Contents
- Causes and Classification
- Risk Stratification
- Initial Management
- Acid Suppression
- Non-Variceal Haemorrhage
- Variceal Haemorrhage
- ICU-Specific Considerations
- Viva Questions
Causes and Classification
Upper GI haemorrhage (UGIH) is defined as bleeding proximal to the ligament of Treitz (duodenojejunal flexure).
Non-Variceal (80%)
| Cause | Proportion |
|---|---|
| Peptic ulcer disease (gastric, duodenal) | ~40–50% |
| Mallory-Weiss tear | ~10–15% |
| Erosive gastritis/duodenitis | ~10% |
| Oesophagitis | ~5–10% |
| Upper GI malignancy | ~2–5% |
| Dieulafoy lesion | Rare; arteriovenous malformation; massive bleeding possible |
| Aorto-enteric fistula | Rare; surgical emergency; consider in patients with aortic grafts |
Variceal (20%)
- Oesophageal varices: from portal hypertension (most commonly cirrhosis)
- Gastric varices: higher rebleeding rate; less amenable to banding
- Gastric antral vascular ectasia (GAVE/"watermelon stomach")
Risk Stratification
Pre-Endoscopy: Glasgow-Blatchford Score (GBS)
Used before endoscopy to identify patients requiring intervention:
Variables: BUN, haemoglobin, SBP, pulse, melaena, syncope, hepatic disease, cardiac failure — each scored; GBS 0 = very low risk (can be managed outpatient); GBS ≥6 = high risk; GBS ≥7 requires urgent inpatient endoscopy.
Post-Endoscopy: Rockall Score
Risk of rebleeding and mortality after endoscopic assessment:
- Variables: age, shock, comorbidity, endoscopic diagnosis, stigmata of recent haemorrhage (SRH)
- Rockall ≥8: high rebleeding and mortality risk
Forrest Classification (Endoscopic Stigmata)
| Class | Finding | Rebleed rate |
|---|---|---|
| Ia | Active spurting haemorrhage | ~90% |
| Ib | Active oozing | ~70% |
| IIa | Non-bleeding visible vessel | ~50% |
| IIb | Adherent clot | ~30% |
| IIc | Haematin on flat base | ~10% |
| III | Clean base | ~5% |
Forrest Ia–IIb: endoscopic therapy indicated
Initial Management
Resuscitation
- IV access: two large-bore cannulae; bloods (FBC, U&E, LFTs, clotting, group and crossmatch)
- Target: systolic BP 90–100 mmHg (haemostatic target — avoid over-resuscitation which dilutes clotting factors)
- Blood transfusion: target Hb ≥70 g/L (TRICC threshold valid here; liberal transfusion increases rebleeding risk — see TRIC journal club)
- Exception: Hb 80–100 in active ischaemic heart disease or significant haemodynamic compromise
- Correction of coagulopathy: INR >1.5 → FFP 4 units; platelets <50 → transfuse; if on warfarin: vitamin K + PCC
- Airway protection: intubation before endoscopy if: GCS ≤8, active vomiting of blood, haemodynamic instability — risk of aspiration during OGD is significant
Timing of Endoscopy
- Emergency endoscopy (<6 hours): active haemorrhage with haemodynamic instability
- Urgent endoscopy (<24 hours): all patients once resuscitated — current UK guideline (BSG)
- Pre-endoscopy erythromycin: 250 mg IV 30–90 minutes before OGD promotes gastric emptying → clears blood from stomach → improves endoscopic views; reduces need for repeat endoscopy
Acid Suppression
PPI Rationale
Gastric acid impairs platelet aggregation and dissolves fibrin clots. Raising gastric pH >6 with high-dose PPI stabilises clots and reduces rebleeding.
Post-Endoscopy PPI Protocol (high-risk lesions — Forrest Ia–IIb)
High-dose IV PPI: omeprazole or pantoprazole 80 mg IV bolus → 8 mg/hour infusion for 72 hours → switch to oral PPI 40 mg daily.
Stress Ulcer Prophylaxis
The SUP-ICU trial (pantoprazole vs placebo, n=3298) showed no mortality benefit from routine PPI prophylaxis in ICU patients, with lower clinically important GI bleeding (2.5% vs 4.2%). Risk-benefit should be individualised: patients with coagulopathy, mechanical ventilation, shock, or recent GI bleed are at higher risk and prophylaxis is appropriate. Routine use in all ICU patients is not supported.
Non-Variceal Haemorrhage
Endoscopic Therapy
High-risk lesions (Forrest I–IIa): dual therapy — combination of two techniques:
- Injection therapy: adrenaline 1:10,000 (causes tamponade and vasoconstriction)
- Thermal: argon plasma coagulation (APC), heater probe, bipolar electrocoagulation
- Mechanical: endoclip application — preferred when technically feasible; superior long-term haemostasis
- Adrenaline alone is inadequate: always combine with a second modality
Second-Look Endoscopy
Not routinely recommended; reserved for patients with high-risk stigmata or clinical concern for rebleeding.
Rebleeding
- Definition: fresh haematemesis or melaena with haemodynamic compromise after initial haemostasis
- Second endoscopic attempt: appropriate
- If endoscopic control fails: interventional radiology (IR) — transarterial embolisation; high success rate (~90%) for peptic ulcer bleeding from GDA or branches
- Surgery: reserved for failure of endoscopic and IR control; decreasing frequency with improved IR
H. pylori
All peptic ulcer patients: test and treat H. pylori (CLO test at endoscopy, stool antigen, or 13C-UBT); eradication dramatically reduces rebleeding risk.
Variceal Haemorrhage
Variceal haemorrhage carries high mortality (~15–20% per episode) and high rebleeding rate. Management differs from non-variceal bleeding.
Vasoactive Agents — Start Before Endoscopy
- Terlipressin 2 mg IV 4-6-hourly (or 1 mg 4-hourly if weight <50 kg): splanchnic vasoconstrictors → ↓ portal pressure; demonstrated mortality benefit in RCTs; start immediately on suspicion of variceal bleed
- Octreotide (or somatostatin): alternative; 50 mcg bolus → 50 mcg/hour infusion
- Continue for 3–5 days
Endoscopic Variceal Band Ligation (EVBL)
- First-line endoscopic treatment for oesophageal varices
- Superior to sclerotherapy in efficacy and safety
- Gastric varices: EVBL less effective; tissue adhesive (cyanoacrylate glue) injection preferred; TIPS more often required
Antibiotics
- Ceftriaxone 1 g IV 24-hourly × 7 days (or norfloxacin 400 mg BD PO if available): reduces SBP (spontaneous bacterial peritonitis) risk, reduces 30-day mortality — mandatory in all patients with cirrhosis and UGIH
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
- Radiologically placed stent between hepatic vein and portal vein → decompresses portal system
- Indications:
- Emergency TIPS: if rebleeding after two endoscopic attempts; also considered in Child-Pugh C cirrhosis or HVPG >20 mmHg as early (within 72h) intervention in high-risk patients
- Elective: prevention of rebleeding after initial control
- Complications: hepatic encephalopathy (shunting bypasses hepatic metabolism of ammonia), stent occlusion
Sengstaken-Blakemore Tube (Balloon Tamponade)
- Four-lumen tube with gastric and oesophageal balloons: inflation of gastric balloon arrests bleeding
- Reserved for massive, life-threatening variceal haemorrhage not controlled by endoscopy — bridge to TIPS or surgery
- Risk: oesophageal rupture, aspiration; only used in intubated patients
- Maximum 24 hours of gastric balloon inflation; oesophageal balloon only as last resort and with extreme caution
Secondary Prevention
- EVBL + non-selective beta-blocker (propranolol or carvedilol): reduces portal pressure and variceal rebleeding; start once acute bleed controlled
ICU-Specific Considerations
Airway and Aspiration
- Massive UGIH with haematemesis → high aspiration risk during endoscopy
- Intubate before endoscopy if: reduced consciousness, haemodynamic instability, inability to protect airway
- RSI with cricoid pressure; suction immediately available
Coagulopathy in Cirrhosis
- Cirrhotic coagulopathy is complex: INR elevated but does not predict bleeding risk (INR measures PT which is dependent on liver-produced clotting factors; does not account for reduced protein C/S or dysfunctional platelets)
- TEG/ROTEM-guided transfusion is preferred over PT-based triggers in cirrhosis
- Platelet transfusion threshold: <50 ×10⁹/L with active bleeding
- Avoid excessive FFP (increases portal venous pressure, worsens portal hypertension)
Viva Questions
1. A patient with cirrhosis presents with massive haematemesis and a GCS of 14. How do you manage them?
Immediately: A — assess and protect airway; this patient is at high risk of aspiration given haematemesis and reduced GCS — I have a low threshold to intubate before endoscopy. B — high-flow oxygen. C — two large-bore cannulae; bloods including group and crossmatch, coagulation, LFTs, FBC; begin fluid resuscitation but avoid over-resuscitation (target SBP ~90, Hb ~70 after transfusion — liberal transfusion worsens portal pressure). Start terlipressin immediately (2 mg IV) — vasoactive therapy before endoscopy reduces portal pressure and mortality. Start ceftriaxone 1 g IV — mandatory antibiotic prophylaxis in cirrhotic GI bleeding. Target INR correction with TEG/ROTEM guidance if available; platelet transfusion if <50. Once stabilised: urgent OGD within 12 hours (sooner if haemodynamic instability persists); pre-endoscopy erythromycin 250 mg IV 30 minutes before. At OGD: variceal band ligation of oesophageal varices if found. If fail after two attempts: consider early TIPS — particularly important in Child-Pugh C cirrhosis or HVPG >20 mmHg. If TIPS not immediately available and massive rebleeding: balloon tamponade as bridge.
2. What is the evidence base for the transfusion threshold in upper GI haemorrhage?
The TRICC trial established that a restrictive transfusion threshold (Hb <70 g/L) is non-inferior to a liberal threshold (<100 g/L) in critically ill patients (see TRIC journal club). For UGIH specifically, a Spanish RCT (Villanueva et al, NEJM 2013) randomised 921 patients with acute UGIH to restrictive (Hb trigger 70 g/L) or liberal (Hb trigger 90 g/L) transfusion. Restrictive strategy was associated with significantly lower 45-day mortality (5% vs 9%), lower rebleeding rate, and fewer complications. The mechanism: over-resuscitation and liberal transfusion raise portal venous pressure in variceal bleeding, increase rebleeding risk. Current UK guideline: target Hb ≥70 g/L in all UGIH; ≥80 g/L in patients with cardiac ischaemia. Avoid raising Hb higher than necessary.
3. What is the role of the Sengstaken-Blakemore tube and what are the risks?
The Sengstaken-Blakemore tube is a rescue device for massive, life-threatening variceal haemorrhage that cannot be controlled endoscopically. It has a gastric balloon (inflated in the stomach to compress gastric varices and tamponade bleeding at the gastro-oesophageal junction) and an oesophageal balloon (less commonly used; compresses oesophageal varices directly). Inflation of the gastric balloon alone controls bleeding in 60–90% of cases. It is a bridge to definitive therapy (TIPS or surgery), not a definitive treatment — bleeding invariably recurs when deflated if the underlying portal hypertension is untreated. Risks are significant: oesophageal rupture (from over-inflation, malposition, or inflation of oesophageal balloon when tube misplaced in oesophagus); aspiration (patient must be intubated); airway obstruction if tube migrates. Given these risks, the SB tube should only be used in intubated patients, by experienced operators, for a maximum of 24 hours, with immediate plans for TIPS or surgical rescue.
