Upper GI haemorrhage

Contents


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.