A 60-year-old man with cirrhosis has INR 1.9, platelet count 70,000/mm3, and fibrinogen 120 mg/dL. He requires dental extraction. His physician notes he has never had abnormal bleeding despite prior procedures. Why is the INR an unreliable predictor of bleeding risk in cirrhosis?
- A INR reflects procoagulant deficiency but ignores elevated factor VIII and reduced protein C, so it misses the rebalanced haemostatic state ✓
- B INR reagents are calibrated only for warfarin-treated patients
- C INR is prolonged by thrombocytopenia through platelet factor 3 depletion
- D INR rises with hypoalbuminaemia because vitamin K dependent factors bind albumin
Explanation
Cirrhosis produces simultaneous reductions in procoagulants (II, VII, IX, X) and anticoagulants (protein C, protein S, antithrombin), along with elevated factor VIII and endothelial-derived von Willebrand factor, yielding a rebalanced haemostatic state. The INR measures only the procoagulant side, so it correlates poorly with actual bleeding risk and was never validated for this purpose in cirrhosis; its legitimate use is as a MELD component. Viscoelastic testing better captures global haemostasis.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
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