IM15.1-18 | GI Bleeding — Practice Quiz

Correct. Acute GI haemorrhage depletes intravascular volume, reducing venous return (preload). Baroreceptors trigger compensatory tachycardia and vasoconstriction. This is the haemorrhagic shock response. In the first 4-6 hours, haematocrit may be deceptively normal due to compensatory vasoconstriction — serial measurements are required.

Haemorrhagic shock follows four progressive phases (I-IV) based on volume lost. Class II shock (loss 750-1500 mL): tachycardia >100, normal BP, prolonged capillary refill. The haematocrit is unreliable within the first 4-6 hours of acute haemorrhage.

Haemorrhagic shock results from acute intravascular volume depletion: reduced venous return lowers cardiac output, triggering compensatory tachycardia and vasoconstriction. The haematocrit may be falsely normal in the first 4-6 hours of acute haemorrhage.

Correct. The Glasgow-Blatchford Score is a pre-endoscopy risk stratification tool that uses: BUN (mmol/L), haemoglobin (g/dL — with different thresholds for men and women), systolic blood pressure, pulse rate, and clinical features (melaena, syncope, hepatic disease, cardiac failure). A score of 0 identifies very-low-risk patients who may be managed as outpatients.

Glasgow-Blatchford Score = pre-endoscopy (identifies need for intervention). Rockall Score = post-endoscopy (predicts rebleeding/mortality). These scores are complementary, not interchangeable. Score 0 on Glasgow-Blatchford = safe for outpatient management.

The Glasgow-Blatchford Score is calculated before endoscopy using: BUN, haemoglobin, systolic blood pressure, pulse, and clinical features (melaena, syncope, hepatic disease, cardiac failure). It is distinct from the Rockall Score, which incorporates endoscopic findings and is used post-endoscopy.

Correct. A BUN:creatinine ratio above 20:1 suggests an upper GI source (digested blood raises BUN). A ratio of 12:1 is within normal range, pointing to a lower GI source. The absence of haematemesis and the presence of bright red rectal blood without melaena further support a lower GI location.

BUN:creatinine ratio >20:1 = upper GI source (digested protein absorbed). Haematemesis/melaena = upper GI. Haematochezia = usually lower GI. Massive upper GI bleeding can mimic lower GI bleeding with haematochezia, but haemodynamic instability and raised BUN:creatinine will be present.

The BUN:creatinine ratio is a useful discriminator: a ratio >20:1 suggests upper GI bleeding (digested blood absorbed raises BUN). A normal ratio (12:1 here), combined with haematochezia and absent haematemesis, points to a lower GI source. Rapid upper GI bleeding can occasionally present with haematochezia but usually shows a raised BUN:creatinine ratio.

Correct. The Forrest classification grades peptic ulcer bleeding stigmata: Ia = spurting arterial haemorrhage (highest rebleed risk, >90%); Ib = oozing haemorrhage; IIa = visible non-bleeding vessel; IIb = adherent clot; IIc = flat pigmented spot; III = clean base (lowest risk, <5%). Forrest Ia and IIa require endoscopic haemostasis and high-dose IV PPI infusion post-procedure.

Forrest classification guides endoscopic intervention: Ia/Ib/IIa = high-risk stigmata requiring dual endoscopic therapy (injection + thermal or clip). Forrest IIc and III = low risk, PPI alone sufficient. High-dose IV PPI post-endoscopy reduces rebleed rate by raising intragastric pH, stabilising the clot.

The Forrest classification: Ia = spurting arterial haemorrhage (highest risk), Ib = oozing, IIa = visible vessel, IIb = adherent clot, IIc = flat spot, III = clean base. Classes Ia, Ib, and IIa require endoscopic therapy. High-dose IV PPI (omeprazole 80 mg bolus then 8 mg/hr infusion) should follow endoscopic haemostasis for high-risk lesions.

Correct. For suspected variceal bleeding, vasoactive therapy should start as soon as the diagnosis is suspected — before endoscopy. Terlipressin (a vasopressin analogue) reduces portal pressure by splanchnic vasoconstriction. Octreotide (somatostatin analogue) inhibits glucagon and reduces splanchnic blood flow. Both are started immediately. Terlipressin is preferred if available as it reduces mortality.

Variceal bleeding bundle (all Level 1A evidence): (1) terlipressin or octreotide — start on admission when variceal bleed suspected; (2) endoscopic band ligation (EVL) — within 12 hours; (3) prophylactic antibiotics (ceftriaxone 1 g/day IV for 5-7 days) — reduce bacterial infection and rebleeding; (4) restrictive transfusion (Hb target 7-8 g/dL).

For suspected variceal UGIB, vasoactive drugs — terlipressin or octreotide — are started immediately upon suspicion, before endoscopic confirmation. High-dose PPI is the correct choice for non-variceal UGIB. Beta-blockers are contraindicated acutely. Vasoactive therapy + band ligation + prophylactic antibiotics is the evidence-based variceal bundle.

Correct. The TRICC trial and subsequent meta-analyses established that a restrictive transfusion threshold (Hb <7 g/dL, target 7-9 g/dL) is superior to a liberal strategy in upper GI bleeding including variceal bleeding. In cardiovascular disease, the threshold is relaxed to Hb <8 g/dL. Liberal transfusion in variceal bleeding increases portal pressure and rebleed risk.

Restrictive transfusion in GI bleeding: PRBCs when Hb <7 g/dL (no CVD) or <8 g/dL (CVD present). Target Hb 7-9 g/dL. Overtransfusion in variceal bleeding raises portal pressure and increases rebleeding. Platelet transfusion threshold: <50 × 10^9/L in active bleeding. FFP: if INR >1.5.

The restrictive transfusion strategy (threshold Hb <7 g/dL, target 7-9 g/dL) is evidence-based for GI bleeding in patients without cardiovascular disease. In those with cardiovascular disease the threshold is <8 g/dL. Liberal transfusion in variceal bleeding paradoxically worsens outcomes by raising portal pressure.

Correct. After endoscopic haemostasis for high-risk peptic ulcer, the evidence-based sequence is: (1) high-dose IV PPI infusion (omeprazole 80 mg bolus then 8 mg/hr for 72 hours) to stabilise the clot; (2) transition to oral PPI; (3) H. pylori eradication — standard first-line triple therapy is PPI + clarithromycin + amoxicillin for 14 days, or bismuth quadruple therapy in clarithromycin-resistance areas. Eradication is confirmed at 4-6 weeks and reduces ulcer recurrence from 70% to <10%.

H. pylori eradication in PUD: first-line = PPI + clarithromycin + amoxicillin (14 days). Confirm eradication by urea breath test or stool antigen at 4-6 weeks (stop PPI 2 weeks before testing). Failure to eradicate is the commonest cause of ulcer recurrence.

Post-endoscopy management of bleeding peptic ulcer with H. pylori: (1) high-dose IV PPI for 72 hours; (2) oral PPI continuation; (3) H. pylori eradication (PPI + clarithromycin + amoxicillin for 14 days, confirmed at 4-6 weeks). Eradication dramatically reduces recurrence from ~70% to <10%. NSAIDs should be stopped if possible.

Correct. A Mallory-Weiss tear is a mucosal laceration at the gastro-oesophageal junction caused by sudden increase in intragastric pressure from retching/vomiting. The classic history is forceful non-bloody vomiting followed by haematemesis. It is the second commonest cause of non-variceal UGIB. Most (90%) stop spontaneously; endoscopic therapy if active bleeding.

Causes of UGIB by frequency: peptic ulcer disease (35-50%), oesophageal varices (10-20%), Mallory-Weiss tear (10-15%), oesophagitis (5-10%), Dieulafoy's lesion (2-5%), gastric cancer (<5%). History of retching before haematemesis = Mallory-Weiss until proven otherwise.

The classic presentation of Mallory-Weiss tear is: forceful non-bloody vomiting (retching) preceding haematemesis. The mucosal tear at the GOJ results from sudden intragastric pressure surge. Varices are associated with stigmata of chronic liver disease. Dieulafoy's lesion presents as massive painless haematemesis without a precipitant. PUD typically has dyspeptic history.

Correct. Postural hypotension — a fall in systolic BP of ≥20 mmHg or diastolic ≥10 mmHg on standing — indicates at least 1000-1500 mL of volume loss (Class II haemorrhage). It is the most sensitive bedside volume assessment tool. A resting hypotension implies Class III haemorrhage (>1500 mL).

Bedside volume assessment sequence: (1) resting BP and pulse; (2) postural blood pressure test (systolic drop ≥20 mmHg = significant volume loss >1 L); (3) capillary refill; (4) skin turgor, mental state. This clinical sequence is more important than initial haematocrit, which may be deceptively normal.

Postural hypotension (systolic drop ≥20 mmHg on standing) indicates at least Class II haemorrhage (>1000-1500 mL loss). Resting tachycardia alone suggests Class I-II; resting hypotension indicates Class III (>30% volume loss). Postural BP assessment is the single most informative bedside sign in volume assessment of GI bleeding.

Correct. Glasgow-Blatchford Score scoring: BUN 7.5-10 mmol/L (note: BUN 28 mg/dL = approximately 10 mmol/L, scores 2); Hb 12-13 g/dL men or 10-11.9 g/dL women (Hb 9 g/dL scores 3 for a man); systolic BP >109 (scores 0); pulse <100 (scores 0); no melaena (0); no syncope (0). Total ≈ 3-5, which requires admission and endoscopy but is not in the emergency range. A score of 0 = outpatient safe.

Glasgow-Blatchford Score of 0 = very low risk (outpatient management). Score 1-5 = moderate risk (admission, endoscopy within 24 hours). Score >6 = high risk (urgent endoscopy). This score outperforms clinical judgment alone for identifying patients who need intervention.

The Glasgow-Blatchford Score is calculated from pre-endoscopy parameters: BUN, haemoglobin, systolic BP, pulse, and clinical features. A score of 0 identifies very low-risk patients for outpatient management. Scores above 0 indicate need for admission and endoscopy. The exact score here places this patient in the moderate-risk admitted category.