ANTICOAGULATION WITH PROSTACYCLIN AND HEPARIN DURING CONTINUOUS VENOVENOUS HEMOFILTRATION

Citation
Sa. Langenecker et al., ANTICOAGULATION WITH PROSTACYCLIN AND HEPARIN DURING CONTINUOUS VENOVENOUS HEMOFILTRATION, Critical care medicine, 22(11), 1994, pp. 1774-1781
Citations number
36
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
00903493
Volume
22
Issue
11
Year of publication
1994
Pages
1774 - 1781
Database
ISI
SICI code
0090-3493(1994)22:11<1774:AWPAHD>2.0.ZU;2-V
Abstract
Objectives: To investigate anticoagulation with prostacyclin (prostagl andin I-2 [PGI(2)]) and/or heparin during continuous venovenous hemofi ltration, and the role of in vitro tests of primary hemostasis in cont rolling anticoagulation.Design: Prospective, randomized, controlled tr ial. Setting: Intensive care unit. Patients: Forty-six consecutive, cr itically ill, mechanically ventilated patients with postoperative acut e renal failure. Interventions: Anticoagulation of the patient's blood was accomplished using heparin (6.0 +/- 0.3 IU/kg/hr for group 1), PG I(2) (7.7 +/- 0.7 ng/kg/min for group 2), or both PGI(2) and heparin ( 6.4 +/- 0.3 ng/kg/min, 5.0 +/- 0.4 IU/kg/hr, respectively, for group 3 ), administered into the extracorporeal line before the hemofilter dur ing continuous venovenous hemofiltration. Measurements and Main Result s: After Ethics Committee approval and informed consent were obtained, tests of primary and secondary hemostasis, plasma concentrations of 6 -ketoprostaglandin F-1 alpha (by radioimmunoassay), and hemodynamic me asurements were performed before hemofiltration and 24 hrs after hemof iltration. In groups 1 and 3, hemodynamic parameters remained stable, whereas in group 2 (the PGI(2) group), there were significant reductio ns in systemic and pulmonary vascular resistances and mean arterial pr essure. Platelet function was unchanged in group 1, and was inhibited in groups 2 and 3. Corresponding with the prolongation of in vitro ble eding time, the 6-ketoprostaglandin F-1 alpha concentration was increa sed, indicating an effective inhibition of platelet aggregation within the hemofilter. Platelet counts remained stable in all patients. Plas ma coagulation tests were stable in groups 2 and 3, and were prolonged in group 1. In all patients, no major bleeding complications were obs erved and there was no clinically important bleeding. Mean hemofilter duration lasted longest in group 3. Blood urea nitrogen and circulatin g creatinine concentrations decreased significantly in groups 2 and 3 within the study period. Conclusions: Patients receiving both PGI(2) a nd heparin showed better hemodynamic profiles and enhanced hemofilter duration compared with the other groups and no bleeding complications were observed. Therefore, we recommend anticoagulation with PGI(2) and heparin during continuous venovenous hemofiltration with close monito ring of platelet function, coagulation profile, and overall hemodynami cs.