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1 Platelet dysfunction in a model of complex military trauma
  1. Herbert Chitambira,
  2. Mark Bates,
  3. Sara Watts and
  4. Emrys Kirkman
  1. CBR Division DSTL Porton Down, JHG (SE)


Background Haemorrhage is a principal contributory factor in trauma-related deaths in military (battlefield) and civilian settings. A significant proportion of severely injured casualties develop an early trauma- induced coagulopathy (TIC), which is an independent predictor of death. One aspect of TIC is an alteration in platelet function. In vivo trauma models are often essential to develop new treatments. The aim of this study was to evaluate whether an established model of trauma incorporates platelet dysfunction.

Method The study was conducted in accordance with the Animals (Scientific Procedures) Act, 1986. Blood was collected from terminally anaesthetised pigs before (Baseline) and 30 minutes after the induction of trauma/haemorrhagic shock (S30), and again after 90 minutes of hypotensive resuscitation (R90) with either 0.9% saline, 1:1 packed red cells and plasma (PRBC:FFP) or whole blood (WB). Platelet function was assessed by aggregometry in response to ADP and TRAP (Multiplate®). Platelet count was obtained using a haematology analyser, and shock was quantified by measuring Actual Base Excess (ABE) of arterial blood.

Results ABE fell significantly from Baseline to S30 and remained negative (-7 ± 1 mM) until R90 in all groups (P<0.001), without significant difference between groups (P=0.4747). Injury, shock and resuscitation were associated with a significant fall in platelet aggregation in response to ADP (P<0.0001) and TRAP (P=0.0006), but no difference between treatment groups (P=0.9388 ADP; P=0.06385 TRAP). The response to TRAP was markedly less than that to ADP. Platelet count fell significantly (P<0.0001), again without significant difference between treatment groups (P=0.8574). After 90 minutes of resuscitation, the response to ADP had fallen to 62% of the baseline response while platelet numbers had only fallen to 85% of baseline over the same period.

Conclusions Our model of trauma results in an attenuation of platelet function that, in the early phase, is independent of resuscitation strategy.

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