Correspondence  |   September 2017
Acute Traumatic Coagulopathy: Thrombin Is the Driver!
Author Notes
  • University of Maryland School of Medicine, Baltimore, Maryland (K.A.T.). ktanaka@som.umaryland.edu
  • (Accepted for publication June 1, 2017.)
    (Accepted for publication June 1, 2017.)×
Article Information
Correspondence
Correspondence   |   September 2017
Acute Traumatic Coagulopathy: Thrombin Is the Driver!
Anesthesiology 9 2017, Vol.127, 585. doi:10.1097/ALN.0000000000001760
Anesthesiology 9 2017, Vol.127, 585. doi:10.1097/ALN.0000000000001760
We read with great interest the article by Davenport et al.1  about activated protein C (aPC)–induced acute trauma coagulopathy (ATC) demonstrated in trauma patients. In their study, the authors state that aPC-induced anticoagulation is not the primary mechanism of ATC and argue that aPC-induced fibrinolytic activity is the central mechanism of fibrinogen depletion in ATC. However, the evidence presented in this article does not fully support their claims due to study design and technical issues, as described below.
First, the authors measured D-dimer as one of the indicators of systemic fibrinolysis. D-dimer is a measurement of plasmin-digested fibrin (after cross-linking by activated factor XIII). No fibrinogen degradation marker was included in this study. Elevated D-dimer here indicated the massive thrombin generation, fibrin formation, and ongoing fibrin degradation. Indeed, prothrombin fragment one plus two and D-dimer levels were higher in those with hypofibrinogenemia and elevated aPC.
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