Cardiopulmonary bypass with a low-molecular-weight heparin fraction (enoxaparin) in a patient with a history of heparin-associated thrombocytopenia

Robitaille, Danielle; Leclerc, Jacques; Laberge, Rémi-Martin; Sahab, P.; Atkinson, Stacey; Cartier, Raymond

doi:10.1016/s0022-5223(19)35009-3

Cited by 43 publications

(18 citation statements)

References 1 publication

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“…54 In two of the three patients no excessive bleeding was reported, in one pa tient blood loss was enhanced. 54 In an overview of 230 HIT patients treated with Orgaran for different indications, 41 52 received Orgaran as anticoagulant cover for a CPB procedure. Of these 52 procedures, 45 were reported adequate, 3 were failures, 4 not evaluable, and 2 deaths occurred as a result of ma jor hemorrhage (overall death rate 25.7%).…”

Section: Cpb Clinical Experience With Lmwhmentioning

confidence: 82%

“…Only a few case reports have been published on LMWH as an anticoagulant during CPB, in each case to replace SH because of previous HIT development. [53][54][55] In all three cases effective anticoagulation was achieved, although clotting started to occur in one case toward the end of the procedure. 54 In two of the three patients no excessive bleeding was reported, in one pa tient blood loss was enhanced.…”

Section: Cpb Clinical Experience With Lmwhmentioning

confidence: 88%

“…[53][54][55] In all three cases effective anticoagulation was achieved, although clotting started to occur in one case toward the end of the procedure. 54 In two of the three patients no excessive bleeding was reported, in one pa tient blood loss was enhanced. 54 In an overview of 230 HIT patients treated with Orgaran for different indications, 41 52 received Orgaran as anticoagulant cover for a CPB procedure.…”

Section: Cpb Clinical Experience With Lmwhmentioning

confidence: 88%

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Anticoagulants and Extracorporeal Circuits

Beijering¹,

Cate²,

Nurmohamed³

et al. 1997

Semin Thromb Hemost

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Anticoagulants are pivotal to achieve circulation in extracorporeal circuits. In this review we discuss several anticoagulants in clinical use or in the preclinical phase. In hemodialysis the low-molecular-weight heparins (LMWHs) appear to be as effective and safe as standard heparin (SH). The main advantages of LMWHs in hemodialysis are the efficacy of a single loading dose, and the lack of laboratory control requirements. Newer anticoagulants such as dermatan sulfate and hirudin have been used in dose-finding studies in hemodialysis, although long-term experience is lacking. LMW heparinoid may be used to replace SH or LMWH in the case of heparin-induced thrombocytopenia. In cardiopulmonary bypass surgery (CPB) heparin-coated extracorporeal circuits are now being commonly applied. Their main advantage is the requirement of lower systemic dosages of heparin. In CPB the place of LMWH or other anticoagulants needs to be investigated.

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Section: Cpb Clinical Experience With Lmwhmentioning

confidence: 82%

Section: Cpb Clinical Experience With Lmwhmentioning

confidence: 88%

Section: Cpb Clinical Experience With Lmwhmentioning

confidence: 88%

See 1 more Smart Citation

Anticoagulants and Extracorporeal Circuits

Beijering¹,

Cate²,

Nurmohamed³

et al. 1997

Semin Thromb Hemost

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“…Similarly, although patients on warfarin preoperatively may bleed after cardiac surgery, two studies demonstrated an inverse relationship between postoperative international normalized ratio and blood loss, which may be secondary to warfarin‐mediated hemostatic system preservation during CPB due to the effects of warfarin to inhibit the DIC process related to CPB 98,99 . The introduction and use of direct thrombin inhibitors (e.g., r‐hirudin, 100,101,102 argatroban, 103 bivalirudin 104 ), dermatan, danaparoid sodium, low‐molecular‐weight heparin compounds, 105‐108 and PLT aggregation inhibitors (e.g., abciximab, 109‐113 eptifibatide, 114 tirofiban, and most importantly long‐acting PLT ADP receptor antagonists such as clopidogrel 115‐126 ), as well as fibrinolytic agents (e.g., recombinant tissue plasminogen activator 49,50 ) can potentially increase bleeding and complicate clinical management. The risk of bleeding related to these agents depends on their relative potency, pharmacodynamic half‐life, time interval for most recent dose before surgery, and whether or not a reversal agent is available.…”

Section: Perioperative Bleedingmentioning

confidence: 99%

A review of transfusion risks and optimal management of perioperative bleeding with cardiac surgery

2008

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A pproximately 10 to 14 million red blood cell (RBC) units 1 and 1.5 million platelet (PLT) transfusions (approx. 85%, single-donor plateletpheresis products; the remainder, pools of six whole-blood-donor PLT concentrates) are administered in the United States each year. Transfusion-related adverse (20% of transfusions) and serious adverse (0.5%) events were estimated by Walker in the 1980s. 2 More recently, serious adverse events have been estimated to occur in 0.1 percent of RBCs and 0.04 percent of PLT transfusions. With early estimates, transfusion-associated adverse events were thought to lead to a short-term (i.e., not including disease transmission-related deaths) mortality of 1 to 1.2 per 100,000 patients, or approximately 35 transfusion-related deaths per year in the United States. With more recent estimates, long-term or total mortality (i.e., including disease transmission-related deaths) is probably higher due to unrecognized or unreported transfusion-related deaths. 1,3 Perioperative signs and symptoms (e.g., fever, hypotension, tachycardia, hypoxemia, microvascular bleeding, hemoglobinuria, low urine output) can accompany any of several serious transfusion-related complications such as acute hemolytic transfusion reactions (HTRs), bacterial contamination, anaphylaxis, transfusion-related acute lung injury (TRALI), or other events (e.g. hyperkalemia, fluid overload, air embolus). Current risks associated with blood and blood component transfusion can be characterized as immune-mediated versus non-immunemediated, hemolytic versus nonhemolytic, or acute versus delayed transfusion reactions, as well as bloodborne disease transmission. Another approach would involve subdividing transfusion risks into those that are the leading causes of mortality versus those that are uncommon causes of transfusion-related mortality. The leading causes of transfusion-related mortalityReports to the US Food and Drug Administration (FDA) 4 and quoted mathematical estimates 1 of transfusionrelated mortality indicate that the leading causes of transfusion-related mortality are (in decreasing order): TRALI, bacterial or viral contamination of blood and blood components, and transfusion of ABO-mismatched blood. Transfusion-associated respiratory distress can be related to one of the following (in order of decreasing frequency): fluid overload (also called transfusion-associated circulatory overload or TACO), allergic reactions, or TRALI. Although the exact incidence of circulatory overload related to transfusion is unknown (e.g., 1 in every 200-10,000 units), 5 it is more likely in older patients with a history of congestive heart failure. Reported estimates of the frequency of TRALI range from 1:400 to 1:50,000 units transfused (i.e., involving plasma, PLTs, or RBCs). 6 This extremely wide estimated range reflects the difficulties in clinical recognition of TRALI with resultant underreporting. Both one-hit (white blood cell [WBC] antibodies) and two-hit mechanisms have been proposed as the etiology of TRALI. Indeed, as TRALI ...

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“…In the years when LMWHs first appeared (1985 to 1995), there were limited reports of their successful use in patients with active clinical HIT. [51][52][53] However, there were also reports of the failure of LMWH treatment in patients with HIT. [53][54][55]…”

Section: Lmwh and Clinical Hitmentioning

confidence: 99%

Decreased Prevalence of Heparin-Induced Thrombocytopenia with Low-Molecular-Weight Heparin and Related Drugs

Walenga

Jeske²,

Prechel³

et al. 2004

Semin Thromb Hemost

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Heparin-induced thrombocytopenia (HIT) Type II represents a disease spectrum associated with a high risk of thrombosis leading to limb loss and death. The pathophysiology of HIT is based on the development of antibodies to the heparin-platelet factor 4 (PF4) complex. Unfractionated heparin (UFH) is heterogeneous in molecular chain length and degree of sulfation accounting in part, for, the heterogeneity of HIT antibodies. Because of its smaller size, low-molecular-weight heparin (LMWH) does not interact with PF4 and platelets as efficiently as does UFH. This translates into a lower risk of immune sensitization with LMWH than with UFH treatment. LMWH is less likely than UFH to cause antibody generation and thus patients do not develop clinical HIT at the same frequency with LMWH as with UFH treatment. The antibodies generated by LMWH treatment are more often immunoglobulin A (IgA) and IgM as opposed to IgG antibodies, which are associated with symptomatic clinical HIT generated by exposure to UFH. However, platelet activation/aggregation can occur from LMWHs in the presence of most pre-existing HIT antibodies that had been generated from UFH exposure, although the response is less than that caused by UFH plus HIT antibody. With the expanded use of LMWH, the frequency of clinical HIT may naturally decline, given that LMWHs are less likely to generate HIT antibody.

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Cardiopulmonary bypass with a low-molecular-weight heparin fraction (enoxaparin) in a patient with a history of heparin-associated thrombocytopenia

Cited by 43 publications

References 1 publication

Anticoagulants and Extracorporeal Circuits

Anticoagulants and Extracorporeal Circuits

A review of transfusion risks and optimal management of perioperative bleeding with cardiac surgery

Decreased Prevalence of Heparin-Induced Thrombocytopenia with Low-Molecular-Weight Heparin and Related Drugs

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