PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 10157544

Improved Coumadin therapy using a continuous quality improvement process.

J Eckhart·P Gilbert
View original source ↗Export metadata ↓

Abstract

Through the Continuous Quality Improvement process, we determined that a significant number of patients were receiving too much Coumadin and having potentially serious side effects. The number of patients studied is limited, and there are only two time intervals reported postintervention. This makes it difficult to draw a definite relationship between the observed rates of Coumadin overdosing and the selected intervention. By educating the physicians on proper Coumadin dosing, we were able to reduce the number of patients experiencing hemorrhage or other complications. Our follow-up data review 1 year later showed that the gain had not been maintained as well as we would have hoped. This demonstrates that active review by Pharmacy and Laboratory on a regular basis and additional physician education would be beneficial. Through this process we gained valuable experience using the FOCUS PDCA method of continuous quality improvement.

Explore related subjects

AnticoagulantsDrug OverdoseHumansIowaLaboratories, HospitalMyocardial InfarctionPharmacy Service, HospitalProthrombin TimeThrombosisTotal Quality ManagementWarfarinJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Eckhart, P Gilbert. Improved Coumadin therapy using a continuous quality improvement process.. https://pubmed.ncbi.nlm.nih.gov/10157544/

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

KEEP EXPLORING

Related citations

PubMed2000

Effects of a fucoidan on the activation of plasminogen by u-PA and t-PA.

The effect of an anticoagulant fucoidan (C-I-H) from the brown seaweed Ecklonia kurome on the fibrinolytic system was studied in vitro using S-2251 as a substrate of plasmin. C-I-H enhanced the activation of Glu- and Lys-plasminogen by high molecular weight urokinase-type plasminogen activator (HMW u-PA) very effectively, but the activation by low molecular weight u-PA was hardly enhanced with C-I-H. C-I-H also potentiated moderately the activation by single- and two-chain tissue-type plasminogen activators (sct- and tct-PA). These effects of C-I-H were higher than those of heparin used. But C-I-H had no effect on the amidolytic activity of plasmin to S-2251. These results indicate that C-I-H promotes the generation of plasmin in the plasminogen activation by HMW u-PA and t-PA, but not the activity of generated plasmin. Kinetic analyses suggest that C-I-H enhances the HMW u-PA-mediated plasminogen activation by increasing the affinity of the activator for Glu- and Lys-plasminogen and by increasing the molecular activity of the activator. On the other hand, C-I-H had no effect on the affinity of tct-PA for both plasminogens. The catalytic efficiencies of HMW u-PA and tct-PA for the activation of both plasminogens were increased with C-I-H about 8- and 2-fold, respectively. The present results suggest that C-I-H has the fibrinolytic activity by stimulating the plasminogen activation by HMW u-PA and t-PA. The mechanism of the enhancement effect of C-I-H on the activation is presumed to be that C-I-H binds to plasminogen, thereby inducing a structural change of plasminogen susceptible to the action of plasminogen activators.

Anticoagulants↗