PubMed Health⌕ Search

PubMed · 681809

Precise anticoagulation for routine hemodialysis.

Abstract

A pharmacokinetic model for minimal dose heparinization for chornic hemodialysis patients was recently described by Gotch and Keen. The model requires the determination of two parameters: dose sensitivity (computed for a given heparin dose from increase in WBPTT above a baseline value) and the heparin elimination constant. This study describes the extension of this model to the more precise control of anticoagulation during routine dialysis. S and K were measured in 30 stable chronic dialysis patients and were found to differ markedly (0.015 less than or equal to S 0.08 sec/unit; 0.04 less than or equal to K less than or equal to 1.7 hr-1). The mean S value was 0.041 +/- 0.002 sec/unit (N = 30) and the mean K value was 0.90 +/- 0.06 hr-1 (N = 30). In addition, the mean t 1/2 of heparin obtained in the group of 30 patients from individual rate constants was 0.86 +/- 0.06 hr, in excellent agreement with values obtained in normal subjects given similar doses of the drug. Variations in sensitivity during dialysis were minimal, but variations in elimination rate of up to 50% were encountered during modeling. However, the large variations in K did not affect the applicability of the model of control clotting times during dialysis when infusion requirements were based on mean values of S and K taken over four to five dialyses. In an initial group of five patients, whose heparin requirements were reduced by an average of 38% +/- 20 (range 13% to 65%), there was no significant change in the degree of dialyzer clotting in comparing premodeling and postmodeling heparin therapy. In most of the remaining patients (N = 22) the pattern was similar: a reduction in total heparin administration without increased dialyzer clotting. In three patients (10%) over-all heparin dose had to be moderately increased (3% to 13%). Heparin modeling has been successfully applied to routine anticoahe technique cannot be extended to other clinical procedures involving either intermittent or continuous infusion of heparin. To assist in the application of heparin modeling, nomograms have been developed.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P C Farrell, R A Ward, K Schindhelm, F Gotch. 1978. Precise anticoagulation for routine hemodialysis.. https://pubmed.ncbi.nlm.nih.gov/681809/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

In vitro kinetics of factor VIII activity in patients with mild haemophilia A and a discrepancy between one-stage and two-stage factor VIII assay results.

In some mild haemophilia A patients (discrepant haemophilia), factor VIII coagulant activity (FVIII:C) levels, by one-stage assay are more than double than those by two-stage assay. This may be due to the longer incubation times (10-12 min) in the two-stage assay. This study aimed to determine the time course of the activation phase of the two-stage assay, using both classical coagulation and chromogenic detection methods. In both systems, for equivalent patients (equivalent FVIII:C levels by one-stage and two-stage assays, n = 6, all different mutations), similar FVIII:C results were obtained with short- or long-incubation times. In contrast, plasma from discrepant patients (n = 8, five different mutations) showed higher FVIII:C at shorter incubation times than after longer incubation times. In the chromogenic assay, FVIII:C levels were higher after incubation for 2 min (23-56%, mean 41%) than after 10 min (19-41%, mean 29%). In the classical coagulation assay, FVIII:C levels were higher at shorter incubation times (21-64%, mean 37%) than with the longer incubation times usually used (13-29%, mean 23%). These time-course experiments have verified that the longer incubation time used in the two-stage assay is at least partly responsible for the lower FVIII:C measured by that assay in discrepant haemophilia.

Blood Coagulation Tests↗

Von Willebrand disease within the collective of haemophilic patients as reason for unexpected bleeding episodes.

In the treatment of haemophilia A and B, recombinant coagulation factors are increasingly replacing plasma-derived factor VIII and IX concentrates. Although provided with replacement therapy, individual patients may exhibit bleeding episodes, which are difficult to control. These bleeds may be caused by von Willebrand disease (VWD) as an additional underlying coagulation disorder. We report in the present study our experience that in the collective of haemophilic patients, VWD must be anticipated at least with the same order of magnitude as it appears in a normal healthy population. Among the patients at our treatment centre, two patients (1.5%) were identified as suffering from VWD in addition to haemophilia A. In the collective of haemophilia B patients at our centre, three patients (10%) with VWD were found. Two of these patients exhibited unexpected severe bleeding episodes, which could only satisfactorily be controlled by the administration of Haemate-P or DDAVP supplementary to the recombinant coagulation factor concentrate.

Blood Coagulation Tests↗