Medicine · Liver Disease (Cirrhosis, Hepatitis, Autoimmune, Wilson's, Hemochromatosis)

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
Correct answer: A. INR reflects procoagulant deficiency but ignores elevated factor VIII and reduced protein C, so it misses the rebalanced haemostatic state

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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