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  • Occurs after heparin has been withdrawn (median time of 14 days after heparin withdrawl)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:
  • Release of procoagulants by activated platelets
  • 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

Deep vein thrombosis (DVT)

• (The classical symptoms of DVT include: Pain, redness and swelling of the affected area, dilation of the surface veins.

Pulmonary embolism

• Three major clinical presentations can exist: difficulty in breathing with or without pleuritic chest pain and blood stained sputum, syncope (associated with massive pulmonary embolism). In the elderly, it may mimick as indolent pneumonia or heart failure. Pulmonary embolism should be suspected in all patients who present with the following symptoms, without an alternative obvious cause.
• Dyspnea (new or worsening)
• Chest pain
• Sustained Hypotension

Limb gangrene

• Can be seen in both upper and lower extremities. However, lower extremities DVT are commoner compared to upper.