Keeping the Circuit Open: Lessons from the Lab

Abstract

Background: Hemofiltration circuits generally require anticoagulation to prevent the membrane from clotting. Understanding the mechanisms involved in premature clotting of the filtration circuit is useful to optimize anticoagulation and maintain filter patency. Aims: To discuss research performed at our institution which throws light on the causes of premature clotting of the hemofilter, and to highlight our approach to anticoagulation. Discussion: Premature clotting of the circuit is related to low baseline levels of antithrombin III (AT-III), heparin co-factor II and tissue factor pathway inhibitor. Clotting is preceded by a precipitous rise in thrombin-antithrombin complexes, suggesting thrombin generation. Our standard anticoagulant is unfractionated heparin, where the primary mode of action is potentiation of endogenous AT-III. However, AT-III levels are diminished in sepsis and other causes of systemic inflammation. To supplement or prevent consumption of AT-III we use fresh frozen plasma or aprotinin (as cheaper alternatives to AT-III) in situations where filter life span is limited and mechanical obstruction has been excluded. Anticoagulation can be managed in heparin-induced thrombocytopenic patients with danaparoid, prostaglandins and/or predilution.

Regional citrate versus systemic heparin anticoagulation for continuous renal replacement in critically ill patients

“…Significantly fewer units of red blood cells (0.17 per day at risk) were transfused in the citrate group compared to the heparin group (0.33 per day at risk), and both of these rates compare favorably to previously published rates of 1.1 units and 1 unit per day using unfractionated heparin [12,33]. Hemofilter clotting is thought to be associated with low baseline levels of AT-III, heparin cofactor II, and tissue factor pathway inhibitor, and a rise in thrombinantithrombin complexes, implicating thrombin generation as a major factor [34,35]. Our finding that AT-III, in a time-dependent fashion, was a strong predictor of hemofilter clotting confirms these findings.…”

A service evaluation comparing CVVH and CVVHDF in minimising circuit failure

“…A recognized problem that occurs during CRRT is premature circuit failure because of thrombosis (Shulman et al, 2002;Brophy et al, 2005;Davies and Leslie, 2006;Kishen et al, 2009;Oudemans-van Straaten et al, 2009). This contributes to treatment interruption times and ineffective clearance (Shulman et al, 2002;Brophy et al, 2005;Davies and Leslie, 2006;Kishen et al, 2009;Oudemans-van Straaten et al, 2009).…”

Coagulation, Fibrinolysis and Inhibitors in Failing Filters during Continuous Venovenous Hemofiltration in Critically Ill Patients with Acute Kidney Injury: Effect of Anticoagulation Modalities

“…Indeed, heparin has been suggested to only partly determine filter survival in previous studies. A poor relation with aPTT is suggested, as found in this study also, possibly following dosing problems or heparin resistance, for instance by low antithrombin levels [9,10,17,23] . We did not observe a difference in filter survival between heparin and citrate as suggested by others [3,[5][6][7] , possibly due to the relatively small number of patients.…”