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Table of Contents
Year : 2012  |  Volume : 15  |  Issue : 2  |  Page : 168-169
Hitting back HIT

Department of Internal Medicine/Critical Care, Medwin Hospital, Nampally, Hyderabad, Andhra Pradesh, India

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Date of Web Publication16-Apr-2012

How to cite this article:
Gude D. Hitting back HIT. Ann Card Anaesth 2012;15:168-9

How to cite this URL:
Gude D. Hitting back HIT. Ann Card Anaesth [serial online] 2012 [cited 2023 Feb 3];15:168-9. Available from:

The Editor,

Heparin-induced thrombocytopenia (HIT) is an entity associated with the development of heparin/platelet factor (PF4) antibodies with a prothrombotic state leading to diverse complications. About 25-50% of postcardiac surgery patients on heparin develop heparin-dependent antibodies, [1] with the risk of HIT being 1-3%.

Although the sensitivity of readily available antibody immunoassays to diagnose HIT is high, specificity is quite low. A study recommends the use of the Warkentin 4Ts clinical score (Thrombocytopenia, Timing of platelet decrease, Thrombotic complications and other causes for thrombocytopenia) in combination with the PF4/heparin immunoassay, in which case the sensitivity and specificity of HIT testing is greater (100% and 70% respectively) compared with the PF4/heparin immunoassay alone (100% and 26%). In cases of intermediate 4Ts score and positive PF4/heparin antibody test, the serotonin release assay (SRA) may be confirmatory. [2] In surgical intensive care unit (ICU) patients, a PF4≥2.0 optical density (OD) is preferable, unlike the general recommendation of PF4≥0.4 OD. [3] Surgical ICU patients with HIT sport increased morbidity rates compared with others, and the platelet count at its lowest is independently associated with a higher risk of in-hospital death in these patients.

Direct thrombin inhibitors are the mainstay of treatment for HIT, and include the bivalent (bind to both active site and exosite-1 of thrombin) hirudin derivatives - bivalirudin, lepirudin and desirudin - and the univalent (bind only to active site) argatroban, melagatran and dabigatran. The strengths of recommendations by the American College of Chest Physicians on use of alternative, nonheparin anticoagulants in HIT are: Danaparoid-Grade 1B, lepirudin-Grade 1C, argatroban-Grade 1C, fondaparinux-Grade 2C, bivalirudin-Grade 2C and initiation/continuation of vitamin K antagonists (after platelet count recovery to >1.5 L)-Grade 1B. [4]

Danaparoid (comprising heparan sulfate, dermatan sulfate and chondroitin sulfate) is known to disrupt PF4-containing immune complexes, interfering with the pathogenesis of HIT. Lepirudin has established efficacy (HAT trials 1, 2 and 3) in HIT, but the rate of major bleeding (17.6%) can be curbed by reducing the initial dose to 0.1 mg/kg/h. [5]

Argatroban was used to provide anticoagulation in patients who needed continuous veno-venous hemofiltration and intermittent hemodialysis in patients who developed HIT after cardiovascular surgery, and was found to provide reliable, safe and effective anticoagulation. [6] Addition of nafamostat mesilate (shorter half-life) to argatroban might prolong the anticoagulant effect.

Although fondaparinux (synthetic heparin-mimicking pentasaccharide) has shown efficacy in HIT, there are reports of it causing HIT as well.

Bivalirudin has been used in HIT associated with antiphospholipid antibody syndrome [7] as well as in cardiopulmonary-bypass patients with confirmed or suspected HIT and anti-PF4/H antibodies (CHOOSE-ON trial). Studies on desirudin in patients undergoing Coronary Artery Bypass Graft (CABG) showed no major bleeding events or postoperative HIT.

Dabigatran etexilate is comparable to enoxaparin in the prevention of venous thromboembolism (after major orthopedic surgery) and to warfarin in stroke prevention in those with atrial fibrillation (with lower rates of hemorrhage).

HIT, especially in settings like cardiopulmonary bypass, warrants prompt diagnosis and management as cessation of heparin and emergent therapy with alternative anticoagulation can be life-saving.

   References Top

1.Arepally GM, Ortel TL. Clinical practice. Heparin-induced thrombocytopenia. N Engl J Med 2006;355:809-17.  Back to cited text no. 1
2.Demma LJ, Winkler AM, Levy JH. A diagnosis of heparin-induced thrombocytopenia with combined clinical and laboratory methods in cardiothoracic surgical intensive care unit patients. Anesth Analg 2011;113:697-702.  Back to cited text no. 2
3.Berry C, Tcherniantchouk O, Ley EJ, Salim A, Mirocha J, Martin-Stone S, et al. Overdiagnosis of heparin-induced thrombocytopenia in surgical ICU patients. J Am Coll Surg 2011;213:10-7; discussion 17-8.  Back to cited text no. 3
4.Warkentin TE, Greinacher A, Koster A, Lincoff AM; American College of Chest Physicians. Treatment and prevention of heparin-induced thrombocytopenia: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8 th Edition). Chest 2008;133(6 Suppl):340S-80S.  Back to cited text no. 4
5.Lubenow N, Eichler P, Lietz T, Greinacher A; Hit Investigators Group. Lepirudin in patients with heparin-induced thrombocytopenia - results of the third prospective study (HAT-3) and a combined analysis of HAT-1, HAT-2, and HAT-3. J Thromb Haemost 2005;3:2428-36.  Back to cited text no. 5
6.Koster A, Hentschel T, Groman T, Kuppe H, Hetzer R, Harder S, et al. Argatroban anticoagulation for renal replacement therapy in patients with heparin-induced thrombocytopenia after cardiovascular surgery. J Thorac Cardiovasc Surg 2007;133:1376-7.  Back to cited text no. 6
7.Sharma VK, Chaturvedi R, Manoj Luthra V. Antiphospholipid syndrome, cardiac surgery and cardiopulmonary bypass. Ann Card Anaesth 2011;14:146-9.  Back to cited text no. 7
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Correspondence Address:
Dilip Gude
AMC, 3rd Floor, Medwin Hospital, Chirag Ali Lane, Nampally, Hyderabad, Andhra Pradesh 500 001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.95088

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