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Critically ill patients receiving continuous renal replacement therapy are frequently given heparin to maintain circuit patency. In the presence of active HIT-II or HITT, even in the absence of clinical thrombosis, systemic anticoagulation with a direct thrombin inhibitor (DTI) decreases the incidence of thrombotic complications, if given until thrombocytopenia has resolved. In this scenario, anticoagulation to maintain CRRT circuit patency is a bonus. In critically ill patients requiring CRRT with a history of HIT-II, but not active thrombocytopenia or thrombosis, avoidance of heparin exposure is still recommended, and argatroban is currently a common choice of DTI if systemic anticoagulation is required. As this is a drug that nephrologists need to be very familiar with, here’s a list of essential facts about argatroban in the form of a mnemonic, for those of you who get off on that kind of thing.

A nticoagulant of choice in active HIT-II or HITT.
R enal dose adjustment not necessary – hepatically cleared only.
G oal aPTT is 2-3 times above baseline (as for heparin).
A ctivated PTT is monitoring test of choice, but note argatroban increases ACT and PT/INR also.
T wo mcg per kg per minute is the usual starting dose (2mcg/kg/min)
R eversal not possible, so careful monitoring essential.
O .5 mcg/kg/min starting dose in liver disease (0.5mcg/kg/min)
B olus not required before infusion (unlike heparin). Steady state within 3 hours.
A lbumin: Low albumin is an important clue to hepatic synthetic dysfunction. Reduce starting dose by 75% if present.
N ormalised ratio: When transitioning to warfarin, once the INR is 4 while on both drugs, the INR will be therapeutic once the argatroban infusion is stopped. The alternative is the measure the chromogenic factor x level (goal less than 45% for efficacy).

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