Translate

Πέμπτη 30 Μαΐου 2019


Variability in international normalized ratio and activated partial thromboplastin time after injury are not explained by coagulation factor deficits
Introduction Conventional coagulation assays (CCAs), PT/INR (prothrombin time/international normalized ratio) and aPTT (activated partial thromboplastin time), detect clotting factor (CF) deficiencies in hematologic disorders. However, there is controversy about how these CCAs should be used to diagnose, treat and monitor trauma-induced coagulopathy. Study objectives were to determine whether CCA abnormalities are reflective of deficiencies of coagulation factor activity in the setting of severe injury. Methods Patients without previous CF deficiency within a prospective database at an ACS verified Level 1 trauma center had CF activity levels, PT/INR, aPTT, and fibrinogen levels measured upon Emergency Department arrival from 2014-2017. Linear regression assessed how CF activity explained the aPTT and PT/INR variation. Prolonged CCA values were set as INR>1.3 and aPTT>34sec. CF deficiency was defined as <30% activity, except for fibrinogen, defined as <150mg/dL. Results Sixty patients with a mean age of 35.8 (std dev:13.6) years and median new injury severity score (NISS) of 32 (IQR:12-43) were included; 53.3% sustained blunt injuries, 23.3% required massive transfusion, and mortality was 11.67%. Overall, 44.6% of the PT/INR variance and 49.5% of the aPTT variance remained unexplained by CF activity. Deficiencies of CFs were: common pathway 25%; extrinsic pathway 1.7%, and intrinsic pathway 6.7%. The positive predictive value for CF deficiencies were: 1)PT/INR>1.3:4.4% for extrinsic pathway, 56.5% for the common pathway; 2) aPTT>34 sec:16.7% for the intrinsic pathway, 73.7% for the common pathway. Conclusion Almost half of the variances of PT/INR and aPTT were unexplained by CF activity. Prolonged PT/INR and aPTT were poor predictors of deficiencies in the intrinsic or extrinsic pathways, however, they were indicators of common pathway deficiencies. Corresponding Author: Ernest E Moore, MD, Email: ernest.moore@dhha.org Phone: 303-724-2685, Fax: 303-720-2682, Mailing Address: 655 Bannock Street Denver, CO 80203 Disclosure: Research reported in this publication was supported in part by the National Institute of General Medical Sciences grants: T32-GM008315 and P50-GM49222, the National Heart Lung and Blood Institute UM1-HL120877, in addition to the Department of Defense USAMRAA and W81XWH-12-2-0028. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, the National Heart, Lung, and Blood institute, or the Department of Defense. Additional research support was provided by Haemonetics (Haemonetics, Niles, IL, USA) with shared intellectual property. © 2019 Lippincott Williams & Wilkins, Inc.

Δεν υπάρχουν σχόλια:

Δημοσίευση σχολίου

Αρχειοθήκη ιστολογίου

Translate