Heparin-Induced Thrombocytopenia in Healthy Individuals with Continuous Heparin Infusion.

Sheila Driscoll,Elizabeth Klerman,Paula Autori,Samuel Goldhaber,Molly Connors,Karine Scheuermaier,Marjorie Kozak,Gregory Piazza,Jonathan Williams,Stephen Kidd,Frank Scheer,Charles Czeisler,Jeanne Duffy

doi:10.1055/s-0038-1624565

Abstract

The risk for developing heparin-induced thrombocytopenia in healthy individuals is thought to be low, but monitoring recommendations remain controversial. Therefore, a retrospective cohort study was conducted to identify the incidence of thrombocytopenic events in a healthy research population exposed and re-exposed to continuous intravenous (IV) unfractionated heparin. The Division of Sleep Medicine and the Centre for Clinical Investigations at Brigham and Women's Hospital, Boston, Massachusetts, United States, instituted a standardized platelet monitoring procedure for all research protocols that involved heparin to detect platelet count decreases. Protocol-related frequent blood sampling required use of continuous IV unfractionated heparin infusion (5,000 unit/L in 0.45% saline at 40 mL/h) to maintain line patency over extended periods of IV access. From the years 2009 to 2012, a total of 273 healthy volunteers enrolled in Sleep Medicine research protocols met study criteria as having been exposed and/or re-exposed to continuously infused intravenous heparin for at least 4 hours. The mean continuous heparin exposure time was 88 ± 82 SD hours with a total of 397 heparin exposure and re-exposure events. Platelet count measurements were obtained on 629 occasions, representing a range from 2 to 9 draws per participant. No platelet count decrease of more than 50% was detected. There were no detected adverse bleeding or thrombotic events. In this retrospective study of healthy volunteers involved in a rigorously applied inpatient platelet monitoring protocol, heparin exposure and re-exposure did not lower platelet concentration and, therefore, does not appear to be associated with increased risk of HIT in this population.

Highlights

Heparin-induced thrombocytopenia (HIT) is a prothrombotic immune reaction to unfractionated and low-molecularweight heparin (LMWH) products mediated by platelet-activating antibodies against complexes of platelet factor 4 (PF4) and heparin.[1,2]
Case detection of HIT is based on three recognized types of presentation: (1) typical-onset thrombocytopenia ($65% of HIT cases) that occurs between 4 and 14 days of exposure, (2) rapid-onset thrombocytopenia ($30%) that occurs within 100 days of heparin re-exposure and leads to abrupt platelet decrease in less than 24 hours, and (3) delayed-onset thrombocytopenia ($5%) that occurs within a median of 9 days following discontinuation of heparin
A total of 629 platelet count measurements were recorded at times varying from 24 to greater than 264 hours after initiation of the heparin infusion

Summary

Introduction

Heparin-induced thrombocytopenia (HIT) is a prothrombotic immune reaction to unfractionated and low-molecularweight heparin (LMWH) products mediated by platelet-activating antibodies against complexes of platelet factor 4 (PF4) and heparin.[1,2] Though venous thromboembolism is most common in medical patients, arterial thromboembolism can occur and is associated with an increased risk of mortality and morbidity, including limb ischemia, amputation, and stroke.[1] HIT is suspected when the baseline platelet count decreases by 50%. It is postulated that the development of HIT requires additional patient-specific factors related to comorbid illness or severity of disease.[3,4] The incidence is up to 10 times higher among patients receiving unfractionated heparin versus LMWH.[3,5] HIT occurs more frequently among patients who have had major surgery (especially cardiac surgery) than among patients who have had minor surgery[3,5] or those only receiving medical therapy.[6] It is rare in otherwise healthy obstetrical patients, outside of pregnancy, women are at slightly higher risk than men.[6]

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Conclusion