Academe Learn
CBME Curriculum Preview

Page 19 of 19

IM15.1-18 | GI Bleeding — PBL Case

CLINICAL SETTING

It is 1 AM in the General Medicine emergency ward of a tertiary teaching hospital in Chennai. Dr Preethi, the second-year resident, is on call. A final-year MBBS student, Arjun, is accompanying her for his emergency posting. The emergency nurse calls: 'New patient — large vomit of blood, relatives are panicking.' Mr Durai, a 48-year-old autorickshaw driver from Tambaram, is brought in by his wife and two sons. He is sitting up on the stretcher, pale and sweating, a blood-soaked towel in his hand. His wife says: 'He vomited blood twice at home — the first time was a small amount, the second time was a lot, maybe a full bowl. He has had some dark stools for two days also.' Mr Durai denies any chest pain. He says he occasionally drinks alcohol at weddings — 'not more than once a month.' He takes no regular medications and has no known medical history. He has never had a hospital admission. Dr Preethi turns to Arjun: 'Before we touch him — what is the first thing you need to establish, and what do you need in the next 60 seconds?'

Trigger 1: First 60 Seconds — Stabilisation and the Primary Survey

Arjun rapidly assesses Mr Durai. Vital signs: BP 92/58 mmHg, pulse 124/min, respiratory rate 22/min, SpO2 96% on air, GCS 14/15 (confused about date). He is pale, cold, and clammy. Capillary refill is 4 seconds. There is no haematemesis at this moment. Dr Preethi inserts two large-bore IV cannulae, draws blood simultaneously, and hangs a rapid saline infusion. She sends bloods: CBC, LFT, PT/INR, U&E/creatinine, blood group and cross-match. She also asks for a urinalysis dipstick. While waiting, Arjun performs a rapid bedside examination. He notes: the abdomen is mildly distended with shifting dullness; the flanks are slightly full. He notices two or three small spider naevi on the upper chest. The hands show mild palmar erythema. Mr Durai's wife, standing nervously by the bed, asks: 'Doctor, is this very serious? He never had any problem before — he is completely healthy.'

DISCUSSION POINTS

  • Using the vital signs provided, classify Mr Durai's haemorrhagic shock. What volume of blood loss does this represent, and what is the physiological mechanism underlying his tachycardia and hypotension?
  • The physical examination reveals shifting dullness, spider naevi, and palmar erythema in a man with no known liver disease. What is the diagnostic significance of these findings, and how do they change your differential diagnosis from peptic ulcer disease to variceal haemorrhage?
  • How would you respond to the wife's question in an empathetic, non-judgmental manner, without withholding information or overwhelming a distressed family?
Click to reveal Trigger 2: Laboratory Results and the Glasgow-Blatchford Score (discuss previous trigger first!)

Trigger 2: Laboratory Results and the Glasgow-Blatchford Score

Results return 40 minutes later. CBC: Hb 6.8 g/dL, WCC 9.2 × 10^9/L, platelets 88 × 10^9/L. PT/INR: 1.8. LFT: bilirubin 44 micromol/L, ALT 52 U/L, AST 78 U/L, albumin 26 g/L, ALP 180 U/L. U&E: sodium 132 mEq/L, potassium 3.2 mEq/L, BUN 42 mg/dL (15 mmol/L), creatinine 0.9 mg/dL. Blood group: O positive. Dr Preethi looks at the results and says: 'Everything here tells me this is NOT a simple peptic ulcer.' She calculates the Glasgow-Blatchford Score and finds it is 14. She asks Arjun: 'What does this score tell us about what we need to do next, and how is it different from the Rockall Score?' The gastroenterology registrar is called. While waiting, Dr Preethi asks Arjun to re-examine Mr Durai and specifically look for signs of portal hypertension and hepatic decompensation.

DISCUSSION POINTS

  • Calculate the Child-Pugh Score from the laboratory results and clinical findings. What class does this correspond to, and what does this imply about Mr Durai's liver reserve and risk from this bleeding episode?
  • The Glasgow-Blatchford Score is 14. What action does this score mandate? Contrast the Glasgow-Blatchford Score with the Rockall Score: what does each measure, when is each applied, and why are they complementary rather than interchangeable?
  • The platelets are 88 × 10^9/L and INR is 1.8. What is the threshold for platelet transfusion and FFP in active GI bleeding? How does coagulopathy in cirrhosis (due to reduced synthetic function) differ from other causes of coagulopathy in terms of transfusion decisions?
Click to reveal Trigger 3: Variceal Bundle and the Emergency Endoscopy (discuss previous trigger first!)

Trigger 3: Variceal Bundle and the Emergency Endoscopy

The gastroenterology team arrives. Before taking Mr Durai to endoscopy, Dr Preethi asks Arjun to list the components of the variceal bleeding management bundle. Arjun hesitates — he remembers 'a drip and a scope' but is unsure of the specific drugs and doses. The gastroenterology registrar, Dr Sundar, explains: 'There are four components of the bundle. We have done two — resuscitation and calling the team. What are the two pharmacological components?' Terlipressin 2 mg IV is given immediately. IV ceftriaxone 1 g is started. Mr Durai is taken to endoscopy. Report: Active spurting from a large oesophageal varix at 30 cm from the incisors. Three band ligation rings applied. Haemostasis achieved. Dr Sundar returns and tells Arjun: 'We got the bleeding to stop, but the fight is not over. This man will rebleed in 48 hours if we do not do two more things correctly.' He asks Arjun what those two things are.

DISCUSSION POINTS

  • State all four components of the variceal bleeding management bundle, with the specific drug, dose, and route for each pharmacological component. What is the mechanism by which terlipressin reduces variceal bleeding?
  • Prophylactic antibiotics (ceftriaxone) were started before endoscopy. Explain why antibiotics are a mandatory component of variceal bleed management — what is the pathophysiological link between cirrhosis, bacterial translocation, and rebleeding?
  • The gastroenterologist warns of high rebleeding risk in 48 hours. What are the two interventions that must be optimised post-endoscopy to reduce the rebleeding risk? What would be the next step if Mr Durai rebleeds despite optimal endoscopic and pharmacological management?
Click to reveal Trigger 4: Transfusion Decision and the Restrictive Strategy (discuss previous trigger first!)

Trigger 4: Transfusion Decision and the Restrictive Strategy

Mr Durai returns to the HDU. His Hb on repeat testing is 6.4 g/dL. The nursing staff asks Dr Preethi: 'Should we transfuse him now? His Hb is 6.4 — it has dropped further.' Dr Preethi turns to Arjun. Before he can answer, the night intern says: 'I read that we should transfuse to at least 10 g/dL in a sick patient like this — he is a cirrhotic.' Dr Preethi corrects the intern: 'That would kill him.' She asks Arjun to explain to the intern, clearly and specifically, why the standard teaching about liberal transfusion is wrong in variceal bleeding, and what the correct threshold and target haemoglobin are. Mr Durai's wife approaches again: 'Doctor, they told me he needs blood — is it from a stranger? Can we give our blood? And is there any risk of HIV or hepatitis from this blood?'

DISCUSSION POINTS

  • Explain, using the underlying pathophysiology of portal hypertension, why liberal transfusion (targeting Hb 10 g/dL) worsens outcomes in variceal UGIB. What is the correct transfusion threshold and target, and how does this differ in a patient with concurrent cardiovascular disease?
  • The wife asks about blood transfusion safety, including the risk of HIV and hepatitis. How would you explain blood screening procedures in India (NACO guidelines for blood bank testing) and manage her concerns in a truthful yet reassuring way?
  • Mr Durai's platelets are 88 × 10^9/L and INR 1.8. Should he receive platelet concentrate and FFP? State the specific triggers for each, and explain whether the coagulopathy of cirrhosis behaves differently from anticoagulant-induced coagulopathy in terms of need for FFP.

Group Task Assignments

  • Construct the complete four-component variceal bleeding bundle for Mr Durai: drug names, doses, routes, timing, and evidence level for each component. Explain which component, if omitted, would cause the greatest increase in 30-day mortality, and justify your reasoning.
  • Calculate Mr Durai's Child-Pugh Score and MELD Score from the given data. Based on these scores, draft a discharge plan that includes: (a) secondary prophylaxis for variceal rebleeding, (b) referral criteria, and (c) lifestyle counselling including alcohol cessation framing for a patient who minimises his intake.
  • Develop a counselling script for Mr Durai and his family that covers: (a) the new diagnosis of cirrhosis; (b) the treatment given and why it was necessary; (c) the risk of rebleeding and how it will be monitored; (d) lifestyle changes including alcohol, diet, and medication review. The script should be in plain Tamil-accessible language (no medical jargon) and demonstrate empathetic, non-judgmental communication.
  • Compare the management of Mr Durai (suspected variceal UGIB in undiagnosed cirrhosis) with the management of a patient with a NSAID-induced duodenal ulcer (Forrest IIa) who presents with the same vital signs. Produce a parallel management table showing the five key differences in pharmacotherapy, transfusion strategy, endoscopic technique, post-procedure monitoring, and secondary prevention.

Learning Issues

Research these questions and bring your findings to the discussion.

  1. [IM15.3] What are the four phases of haemorrhagic shock, and how does the physiology of portal hypertension in cirrhosis alter the haemodynamic response to acute blood loss compared to a non-cirrhotic patient?
  2. [IM15.2] What are the parameters of the Glasgow-Blatchford Score, and how does it differ from the Rockall Score in terms of timing, parameters, and clinical purpose?
  3. [IM15.14] What is the mechanism of action of terlipressin in variceal haemorrhage, what are its contraindications and side effects, and what is the alternative if terlipressin is not available?
  4. [IM15.11] Why does a liberal transfusion strategy worsen outcomes in variceal UGIB? What is the evidence base for the restrictive transfusion threshold of Hb <7 g/dL, and when is this threshold modified?
  5. [IM15.12] What are the indications for FFP, platelet concentrate, and cryoprecipitate in acute GI bleeding? How does the coagulopathy of cirrhosis differ from other causes of raised INR in terms of clinical significance and transfusion decision-making?
  6. [IM15.17] At what point in the management of variceal UGIB should a TIPS (transjugular intrahepatic portosystemic shunt) referral be considered, and what Child-Pugh or MELD score threshold guides this decision?
  7. [IM15.18] How should the new diagnosis of cirrhosis be communicated to a patient and family who had no prior awareness of liver disease? What specific communication strategies support non-judgmental, patient-centred counselling about alcohol use?