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Home > Blogs > Trauma Research Blog > Early coagulopathy in trauma patients: An on-scene and hospital admission study.

PubMed ID: 21112053
Injury. 2010 Nov 25. [Epub ahead of print]
Authors: Floccard B, Rugeri L, Faure A, Denis MS, Boyle EM, Peguet O, Levrat A, Guillaume C, Marcotte G, Vulliez A, Hautin E, David JS, Négrier C, Allaouchiche B.

Abstract:

PURPOSE: Amongst trauma patients, early coagulopathy is common on hospital admission. No studies have evaluated the initial coagulation status in the pre-hospital setting. We hypothesise that the coagulopathic process begins at the time of trauma. We studied the on-scene and on hospital arrival coagulation profile of trauma patients.

METHODS: Prospective, observational study investigating the on-scene coagulation profile and its time course. We studied 45 patients at the scene of the accident, before fluid administration, and on hospital admission and classified their coagulopathy using the International Society on Thrombosis and Haemostasis score during a 2-month period. Prothrombin time, activated partial thromboplastin time, fibrinogen concentration, factors II, V and VII activity, fibrin degradation products, antithrombin and protein C activities, platelet counts and base deficit were measured.

RESULTS: The median injury severity score was 25 (13-35). On-scene, coagulation status was abnormal in 56% of patients. Protein C activities were decreased in the trauma-associated coagulopathy group (p=.02). Drops in protein C activities were associated with changes in activated partial thromboplastin time, prothrombin time, fibrinogen concentration, factor V and antithrombin activities. Only factor V levels decreased significantly with the severity of the trauma. On hospital admission, coagulation status was abnormal in 60% of patients. The on-scene coagulopathy was spontaneously normalised only in 2 patients whereas others had the same or a poorer coagulopathy status. All parameters of coagulation were significantly abnormal comparing to the on-scene phase. Decreases in protein C activities were related to the coagulation status (p<.0001) and changes in other coagulation parameters. Patients with base deficit ≤-6mmol/L had changes in antithrombin, factor V and protein C activities but no significant coagulopathy.

CONCLUSION: Coagulopathy occurs very early after injury, before fluid administration, at the site of accident. Coagulation and fibrinolytic systems are activated early. The incidence of coagulopathy is high and its severity is related to the injury and not to hypoperfusion.

Notes & Commentary:

Acute Traumatic Coagulopathy (ATC) has been described as present in 10-25% of trauma patients on arrival in the emergency department.  This is the first on-scene study of ATC and identifies a very high incidence of 56% when measured in 45 patients. These were patients managed by SAMU and a more severely injured group of patients (average ISS 25) but this remains a very high incidence.   UNfortunately the authors use a DIC score to define ATC.  ATC is not a DIC-type coagulopathy and ATC was not included in the development of the ISTH DIC score.  Nevertheless ATC clearly develops very soon after injury (25 minutes on average in this study) as shown by a fall in Protein C and Factor V levels as we have previously shown (PMID:18212647).   This study adds to the evidence that ATC is endogenous as this was before significant dilution or other iatrogenic interntion.  The speed at which dysfunction of coagulation and inflammation develops continues to surprise and challenge pre-existing conceptions of the pathophysiology of trauma.

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