Low Incidence of Clinically Significant Heparin Induced Thrombocytopenia after Cardiopulmonary Bypass SurgeryAbhinav B Chandra*, Navneet Mittal, Shilpa Sambidi, Anuradha Belur, Swati Pathak, Himanshu Pathak and Yiqing Xu
Division of Hematology and Oncology, Department of Internal Medicine, Maimonides Medical Center, Brooklyn, New York, USA
- *Corresponding Author:
- Abhinav B Chandra
Division of Hematology and Oncology
Department of Internal Medicine
Maimonides Medical Center
Brooklyn, 4802 Tenth Avenue
Brooklyn, NY 11219, New York, USA
E-mail: [email protected]
Received date: October 23, 2013; Accepted date: December 10, 2013; Published date: December 12, 2013
Citation: Chandra AB, Mittal N, Sambidi S, Belur A, Pathak S, et al. (2013) Low Incidence of Clinically Significant Heparin Induced Thrombocytopenia after Cardiopulmonary Bypass Surgery. J Blood Disord Transfus 5:180. doi: 10.4172/2155-9864.1000180
Copyright: © 2013 Chandra AB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Introduction: Thrombocytopenia after cardiopulmonary bypass (CPB) is common, and the diagnosis of heparin induced thrombocytopenia (HIT) remains a challenge in clinical practice despite the guidance from the “4T” diagnostic scoring criteria and the laboratory tests. Objectives: This study aims to evaluate (i) the temporal laboratory characteristics of thrombocytopenia after CPB and (ii) the incidence of clinically significant HIT based on clinical assessment. Methods: A retrospective data review of patients undergoing coronary artery bypass graft surgery or valve surgery who were also placed on bypass pump and received intra-operative heparin. Results: Among 450 study patients, 142 (31.5%) patients developed decrease of platelet counts at least 33% below base line following surgery, with a median degree of 61%. The initial platelet nadir occurred between day 0 to day 4 (median 1 day). The cumulative percentage of patients demonstrating recovery of their platelet count was 44% by day 4, 80% by day 5 and 100% by day 10. Only 9 patients (2%) showed a second decrease in platelet count. By clinical assessment, including clinical outcome, platelet recovery, Doppler test results and the need for use of direct thrombin inhibitors, not a single case of clinically significant HIT was diagnosed. Heparin associated platelet factor 4 (H-PF4) antibody test was positive in 10% and 0% of patients who developed platelet count decrease in the first and second phase, respectively. Conclusion: A very low incidence of clinically significant HIT after CABG using clinical assessment was observed and further prospective trials are warranted to confirm this observation.