CONTINUOUS VENOVENOUS HEMOFILTRATION USING POLYACRYLONITRILE FILTERS DOES NOT ACTIVATE CONTACT SYSTEM AND INTRINSIC COAGULATION PATHWAYS

Objectives: To investigate whether continuous venovenous haemofiltrati on using polyacrylonitrile filters causes activation of the contact sy stem and intrinsic coagulation path ways and if this, and/or low plasm a levels of endogenous anticoagulants, influences filter lifespan. Des ign: Observational study. Setting: University Teaching Hospital Intens ive Care Unit. Patients: Twelve critically ill patients with acute ren al failure receiving continuous venovenous haemofiltration. Interventi ons: Blood samples were taken before starting haemofiltration, at 15 m in, 1 h, 3-4 h, 8-12 h, 24 h and at 24-h intervals thereafter until fi lter blockage occurred. Measurement was made of the contact and intrin sic coagulation system proteins factor XII, activated factor XII and p rekallikrein and the protease inhibitors antithrombin III, heparin co- factor II, alpha(2)-macroglobulin and Cl-esterase inhibitor. Thrombin- antithrombin complex levels were measured to provide evidence of throm bin generation. Results: (i) Factor XII, prekallikrein and contact sys tem inhibitors were subnormal in 10/12 and activated factor XII raised in 11/12 patients at baseline, implying pre-existing contact pathway activation. (ii) No change occurred during haemofiltration in the intr insic coagulation pathway factor or inhibitor levels. (iii) Clotting o f the filter circuit within the first 24 h occurred in 5/12 and was as sociated with low baseline levels of antithrombin III and heparin co-f actor II. Only in these patients did thromibin-antithrombin complex le vels rise significantly. Conclusions: The contact system was not activ ated further by continuous venovenous haemofiltration using polyacrylo nitrile filters in critically ill patients. Premature clotting of the haemofilter circuit was more common in patients with very low levels o f antithrombin III and heparin co-factor II; although this was related to thrombin generation, the intrinsic coagulation pathway does not ap pear to be implicated.