Objectives: Behind armour blunt trauma (BABT) to the thorax results from motion of the body wall arising from the defeat of high-energy projectiles by body armour. NATO predicts that BABT will increase in future conflicts. This study aims to define biomechanical tolerance levels for BABT to the lateral thorax.

Methods: Terminally anaesthetised pigs (n=19) were subjected to 4 levels of severity of BABT (Table). Two types of armour plates were used. Group 1 were subjected to a 7.62 mm round (INIBA armour) whilst group 2 was subjected to a 12.7 mm round (EBA armour) the latter group being further subdivided by the presence or absence of two thicknesses of trauma attenuating backing (TAB). Accelerometers were attached to the pleural aspect of ribs 7, 8 and 9 mid-way between the spine and the sternum.

Results: Outcome was assessed by classifying severity of injury, in terms of mortality, into 3 groups – survivors (animals surviving to 6 h post-impact), early (0–30 min) and late deaths (> 30 min–6 h). The peak acceleration values were obtained from the accelerometer closest to the point of impact. Mean peak acceleration was significantly higher in the early death group (1070 km/s²) compared to survivors (591 km/s²) (p< 0.05).

There were 6 early deaths, 5 late deaths and 8 survivors. In terms of outcome Group 1 represented the lowest threat with 5 survivors and 1 late death. The animals in Group 2 with no TAB fared worst with 2 early deaths, one late death and no survivors. Deaths were due to respiratory failure/apnoea (n=4), pneumothorax (n=2), haemothorax (n=1), respiratory failure/pulmonary contusion (n=3) and ventricular fibrillation (n=1).

Conclusions: Peak acceleration of the body wall may be used to rank the outcome following BABT. There is a significant difference in peak acceleration at the extremes of the injury scale.

Phosgene has been deployed as a CW and is also widely used in the chemical industry. Following exposure, acute lung injury (ALI) occurs after a latency period of 6 – 12 h, with pulmonary oedema ensuing. Death may occur 6–24 h after exposure. There is no specific therapy.

Conventional ventilation strategies (VS) for the treatment of ALI and ARDS utilise tidal volumes of 10 – 12 ml.Kg⁻¹ with variable PEEP. A recent multinational clinical trial advocates a protective VS (PVS) combining reduced tidal volume and increased PEEP, which resulted in a significant reduction in mortality.

The purpose of this study is to determine if a similar strategy is beneficial in the treatment of PIALI.

Twenty female pigs were anaesthetised and instrumented for the collection of physiological and biochemical data. Following surgery the animals equilibrated for 1 hour, and exposed to air (Control) or Phosgene (10 min). At 30 minutes post exposure, ventilation was initiated and the animals further divided into treatment groups prior to monitoring for up to 24 hours.

Preliminary results show that, utilising a PVS, there is an increase in oxygenation together with reduced mortality at 24 hour post exposure. Post mortem showed a decrease in severity of pathology and lung wet weight/ body weight ratio.

These results would indicate that in a clinical situation this strategy would be of benefit in the treatment of PIALI.