Plasmapheresis and Heparin Reexposure as a Management Strategy for Cardiac Surgical Patients with Heparin-Induced Thrombocytopenia

Welsby, Ian J.; Um, J.; Milano, Carmelo A.; Ortel, Thomas L.; Arepally, Gowthami M.

doi:10.1213/ane.0b013e3181c3c1cd

Cited by 101 publications

(92 citation statements)

References 37 publications

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“…For these patients, management approaches extend from delaying surgery, if possible, to the use of plasmapheresis. 43 Prospective studies could help delineate optimal management strategies for this high risk patient population. 12 patients with HIT (■) and 36 control patients who were PF4/H seropositive but did not have HIT (□) were monitored after orthopedic surgery for PF4/H antibodies, thrombocytopenia, and thrombosis.…”

Section: What Is the Optimal Management Strategy In Cardiac Surgery Pmentioning

confidence: 99%

Heparin-induced thrombocytopenia

Arepally

2017

Blood

337

362

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Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder caused by antibodies that recognize complexes of platelet factor 4 (PF4) and heparin. HIT is frequently considered in the differential diagnosis of thrombocytopenia occurring in patients on heparin therapy. HIT is a challenging diagnosis because of routine heparin use in hospitalized patients, the common occurrence of thrombocytopenia, and high rates of anti-PF4/heparin seroconversions in patients treated with heparin. This chapter will summarize our diagnostic approach to HIT by underscoring critical elements of the clinical and laboratory evaluation. Keywordsplatelet factor 4; PF4; heparin; PF4/H complexes; HIT Heparin-induced thrombocytopenia (HIT) is a potentially life-threatening immune complication which occurs after exposure to unfractionated heparin (UFH) or less commonly, to low-molecular weight heparins (LMWHs). 1 It is characterized by declining platelet counts beginning 5-14 days after heparin exposure occurring in isolation (isolated HIT) or concurrent with new arterial and venous thrombotic complications. 2 HIT is caused by antibodies directed against complexes formed by a platelet protein, platelet factor 4, and heparin (PF4/H). Circulating immune complexes containing IgG and PF4/H complexes bind to platelet and monocyte Fc receptors and promote cellular activation leading to procoagulant microparticle release and thrombin generation. 3,4 Historically, the challenge associated with HIT was lack of awareness of the syndrome and its pursuant complications; the challenge now is in over-diagnosis and treatment of HIT. With the widespread availability of screening immunoassays and the desire of clinicians to avoid the thrombotic consequences associated with true disease, many patients without HIT Correspondence to: Gowthami M. Arepally, arepa001@mc.duke.edu. now suffer needless morbidity due to bleeding complications from use of alternative anticoagulants. To avoid a reflexive diagnosis of HIT in the heparinized thrombocytopenic patient, clinicians must have a sound understanding of the clinical and laboratory diagnostic elements essential for a diagnosis of HIT. This paper reviews our diagnostic and management strategy in evaluating the common presentation of thrombocytopenia in a heparinized patient. NIH Public Access Diagnosing HIT: the clinical challengeHIT is a challenging clinical diagnosis. The increasing use of UFH/LMWH for thromboprophylaxis in hospitalized patients 5 coupled with the frequency of thrombocytopenia, particularly among critically ill patients, 6 results in a significant overlap of patients suspected of HIT. In a recent registry of ~1000 patients treated with thromboprophylactic dosed heparin, 19% (n = 190) met thrombocytopenia criteria compatible with a diagnosis of HIT (as defined by a platelet count < 150 × 10 9 /L or > 50% drop in platelet counts), but only 5% of patients were diagnosed with HIT. 6 This study and clinical experience suggest that other causes of thrombocytopenia, such as infection, medi...

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Section: What Is the Optimal Management Strategy In Cardiac Surgery Pmentioning

confidence: 99%

Heparin-induced thrombocytopenia

Arepally

2017

Blood

337

362

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“…Welsby and colleagues 36 used intraoperative TPE to decrease anti-PF4/heparin antibody levels in patients with recent HIT who were given UFH for heart transplantation despite being EIA positive (but platelet aggregation test negative) at surgery. None of the patients developed recurrent HIT using this management strategy.…”

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confidence: 99%

How I treat patients with a history of heparin-induced thrombocytopenia

Warkentin

Anderson

2016

Blood

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Heparin-induced thrombocytopenia (HIT) is a relatively common prothrombotic adverse drug reaction of unusual pathogenesis that features platelet-activating immunoglobulin G antibodies. The HIT immune response is remarkably transient, with heparin-dependent antibodies no longer detectable 40 to 100 days (median) after an episode of HIT, depending on the assay performed. Moreover, the minimum interval from an immunizing heparin exposure to the development of HIT is 5 days irrespective of the patient’s previous heparin exposure status or history of HIT. This means that short-term heparin reexposure can be safely performed if platelet-activating antibodies are no longer detectable at reexposure baseline and is recommended when heparin is the clear anticoagulant of choice, such as for cardiac or vascular surgery. The risk of recurrent HIT 1 to 2 weeks after heparin reexposure is ∼2% to 5% and is attributable to formation of delayed-onset (or autoimmune-like) HIT antibodies that activate platelets even in the absence of pharmacologic heparin. Some studies suggest that longer-term heparin reexposure (eg, for chronic hemodialysis) may also be reasonable. However, for other antithrombotic indications that involve patients with a history of HIT (eg, treatment of venous thromboembolism or acute coronary syndrome), preference should be given to non-heparin agents such as fondaparinux, danaparoid, argatroban, bivalirudin, or one of the new direct-acting oral anticoagulants as appropriate.

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“…Although both the patients had very similar backgrounds and required massive transfusion support for severe intraoperative and postoperative bleeding, the blood loss in Case 2 was much lesser than that in Case 1. Welsby et al reported that an alternative management strategy using intraoperative plasmaphaeresis for patients scheduled for cardiac surgery with acute or subacute HIT can reduce antibody load and decrease the thrombotic risk associated with high anti-HPF4 titers [16]. But we are not convinced that plasmapheresis may be effective in the removal of argatroban because of no blood concentration measurement for argatroban at all.…”

Section: Discussionmentioning

confidence: 98%

Anticoagulant Managements of Left Ventricular Assist Device Implantation in Two Patients with Heparin-Induced Thrombocytopenia (HIT): Use of Argatroban as an Anticoagulant for Cardiopulmonary Bypass

Toyama¹

2015

J Anesth Clin Res

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Heparin-induced thrombocytopenia (HIT) can cause fatal arterial or venous thrombosis/thromboembolism. In high-risk cases, heparin should be immediately discontinued and an alternative administered; the only alternative permitted in Japan is argatroban, a direct thrombin inhibitor. Anticoagulation in patients with recent HIT requiring cardiopulmonary bypass (CPB) surgery is challenging, because it is sometimes difficult to find out appropriate dosage of argatroban using ACT based monitoring calculation.Two dilated cardiomyopathy patients with HIT were administered argatroban as the anticoagulant for the CPB in left ventricular assist device (LVAD) implantation. After discontinuing argatroban, blood coagulopathy persisted beyond its expected half-life, leading to abnormal haemostasis. Because of severe intraoperative and postoperative bleeding, both patients required massive transfusion support, despite the case 2 performed plasmapheresis to eliminate argatroban at the weaning from CPB. However, blood loss in case 2 (18,159 ml) was significantly lower than that in case 1 (31,292 ml), which might be contributed by the smaller dosage of argatroban (242 mg in case 2 vs. 489 mg in case 1) and plasmapheresis.Prolongation of ACT is multifactorial and affected by platelet count, fibrinogen concentration and, particularly total dose of argatroban. Furthermore, literatures and our experienses revealed that the recovery time to baseline ACT after stopping argatroban was significantly correlated with the total dose of argatroban (r=0.927). But, we could not authenticate the potency of plasmapheresis to eliminate argatroban and HIT antibodies.Because no specific antidotes are available for argatroban, surgical teams should carefully monitor timing of argatroban administration and the total dosage.

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Plasmapheresis and Heparin Reexposure as a Management Strategy for Cardiac Surgical Patients with Heparin-Induced Thrombocytopenia

Cited by 101 publications

References 37 publications

Heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia

How I treat patients with a history of heparin-induced thrombocytopenia

Anticoagulant Managements of Left Ventricular Assist Device Implantation in Two Patients with Heparin-Induced Thrombocytopenia (HIT): Use of Argatroban as an Anticoagulant for Cardiopulmonary Bypass

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