- A potentially life-threatening complication of heparin use
- Platelet count falls 50% or more from baseline.
- 5–10% daily risk for thromboembolism, amputation, and death
- Antibody-mediated prothrombotic disorder initiated by heparin administration
- Unlike other thrombocytopenias, heparin-induced thrombocytopenia (HIT) is an idiosyncratic reaction that results in thrombosis rather than bleeding.
- Two types: nonimmune heparin-associated thrombocytopenia (previously called HIT type I) and heparin-induced thrombocytopenia/thrombosis (HITT) (immune induced; previously called HIT type II)
- Nonimmune heparin-associated thrombocytopenia (HIT): more common, onset 1 to 4 days after starting heparin, mild thrombocytopenia (>100,000/mm3), few complications, platelet count may normalize spontaneously
- Immune HITT: less common, onset 5 to 14 days after primary exposure to heparin, thrombocytopenia often <100,000/mm3, but usually >20,000/mm3; high risk of thrombosis and mortality.
- HIT has three different patterns of onset: rapid, typical, and delayed. HIT has three different patterns of onset: rapid, typical, and delayed.
- Typical pattern is exhibited in 60% of the cases, resulting in fall in platelet decline 5 to 10 days after exposure.
- Rapid pattern is seen in 30% of the cases with decline in platelet count immediately after exposure to any heparin product
- Delayed-onset pattern occurs at an average of 9.2 days from initiation of heparin products. It can develop even after cessation of heparin.
- 0.1–5% of heparin-treated patients will experience thrombocytopenia, regardless of dose, schedule, or route of administration.
Etiology and Pathophysiology
- Nonimmune heparin-associated thrombocytopenia: potentially a result of direct platelet membrane binding with heparin
- HITT: Heparin can cause an increase in the blood concentration of platelet factor 4 (PF4), a chemokine. PF4 will form a complex with heparin, which acts as a substrate for immunoglobulin (IgG) antibodies. IgG antibodies recognize neoepitopes on PF4 and the resulting complex activates monocytes and platelets, resulting in increased production of thrombin and platelet-fibrin thrombi.
- Heparin/PF4 complex can, in turn, stimulate the production of specific antiheparin/PF4 complex antibodies. These antibodies cause platelet activation and a prothrombotic state. Ultimately, this hypercoagulable state leads to thromboembolic complications in many patients.
- Sources of heparin
- Heparin flushes (e.g., for arterial lines or heparin locks)
- Heparin-bonded catheters
- Unfractionated heparin (UFH)
- Low-molecular-weight heparin (LMWH) (enoxaparin, dalteparin)
- Postsurgical > medical > obstetric
- Postcardiopulmonary bypass (CPB) is the most significant risk factor.
- Surgical or trauma patients have a greater risk than medical or intensive care unit patients.
- Bovine UFH > porcine UFH > LMWH; UFH carries a risk 10 times greater than LMWH.
- Female > male
- Heparin duration >5 days
- Therapeutic anticoagulation doses result in a greater reduction in platelet count compared to prophylactic dose.
- Rare in pregnant females
- Inquire about recent heparin exposure and any history of HIT.
- Use of LMWH (vs. unfractionated), for a shorter duration, can reduce the risk of developing HIT.
- Properly document past HIT reactions in patient’s medical record. Develop a HIT recognition and treatment protocol.
- No form of heparin should be administered once the diagnosis of HIT is confirmed.
Commonly Associated Conditions
- Venous thrombosis: deep venous thrombosis (DVT), pulmonary embolism (PE), adrenal vein thrombosis with hemorrhagic infarction; seen more frequently among medical and postoperative orthopedic surgery patients
- Arterial thrombosis: myocardial infarction, stroke, mesenteric infarction, limb ischemia; seen more frequently among vascular and cardiac surgery patients
- Skin lesions (skin necrosis at site of injection)
- Acute systemic reactions
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Domino, Frank J., et al., editors. "Heparin-Induced Thrombocytopenia." 5-Minute Clinical Consult, 27th ed., Wolters Kluwer, 2020. Medicine Central, im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117531/all/Heparin_Induced_Thrombocytopenia.
Heparin-Induced Thrombocytopenia. In: Domino FJF, Baldor RAR, Golding JJ, et al, eds. 5-Minute Clinical Consult. Wolters Kluwer; 2020. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117531/all/Heparin_Induced_Thrombocytopenia. Accessed June 7, 2023.
Heparin-Induced Thrombocytopenia. (2020). In Domino, F. J., Baldor, R. A., Golding, J., & Stephens, M. B. (Eds.), 5-Minute Clinical Consult (27th ed.). Wolters Kluwer. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117531/all/Heparin_Induced_Thrombocytopenia
Heparin-Induced Thrombocytopenia [Internet]. In: Domino FJF, Baldor RAR, Golding JJ, Stephens MBM, editors. 5-Minute Clinical Consult. Wolters Kluwer; 2020. [cited 2023 June 07]. Available from: https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117531/all/Heparin_Induced_Thrombocytopenia.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC T1 - Heparin-Induced Thrombocytopenia ID - 117531 ED - Domino,Frank J, ED - Baldor,Robert A, ED - Golding,Jeremy, ED - Stephens,Mark B, BT - 5-Minute Clinical Consult, Updating UR - https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117531/all/Heparin_Induced_Thrombocytopenia PB - Wolters Kluwer ET - 27 DB - Medicine Central DP - Unbound Medicine ER -