Elsevier

Injury

Volume 43, Issue 1, January 2012, Pages 26-32
Injury

Early coagulopathy in trauma patients: An on-scene and hospital admission study

https://doi.org/10.1016/j.injury.2010.11.003Get rights and content

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 ≤−6 mmol/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.

Introduction

The development of coagulation abnormalities is frequent in severe trauma and contributes significantly to the morbidity and the mortality.14, 33 Haemorrhage accounts for 40% of all trauma deaths.33 In the pre-hospital setting, uncontrolled bleeding is the second most common cause of death after central nervous system injuries26 and the first responsible for early in-hospital mortality from major trauma.33 The triad of coagulopathy, acidosis and hypothermia in trauma patients is associated with a high mortality.8, 34, 36

The pathogenesis of severe post-traumatic coagulopathy is complex and multifactorial.17, 18, 34 Six major events appear as contributing to post-traumatic coagulopathy: tissue trauma, shock, haemodilution, hypothermia, acidemia and inflammation.10, 17 In combination, direct tissue trauma and shock with systemic hypoperfusion appear to be the primary factors responsible for the development of coagulopathy in the immediate post-injury phase. Other factors as acidosis, hypothermia and haemodilution may be important later in the clinical course.17 A profile of coagulopathy secondary to the extravasation of tissue factor and hypoperfusion is associated with poor outcome such as multiple organ failure and death.6, 13, 14, 24 A recent review suggests that most early trauma-associated coagulopathy (TAC) is a result of enhanced activity of plasma coagulation during the initial phase.17 This phenomenon is not a disseminated intravascular coagulation (DIC) as described in sepsis.21 It is marked by early onset, prolonged prothrombin time and activated partial thromboplastin time and a relative sparing of platelets and fibrinogen.17

Recent studies have described an early post-traumatic coagulopathy in 24–36% of trauma patients upon admission to the emergency room.7, 19, 27, 28 In all these studies, the mean time from injury to arrival in the emergency room was 75 min. This early coagulopathy was a marker of injury severity and was related to mortality. However, up to this date there have been no prospective studies evaluating the initial coagulation status in the pre-hospital setting. Our hypothesis was that coagulation abnormalities became apparent very early, at the site of the accident.

The aim of this prospective study was to describe the on-scene and on hospital arrival coagulation profile in trauma patients.

Section snippets

Study sample

This single-centre, prospective, observational study was approved by our hospital research ethics committee. Waived informed consent was authorised by the committee as this study did not impact patient care and did not change local practices. All trauma patients managed by a mobile intensive care unit (SAMU system) and admitted to the trauma resuscitation room (TRU) of our level 1 trauma centre between May and June 2007 were included. The SAMU system has been described elsewhere.31 On-scene

Characteristics of the study sample

During the study period, 45 patients were included. No patients were excluded. General characteristics of the study patients are given in Table 2. The median AIS for head was 1.5 (0–4.5). Fourteen patients (31%) presented a head injury with an AIS ≥3. Times from injury to team's ambulance arrival and from injury to arrival in the emergency room are presented in Table 2. The median systolic arterial pressure was 120 mm Hg (98–130) on-scene and 120 mm Hg (110–130) at the hospital admission. The

Discussion

The present results indicate that in a group with significant injuries more than half of patients presented coagulation abnormalities on-scene. This coagulopathy developed early after injury and before fluid administration. In the TRU, coagulopathy was present in 60% of the patients. Upon hospital admission, the on-scene coagulopathy was spontaneously normalised only in 2 patients when others had the same or a worsened coagulopathy status. The time from injury to arrival in hospital and the

Conclusion

Our results demonstrate that coagulation abnormalities appear very early after injury and are, thus, observed on-scene. This coagulopathy is present before fluid administration. Coagulation status was abnormal in 60% of patients. Upon hospital admission, the on-scene coagulopathy was the same or worsened in 96% of the patients. Every marker of coagulation was modified on hospital admission. Decreases in protein C activities were related to the coagulation status and changes in other coagulation

Conflict of interest statement

All authors attest they have no conflicts of interest.

Role of the funding source

Support was provided only by institutional sources.

References (36)

  • C. Bartal et al.

    The role of thromboelastometry and recombinant factor VIIa in trauma

    Curr Opin Anaesthesiol

    (2009)
  • K. Brohi et al.

    Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway?

    Ann Surg

    (2007)
  • K. Brohi et al.

    Acute traumatic coagulopathy

    J Trauma

    (2003)
  • N. Cosgriff et al.

    Predicting life-threatening coagulopathy in the massively transfused trauma patient: hypothermia and acidoses revisited

    J Trauma

    (1997)
  • J.W. Davis et al.

    Admission base deficit predicts transfusion requirements and risk of complications

    J Trauma

    (1996)
  • D. Fries et al.

    Time for changing coagulation management in trauma-related massive bleeding

    Curr Opin Anaesthesiol

    (2009)
  • S. Gando et al.

    Combined activation of coagulation and inflammation has an important role in multiple organ dysfunction and poor outcome after severe trauma

    Thromb Haemost

    (2002)
  • S. Gando et al.

    Disseminated intravascular coagulation and sustained systemic inflammatory response syndrome predict organ dysfunctions after trauma: application of clinical decision analysis

    Ann Surg

    (1999)
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