Can the Viscoelastic Parameter α-Angle Distinguish Fibrinogen from Platelet Deficiency and Guide Fibrinogen Supplementation?. (August 2015)

• Record Type: Journal Article
• Authors: Solomon, Cristina; Schöchl, Herbert; Ranucci, Marco; Schlimp, Christoph J.
• Is Part Of: Anesthesia & analgesia. Volume 121:Number 2(2015)
• Publication Date: 2015-08
• Subjects: Anesthesiology -- Periodicals; Anesthesia; Anesthesiology; Analgesia; Analgesics; Anesthesiology -- Periodicals; 617.9605
• DOI: 10.1213/ANE.0000000000000738
• Languages: English
• ISSNs: 0003-2999

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <p>Viscoelastic tests such as thrombelastography (TEG®, Haemoscope Inc., Niles, IL) and thromboelastometry (ROTEM®, Tem International GmbH, Munich, Germany), performed in whole blood, are increasingly used at the point-of-care to characterize coagulopathic states and guide hemostatic therapy. An algorithm, based on a mono-analysis (kaolin-activated assay) approach, was proposed in the TEG® patent (issued in 2004) where the α-angle and the maximum amplitude parameters are used to guide fibrinogen supplementation and platelet administration, respectively. Although multiple assays for both the TEG® and ROTEM devices are now available, algorithms based on TEG® mono-analysis are still used in many institutions. In light of more recent findings, we discuss here the limitations and inaccuracies of the mono-analysis approach. Research shows that both α-angle and maximum amplitude parameters reflect the combined contribution of fibrinogen and platelets to clot strength. Therefore, although TEG® mono-analysis is useful for identifying a coagulopathic state, it cannot be used to discriminate between fibrin/fibrinogen and/or platelet deficits, respectively. Conversely, the use of viscoelastic methods where 2 assays can be run simultaneously, one with platelet inhibitors and one without, can effectively allow for the identification of specific coagulopathic states, such as insufficient fibrin formation or an insufficient contribution of platelets to clot strength. Such information is critical for making the appropriate choice of hemostatic therapy.</p> </sec> </abstract>