Varices, ulcers, reflux and lower GI bleeding

Variceal vs Non-Variceal Upper GI Bleeding

Rapid clinical discrimination between non-variceal and variceal haemorrhage dictates initial pharmacotherapy and endoscopic strategy.

Non-Variceal Bleeding (Peptic Ulcers, Tears, Ectasias)

• Aetiology: Peptic ulcer disease ($50\%$), gastroduodenal erosions ($15\%$), Mallory-Weiss tears ($10\%$, mucosal laceration at the gastro-oesophageal junction post-retching), Dieulafoy lesions (aberrant submucosal calibre-persistent artery), and upper GI malignancy ($5\%$).
• Pharmacotherapy: Initiate high-dose intravenous proton pump inhibitor (PPI) therapy upon admission (e.g. pantoprazole 80 mg IV bolus followed by an 8 mg/hour continuous infusion for 72 hours, or $40\text{ mg}$ IV twice daily). Maintaining intragastric $pH > 6$ promotes platelet aggregation and prevents pepsin-mediated clot lysis.
• Endoscopy Timing: Perform upper endoscopy within 24 hours of presentation (within 12 hours if haemodynamically unstable despite fluid resuscitation).
• Endoscopic Haemostasis: Guided by the Forrest Classification:
  • Forrest Ia (Spurting arterial) and Ib (Oozing): High rebleeding risk ($55-90\%$). Mandates dual endoscopic therapy: injection of dilute adrenaline ($1:10,000$) combined with a second mechanical or thermal modality (through-the-scope clips or bipolar electrocoagulation).
  • Forrest IIa (Non-bleeding visible vessel) and IIb (Adherent clot): Moderate to high risk ($25-50\%$). Mandates endoscopic intervention (clot removal and dual therapy).
  • Forrest IIc (Flat pigmented spot) and III (Clean ulcer base): Low rebleeding risk ($< 5\%$). No endoscopic intervention required; switch to oral PPI.

Variceal Bleeding (Portal Hypertension)

• Aetiology: Rupture of dilated submucosal gastro-oesophageal varices driven by elevated portal venous pressure gradient ($HVPG \ge 12\text{ mmHg}$) in patients with cirrhosis.
• Immediate Vasoactive Pharmacotherapy: Must be administered immediately upon suspicion of variceal bleeding, prior to endoscopy:
  • Terlipressin: Synthetic vasopressin analogue with selective $V_1$ receptor agonism causing splanchnic arterial vasoconstriction and rapid reduction in portal inflow. Dose: 2 mg IV stat bolus, then 1-2 mg IV every 4-6 hours for up to 2-5 days.
  • Octreotide: Synthetic somatostatin analogue; alternatives when terlipressin is unavailable or contraindicated (e.g. severe peripheral vascular disease). Dose: $50\ \mu\text{g}$ IV bolus followed by $50\ \mu\text{g/hour}$ infusion.
• Antibiotic Prophylaxis: Mandatory in all cirrhotic patients presenting with upper GI bleeding regardless of ascites. Administer intravenous ceftriaxone 1 g daily for 5 to 7 days. Antibiotic prophylaxis reduces bacterial translocation, prevents spontaneous bacterial peritonitis (SBP), decreases rebleeding, and confers a proven survival advantage.
• Endoscopic Haemostasis: Perform urgent gastroscopy within 12 hours of presentation. The gold standard is Endoscopic Variceal Ligation (EVL / band ligation) for oesophageal varices. Gastric fundal varices are treated with endoscopic cyanoacrylate tissue adhesive glue.
• Rescue Interventions: If endoscopic haemostasis fails or exsanguinating haemorrhage precludes visualization:
  • Balloon Tamponade: Placement of a Sengstaken-Blakemore or Minnesota tube provides mechanical compression of bleeding varices. Used strictly as a temporary bridge ($< 24\text{ hours}$) due to risks of oesophageal necrosis and aspiration.
  • TIPSS: Early Transjugular Intrahepatic Portosystemic Shunt (TIPSS) within 72 hours is indicated for high-risk patients (Child-Pugh C $< 14$ or Child-Pugh B with active bleeding at endoscopy) to decompress the portal circulation.

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Peptic Ulcer Disease (PUD) & Helicobacter pylori

Peptic ulceration results from an imbalance between protective mucosal defense factors (mucus, bicarbonate, prostaglandins, blood flow) and aggressive luminal factors (hydrochloric acid, pepsin).

Major Aetiological Drivers

1. Helicobacter pylori Infection: Microaerophilic, Gram-negative flagellated bacillus residing in the gastric mucous layer. Responsible for $> 85\%$ of duodenal ulcers and $> 65\%$ of gastric ulcers. Urease production hydrolyses urea to ammonia, buffering gastric acid and damaging the surrounding epithelium.
2. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) & Aspirin: Non-selective NSAIDs inhibit cyclooxygenase-1 (COX-1), blocking cytoprotective prostaglandin $E_2$ and $I_2$ synthesis, impairing mucosal microcirculation and bicarbonate secretion.
3. Uncommon Causes: Zollinger-Ellison syndrome (gastrinoma with severe hyperchlorhydria), severe physiological stress (Curling ulcers in major burns; Cushing ulcers in intracranial pathology).

Diagnostic Investigations for H. pylori

• Urea Breath Test (UBT) (Carbon-13 or Carbon-14): Sensitivity / Specificity: $> 95\% / > 95\%$; Clinical Utility & Diagnostic Caveats: Non-invasive test of choice to confirm active infection and verify eradication. False negatives occur if patient has taken a PPI within 2 weeks or antibiotics / bismuth within 4 weeks.
• Faecal Antigen Test (SAT): Sensitivity / Specificity: $> 95\% / > 95\%$; Clinical Utility & Diagnostic Caveats: Excellent alternative non-invasive test detecting active bacterial shed. Same 2-week PPI and 4-week antibiotic cessation requirements as UBT.
• Endoscopic Biopsy & Rapid Urease Test (CLO test): Sensitivity / Specificity: $> 90\% / > 95\%$; Clinical Utility & Diagnostic Caveats: Performed during gastroscopy; biopsy tissue placed into urea-containing agar with phenol red indicator. Subject to false negatives from recent PPI use.
• Histopathology & Culture: Sensitivity / Specificity: $> 95\% / > 98\%$; Clinical Utility & Diagnostic Caveats: Direct microscopic visualization with Giemsa or silver stains. Allows antimicrobial susceptibility profiling in refractory cases.
• Serology (Serum IgG): Sensitivity / Specificity: $80-90\% / 70-80\%$; Clinical Utility & Diagnostic Caveats: Cannot differentiate past resolved infection from active infection. Unreliable for confirming eradication; rarely indicated in modern practice.

AMC Clinical Rule: Gastric ulcers carry a $3-5\%$ risk of underlying gastric adenocarcinoma. Unlike duodenal ulcers, all gastric ulcers require multiple edge and base biopsies during endoscopy, followed by a repeat surveillance gastroscopy in 6 to 8 weeks to confirm complete mucosal healing.

Eradication Regimens per Australian Therapeutic Guidelines (eTG)

• First-Line Triple Therapy (7 to 14 days):
  • Standard-dose PPI twice daily (e.g. esomeprazole $20\text{ mg}$ bd, or omeprazole $20\text{ mg}$ bd)
  • Amoxicillin 1000 mg orally twice daily
  • Clarithromycin 500 mg orally twice daily
  • Penicillin Hypersensitivity: Substitute amoxicillin with metronidazole 400 mg orally twice daily.
• Second-Line / High-Resistance Bismuth Quadruple Therapy (10 to 14 days):
  • Standard-dose PPI twice daily
  • Bismuth subcitrate (or subsalicylate) standard dose
  • Metronidazole 400 mg orally three times daily
  • Tetracycline 500 mg orally four times daily
• Confirmation of Eradication: Mandatory for all patients treated for PUD. Repeat Urea Breath Test or Faecal Antigen Test at least 4 weeks after completing antibiotics and at least 2 weeks after stopping PPI therapy.

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Reflux and indigestion

Heartburn and acid regurgitation can support gastro-oesophageal reflux, with assessment of meals, posture, medicines and weight-related factors. Appropriate lifestyle measures and a time-limited acid-suppression trial can help a low-risk typical presentation, followed by review and the lowest effective regimen. Dysphagia, odynophagia, bleeding, anaemia, involuntary weight loss or persistent atypical symptoms require investigation rather than repeated empirical prescriptions. Chest pain must also be assessed for cardiac causes; response to antacid does not exclude ACS. Dyspepsia can reflect functional disease, ulcer or malignancy. Select H. pylori testing with attention to PPI/antibiotic effects, and arrange endoscopy according to risk and alarm features. Refractory symptoms need diagnostic review, not automatic lifelong dose escalation.

Lower Gastrointestinal Bleeding (LGIB)

Lower GI bleeding accounts for approximately $20-30\%$ of all major GI bleeding presentations. Over $80\%$ of acute LGIB cases resolve spontaneously with supportive measures.

Aetiologies

• Diverticular Bleeding ($30-40\%$): The single most common cause of major acute lower GI bleeding. Arises from rupture of the nutrient arteriole (vasa recta) traversing the dome or neck of a colonic diverticulum. Characteristically presents as sudden, painless, massive haematochezia. True diverticulitis is typically absent during a bleed.
• Angiodysplasia / Vascular Ectasias ($10-15\%$): Acquired, tortuous, thin-walled submucosal arteriovenous malformations predominantly located in the caecum and ascending colon of elderly patients ($> 65\text{ years}$). Associated with aortic stenosis (Heyde syndrome, where shear stress degrades von Willebrand factor multimers) and end-stage renal failure.
• Colitis ($15-20\%$):
  • Ischaemic Colitis: Sudden crampy left iliac fossa pain followed by bloody diarrhoea, characteristically occurring at mesenteric 'watershed' regions (Griffiths' point at the splenic flexure, Sudeck's point at the rectosigmoid junction) following transient systemic hypoperfusion.
  • Infectious Colitis: Campylobacter, Salmonella, Shigella, E. coli O157:H7, Clostridioides difficile.
  • Inflammatory Bowel Disease: Ulcerative colitis, Crohn's disease.
• Haemorrhoids and Anal Fissures ($10-15\%$): Fresh, bright red blood coating the surface of formed stool or dripping into the toilet bowl; rarely causes haemodynamic compromise.
• Neoplasia ($10\%$): Colorectal adenocarcinoma or large polyps; typically presents with occult bleeding, chronic microcytic iron deficiency anaemia, or intermittent altered blood.

Diagnostic & Management Pathway for Acute LGIB

• Localisation: History, examination, haemodynamics and the clinical pattern guide endoscopy or imaging. Nasogastric aspiration is not mandatory and a negative aspirate does not exclude upper-GI bleeding. Unstable haematochezia can be brisk upper-GI bleeding; CT angiography can also help localise active lower bleeding.

1. Haemodynamically Unstable Patient: If active, brisk haematochezia persists with shock despite aggressive fluid resuscitation:
   • Investigation of Choice: Urgent contrast-enhanced Computed Tomography Mesenteric Angiography (CTMA). CTMA can detect active arterial bleeding at extravasation rates as low as $0.3-0.5\text{ mL/min}$ with high anatomical accuracy.
   • Definitive Treatment: If CTMA identifies active contrast extravasation, transfer the patient directly to the interventional radiology suite for transcatheter arterial embolisation (TAE). Emergency segmental colectomy is reserved for failed embolisation or uncontrollable exsanguination.
2. Haemodynamically Stable Patient:
   • Admit to an inpatient ward, optimize haemoglobin, and correct coagulopathies.
   • Perform colonoscopy following rapid oral bowel lavage (e.g. 4 litres of polyethylene glycol solution). Colonoscopy permits mucosal visualization, tissue biopsy, and direct endoscopic haemostasis (haemostatic clips, thermal probe, or argon plasma coagulation for angiodysplasia).

Primary references (checked 7 October 2026): National Blood Authority PCC transition.