HEMOSTATIC ALTERATIONS DURING CONTINUOUS VENOVENOUS HEMOFILTRATION INACUTE-RENAL-FAILURE

Citation
I. Stefanidis et al., HEMOSTATIC ALTERATIONS DURING CONTINUOUS VENOVENOUS HEMOFILTRATION INACUTE-RENAL-FAILURE, Clinical nephrology, 46(3), 1996, pp. 199-205
Citations number
29
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
03010430
Volume
46
Issue
3
Year of publication
1996
Pages
199 - 205
Database
ISI
SICI code
0301-0430(1996)46:3<199:HADCVH>2.0.ZU;2-8
Abstract
In order to determine changes in hemostasis occurring during continuou s venovenous hemofiltration (CVVH), we made a prospective study of 14 patients with acute renal failure. Fibrinopeptide A, thrombin-antithro mbin III complex, P-thromboglobulin and platelet retention were determ ined serially. Fibrinopeptide A ((x) over bar +/- SD: 33 +/- 20 ng/ml, ref. < 3.0) and thrombin-antithrombin III complex (11 +/- 5 ng/ml, re f. 1.0-4.0) were enhanced prior to commencement of treatment but showe d no further increase during therapy. Platelet retention (Hellem II, r ef. 60-99%) fell from 39 +/- 32% before treatment to 16 +/- 15% after treatment, while the beta-thromboglobulin/creatinine ratio (ref. 0.23- 0.41) rose from 0.39 +/- 0.20 to 0.64 +/- 0.44. Via platelet activatio n, CVVH leads to a reinforcement of the existing platelet dysfunction (thrombocytopathy), without influencing plasmatic coagulation. In orde r to analyze the influence of pre-existing hemostatic alterations on f ilter running time during CVVH, 60 patients were examined retrospectiv ely in a second study. Filter running time, global coagulation tests, fibrinogen, antithrombin III, platelet count and hematocrit were regis tered daily. There was no significant correlation between filter runni ng time and fibrinogen concentration, thrombin time, platelet count or hematocrit. Apart from filter occlusion, no thrombotic complications were observed. The frequency of filter occlusion increased with fallin g activated clotting time (ACT) (p < 0.05). Rising platelet count led to an increase in heparin dose (p < 0.05), primarily due to the anti-h eparin effect of platelet factor 4.