Impact of a Pharmacist-Directed Anticoagulation Service on the Quality and Safety of Heparin-Induced Thrombocytopenia Management

To, Long; Schillig, Jessica; DeSmet, Brian D; Kuriakose, Philip; Szandzik, Edward G.; Kalus, James S.

doi:10.1345/aph.1p503

Cited by 18 publications

(12 citation statements)

References 14 publications

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“…stopped and replaced with an alternative anticoagulant, which may be associated with a higher risk of bleeding and may be difficult to monitor [21,[25][26][27][28][29]. Our data showed that 20.9% of all samples referred for HIT investigation to a reference laboratory were positive in the EIA but negative in the SRA (presumed false-positive HIT test).…”

Section: Discussionmentioning

confidence: 79%

Pitfalls in the diagnosis of heparin‐Induced thrombocytopenia: A 6‐year experience from a reference laboratory

et al. 2015

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Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating antibodies against complexes of platelet factor 4 (PF4) and heparin. The diagnosis of HIT is contingent on accurate and timely laboratory testing. Recently, alternative anticoagulants for the treatment of HIT have been introduced along with algorithms for better HIT diagnosis. However, the increased reliance on immunoassays for the diagnosis of HIT may have harmful consequences due to the high rate of false positive results. To compare trends and implications of current HIT testing approaches, we analyzed results over a six-year period from the McMaster University Platelet Immunology Reference Laboratory. From 2008 to 2013, 8,546 samples were investigated for HIT using both an in-house IgG-specific anti-PF4/heparin enzyme immunoassay (EIA) and the serotoninrelease assay (SRA). Of 8,546 samples tested, 13.4% were true-positives (positive in both assays); 65.6% were true-negatives (negative in both assays); 20.9% were presumed false positive for HIT (EIA-positive/SRAnegative); and 0.2% were EIA-negative/SRA-positive. The frequency of EIA-positive/SRA-negative results increased over time (from 12.9% in 2008 to 22.9% in 2013). We found that the number of SRA-negative samples was reduced from referring centers that used an immunoassay as an initial screen; however, 41% of those samples tested negative in the immunoassay and in the SRA at the reference laboratory. The suspicion of HIT continues at a high rate and the agreement between the EIA and SRA test results remains problematic.

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Section: Discussionmentioning

confidence: 79%

Pitfalls in the diagnosis of heparin‐Induced thrombocytopenia: A 6‐year experience from a reference laboratory

et al. 2015

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“…Indeed, these drugs are sufficiently complex that many institutions have reassigned primary responsibility for their management to dedicated pharmacist-directed anticoagulation services. 89 Desirudin and fondaparinux offer hope of reducing therapeutic complexity. Neither appears to require routine laboratory monitoring or dose adjustment.…”

Section: Limitations Of Currently Available Agentsmentioning

confidence: 99%

How I treat heparin-induced thrombocytopenia

Cuker

Cines

2012

Blood

141

159

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Heparin-induced thrombocytopenia is a prothrombotic adverse drug effect induced by platelet-activating antibodies against multimolecular complexes of platelet factor 4 and heparin. Diagnosis rests on a clinical assessment of disease probability and laboratory testing. Management involves immediate discontinuation of heparin and initiation of an alternative anticoagulant. Because of the frequency of thrombocytopenia among heparinized patients, the limited specificity of widely available immunoassays, the limited availability of more specific functional assays, and clinicians' fears of missing a case of true disease, overtesting, overdiagnosis, and overtreatment have become common. As a result, a substantial number of thrombocytopenic patients are unnecessarily exposed to costly alternative anticoagulants and their attendant risk of bleeding. In this review, we describe not only our approach to the evaluation and management of patients with heparin-induced thrombocytopenia, but also the measures we use to minimize misdiagnosis and unnecessary treatment of patients without the disease. In addition, we propose areas of investigation for improvement of the diagnosis and management of this potentially fatal disorder. (Blood. 2012;119(10):2209-2218)

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“…When PDAS was not available, DTIs were managed by the other pharmacists, assuring a 24/7 coverage by a pharmacist. 15…”

Section: Study Methodsmentioning

confidence: 99%

Impact of Platelet Functional Assays on the Cost of Treating Suspected Heparin-Induced Thrombocytopenia

Sadik

Jennings

Nemerovski

et al. 2014

Journal of Pharmacy Practice

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Impact of a Pharmacist-Directed Anticoagulation Service on the Quality and Safety of Heparin-Induced Thrombocytopenia Management

Abstract: Implementation of a focused inpatient PDAS was associated with improved efficiency of dosing, improved monitoring, and low bleeding risk.

Cited by 18 publications

References 14 publications

Pitfalls in the diagnosis of heparin‐Induced thrombocytopenia: A 6‐year experience from a reference laboratory

Pitfalls in the diagnosis of heparin‐Induced thrombocytopenia: A 6‐year experience from a reference laboratory

How I treat heparin-induced thrombocytopenia

Impact of Platelet Functional Assays on the Cost of Treating Suspected Heparin-Induced Thrombocytopenia

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