Gastrointestinal Bleeding — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Margaret O'Brien, 76 years old. [1]

Presenting complaint: Three episodes of haematemesis (bright red with clots) and dark melaena over the past 12 hours. Felt dizzy on standing this morning and nearly collapsed in the bathroom. [1]

Past history:

• Paroxysmal atrial fibrillation — on apixaban 5 mg BD (CHA2DS2-VASc 4)
• Ischaemic heart disease — NSTEMI 3 years ago, DES to LAD, on aspirin 100 mg daily
• Type 2 diabetes (HbA1c 62 mmol/mol) — on metformin
• Hypertension
• Osteoarthritis — started naproxen 500 mg BD two weeks ago for knee pain
• Stage 3a CKD (baseline creatinine 120, eGFR 48) [1]

Current medications: apixaban 5 mg BD, aspirin 100 mg daily, atorvastatin 40 mg, metformin 1 g BD, perindopril 5 mg, naproxen 500 mg BD. [1]

Examination findings (trainee elicits):

• Pale, cool peripheries, capillary refill 3 seconds
• Blood pressure 96/60 supine, 82/52 standing (postural drop); pulse 108/min irregularly irregular
• Abdomen soft, non-tender, no organomegaly, bowel sounds present
• Rectal examination: melaena
• No stigmata of chronic liver disease [1]

Investigations:

• Hb 74 g/L (baseline 128 six months ago), MCV 78, platelets 198, WCC 11.2
• Urea 15.8 mmol/L, creatinine 142 micromol/L, eGFR 40
• INR 1.2, APTT 32, albumin 33, normal LFTs
• Troponin 24 (background, no chest pain)
• ECG: AF, HR 108, old anterior T wave changes [1]

Candidate's structured presentation (model)

Opening statement (SASPOP): [1]

"Mrs O'Brien is a 76-year-old woman who presents with an acute upper gastrointestinal bleed — haematemesis and melaena with a postural drop — over 12 hours. She has a background of paroxysmal atrial fibrillation on apixaban, ischaemic heart disease with a prior stent on aspirin, type 2 diabetes, hypertension, stage 3 CKD, and she recently started naproxen for osteoarthritis. [1]

Her main problems are:

1. Acute upper GI haemorrhage with shock — most likely a peptic ulcer given the naproxen and aspirin, though the differential includes erosive gastritis
2. Haemodynamic compromise — postural drop, tachycardia, cool peripheries
3. Anticoagulation with apixaban and antiplatelet therapy with aspirin — bleeding versus thrombotic risk
4. Ischaemic heart disease with a prior DES — the cardiovascular risk of anaemia and of stopping antiplatelets
5. CKD stage 3a — contributing to anaemia and drug handling
6. Multi-morbidity and polypharmacy requiring coordinated care"* [1]

Investigation summary: [1]

"Her bloods confirm a significant bleed — haemoglobin 74 with microcytosis suggesting some chronic component, urea of 15.8 disproportionately high relative to creatinine of 142, confirming an upper GI source. Her renal function has deteriorated from baseline, likely pre-renal from hypovolaemia. Her troponin is mildly elevated at 24, consistent with a type 2 myocardial injury from demand ischaemia in the setting of hypovolaemia and AF." [1]

Management plan: [1]

1. Resuscitation: two large-bore cannulae, crystalloid bolus, cross-match four units, urinary catheter to monitor perfusion. [1]

2. Restrictive transfusion: transfuse to a target of 80 to 90 g/L — she has ischaemic heart disease, so I use a higher threshold than the standard 70 g/L. Villanueva et al. (NEJM 2013) established restrictive transfusion improves survival, with acute coronary syndrome as the key exception. [1]

3. Anticoagulation: withhold apixaban immediately. For this life-threatening bleed, discuss reversal with haematology — andexanet alfa or prothrombin complex concentrate. Plan to resume apixaban in 7 to 14 days once haemostasis is secure, balancing her CHA2DS2-VASc thrombotic risk. [1]

4. Antiplatelet: continue aspirin for secondary cardiovascular prevention if possible; the risk of stent thrombosis outweighs the bleeding risk once haemostasis is achieved. Stop naproxen permanently. [1]

5. PPI infusion: esomeprazole 80 mg IV bolus then 8 mg/hour infusion — give the bolus now, before endoscopy. [1]

6. Endoscopy within 24 hours: if a bleeding ulcer is found, dual therapy (adrenaline + clip/thermal) followed by the 72-hour PPI infusion (Lau et al., NEJM 2000). [1]

7. Ongoing care: monitor for rebleeding, manage her AF rate, and coordinate multidisciplinary care across gastroenterology, cardiology, haematology, and nephrology. [1]

Examiner discussion questions

Q: "Her GBS is 13. What does that tell you?" [1]

"A Glasgow-Blatchford Score of 13 confirms she is high risk and requires admission, endoscopic therapy, and close monitoring. The GBS predicts the need for intervention — transfusion, endoscopic therapy, or surgery — and its strength is identifying low-risk patients suitable for outpatient care. A score this high means the probability of needing an intervention is very high. After endoscopy I will calculate her full Rockall score, which predicts mortality and will guide her level of care." [1]

Q: "Her troponin is 24. Is this an NSTEMI?" [1]

"In the setting of acute hypovolaemia from GI bleeding with atrial fibrillation at a rapid rate, the most likely explanation is a type 2 myocardial injury — demand ischaemia from reduced oxygen delivery relative to demand, rather than a type 1 plaque rupture. I would trend the troponin rather than treating it as an NSTEMI with antiplatelet intensification or anticoagulation, which would worsen her bleeding. The management is to correct the underlying problem — restore circulating volume with restrictive transfusion and control her heart rate — and the troponin should settle. If it rises steeply with chest pain or ECG changes, I would involve cardiology." [1]

Q: "When will you restart her apixaban?" [1]

"I will resume apixaban once haemostasis is secure and the bleeding source has been treated — typically 7 to 14 days after the bleed, weighing her thrombotic risk (CHA2DS2-VASc 4) against rebleeding risk. Premature permanent cessation is a common error that exposes her to stroke. If she needs to restart sooner because of very high thrombotic risk, I would discuss the timing with cardiology and haematology. While held, she should be monitored for thromboembolism." [1]

Q: "Endoscopy shows a duodenal ulcer with a visible vessel. What is your endoscopic and pharmacological management?" [1]

"Dual endoscopic therapy — adrenaline submucosal injection plus a haemoclip or thermal coagulation — because adrenaline alone has a high rebleeding rate. I will then continue the high-dose PPI infusion (80 mg bolus already given, then 8 mg/hour for 72 hours), which Lau et al. showed reduces rebleeding from 22 percent to under 7 percent. I will monitor her closely for 72 hours, as most rebleeding occurs in that window. After discharge I will test and treat H. pylori and continue a maintenance PPI, especially since she will resume aspirin and apixaban." [1]

DCE Short Case — Abdominal Examination

Instruction

"Examine this patient's abdomen. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates (cirrhotic model)

• Spider naevi on the anterior chest wall and neck (with central arteriole)
• Palmar erythema affecting the thenar and hypothenar eminences
• Jaundice — scleral icterus
• Palpable spleen — 2 cm below the costal margin (splenomegaly from portal hypertension)
• Firm, enlarged liver edge — or a small shrunken liver in advanced cirrhosis
• Ascites — shifting dullness, fluid thrill
• Caput medusae — dilated paraumbilical veins
• Asterixis — liver flap if encephalopathic [1]

Examination routine (step by step)

1. Approach and positioning: introduce, explain, position the patient supine with one pillow, expose the abdomen from xiphisternum to pubic symphysis. Ensure warm hands and good lighting.
2. General inspection from the end of the bed: note pallor, jaundice, cachexia, the use of accessory muscles, and any obvious distension.
3. Hands and arms: inspect for palmar erythema, clubbing, leukonychia, asterixis (ask the patient to hold their hands out with wrists cocked for 30 seconds). Take the pulse (irregular in AF).
4. Face and neck: sclerae for jaundice, eyes for anaemia, mouth for angular stomatitis and glossitis, neck for lymphadenopathy and JVP.
5. Chest: spider naevi (central arteriole that blanches on pressure and refills on release — pathognomonic of liver disease), gynaecomastia.
6. Abdominal inspection: distension, visible veins (caput medusae), scars, visible peristalsis.
7. Palpation: start away from any tender area, light then deep. Feel for the liver edge (firm, enlarged, or shrunken and impalpable), spleen, and any masses. Check for shifting dullness and a fluid thrill if ascites suspected.
8. Percussion and auscultation: percuss the liver span, check for shifting dullness, and listen for bowel sounds and a hepatic bruit. [1]

Presentation template

"I examined Mrs O'Brien's abdomen. On general inspection she is pale and has spider naevi on the anterior chest wall. There is palmar erythema and a liver flap is present. The pulse is irregularly irregular at 96 per minute. [1]

The abdomen is soft and non-tender. The liver edge is firm and palpable 3 cm below the costal margin. The spleen is palpable 2 cm below the costal margin. There is shifting dullness in the flanks consistent with ascites. Dilated veins radiate from the umbilicus — caput medusae. Rectal examination reveals melaena. [1]

In summary, these findings are consistent with decompensated chronic liver disease with portal hypertension presenting with an acute upper gastrointestinal bleed." [1]

Discussion questions

Examiner: "What is the differential of these findings?" [1]

"The combination of splenomegaly, ascites, caput medusae, and spider naevi points to portal hypertension from chronic liver disease, most commonly cirrhosis. The acute GI bleed is most likely variceal in this context, though peptic ulcer disease remains a possibility and would be distinguished at endoscopy. The differential for portal hypertension itself includes pre-hepatic causes (portal vein thrombosis), intra-hepatic causes (cirrhosis — the most common), and post-hepatic causes (right heart failure, Budd-Chiari)." [1]

Examiner: "What level of care does this patient need?" [1]

"Given the haemodynamic instability and high rebleeding risk, she needs a high-dependency or ICU-level bed for close monitoring in the first 24 to 72 hours — continuous observations, invasive blood pressure monitoring if shock persists, and rapid access to repeat endoscopy or interventional radiology if she rebleeds. The full Rockall score will quantify her mortality risk and support that decision." [1]