB in children.
3. Posterior duodenal ulcer erodes the gastroduodenal artery → massive bleed.
4. Raised urea with normal creatinine = clue to UGIB.
5. Resuscitate first (two wide-bore lines), then scope; OGD within 24 h, within 12 h if variceal/unstable.
6. Transfuse restrictively at Hb < 7 g/dL.
7. GBS = pre-endoscopy discharge tool; Rockall = post-endoscopy mortality/rebleed; Forrest = ulcer rebleed risk.
8. Non-variceal: high-dose IV PPI + dual endoscopic therapy (adrenaline + second method).
9. Variceal: terlipressin + ceftriaxone + band ligation; balloon tamponade as bridge; TIPS as rescue.
10. Gastric varices → cyanoacrylate glue; oesophageal → band ligation.
11. Heyde syndrome = aortic stenosis + angiodysplasia + acquired vWD.
12. Tagged RBC scan is the most sensitive bleed-detection test (0.1 mL/min) but only regionalises; angiography lets you embolise.