Heparin-induced thrombocytopenia history and symptoms

Heparin-induced thrombocytopenia
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Heparin-induced thrombocytopenia is diagnosed when the platelet count falls by > 50% typically after 5-10 days of heparin therapy. Unlike other immune mediated thrombocytopenia (idiopathic thrombocytopenic purpura), the levels of platelet stays > 20,000 microl, thus frank clinical bleeding is less common in HIT when compared to other conditions, where the platelet may fall below 10,000/ microl.

History

Heparin therapy

• Occurs commonly after 5-10 days of initiation of heparin therapy. Onset of HIT after 2 weeks of heparin therapy is uncommon. Earlier onset of HIT is usually seen in patients who have been previously treated with heparin (1-3 months back) and have circulating HIT antibodies in them. In these patients the median time of platelet fall is less than 12 hours after the start of heparin administration
• Delayed onset HIT:
  • Occurs after heparin has been withdrawn (median time of 14 days after heparin withdrawl)
  • High titer platelet-activating antibodies that have both increased heparin-dependent and heparin independent platelet activation
  • The phenomena is sometimes explained by the fact that unusually high antibody levels react with platelet-associated Platelet Factor 4 (PF4) bound to non-heparin glycosaminoglycans like chondroitin sulfate and not to heparin.
• The incidence of delayed onset HIT are less compared to other forms of HIT.

Cardiac surgery

• In cardiac surgery patients, decrease in the platelet count by > 50 % can occur within 3 days of surgery. This may be attributed to prolonged contact of platelets with the artificial surface and administration of large amount of unfractionated heparin (UFH). However, a diagnosis of HIT is more probable if a fall in the platelet counts ≥50 % is seen after 5-10 days of heparin therapy.

Symptoms

• Presents with symptoms suggestive of arterial and venous thrombosis. The increased incidences of thrombosis may be attributed to:
  • Activated platelets release procoagulants
  • Release of platelet membranes that in turn activates coagulation pathways
  • HIT antibodies bind and activate endothelial cells resulting in release of tissue factor and thrombin
• Venous thrombosis