Heparin-induced thrombocytopenia overview
|
Heparin-induced thrombocytopenia |
|
Differentiating Heparin-induced thrombocytopenia from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Heparin-induced thrombocytopenia overview On the Web |
|
American Roentgen Ray Society Images of Heparin-induced thrombocytopenia overview |
|
Directions to Hospitals Treating Heparin-induced thrombocytopenia |
|
Risk calculators and risk factors for Heparin-induced thrombocytopenia overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2] Shyam Patel [3]
Overview
Heparin-induced thrombocytopenia, or HIT, is a transient yet potentially life-threatening thrombotic disease characterized by low platelet count and paradoxical blood clot formation after exposure to the anticoagulant heparin or its derivatives.[1] Typical manifestations include thrombocytopenia with > 50% drop in platelet count after 5-14 days of receiving heparin.[1] Though there is a large reduction in the platelet count, platelet counts less than 20,000 per microliter are quite unusual for the syndrome.[2] Given that the nadir in the platelet count is not extremely low, clinically significant bleeding is rarely associated with HIT. On the contrary, HIT is primarily a thrombotic disorder, with very high rates of thrombosis in the arteries with or without venous complications.
Historical Perspective
In the 1950s, Rodger Weissman and Richard Tobin of Dartmouth Medical School describes the phenomenon of HIT.[3] [1] They noted an alarming increase in the incidence of peripheral arterial embolism after systemic heparin therapy.[3] They reported 10 cases of embolism and thrombotic complications after heparin. [3] Emboli were noted in the femoral, popliteal, and cerebral circulation. This seminal study paved the way for future investigations into the pathophysiology of HIT.
Classification
There are two types of HIT, type I and type II. Type I HIT patients characteristically have a transient decrease in platelet count (rarely <100,000) without any further symptoms and can recover even if heparin is continued to be administered. It occurs in 10-20% of all patients on heparin and is not due to an immune reaction and antibodies are not found upon investigation. HIT-1 is due to heparin-induced platelet clumping; it is innocuous. Type II is due to an autoimmune reaction with antibodies formed against platelet factor 4 (PF4), neutrophil-activating peptide 2 (NAP-2) and interleukin 8 (IL8) which form complexes with heparin.
Pathophysiology
It is caused by antibodies to complexes between heparin and platelet factor 4 (PF4). These antibody complexes stimulates the procoagulant pathways due to activation of platelet and endothelium.
Causes
Heparin-induced thrombocytopenia (HIT) with or without thrombosis (HITT) is thrombocytopenia (low platelet counts) due to the administration of heparin. While it is mainly associated with unfractionated heparin (UFH), it can also occur with exposure to low-molecular weight heparin (LMWH), but at significantly lower rates.
Differentiating Heparin-induced thrombocytopenia from other Diseases
Epidemiology and Demographics
It has been found to occur with increased frequencies in females, white population and patients over age of 60 years. An episode of Heparin-induced thrombocytopenia increases risks for other future thrombo-embolic events.
Risk Factors
Screening
Natural History, Complications, and Prognosis
Natural History
Complications
Prognosis
Diagnosis
History and symptoms
HIT typically develops 4-14 days after the administration of heparin. The onset of thrombocytopenia in less than 4-5 days after the initiation of heparin treatment is extremely rare due to the time required for antibody production, and alternative explanations should be sought for the development of thrombocytopenia this early in therapy. The primary exception to this is in the case of recent heparin exposures (<100 days) where the patient may have pre-existing antibodies against the heparin-PF4 complex.[4]
Physical Examination
Laboratory Findings
The four commonest diagnostic tests used for heparin-induced thrombocytopenia (HIT) are Serotonin release assay, heparin-induced platelet aggregation assay, solid phase immunoassay (enzyme-linked immunosorbent assay), and particle gel immunoassay.
Imaging Findings
Other Diagnostic Studies
Treatment
=Medical Therapy
Treatment is by prompt withdrawal of heparin and replacement with a suitable alternative anticoagulant. Lepirudin, fondaparinux, bivalirudin, argatroban, danaparoid or other direct thrombin inhibitors are used to treat the thrombotic state. Out of these lepirudin and argatroban are available for use in USA.
Prevention
Patients with HIT should be treated with Bivalirudin, a direct thrombin inhibitor to support future procedures.
References
- ↑ 1.0 1.1 1.2 Lee GM, Arepally GM (2013). "Diagnosis and management of heparin-induced thrombocytopenia". Hematol Oncol Clin North Am. 27 (3): 541–63. doi:10.1016/j.hoc.2013.02.001. PMC 3668315. PMID 23714311.
- ↑ Arepally GM, Ortel TL (2010). "Heparin-induced thrombocytopenia". Annu. Rev. Med. 61: 77–90. doi:10.1146/annurev.med.042808.171814. PMID 20059332.
- ↑ 3.0 3.1 3.2 WEISMANN RE, TOBIN RW (1958). "Arterial embolism occurring during systemic heparin therapy". AMA Arch Surg. 76 (2): 219–25, discussion 225-7. PMID PMID13497418 Check
|pmid=value (help). - ↑ Arepally GM, Ortel TL (2006). "Clinical practice. Heparin-induced thrombocytopenia". N. Engl. J. Med. 355 (8): 809–17. doi:10.1056/NEJMcp052967. PMID 16928996. Unknown parameter
|month=ignored (help)