Upper GI Bleeding

Acute upper GI bleeding (UGIB) is a common cause of UK hospital admission with a mortality of ~10%. Patients present with haematemesis (vomiting blood, which may be 'coffee-ground' due to acid exposure) or melaena (black, tarry, offensive-smelling stools). Major causes include Peptic Ulcer Disease (50%), Oesophageal Varices (associated with cirrhosis), Mallory-Weiss tears (mucosal tear at the GOJ due to forceful vomiting), and Gastritis/Oesophagitis. Initial management must prioritize haemodynamic stability using the ABCDE approach. Small-volume bleeds can be assessed using the Glasgow-Blatchford Score (GBS) in the A&E; a score of 0-1 allows for outpatient management. All others require admission and urgent OGD (within 24 hours). For suspected variceal bleeding (e.g., in a patient with liver disease), Terlipressin and prophylactic antibiotics must be started immediately before endoscopy. Following endoscopy, the Rockall Score is used to calculate the risk of re-bleeding and mortality. Endoscopic treatments include adrenaline injection, thermal coagulation, or clipping for ulcers, and band ligation for varices.

The high mortality in UGIB is often due to hypovolaemic shock and subsequent multi-organ failure. Blood loss leads to a drop in stroke volume; compensatory mechanisms (tachycardia and vasoconstriction) maintain BP initially (Class I/II shock), but eventually, MAP falls (Class III/IV shock). In variceal bleeding, the cause is portal hypertension, which causes thin-walled collateral vessels to form at the gastro-oesophageal junction. When portal pressure exceeds a certain threshold, these vessels rupture, leading to massive, often fatal haemorrhage. Mallory-Weiss tears are longitudinal mucosal lacerations caused by a sudden rise in intra-abdominal pressure (e.g., coughing, retching). Peptic ulcers bleed when the ulcer erodes into an underlying artery (e.g., the gastroduodenal artery in posterior duodenal ulcers).

Assess for shock: Tachycardia, hypotension, and cool peripheries. History: Ask about NSAID use, alcohol, previous ulcers, or anticoagulant/antiplatelet use. Examination: Look for stigmata of chronic liver disease, abdominal masses, or epigastric tenderness. Perform DRE to confirm melaena (note: iron supplements and bismuth cause black stools that are not melaena). Scorings: Glasgow-Blatchford Score (GBS) integrates Urea, Hemoglobin, Systolic BP, Heart Rate, and comorbidities. A GBS of 0-1 is 'low risk' and suitable for early discharge and outpatient OGD. Post-OGD Rockall score uses age, shock, comorbidities, and endoscopic findings (e.g., visible vessel or clot).

Bedside: ECG (exclude MI triggered by anaemia), Hourly observations, Urine output (catheterization). Bloods: FBC (Hb may be normal in early acute bleed), U&Es (looking for raised Urea/Creatinine ratio), LFTs, Coagulation (INR/PT), Group and Save or Cross-match (minimum 2-4 units). Imaging: Erect CXR (if perforation suspected). Diagnostic Gold Standard: OGD (should be done within 24 hours of admission, or immediately if hemodynamically unstable).

General: ABCDE. High-flow oxygen. Large-bore IV access (x2) and fluid resuscitation (crystalloid). Transfuse blood if Hb <70g/L (target 70-90g/L, unless IHD). Correct coagulopathy (Vitamin K, Prothrombin complex). Non-Variceal (Ulcer): OGD + endotherapy (dual therapy e.g. adrenaline + clips/cautery). Start high-dose IV PPI (e.g. Omeprazole 80mg bolus then infusion) *only after* OGD. Variceal Bleed (Specific): Start Terlipressin (vasoconstrictor) and IV Antibiotics (Ceftriaxone) *before* OGD. Urgent OGD for Band Ligation. If band ligation fails, use a Sengstaken-Blakemore tube or TIPS procedure. Mallory-Weiss: Usually stops spontaneously; OGD used if persistent.