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TRAUMATIC COAGULOPATHY INFLUENCES OUTCOME IN PATIENTS WITH ISOLATED TRAUMATIC BRAIN INJURY
  1. A Kehoe2,
  2. R Bullough1,
  3. K Ainsley1,
  4. O Wigginton1
  1. 1Derriford Hospital, Plymouth, UK
  2. 2Plymouth University, Plymouth, UK

Abstract

Objectives & Background The coagulopathy associated with severe trauma and shock (ACOTS) has been well-described over the last decade. Recently a similar coagulopathy has been identified in patients with isolated traumatic brain injury (iTBI) in the absence of shock. The aim of this study was to identify whether or not ACOTS is detectable on admission in patients with iTBI admitted to a UK Major Trauma Centre and to explore associations with outcome.

Table 1

Methods A retrospective search of the local Trauma Audit Research Network (TARN) dataset was undertaken to identify patients with iTBI (AIS head>2, no other injury AIS>2) who presented to Derriford Hospital from 01 January to 31 December 2014. Demographic, mechanistic, physiological, resource utilisation and outcome data were recorded alongside admission laboratory blood test results. Cases were included if they had a FBC and lab coagulation screen performed on the day of admission. Cases therapeutically anticoagulated prior to admission or those transferred more than 24 hours following injury were excluded from analysis. ACOTS was defined as either PT>1.5s or APTT>35s or INR>1.2 or platelets <100 or fibrinogen <1, consistent with previous studies. Cases were categorised into 2 groups according to the presence or absence of ACOTS. Data were compared between the two groups using standard statistical tests.

Results 108 cases met the inclusion criteria whose data are presented in Table 1. ACOTS was identified in 52 (48.1%). ACOTS occurred independently of age, gender, mechanism of injury, AIS head, intracranial injury type and admission GCS but was associated with higher mortality (26.9% vs 5.4% p=0.002) than those without. Admission CRP was available in 23 cases and was significantly higher in cases with ACOTS.

Conclusion ACOTS occurs commonly in patients with iTBI and can be detected on admission using standard laboratory tests. It is associated with an increased absolute risk of death of 21.5% in patients presenting to our MTC. It does not seem to be driven by type or severity of anatomical injury and appears to involve systemic inflammatory activation. Further work is justified to describe these observations in greater detail. Therapeutic trials of coagulopathy reversal in iTBI patients with ACOTS may offer the potential to improve outcomes.

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