4.1 Upper Gastrointestinal Bleeding & Dyspepsia

Upper Gastrointestinal Bleeding & Dyspepsia

Acute upper gastrointestinal bleeding (UGIB) is defined as intraluminal haemorrhage arising proximal to the ligament of Treitz (the suspensory muscle of the duodenum). In the United Kingdom, UGIB accounts for approximately 50 to 70 hospital admissions per 100,000 adults annually, carrying an overall inpatient mortality of 8% to 10%. Clinical success hinges on rapid hemodynamic resuscitation, accurate pre-endoscopy risk stratification, timely pharmacological intervention, and urgent therapeutic endoscopy.

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1. Clinical Presentation & Differential Aetiology

UGIB classically presents with:

• Haematemesis: Vomiting of frank bright red blood or dark "coffee-ground" altered blood (haematin produced by gastric acid oxidation).
• Melaena: Passage of black, tarry, foul-smelling stools resulting from bacterial degradation of haemoglobin over transit through the small and large bowel.
• Haematochezia: Brisk passage of fresh red rectal blood, typically seen in massive, exsanguinating upper GI haemorrhage accompanied by hemodynamic shock.

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2. Emergency Resuscitation & Transfusion Strategy

Initial resuscitation must proceed according to the systematic ABCDE algorithm:

1. Vascular Access: Immediately insert two large-bore peripheral intravenous cannulae (14G or 16G) into the antecubital fossae. Central venous access should not delay peripheral wide-bore cannulation.
2. Urgent Blood Sampling: Full blood count, urea and electrolytes (U&Es), liver function tests, coagulation screen (INR, prothrombin time, fibrinogen), and cross-match for 2 to 4 units of packed red blood cells (or activate the local hospital Major Haemorrhage Protocol if massive bleeding and hemodynamic instability are present).
3. Biochemical Hallmark: The urea-to-creatinine ratio is characteristically disproportionately elevated. Digestion and intestinal absorption of blood proteins, combined with hypovolaemic prerenal azotaemia, leads to a markedly elevated blood urea while serum creatinine remains comparatively stable.

Restrictive Red Blood Cell Transfusion Strategy

Both NICE clinical guidelines (CG141) and the British Society of Gastroenterology (BSG) mandate a restrictive transfusion strategy:

• Standard Threshold: Once major haemorrhage is controlled, transfuse red cells when haemoglobin is below 70 g/L, targeting a post-transfusion haemoglobin of 70–90 g/L (NICE NG24 restrictive thresholds; BSG uses the same 70 g/L trigger). During massive haemorrhage, transfusion follows the major haemorrhage protocol and clinical response, not a number.
• Cardiovascular Disease Exception: In patients with known, significant ischaemic heart disease or active acute coronary syndrome, use a transfusion trigger of <80 g/L, targeting 80–100 g/L.

Coagulopathy & Reversal Protocols

• Platelets: Transfuse adult therapeutic doses of platelets only if actively bleeding with a platelet count <50 × 10⁹/L.
• Fresh Frozen Plasma (FFP): Administer FFP (15 mL/kg) if the INR is >1.5 in the context of active major haemorrhage.
• Warfarin Reversal: Administer Prothrombin Complex Concentrate (PCC) (e.g. Beriplex, 25–50 IU/kg) and intravenous Vitamin K (phytomenadione 5–10 mg) for immediate reversal in life-threatening bleeding.
• DOAC Reversal: Specific reversal agents include idarucizumab for dabigatran, or andexanet alfa (or PCC 50 IU/kg) for factor Xa inhibitors (apixaban, rivaroxaban).

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3. Pre-Endoscopy vs Post-Endoscopy Risk Stratification

Clinical risk scores differentiate patients requiring urgent critical care and immediate endoscopy from those suitable for outpatient management.

Glasgow-Blatchford Bleeding Score (GBS)

The Glasgow-Blatchford Score is calculated pre-endoscopy using routine bedside clinical and laboratory parameters. It assesses the risk of requiring intervention (transfusion, endoscopic therapy, or surgery) or dying.

Full Rockall Score

The Full Rockall Score is calculated post-endoscopy to quantify the risk of rebleeding and all-cause mortality. It integrates:

1. Age: (<60 = 0; 60–79 = 1; ≥80 = 2)
2. Shock: (No shock = 0; Tachycardia HR >100 = 1; Hypotension SBP <100 = 2)
3. Co-morbidity: (None = 0; CAD/Heart failure = 2; Renal failure/Liver failure/Metastatic malignancy = 3)
4. Endoscopic Diagnosis: (Mallory-Weiss/No lesion = 0; PUD/Erosions = 1; Upper GI malignancy = 2)
5. Stigmata of Recent Haemorrhage: (Clean base/Flat spot = 0; Blood in stomach/Adherent clot/Visible spurting vessel = 2)

A post-endoscopy Rockall score <3 denotes low risk of death (<5%), whereas a score ≥8 confers a mortality exceeding 40%.

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4. Suspected Variceal Haemorrhage Protocol

Any patient presenting with upper GI bleeding who exhibits stigmata of chronic liver disease (spider naevi, palmar erythema, jaundice, ascites, caput medusae, splenomegaly) or a history of cirrhosis must be treated as a suspected variceal haemorrhage immediately.

Pharmacological Pre-Endoscopic Management

1. Intravenous Terlipressin: Administer 2 mg IV bolus immediately upon suspicion, continued at 1–2 mg every 4–6 hours (or QDS) for up to 48–72 hours until haemostasis is secure. Terlipressin is a synthetic vasopressin analogue that induces splanchnic vasoconstriction, reducing portal venous inflow and decreasing variceal pressure. Adverse effects: Peripheral ischaemia, bradycardia, coronary vasospasm, and hyponatraemia.
2. Prophylactic Broad-Spectrum Antibiotics: Administer intravenous ceftriaxone (1 g once daily) or co-amoxiclav prior to endoscopy. Cirrhotic patients experiencing UGIB are at extreme risk of bacterial translocation and spontaneous bacterial peritonitis. Prophylactic antibiotics significantly reduce rebleeding rates and decrease all-cause mortality.
3. Proton Pump Inhibitors: Routine pre-endoscopic PPI infusions are not indicated for variceal bleeding and should be withheld until diagnostic endoscopy clarifies the mucosal pathology.

Endoscopic & Interventional Rescue

• First-Line Endoscopy: Must be performed within 24 hours of presentation (or emergently once resuscitated if persistently hypotensive). The definitive treatment of choice for oesophageal varices is Endoscopic Variceal Band Ligation (EVBL). Sclerotherapy is reserved only when band ligation is technically unfeasible.
• Gastric Variceal Bleeding: Managed with endoscopic injection of N-butyl-2-cyanoacrylate tissue glue (histoacryl) mixed with Lipiodol.
• Balloon Tamponade (Sengstaken-Blakemore Tube): Employed strictly as a temporary bridge to definitive care in catastrophic, uncontrolled exsanguinating bleeding. The gastric balloon is inflated with 200–250 mL of air and gentle traction is applied to compress the gastro-oesophageal junction. The oesophageal balloon is inflated only if bleeding continues. Due to risk of pressure necrosis and oesophageal rupture, tamponade must never exceed 24 hours. The patient must be endotracheally intubated prior to tube insertion to prevent pulmonary aspiration.
• Transjugular Intrahepatic Portosystemic Shunt (TIPS): Radiological creation of a low-resistance channel between the hepatic vein and an intrahepatic branch of the portal vein using an expandable covered stent. Indicated as "pre-emptive/early TIPS" within 72 hours for high-risk patients (Child-Pugh C or Child-Pugh B with active bleeding) or as salvage rescue for failed endoscopic haemostasis.
• Secondary Prevention: Once stabilized, commence oral non-selective beta-blockers (carvedilol 6.25–12.5 mg daily or propranolol) alongside repeated elective outpatient band ligation every 2 to 4 weeks until varices are completely obliterated.

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5. Non-Variceal Peptic Ulcer Haemorrhage

Peptic ulcer disease accounts for half of all UGIB cases. Management focuses on targeted endoscopic haemostasis and acid suppression.

Forrest Classification & Endoscopic Stigmata

• Forrest Ia (Arterial spurting) & Ib (Oozing haemorrhage): High rebleeding risk (~80%); mandates dual endoscopic haemostasis.
• Forrest IIa (Non-bleeding visible vessel): High rebleeding risk (~50%); mandates dual endoscopic haemostasis.
• Forrest IIb (Adherent clot): Intermediate rebleeding risk; endoscopic clot removal and underlying vessel treatment.
• Forrest IIc (Flat pigmented spot) & III (Clean ulcer base): Low rebleeding risk (<5%); no endoscopic intervention required; early oral re-feeding and discharge.

Dual-Modality Endoscopic Haemostasis

Monotherapy with adrenaline injection is inadequate because adrenaline provides only temporary vasospasm and local mechanical tamponade without definitive vessel thrombosis. Guidelines strictly mandate dual-modality therapy:

• Adrenaline (1:10,000) injection PLUS
• Mechanical modality: Endoscopic hemoclips (through-the-scope clips or over-the-scope clips), OR
• Thermal contact coagulation: Bipolar electrocoagulation or heater probe coagulation.

High-Dose Post-Endoscopy Proton Pump Inhibitors

Following successful endoscopic haemostasis for high-risk ulcer stigmata (Forrest Ia–IIa), administer high-dose intravenous PPI therapy (e.g. omeprazole 80 mg IV bolus followed by 8 mg/hour continuous infusion for 72 hours, or high-dose intermittent IV omeprazole 40 mg twice daily). Suppressing gastric acidity to maintain intragastric pH >6 prevents pepsin activation and promotes platelet aggregation and fibrin clot stabilization.

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6. Dyspepsia & Peptic Ulcer Disease: Investigation & Eradication

Dyspepsia refers to a complex of upper abdominal symptoms including epigastric pain or discomfort, heartburn, acid regurgitation, early satiety, and nausea.

NICE NG12 Upper GI Cancer Criteria

NICE NG12 (Suspected cancer: recognition and referral) uses the suspected cancer pathway (the referral route formerly called the "2-week wait"):

• Urgent direct-access upper GI endoscopy (within 2 weeks): dysphagia at any age, or age 55 or over with weight loss AND any of upper abdominal pain, reflux or dyspepsia.
• Suspected cancer pathway referral (consider): an upper abdominal mass consistent with stomach cancer.
• Non-urgent direct-access endoscopy (consider), age 55 or over: treatment-resistant dyspepsia; upper abdominal pain with low haemoglobin; raised platelet count with nausea, vomiting, weight loss, reflux, dyspepsia or upper abdominal pain; or nausea or vomiting with weight loss, reflux, dyspepsia or upper abdominal pain.

Uncomplicated Dyspepsia (No Red Flags, NICE CG184)

1. Review medicines (stop NSAIDs or aspirin if possible) and offer lifestyle advice (weight loss, smoking cessation, alcohol reduction, avoiding late meals).
2. Offer either "test and treat" for H. pylori (carbon-13 urea breath test or stool antigen) or a full-dose PPI for 4 weeks; if symptoms continue, try the other approach.
3. H. pylori positive: 7-day triple eradication therapy (PPI plus amoxicillin plus clarithromycin or metronidazole). Retest only if symptoms persist or there is a specific indication (for example a peptic ulcer).

Helicobacter pylori Diagnostic Testing

• Carbon-13 Urea Breath Test (¹³C-UBT) or Stool Antigen Test (SAT): High sensitivity and specificity (>95%).
• Critical Pre-Test Requirement: Patients must stop taking proton pump inhibitors for at least 2 weeks and antibiotics for at least 4 weeks prior to breath or stool testing. Failure to withhold these agents suppresses bacterial load and causes false-negative results.
• Serology (Serum IgG): Demonstrates past exposure; cannot differentiate active infection from successfully treated infection. Not recommended for clinical management.

First-Line 7-Day H. pylori Eradication Triple Therapy

In the UK, first-line eradication therapy consists of a 7-day twice-daily oral regimen:

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Reflux, Barrett's Oesophagus, Hiatus Hernia & Upper GI Cancer

• Gastro-oesophageal reflux disease (NICE CG184): heartburn and regurgitation; offer lifestyle advice and a full-dose PPI for 4 weeks (8 weeks for severe oesophagitis), then the lowest dose that controls symptoms. Alarm features (dysphagia, weight loss, anaemia, persistent vomiting, age 55 or over with new symptoms) need endoscopy under NICE NG12.
• Barrett's oesophagus: columnar metaplasia of the lower oesophagus from chronic reflux; it is the precursor of oesophageal adenocarcinoma. Patients have PPI treatment and endoscopic surveillance; dysplasia is treated endoscopically (resection and ablation).
• Hiatus hernia: sliding hernias (most common) worsen reflux; rolling (para-oesophageal) hernias can twist or strangulate (gastric volvulus) and are repaired surgically if symptomatic.
• Oesophageal cancer: adenocarcinoma of the lower third (reflux, Barrett's, obesity) or squamous cell carcinoma of the upper and middle thirds (smoking, alcohol). It presents with progressive dysphagia (solids, then liquids) and weight loss; dysphagia at any age needs urgent direct-access endoscopy.
• Gastric cancer: adenocarcinoma linked to H. pylori, smoking and diet; presents with dyspepsia, weight loss, anaemia, vomiting or an epigastric mass, and sometimes a left supraclavicular node (Virchow's node, Troisier's sign).