Upper and lower GI bleeding (variceal and non-variceal)

Overview

Gastrointestinal (GI) bleeding is divided by the ligament of Treitz (duodenojejunal flexure):

• Upper GI bleeding (UGIB): oesophagus, stomach, duodenum. Presents with haematemesis (fresh blood or "coffee grounds") and/or melaena (black, tarry, sticky, foul stool from digested blood).
• Lower GI bleeding (LGIB): below the ligament. Presents with haematochezia (fresh or maroon blood per rectum).

A brisk upper GI bleed can also produce fresh red blood per rectum, usually with shock. Most bleeds (about 85% of upper GI bleeds) stop on their own, but bleeding varices and large-vessel ulcer bleeds can kill quickly. The rule is resuscitate first, then find and treat the source.

Upper GI bleeding

Causes

Clinical assessment

• History: NSAIDs, aspirin, anticoagulants and antiplatelets, steroids with NSAIDs, alcohol, liver disease, previous bleeds or ulcers, retching, weight loss, aortic graft.
• Shock: tachycardia, postural drop, cold peripheries, low urine output, confusion. Hypotension is late in young patients. Beta-blockers mask the tachycardia.
• Rectal examination: melaena confirms the bleed.
• Signs of chronic liver disease suggest varices.

Risk scoring

• Glasgow-Blatchford score (before endoscopy): uses blood urea, haemoglobin, systolic BP, pulse, melaena, syncope, liver disease and heart failure. It predicts the need for transfusion, endoscopic therapy or surgery. A score of 0 identifies patients who can be managed as outpatients.
• Rockall score: age, shock, comorbidity, endoscopic diagnosis and stigmata of recent haemorrhage. A pre-endoscopy (clinical) part and a full post-endoscopy score predict rebleeding and death.

Immediate management (all upper GI bleeds)

1. Airway and breathing: oxygen; protect the airway in massive haematemesis or reduced consciousness.
2. Two large-bore cannulae; send Hb, platelets, urea and electrolytes, liver tests, clotting, group and crossmatch.
3. Fluids: crystalloid boluses for hypotension, then blood.
4. Transfusion: a restrictive approach is safer; transfuse when Hb is below 70 g/L in most patients (a higher threshold, around 80–90 g/L, in heart disease). In massive bleeding, use a major haemorrhage protocol.
5. Correct clotting: platelets if under 50 × 10⁹/L and bleeding; fresh frozen plasma if INR or APTT is over 1.5 times normal; prothrombin complex concentrate for warfarin; stop DOACs (idarucizumab reverses dabigatran).
6. Stop NSAIDs, aspirin and anticoagulants (discuss antiplatelets with cardiology if the patient has stents).
7. Keep nil by mouth until endoscopy; monitor pulse, BP and urine output closely; catheterise in severe bleeds.
8. Endoscopy: immediately after resuscitation if unstable; within 24 hours for all others.

Peptic ulcer bleeding

At endoscopy (Forrest description of the ulcer base):

• Endoscopic haemostasis: combine two methods: adrenaline injection plus a thermal method (heater probe, bipolar probe, argon plasma) or clips. Adrenaline alone is not enough. Haemostatic powder sprays help with difficult or tumour bleeds.
• After endoscopy: for high-risk ulcers, high-dose IV PPI (Kumar: omeprazole 80 mg, then 8 mg/hour for 72 hours), then oral PPI. Acid inhibition stabilises the clot.
• Biopsy and test for H. pylori; eradicate if positive and confirm eradication. A negative urease test during an acute bleed may be false, so check histology.
• Rebleeding: repeat endoscopy once; if it fails, interventional radiology (angiographic embolisation); if that is not available or fails, surgery.
• Surgery (Bailey): continued bleeding or a significant rebleed despite endoscopy, or high transfusion needs (more than about 6 units). For a duodenal ulcer, open the duodenum and under-run the bleeding vessel (gastroduodenal artery); for a gastric ulcer, excise or under-run the ulcer and send tissue for histology.

Variceal bleeding

Background

• Portal hypertension: normal portal pressure is 5–8 mmHg. A hepatic venous pressure gradient of 10 mmHg or more is clinically significant; varices bleed when it rises above about 12 mmHg.
• Varices form at portosystemic connections; oesophageal varices (from the left gastric vein to oesophageal veins) are superficial and bleed most.
• About 90% of cirrhotics develop varices over 10 years; about a third of these bleed. Bleeding is likelier with large varices, red signs and poor liver function.
• Kumar: 6-week mortality is 15–25%, reaching 50% in Child C.

Acute management

1. Resuscitate but do not over-transfuse: overfilling raises portal pressure and causes rebleeding. Aim for Hb around 70–80 g/L.
2. Vasoconstrictor before endoscopy: terlipressin (Kumar: 2 mg IV 6-hourly, reducing after 48 hours, for up to 5 days). It constricts splanchnic arteries and lowers portal inflow; it is the vasoconstrictor shown to reduce mortality. Avoid in ischaemic heart disease and peripheral vascular disease. Somatostatin or octreotide are alternatives.
3. Prophylactic antibiotics (e.g. IV ceftriaxone): reduce infection (including SBP), rebleeding and death.
4. Urgent endoscopy: band ligation for oesophageal varices (now preferred to sclerotherapy). Gastric (fundal) varices: cyanoacrylate glue injection.
5. Balloon tamponade (Sengstaken-Blakemore tube) if bleeding cannot be controlled: inflate the gastric balloon first and pull it against the gastro-oesophageal junction; the oesophageal balloon only if needed. Leave no longer than about 12 hours; protect the airway (intubate). Risks: aspiration, oesophageal rupture, ulceration. A removable covered oesophageal stent is an alternative bridge.
6. TIPS (transjugular intrahepatic portosystemic shunt): a stent between a hepatic vein and a branch of the portal vein, placed via the jugular vein. Used when bleeding cannot be controlled or rebleeds; early TIPS helps high-risk (Child C or B with active bleeding) patients. Main risk: encephalopathy.
7. Prevent encephalopathy (lactulose), give thiamine in drinkers, manage alcohol withdrawal (lorazepam or oxazepam), tap ascites.

Preventing the first bleed (primary prophylaxis)

• Screen cirrhotics by endoscopy (or by elastography and platelet count).
• Large varices or red signs: non-selective beta-blocker (propranolol or carvedilol) or band ligation.
• Non-selective beta-blockers lower portal pressure by reducing cardiac output (β1) and by blocking β2-mediated splanchnic vasodilatation, leaving α-mediated vasoconstriction unopposed. Target a resting pulse fall of about 25%.

Preventing rebleeding (secondary prophylaxis)

• Without prophylaxis, rebleeding occurs in 60–80% within 2 years.
• Non-selective beta-blocker plus repeated banding (about every 2 weeks) until varices are obliterated, then surveillance endoscopy.
• TIPS or liver transplant for repeated failure.

Non-cirrhotic causes of varices

Lower GI bleeding

Causes

Management

• Resuscitate as for upper GI bleeding. If the patient is shocked with fresh rectal blood, exclude an upper GI source (urea, OGD).
• Digital rectal examination and proctoscopy.
• Flexible sigmoidoscopy or colonoscopy after bowel preparation when stable. Young patients (under about 45) with a single small rectal bleed usually need only rectal examination and flexible sigmoidoscopy, unless there are risk factors.
• CT angiography localises active bleeding; then mesenteric angiography and embolisation.
• Capsule endoscopy and enteroscopy for small bowel bleeding when upper and lower endoscopy are normal.
• Surgery is rarely needed: segmental resection if the site is known; subtotal colectomy as a last resort if not.

Chronic (occult) GI bleeding

Iron deficiency anaemia in a man or post-menopausal woman is presumed to be GI blood loss: do upper GI endoscopy (with duodenal biopsies for coeliac disease) and colonoscopy. Worldwide, hookworm is the commonest cause of chronic GI blood loss. Varices rarely cause slow bleeding.

Quick revision

• UGIB: peptic ulcer commonest; varices most lethal; Mallory-Weiss after retching.
• Resuscitate: two large cannulae, crossmatch, restrictive transfusion (Hb below 70 g/L).
• Glasgow-Blatchford 0 → outpatient; Rockall predicts rebleeding and death.
• Endoscopy within 24 h (immediately if unstable).
• Ulcer: adrenaline + clips/heat; IV PPI for 72 h; H. pylori eradication; embolisation then surgery.
• Varices: terlipressin + antibiotics, banding, glue for gastric varices; tamponade then TIPS.
• Prevent: non-selective beta-blocker ± banding.
• Splenic vein thrombosis → isolated gastric varices → splenectomy.
• LGIB: diverticular (painless, large), angiodysplasia (right colon, aortic stenosis), Meckel's in the young.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine; Bailey & Love's surgery textbook).

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