Discuss the causes, clinical assessment and management of upper gastrointestinal bleeding.

Definition

Upper gastrointestinal (GI) bleeding is bleeding from a source proximal to the ligament of Treitz. It presents as haematemesis (vomiting fresh or "coffee-ground" blood), melaena (black, tarry, offensive stool — requiring as little as 50–100 mL of blood), or, with brisk bleeding, haematochezia with haemodynamic compromise. It is a medical emergency with significant mortality, particularly in the elderly and in those with comorbidity.

Causes

Clinical Assessment

History:

• volume and nature of the bleed
• previous dyspepsia or ulcer
• NSAID, aspirin, anticoagulant and steroid use
• alcohol and known liver disease
• retching before haematemesis (Mallory–Weiss)
• weight loss and dysphagia (malignancy)
• previous aortic surgery
• comorbidity.

Examination — the first priority is haemodynamic status, not the source:

• Pulse, blood pressure, postural drop, capillary refill, mental state and urine output.
• Tachycardia precedes hypotension — a resting tachycardia in a bleeding patient means significant loss.
• Look for stigmata of chronic liver disease — this changes management entirely.
• Per rectal examination to confirm melaena.
• Nasogastric aspiration is no longer routinely recommended.

Risk scores: the Glasgow–Blatchford score (using urea, haemoglobin, systolic pressure, pulse, melaena, syncope, hepatic disease and cardiac failure) identifies very low-risk patients suitable for outpatient management; the Rockall score predicts rebleeding and mortality after endoscopy.

Investigations

• CBC — note that haemoglobin may be normal initially in acute bleeding before haemodilution occurs; it is not a measure of the volume lost in the first hours.
• Urea and creatinine — a disproportionately raised urea with normal creatinine reflects absorbed blood protein and supports an upper GI source.
• Liver function, coagulation profile, blood grouping and cross-match (at least 2–4 units).
• ECG and troponin in the elderly or those with cardiac disease — bleeding precipitates myocardial ischaemia.
• Upper GI endoscopy — both diagnostic and therapeutic; performed within 24 hours in most patients, and urgently (within 12 hours) in variceal bleeding or haemodynamic instability after resuscitation.
• CT angiography or catheter angiography if bleeding continues and endoscopy is non-diagnostic.

Management

1. Resuscitation FIRST — before any diagnostic effort

• Two large-bore intravenous cannulae; crystalloid while awaiting blood.
• Blood transfusion with a RESTRICTIVE strategy — transfusing at a lower haemoglobin threshold improves survival compared with liberal transfusion, particularly in variceal bleeding, where over-transfusion raises portal pressure and precipitates rebleeding.
• Correct coagulopathy — vitamin K, prothrombin complex concentrate or fresh frozen plasma; platelets for significant thrombocytopenia; reverse anticoagulants where the bleeding is life-threatening.
• Protect the airway — intubate for massive haematemesis or altered consciousness, since aspiration is a major cause of death.
• Keep nil by mouth, monitor closely with urine output, and involve gastroenterology and surgery early.

2. Pharmacological therapy

• High-dose proton pump inhibitor — intravenous, started before endoscopy in suspected ulcer bleeding; it stabilises clot by raising gastric pH, reduces the need for endoscopic therapy, and is continued as an infusion after treatment of high-risk lesions.
• Vasoactive drugs for suspected variceal bleeding — terlipressin or octreotide/somatostatin — started IMMEDIATELY on suspicion, before endoscopy, as they reduce portal pressure and improve control of bleeding.
• Prophylactic antibiotics (ceftriaxone) in ALL cirrhotic patients with GI bleeding — this reduces infection, rebleeding and mortality, and is one of the most robust interventions in the field, yet is frequently omitted.

3. Endoscopic therapy

• Ulcers: treatment is guided by the Forrest classification of stigmata (active spurting, oozing, visible vessel, adherent clot, flat pigmented spot, clean base). High-risk lesions receive combination therapy — adrenaline injection PLUS a second modality (thermal coagulation, haemoclips); adrenaline alone is inadequate.
• Oesophageal varices: endoscopic band ligation (superior to sclerotherapy).
• Gastric varices: cyanoacrylate glue injection.

4. Failure to control bleeding

• Balloon tamponade (Sengstaken–Blakemore or Minnesota tube) — a temporary bridge for no more than 24 hours in exsanguinating variceal bleeding, with the airway protected; risks oesophageal necrosis and rupture.
• TIPS (transjugular intrahepatic portosystemic shunt) — for refractory or early rebleeding variceal haemorrhage; early "pre-emptive" TIPS improves survival in high-risk patients. Risk of precipitating encephalopathy.
• Interventional radiology — angiographic embolisation for non-variceal bleeding.
• Surgery — now rarely required, for uncontrolled bleeding despite the above.

5. After the bleed — preventing recurrence

• Test and eradicate *H. pylori* in ulcer disease, and confirm eradication.
• Stop NSAIDs and aspirin where possible; if antiplatelet therapy is essential (for example after coronary stenting), restart early with proton pump inhibitor cover — the risk of stopping it may exceed the risk of rebleeding.
• Repeat endoscopy to confirm healing of gastric ulcers and exclude malignancy — a gastric ulcer must always be biopsied.
• Variceal bleeding: secondary prophylaxis with a non-selective beta-blocker PLUS repeated band ligation until varices are eradicated, and referral for transplant assessment.