Improvised explosive devices (IEDs) came to prominence in Iraq and became the
primary weapon used by insurgent forces in Afghanistan against coalition troops and
vehicles in the late 20th and early 21st century. IEDs caused over 50% of all UK combat
fatalities in these conflicts, many of whom suffered extremity traumatic amputations
(TAs). To date, understanding of the mechanism of blast-mediated TA has been based
on limited anatomical and minimal radiological injury data.
Blast-mediated TAs were first thought to be solely attributable to limb flail caused by a blast wind of sufficient velocity to bring about extremity avulsion. This injury mechanism theory was significantly modified in 1996 following UK military medical research: the shockwave – ‘primary blast injury’ – was thought to be pivotal in the
creation of blast-mediated TAs, coupling directly into the limb and causing a long bone
fracture prior to gross limb movement, with the blast wind – ‘tertiary blast injury’ -
subsequently displacing the limb causing amputation through the aforementioned
fracture. A strong link was believed to exist between TA and exposure to lethal levels
of primary blast loading. Guillotine-type TAs were also seen due to large fragments
energised by the blast (secondary blast injury).
Modern battlefield blast casualty (survivors and fatalities) analysis, combined with
incident data analysis of each blast event, has not shown the previously asserted link
between TA and primary blast lung injury. Furthermore, the high proportion of through
joint TAs (22.4% in fatalities vs. 1.3% reported previously), determined by
postmortem CT imaging, has indicated pure flail as a valid injury mechanism. These
injuries thus appear to have multiple blast injury mechanisms - primary and tertiary,
secondary, and (previously unappreciated) pure tertiary – and a greater understanding
of these injury modalities has significant implications for mitigation and prevention
strategies.