Page 1 of 1: Pulmonary embolism

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A 35-year old woman comes to the urgent care clinic with a 3-day history of right lower extremity swelling. She first noticed the swelling after returning from Spain via a transatlantic flight. She also reports mild shortness of breath. Her past medical history is significant only for tobacco abuse. Her only medication is oral contraceptive pills. Her vitals signs are normal.You obtain a V/Q scan that demonstrates a segmental pulmonary embolism. You admit the patient and begin an unfractionated heparin drip and warfarin. On hospital day 5 with continued heparin and warfarin, you notice that her platelet count has decreased from an admission count of 250,000/ml to the current value of 50,000/ml. Her hematocrit remains stable at 38% and she has no evidence of bleed. Which of the following is the mechanism that accounts for the thrombocytopenia?

A.Bleed from an undetermined site because of the heparin and warfarin

B.Decreased megakaryocyte production in the bone marrow

C.Direct effect of heparin on platelet activation

D.Formation of antibodies against platelet factor 4 complex

E.Formation of antibodies against platelet factor 8 complex

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D.Formation of antibodies against platelet factor 4 complex

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Heparin-induced thrombocytopenia represents one of the most severe drug-induced disorders of platelets. This syndrome is believed to be mediated through antibodies generated against a heparin-platelet factor 4 complex. Complexation of a sulfated mucopolysaccharide chain of heparin with a platelet granular protein (platelet factor 4) produces an allosteric modification of platelet factor 4 resulting in neoepitope formation and the generation of antiheparin-platelet factor 4 antibodies. These antibodies are capable of activating platelets by binding to heparin, platelet factor 4 and the Fc receptor on platelets, resulting in a complex pathophysiology involving ischemic, thrombotic, and inflammatory processes

D.Formation of antibodies against platelet factor 4 complex

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Right but the answer could have been C as well except for the following reasons:

There are two types of heparin-induced thrombocytopenia (HIT), HIT I and HIT II. HIT I is the more benign form and occurs from a direct effect of heparin on platelet activation. Additionally, HIT I occurs in 10 to 20% of patients exposed to heparin and occurs 1 to 4 days after exposure to heparin. The nadir platelet count is typically around 100,000/ml. In contrast, HIT II is mediated by the formation of antibodies against platelet factor complex 4, not platelet factor 8 (choice E) complex. The Fc portion of these antibodies then binds to receptors present on platelets, leading to further release of factor 4 and further positive FEEDBACK . Additionally, HIT II is characterized by an incidence of 1 to 3% of patients exposed to unfractionated heparin and a nadir platelet count of 35,000 to 55,000/ml. Further, HIT II occurs after 5 to 10 days of exposure to heparin. In this case the presentation is classical for HIT II, with thrombocytopenia developing after 5 days of heparin exposure and the patient having a platelet count of 50,000/ml.

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C.Direct effect of heparin on platelet activation

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C.Direct effect of heparin on platelet activation

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