Unsuitable Approaches

Low Molecular Weight Heparin

LMWH is not recommended as an alternative anticoagulant for managing acute HIT. In vitro tests for HIT antibodies show a high degree of cross-reactivity between UFH and LMWH (Greinacher et al., 1992b; Vun et al., 1996). Furthermore, in vivo cross-reactivity manifesting as persistent or recurrent thrombocytopenia or thrombosis during LMWH treatment of HIT appears to be common (Greinacher et al., 1992a; Horellou et al., 1984; Roussi et al., 1984). Because non-heparin anticoagulants are available, LMWH probably should not be used even if in vitro cross-reactivity is reported to be negative.

Regional Heparinization

Regional heparinization is defined as application of heparin at the inlet of the extracorporeal circuit and its neutralization by protamine at the outlet of the circuit. However, its use in HIT is problematic because of the potential for heparin "contamination" of the patient, as well as for heparin "rebound anticoagulation" (recurrence of heparin anticoagulation owing to shorter half-life of protamine compared with heparin) (Blaufox et al., 1966). Moreover, direct injurious effects of protamine on the clotting cascade can occur. Consequently, this regimen is not recommended for HD of patients with HIT.

Aspirin

Acetylsalicylic acid has been used as an antiplatelet agent together with continued anticoagulation with UFH for HD of patients with HIT (Hall et al., 1992; Janson et al., 1983; Matsuo et al., 1989). This approach is not recommended for at least two reasons: (1) protection against heparin-induced platelet activation may be incomplete or absent, as aspirin's effects on blocking the thromboxane-dependent pathway of platelet activation does not reliably inhibit platelet activation by HIT antibodies (Kappa et al., 1987; Polgâr et al., 1998; Selleng et al., 2005); and (2) the bleeding risk of uremic patients is increased.

HD Without Anticoagulant

HD without an anticoagulant (Romao et al., 1997) is not ideal for maintenance HD. Without anticoagulation, the artificial surfaces become coated, first by plasma proteins, followed by adhesion and activation of platelets, with accompanying activation of the coagulation cascade (Basmadjian et al., 1997). This will markedly reduce dialysis quality in removal of fluid and solutes long before clotting of the circuit is visible. Moreover, this approach may aggravate HIT-associated thrombosis. However, in patients at high risk of bleeding (e.g., owing to hepatic disorders or multiorgan failure, or those requiring surgery), temporary HD without anticoagulant may be appropriate.

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