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ABSTRACT
Behind Armour Blunt Trauma (BABT)
is the non-penetrating injury resulting
from the rapid deformation of armours
covering the body. The deformation of
the surface of an armour in contact with
the body wall arises from the impact of a
bullet or other projectile on its front
face. The deformation is part of the
retardation and energy absorbing
process that captures the projectile. In
extreme circumstances, the BABT may
result in death, even though the
projectile has not perforated the
armour. An escalation of the available
energy of bullets and the desire of
armour designers to minimise the
weight and bulk of personal armour
systems will increase the risk of BABT
in military and security forces
personnel.
In order to develop materials that can
be interposed between the armour and
the body wall to attenuate the transfer of
energy into the body, it is essential that
the mechanism of BABT is known.
There is a great deal of activity within
UK and NATO to unravel the
interactions; the mechanism is likely to
be a combination of stress (pressure)
waves generated by the rapid initial
motion of the rear of the armour, and
shear deformation to viscera produced
by gross deflection of the body wall.
Physical and computer model systems
are under development to characterise
the biophysical processes and provide
performance targets for materials to be
placed between armours and the body
wall in order to attenuate the injuries
(trauma attenuating backings - TABs).
The patho-physiological consequences
of BABT are being clarified by research,
but the injuries will have some of the
features of blunt chest trauma observed
in road traffic accidents and other forms
of civilian blunt impact injury. The
injuries also have characteristics of
primary blast injury. An overview
diagnosis and treatment is described.
Introduction
Behind armour blunt trauma (BABT) is
the spectrum of non-penetrating injuries to
the torso resulting from the impact of
projectiles on personal armours. Although
the armour may stop the actual penetration
of the projectile through the armour, the
energy deposited in the armour by the
retarded projectile may be transferred
through the armour backing and body wall.
It may produce serious injury to the thoracic
and abdominal contents behind the plate.
With very high energy bullet impacts, the
thoracic injuries may result in death.
The existence of BABT as a clinical entity
was first reported in 1978 by Carroll and
Soderstrom among police officers wearing
flexible body armour struck by handgun
bullets. BABT may occur behind flexible
textile-based armours and also behind rigid
armours, principally constructed from
ceramic materials.
BABT has been identified as an emerging
problem that has implications for the
designers of personal armour systems, the
operational performance of soldiers and for
medical management of casualties.There are
two principal reasons for its growing
prominence:
• An increase in the calibre and available
energy of bullets that may be used in
peace-keeping and other operational
scenarios;
• The desire of the designers of personal
armour systems to reduce the weight and
thickness of soft armours and armour
plates - a strategy that plainly will buy
benefit in terms of the burden on military
personnel, but will exacerbate the problem
of dissipating the energy in the armour
system. Armours are designed to absorb
energy but the rapid deformations of the
armours may result in a greater proportion
of the energy of the retarded projectile
being propagated into the body.
The energy transferred from armours may
be absorbed, dissipated or redistributed
using materials placed between the armour
system and the body - these materials are
called Trauma Attenuating Backings (TABs).
There is research activity within NATO to
develop the scientific basis for the design of
TABs.
This paper outlines the current views on
the pathophysiology and biophysical
mechanisms of BABT, and describes
Surg Lt Cdr
L Cannon, BSc MB BS
FRCS Dip Sports Med
RN
Orthopaedic Specialist
Registrar
Orthopaedic Dept,
Queen Alexandra
Hospital, Cosham,
Hants, PO6 3LY
J R Army Med Corps 2001; 147: 87-96
Behind Armour Blunt Trauma -
an emerging problem
L Cannon
technical approaches to developing model
systems to characterise the BABT threat
behind armours. A brief overview on the
medical management of blunt injury to the
thorax is also presented.
The ballistic threat against
armour plates
The ballistic threat against soldiers continues
to rise, both in terms of bullet calibre and
available energy. United Kingdom armed
forces use rifles that fire bullets of principally
5.56mm calibre (e.g. the SA-80); the most
ubiquitous weapons deployed by irregular
forces fire 7.62 mm calibre projectiles (e.g.
the AK-47). Rifles are available which fire
bullets of 12.7mm calibre; this calibre was
largely developed to fire ball and armour
piercing rounds against vehicles and lightly
defended structures. Rifles and other types of
gun firing 12.7 mm bullets are in service with
the majority of major armies (Jane’s Infantry
Weapons 1999). During the early 1990’s,
12.7 mm rounds were fired against British
soldiers in Northern Ireland (Gotts 1998a),
and caused fatalities. It has been reported in
the press that the Royal Ulster Constabulary
believe that the Provisional Irish Republican
Army (PIRA) are in possession of a number
of Barratt rifles that fire 12.7mm rounds
(The Sunday Times 7 May 2000).
The 12.7 mm calibre bullet is emerging as
a direct anti-personnel weapon. Modern
armies routinely deploy armour plates that
are designed to stop 5.56/7.62 mm calibre
bullets.The significantly higher energy of the
12.7 mm bullet will inevitably result in
perforation of these plates. It is technically
feasible to develop armour plates that will
stop 12.7 mm ammunition, but the
dissipation of the enormous quantities of
energy raises the issue of BABT injury, which
in extreme cases may result in death.
Representative available energies at the gun
muzzle for 7.62mm (standard NATO issue)
and 12.7mm (Soviet B-32, armour piercing
incendiary) are 3.5kJ and 14 kJ respectively.
NATO has reviewed the threat from
BABT in military operations. A Specialist
Team on Body Armour (Knudsen 1996)
concluded from the available knowledge
that:
• the BABT injury potential of defeated
high-energy bullets (i.e. 12.7mm calibre)
was significant;
• that of 7.62 mm bullets was largely
dependent on the armour design;
• there was no evidence of significant BABT
injury from 5.56 mm military bullets.
Another potential source of BABT injury
arises from the detonation of explosives
encased within metal containers. Although
conventional munitions are designed to
produce very large numbers of small
fragments with uniform mass and low
energy, certain improvised explosive devices
may generate large metallic fragments with
very high available energies. The impact of
these fragments either individually, or as a
shower upon the armour plates of Explosive
Ordnance Disposal (EOD) suits may
transfer sufficient energy during the
retardation process to produce BABT
injuries.
Personal body armour design
The use of body armour dates to antiquity.
The development of body armour for
protection against bullets and fragments
began during the American Civil War
(Peterson 1950) with the Korean War
providing the catalyst for modern scientific
study (Coates and Beyer 1962).The current
commercially available body armours share
similar features.The main types of armour in
service with the British Army include ‘soft’,
flexible armours and ceramic-based, ‘rigid’
armour plates.
The flexible armours comprise layers of
aramid and/or nylon to dissipate the kinetic
energy of a projectile (either low-energy
bullets or fragments) by stretching fibres.The
most common aramid - Kevlar® - was
originally developed by DuPont (USA) as a
replacement for steel belting in vehicle tyres
but the research division of the US National
Institute of Justice (NIJ) recognised that it
might prove a replacement for nylon in
personal armours. It became apparent that it
was superior to nylon and its use is now
ubiquitous.
Rigid plates usually have three
components: a hard, brittle ceramic strike
face acting as a bullet eroder and energy
dissipater, an energy absorbing backing to
the ceramic (frequently an aramid
composite) and the adhesive binding the two
materials. Improved Northern Ireland Body
Armour (INIBA) plates are composed of an
alumina ceramic (Al
2
O
3
) and will defeat
7.62mm rounds. A commercially available
boron carbide plate capable of stopping a
88 Behind Armour Blunt Trauma
Fig 1. A commercial boron carbide armour plate capable of stopping 12.7 mm bullets.
12.7 mm bullet is shown in Figure 1. As the
projectile strikes the plate, the ceramic is
fractured (Figure 2) and deforms in a cone-
shaped fashion (Gotts 1998b). The armour
plate backing maintains this conoid as the
bullet is eroded by the ceramic (Figure 3).
The backing also distributes the energy of
the eroded bullet and ceramic fragments
from the localised impact over a larger area.
Finally, the aramid composite backing
absorbs the energy of the eroded bullet and
ceramic by stretching aramid fibres and
thereby deforming. The strike face also has
an aramid cover that acts as a spall shield to
limit the scatter of ceramic fragments upon
initial impact, thereby reducing the risk of
facial injuries.
Evidence of BABT in civilian
and military conflict
The earliest case report of the lethal
indirect effect of a high-energy round can be
found in an article by Shepard et al (1969).
He describes the case of a US Army sergeant
accidentally shot with an M-16 round at
close range during the Vietnam War.There is
no mention of ‘rigid’ body armour or other
retardation but the round did not penetrate
the pleural cavity. After a short period of
respiratory and haemodynamic stability the
patient rapidly deteriorated and died within
45 minutes of admission. Massive
pulmonary contusions alone were seen at
post-mortem.
In a civilian setting, Carroll and
Soderstrom (1978) described 5 cases of
BABT in police officers wearing Kevlar®
soft body armour struck by handgun bullets.
All survived with no significant
cardiorespiratory sequelae.
The lethal effects of a higher energy round
(.45 inch) fired at close range against soft
armour (undefeated) were reported by
Thomas (1982). The energy transfer greatly
exceeded the limits of the vest but these cases
do exemplify that over a certain range of
energy transfers to the chest, a clinical
picture will develop anywhere on the
spectrum between minor and non-survivable
injury.
One of the few accurately documented
examples of significant but survivable BABT
was presented as recently as 1995 (Jourdan
1995). A humanitarian aid worker in
Sarajevo was struck by a Soviet 14.5mm
bullet (at unknown range) while wearing
‘complete’ body armour. Apart from skin
and muscle damage his cardio-respiratory
status was stable.A chest radiograph revealed
no rib fractures and a small haemothorax
only, which was managed with a chest drain.
A subsequent radiograph on the same day
revealed a developing pulmonary contusion
corresponding to the site of impact. The
patient made an uneventful recovery.
Body armour reduces the incidence of
torso injury while shifting the worst injured
areas to the extremities (Mehran 1995).This
shift has been confirmed by the Canadian
Casualty Database Project which has been
gathering casualty statistics from the former
Yugoslavia since 1992 (Gotts 1998a). The
Canadians have also concluded that wearing
body armour decreases wounding potential
(from fragmentation injury as well as bullets)
and that there have been no reported
instances where the wearing of armour has
exacerbated injury.
The important issue with BABT is that
historically it has been associated with the
defeat of low energy bullets (such as from
hand-guns) by flexible textile armour
systems. Many armour manufacturers offer
“trauma backings” to reduce these injuries
behind soft armours. However, it is now
emerging as a significant military problem,
particularly behind rigid armour plates
designed to defeat high energy bullets.There
is little biophysical and pathophysiological
L Cannon 89
Fig 2.The brittle fracture on the impact face of a boron carbide plate (the black aramid spall
shield has been removed).
Fig 3. Retardation of a projectile by a ceramic facing on a
composite backing.
information on which to base designs for
TABs to counter the very high rates of energy
transfer to the body under these
circumstances.
Mechanism of thoracic injury
from BABT
BABT is a specific form of blunt chest
trauma (BCT). Experimental studies on
animal models, computer modelling of the
transfer of energy into the body and review
of clinical data have enabled an
understanding of the biophysical principles
of BCT (Cooper and Taylor 1989).
General principles of blunt impacts to the body
A blunt impact to the body may produce
local and distant injuries. Motion of the
body wall transfers energy from the
impactor to the viscera, and the
characterisation of this motion is the key to
understanding the aetiology of the internal
injuries. The type and severity of visceral
injuries from blunt impact are dependent
upon the magnitude of the deflection of the
body wall, and most importantly upon the
rate of the deflection.
An impact produces a force on the body
wall, and consequently the body wall
accelerates and its velocity increases. A
bending load will be applied to structures
within the body wall (such as ribs) and the
local deflection arising from its motion will
apply shear to the local underlying tissues.
Depending upon the magnitude of this
shear, local tissues may be lacerated or
contused.
The increase in velocity of the body wall
leads to the generation of stress (pressure)
waves. The stress waves will propagate
through the tissues and will reflect from
effectively rigid structures within the body
(such as the mediastinum or cranial vault) to
result in a complex pressure environment
within body compartments. The
enhancement of stress waves by reflection
and reinforcement may lead to “stress
concentration” at particular foci, such as the
contre-coup site in head injury, or the
anterior borders of the lung. Stress waves
lose energy when they encounter materials
of different mechanical properties (the
acoustic impedance - a function of the
density and wave speed in the material).
Tissue/air interfaces within lung
parenchyma are particularly susceptible to
energy transfer from stress waves.
Disruption of the alveolar/capillary interface
by the transferred energy will result in
pulmonary contusion. Stress waves do not
produce gross motion, but the forces within
the tissue may be very high.
The propagated stress waves account for
many of the distant injuries observed in
high-speed BCT. Distant injuries may also
be caused by shear waves. These are low
velocity waves that cause gross motion of
internal organs; a useful analogy is the wave
that travels down a rope when it is whipped.
The motion produced by shear may lead to
strain (stretching) between organs and their
sites of attachment, or produce local strain
within organs resulting in contusion or
laceration.
As a general principle therefore, in the
characterisation of any type of non-
penetrating impact, the deflection of the
body wall and the rate of the deflection
(defined either by the peak acceleration or
peak velocity of the body wall) must be
defined. For slow, high momentum impacts
such as those occurring in Road Traffic
Accidents (RTA’s), the peak velocity of the
body wall may be relatively small, but the
body wall deflection will be large (i.e. high
local shear).The deflection may take tens of
milliseconds to reach its maximum. At the
other extreme, the impact of a very fast but
lightweight blunt projectile (low
momentum) will lead to very high body wall
velocities (i.e. intense stress waves), but
small body wall deflections. The time to
peak body wall deflection may be only 1 or 2
milliseconds. The pathology arising from
these two impact extremes may be different.
The challenge for developing protective
measures to reduce the incidence and
severity of BABT is to characterise the
motion of the body wall behind the armours
and thereby define the balance of local
shear, stress waves and shear waves in the
production of the injuries.
Lateral thoracic impacts
Much of the available knowledge of blunt
injury mechanisms has been generated by
the automobile industry. As discussed above,
the injury mechanisms following RTA are
characterised by low speed, large mass
impacts transferring energy to the chest over
a comparatively long time period. This is in
direct contrast to ballistic impacts on
ceramic plates, nevertheless some of the
biophysical data from research aimed at
reducing the incidence and severity of
thoracic trauma from RTAs provides insight
into the dynamic response of the chest to
impact.
The chest wall under the impact point will
accelerate to a peak velocity, which then
decreases back to zero when the peak
deformation is attained. It is the rate at
which this deformation occurs and not its
magnitude that is the injurious event. This
feature was exemplified by experiments in
which human volunteers had their chests
compressed at 1 m/s by up to 20% [this
value is a relative deflection - the percentage
reduction in chest dimensions in the same
axis as the applied force] (Kroell 1976).
They suffered no ill effects. In contrast, pigs
showed an almost 100% probability of lung
injury with 20% compression at a chest wall
90 Behind Armour Blunt Trauma
velocity of 10 m/s (Viano and Lau 1988).
Relative chest wall displacements in pig
thoraces of 27% (with attendant rib
fractures) have been recorded following
impacts with 12.7mm rounds (Figure 4).
The human body is visco-elastic: its
effective stiffness is dependent upon the rate
at which it is compressed. Reflecting this
behaviour, a ‘Viscous Criterion’ of blunt
injury prediction to soft tissue was proposed
in 1983 (Viano and Lau 1983).This criterion
is the product of the time varying percentage
of chest compression and the velocity of
body wall deformation. The upper extreme
of the criterion’s validity with respect to
velocity is approximately 30 m/s (Viano and
Lau 1988). Its validity in predicting injury as
a result of BABT may be limited because
body wall velocities may exceed this value
From first principles, the rate of rise of a
stress wave generated in the body is probably
dependent upon the peak acceleration
attained by the chest wall following impact. It
is possible therefore that peak body wall
acceleration may be an appropriate index of
the severity of injury from stress waves.
Whole body peak acceleration has not been
shown to be a satisfactory correlate or causal
factor in RTA type lateral impacts (Kroell et
al 1981) - undoubtedly because these
impacts are relatively low speed, and whole
body acceleration does not adequately
represent the local acceleration of the body
wall. In a study into the effects of air bag
deployments, Lau et al (1993) used the
premise that body wall acceleration was an
important factor. Using computer
modelling, peak chest wall acceleration was
predicted to correlate with lung injury
following high-speed blunt projectile impacts
to the chest (Bush and Challener 1988).
In work on primary blast injuries, a good
correlation was achieved between peak chest
wall acceleration (above 10km/s/s) and the
increase in lung weight - an index of the
degree of haemorrhage and oedema in the
lung (Cooper et al 1996a). One important
difference between blast and BABT
biomechanics is that an explosion will
normally produce a shock wave loading that
encompasses the whole thorax and is
relatively uniform over the surface facing the
explosion. However, thoracic stress wave
loading from a BABT impact will originate
from a specific locus on the thoracic wall (the
impact point) and will propagate as a
hemispherical wave from that point. Another
important difference is that pulmonary
contusions from blast interactions may be
entirely dependent upon the propagation and
interaction of stress waves (and therefore
characterised by the peak acceleration or
velocity of the body wall) with the gross
deflection of the thoracic wall contributing
little to aetiology of the injury (Cooper et al
1991). This is not likely to pertain to BABT
where, because of the more localised loading,
the gross deflection will be notable and will
contribute to the observed pathology.
Anterior thoracic impacts
Less research has been undertaken on the
biomechanical response of high speed
impacts to the anterior thorax. The Viscous
Criterion (VC) has been validated for
predicting soft tissue injury following
anterior RTA-type impacts (Viano and Lau
1988). With regard to peak acceleration,
Nahum et al (1975) concluded that for RTA-
type impacts, sternal acceleration did not
correlate with injury severity. However in
later experiments, an association was found
between fatal ventricular fibrillation (VF)
and peak acceleration (Viano and Artinan
1978). The production of dysrhythmias may
be more important clinically than the
presence of some types of cardiac damage as
it is well recognised that cardiac contusions
are usually well tolerated. The clinical signs
are transient and difficult to recognise and
the electro-physiological effects they produce
are often idiosyncratic (Parmley 1958).
Probable mechanism of BABT injury
The biophysical principles of BABT injury
L Cannon 91
Fig 4. Deflection of the internal aspect of the left lateral thoracic wall following 12.7 mm bullet
impact on a boron carbide plate placed on the external body wall.The model is the eviscerated
thorax of a pig and the camera view is from the approximate position of the abdomen, looking
anteriorly.The spine is at the bottom of the picture. Marker beads to track the motion of the
internal aspect of the left body wall are attached to the pleural surface of the thorax (the beads
are on the right side of the image).The pre-impact view is shown in the upper image. The
deflection of the body wall a few milliseconds after the non-penetrating impact of the bullet on
a plate placed over the left thorax is shown in the lower image. Fractured, displaced ribs are
evident with gross intrusion of the body wall into the thoracic cavity.
are the subject of current research, but the
following sequence is an informed prediction
of events following the impact of a high
energy bullet on a ceramic armour plate
directly against the body wall:
• The contact of the bullet on the hard face
of the ceramic plate generates a very short
duration stress wave (van Bree and van der
Heiden 1996). This wave propagates
through the plate and its backing, and
couples directly into the body. This is an
extremely fast event with no significant
gross motion of the plate or body wall.
• The debris from the erosion of the bullet
by the ceramic applies a load to the
backing of the plate and the rear of the
backing accelerates and deforms locally
beneath the bullet contact point. The
residual deformation may be relatively
small (Figure 5), but the dynamic
deflection will be greater, and occurs at
high speed.
• The localised motion of the plate backing
applies a load to the surface of the body
wall. The superficial tissues of the body
wall compress, reducing the thickness of
the body wall.The inner aspect of the body
wall starts to accelerate and soon attains a
peak velocity. This dynamic motion
generates a second stress wave that is
propagated into the body and may produce
pathology both locally and at distant sites,
and electro-physiological effects.
• The gross deflection of the body wall
increases and applies local shear to tissues
immediately underneath the deflection - for
example: pulmonary contusion; myocardial
contusion; liver laceration, depending on
impact location. Figure 4 shows the gross
deflection of the interior aspect of the
thoracic wall following non-penetrating
impact of a 12.7 mm round on a ceramic
plate placed on the outside of the thorax.
• As the deflection increases, shear waves are
propagated through tissues leading to gross
motion of organs. Ribs (or sternum) may
be fractured by the high forces within the
body wall and displaced through the inner
aspect to produce local lacerations to
underlying tissue.
• The plate as a whole will also gain velocity
imparted by the impact of the bullet (the
conservation of momentum) and the
whole plate may then apply a more
distributed load to the body.
Thus, the aetiology of BABT is complex
and its prevention requires an integrated
approach to dissipate and absorb energy over
different time-scales. Attenuating one form
of energy transfer may exacerbate another
form. It is also necessary to ensure that
methods used to alleviate the biological
effects of the energy by placing materials
between the armour plate backing and the
body wall do not compromise the
performance of the plate with regard to
stopping the projectile.
Pathophysiology of BCT
The pathophysiological consequences of
BABT from high available energy impacts
are currently under investigation, but an
overview of BCT from general non-
penetrating impacts will offer insight into the
likely pathology.
Chest wall
A range of soft tissue and bony injuries can
result following BCT. There may be no
outward signs of chest wall injury despite
marked pulmonary insufficiency (Alfano and
Hale1965). While rib fractures are merely
used as a guide to visceral damage following
civilian accidents, the presence of rib
fractures in combat troops may result in
military incapacitation. An important point
to be made is that the extent of injuries to the
chest wall cannot be used to predict the
extent and nature of intrathoracic injuries,
such is the idiosyncratic nature of the
production of indirect injuries following
BABT (Carroll and Soderstrom 1978).
Indeed, even in experimental models
subjected to apparently identical energy
transfers, the degree and pattern of injury
can be unpredictable (Baosong et al 1996).
Lung
Although a wide range of pulmonary injuries
can result following BCT, the typical if not
pathognomonic lesion is the lung contusion.
Little attention was paid to contusions until a
number of reports emerged during and after
WW II as a result of studies into the effects
of blast waves (Ross 1941, King and Curtis
1942). The characteristic histological
findings consist of localised haemorrhage
and oedema in the alveoli and the interstitial
spaces (Alfano and Hale 1965), Fulton and
Peter 1970). In a departure from this
histopathological description, Wagner et al
(1988) used computerised tomography (CT)
to investigate clinical cases of BCT and
found that the basic component of the
majority of lung contusions were lacerations
of the alveoli or alveolar septae.The cause of
this epithelial-endothelial disruption has
been attributed to stress waves (Cooper and
Taylor 1989, Baosong et al 1996) and tensile
forces across the alveoli (Fung et al 1988).
Acute respiratory distress syndrome
(ARDS) complicates up to 26% of cases of
92 Behind Armour Blunt Trauma
Fig 5. Residual deformation of 20 mm of the rear of a boron carbide plate - the dynamic
deformation was greater.
significant BCT associated with pulmonary
contusions (Pepe 1989). First recognised
during WW II (Burford and Burbank 1945),
the condition has been described by a variety
of names including ‘contusion pneumonitis’
and ‘traumatic wet lung’. Pneumonia may
complicate BCT in 5-10% or more of cases
(Pepe 1989) rising to 85% if there is a co-
existing flail segment (Clark et al 1988).This
is in contrast to an incidence of less than 5%
following penetrating chest trauma (Pepe
1989). Pulmonary contusions may pre-
dispose to pulmonary infection by producing
a reduced ability to cough and thus to clear
secretions and by directly reducing the
clearance of bacteria (Richardson et al 1979).
Heart
Following RTA-type impacts, the
anteroposterior (AP) displacement of the
chest wall is large (often exceeding 50%) and
the cardiac injury pattern is thus
predominated by crushing (local shear). The
principal consequence of RTA BCT
affecting the heart is trauma to the
myocardium accounting for more than 90%
of all cardiac lesions (Parmley et al 1958). In
experiments on anaesthetised pigs using high
speed blunt projectiles, 54% were found to
have areas of contusion with ruptures in
29%. A number of contusions were situated
adjacent to the coronary vessels as well as in
seemingly random areas (Cooper et al 1982).
This led the authors to speculate in later
papers (Cooper et al 1984, Cooper and
Taylor 1989) that this distribution of
contusions was dictated by the propagation
of stress and shear waves rather than direct
trauma.
Cardiac contusion may lead to
dysrhythmias, due to altered electrical
characteristics with respect to normal
myocardium (Pearce and Blair 1976).
Tachyarrhythmias, bradyarrhythmias and
ventricular ectopic foci may arise from these
areas. The other effect of large areas of
contusions is myocardial pump failure. This
feature includes a spectrum of outcomes
encompassing transient cardiac depression
and cardiogenic shock.
In addition to the coronary arteries, the
thoracic aorta and its arch divisions can be
injured in BCT. The location and type of
vessel injury depends on the forces acting
upon them and the degree of displacement of
the vessel. The aortic isthmus is particularly
prone to injury as it marks the junction
between the relatively mobile aortic arch and
the fixed descending aorta. In patients with
thoracic aortic trauma due to BCT, isthmic
damage is present in 80-90% of patients
(Pretre and Chilcott 1997).
The early dysrhythmias constitute the most
immediate and life-threatening situation
(other than myocardial rupture) to arise from
BCT affecting the heart. Ventricular
fibrillation (VF) and transient complete
heart block are the two most commonly
encountered in experimental pig models
(Cooper et al 1982, Link et al 1998).Variable
periods of transient ‘cardiac standstill’ are
often seen which do not appear to result in
any significant degree of morbidity. VF is the
more common, and the one most likely to
result in death if defibrillation is not
attempted. If the human patient survives the
initial impact, a plethora of other rhythm
disturbances may follow.These include atrial
fibrillation, premature ventricular
contractions, bundle branch blocks and sinus
bradycardia (Baxter et al 1989). These
complications invariably occur within the
first 12 hours post-impact.
Thoracic surrogates for
prediction of BABT
The current standard for the predicted
occurrence of BABT behind armours is
promulgated by the US National Institute of
Justice (NIJ, 1987). This standard stipulates
a maximum level of post-impact static
indentation in clay of 44 mm; this is taken as
a pass/fail criterion for BABT. The standard
principally addresses the deformation of soft,
flexible body armours attacked by low
energy-transfer bullets. This standard does
not address a key feature of BABT - that the
impact is a dynamic event and the motion of
the body wall is the prime factor coupling
energy into the body. Plainly, measurement
of a static indentation in a medium such as
clay cannot represent this event. This
deficiency is widely recognised, but in the
absence of data defining the relationship of
the dynamic response of the body wall to
loading by the rear face of an armour and
BABT, the standard does at least offer the
commercial developers of armours a
performance target to reduce the trauma
from localised thoracic wall deflection.
A physical model simulating the effects of
blast on the thorax has been developed by
DERA Porton Down (Cooper et al 1996b); it
uses peak acceleration of a physical
representation of the body wall as the sole
measured output for simple blast waves (a
different biophysical indicator is used for
complex blast waves). The peak acceleration
of the wall of the model correlates with the
severity of lung contusion (assessed by an
increase in lung weight). This approach is
now being extended to design a thoracic wall
material that will replicate the deflection and
motion of a pig thoracic wall subjected to
BABT loading (Tam 1999). The BABT rig
(Figure 6) consists of a silicone rubber ‘chest
wall’ mounted in a support system. The
required mechanical properties of the model
wall were determined by reviewing historical
data on the response of the lateral thoracic
wall of anaesthetised pigs to high-speed non-
penetrating impacts, limited BABT data
from dead pig models and mathematical
L Cannon 93
models of body wall dynamics developed
from these data. The motion of the rear of
the model body wall is determined by a non-
contacting laser system that tracks its
motion. The wall velocity and acceleration
can be calculated from this data.The system
as currently implemented can rank the
BABT potential of armour plates and TABs.
It is being enhanced to enable an absolute
prediction of BABT injury, and thereby offer
dynamic performance targets for protection
from BABT.
Other workers have also realised the need
for specific, validated models of localised,
non-penetrating chest trauma. One such
system, termed the 3-rib chest structure, has
been designed to study the injury potential of
non-lethal weapons (such as riot control
projectiles). Its output is peak velocity from
which the maximum Viscous Criterion
(VC
max
) can be calculated and as its designers
point out,VC
max
can only predict injury if the
chest wall deformation velocity is between 3
and 30 m/s (Bir and Viano 1998).
Experiments at Porton Down have measured
peak inner chest wall velocities following
12.7mm bullet impact in excess of 50m/s.
Haley et al (1996) used the Hybrid III
anthropomorphic ‘crash test dummy’ in a
BABT test in which 12.7 mm calibre rounds
were fired against ceramic plates. They
recorded the average displacement of the
rear of the armour plate as 0.7-0.8 inches.
They recognised that a significant time span
elapsed between frames and commented that
an element of rebound of the chest wall may
have occurred in the time span between
frames. Also, the residual permanent
deformation may not reliably represent the
extent of true deformation because it takes
no account of the dynamic nature of the
deformation.
Jonsson et al (1988) used a modified
version of the Hybrid III dummy to predict
lung injury following BABT. They placed
pressure transducers into foam lung models
within the Hybrid III thorax and recorded
the pressure profiles following various levels
of BABT loading. They made the
assumption that the injury patterns following
blast were similar to those following BABT.
They found no direct proportionality
between projectile mass, velocity or Kinetic
Energy and intrathoracic pressure - an index
of blunt injury potential.
Guidelines for the clinical
management of high energy
BCT
Diagnosis
The management of BCT in field conditions
relies totally on the recognition of the
condition and the diagnostic aids available.
The immediately life threatening thoracic
injuries can all be diagnosed on clinical
examination and imaging should play little or
no role in the diagnosis of these injuries.The
injuries presenting to the field medical officer
are probably self-selecting and those with
gross injuries are usually apparent. The
difficulty will lie in those patients with little in
the way of early pathology, but in whom
pathology may evolve over a period of hours.
The diagnosis of chest wall and thoracic
organ injury by special investigations in
terms of civilian BCT is still a matter for
considerable debate.The main reason for this
is the often inconsistent correlation between
detectable injury and clinical effects.
Lung injuries
The supine anteroposterior chest radiograph
is one of the initial investigations routinely
performed on the trauma victim. The
limitations of this investigation are well
documented. Approximately 30% of
traumatic pneumothoraces are missed on
supine radiographs (Wall et al 1983) and on
erect radiographs it has been shown that 500
ml of blood is required to fill the
costophrenic recess sufficiently to allow the
diagnosis of haemothorax to be made
(Collins et al 1972). Similarly, 21% of
experimentally produced pulmonary
contusions in dogs were missed by
radiographs 6 hours post-injury although all
were visible on computerised tomography
(CT) scans (Schild et al 1989).
Heart injuries
Virtually every type of electrocardiograph
(ECG) change has been associated with
BCT to the heart but no change is
pathognomonic (Unkle et al 1989). ECG’s
have a high false-positive and false-negative
rate for BCT. Parmley et al (1958) induced
chest trauma to animals and recorded a
94 Behind Armour Blunt Trauma
Fig 6. The BABT rig: a boron carbide plate and flexible
combat armour system have been placed over the white
silicone rubber wall that replicates the dynamic motion of
the pig body wall.The rapid deflection of the wall is detected
by sequential obstruction of an fan of laser beams behind it
(not visible in the image).
variety of ECG changes despite the absence
of injury at autopsy. Conversely, Blair et al
(1971) described patients with normal
ECGs and autopsy-proven myocardial
contusion (the patients dying of
comorbidity). However, the ECG does have
an important role to play in the
management, if not the diagnosis, of cardiac
BCT - it is the haemodynamic compromise
resulting from the dysrhythmia that is
important, not necessarily the absolute
diagnosis of contusions (Baxter et al 1989,
Healey et al 1990).
More recently, the role of helical CT has
been investigated. It was found to give a level
of 100% sensitivity and 99.7-99.8%
specificity (Mirvis et al 1998, Wicky et al
1998). One group recommends that all
trauma patients with suspected aortic injury
undergo helical CT evaluation and that it
should replace aortography as a screening
tool (Demetriades et al 1998). As mobile
helical CT scanners are to be deployed with
UK forces in the near future, its use in the
evaluation of BCT needs to be examined.
Treatment
Following recognition of the extent of the
injuries, the treatment of BCT (BABT)
injuries will be largely supportive. Drainage
of a haemopneumothorax and cardiac
monitoring have been employed (Jourdan
1995) and are within the skills of most
medical officers. Following civilian BCT and
because of the variability in electrophysiology
and the poor sensitivities and specificities of
diagnostic tests, some authors argue that
cardiac monitoring for a 24-hour period is a
pragmatic and sensible approach (Baxter et al
1989, Healey et al 1990). This would seem a
sensible approach for BABT injuries (local
circumstances permitting).
Concluding remarks
It is a false assumption that eliminating the
penetration of a projectile into the body by
using a personal armour system absolves the
wearer from serious injury or death. The
kinetic energy of the projectile must be
dissipated; the key is to ensure that the
proportion of this energy which is coupled
into the body is minimised, or is transferred
over an extended time-scale or surface area.
However, the design of a trauma attenuating
backing placed between an armour plate and
the body to enable this re-distribution of
energy, must also ensure that the ballistic
performance of the plate is not compromised.
This is a very difficult balance, and the trade-
offs can only be determined with knowledge
of the biophysical principles of the transfer of
the energy of the projectile into the body.
There are a number of co-ordinated research
activities within NATO addressing this issue.
Behind Armour Blunt Trauma is not an
insurmountable problem but its emergence
requires innovative technical solutions. The
art is to attenuate the injury using solutions
that do not increase the burden to the soldier,
but offer to the designers of heavy, rigid
ballistic plates an opportunity to reduce plate
weight and bulk. This may only be achieved
with control over how and where the energy
of the bullet will be dissipated safely.
References
Alfano GS, Hale HW. Pulmonary contusion. J Trauma
1965; 5(5): 647-656.
Baosong L, Zhengguo W, Huaguang L, Zhihuan Y,
Xiaoyan L. Studies on the mechanisms of stress wave
propagation in chest subjected to impact and lung
injuries. J Trauma 1996; 40(3): S53-55.
Baxter BT, Moore EE, Moore FA et al. A plea for
sensible management of myocardial contusion. Am J
Surg 1989; 158: 557-561.
Bir CA, Lyon DH, Viano DC. Development of a low-
cost, portable surrogate – the 3-rib chest structure.
Non-lethal defense meeting III. Johns Hopkins Applied
Physics Lab, 1998: 25-26.
Blair E, Topuzulu C, Davis JH. Delayed or missed
diagnosis of cardiac damage in blunt chest trauma. J
Trauma 1971; 11: 129.
Burford TH, Burbank B. Traumatic wet lung:
observations on certain physiologic fundamentals of
thoracic trauma. J Thorac Surg 1945; 14: 415-424.
Bush IS, Callener SA. Finite element modelling of
non-penetrating thoracic impact. In Proceedings of the
1988 conference of the International Research
Committee on Biokinetics of Impacts (IRCOBI),
September 1988.
Carroll AW, Soderstrom CA. A new non-penetrating
ballistic injury. Annals of surgery 1978; 188(6): 735-7.
Clark GC, Schecter WP, Trunkey DD. Variables
affecting outcome in blunt chest trauma: Flail chest v’s
pulmonary contusions. J Trauma 1988; 28: 298-304.
Coates JB, Beyer JC. Wound ballistics. Office of the
Surgeon General. Department of the Army.
Washington, DC, 1962.
Collins JD, Burwell D, Furmanski S et al Minimal
detectable pleural effusions. A roentgen pathology
model. Radiology 1972; 105: 51-53.
Cooper GJ, Maynard RL, Pearce BP, Stainer MC,
Taylor DEM . The biomechanical response of the
thorax to nonpenetrating impact with particular
reference to cardiac injuries. J Trauma 1982; 22(12):
994-1008.
Cooper GJ, Maynard RL, Pearce BP, Stainer MC,
Taylor DEM. Cardiovascular distortion in
experimental nonpenetrating chest impacts. J Trauma
1984; 24(3): 188-200.
Cooper GJ, Pearce BP, Sedman AJ et al Experimental
evaluation of a rig to simulate the response of the thorax
to blast loading. J Trauma 1996b; 40(3) Suppl : S38-41.
Cooper GJ, Taylor DEM. Biophysics of impact injury
to the chest and abdomen. J R Army Med Corps 1989;
135:58-67.
Cooper GJ, Townend DJ, Cater SR et al. The role of
stress waves in thoracic visceral injury from blast
loading: modification of stress transmission by foams
and high-density material. J Biomechanics 1991; 24:
273-285.
Cooper GJ. Protection of the lung from blast
overpressure by thoracic stress wave decouplers. J
Trauma 1996a; 40(3): S105-110.
Demetriades D, Gomez H, Velmahos G et al. Routine
helical computed tomographic evaluation of the
mediastinum in high-risk blunt trauma patients. Arch
Surg 1998; 133: 1084-1088.
Fulton RL, Peter ET. The progressive nature of
pulmonary contusion. Surgery 1970; 67(3): 499-506.
Fung YC,Yen RT,Tao ZL, Liu SQ. A hypothesis on the
mechanisms of trauma of lung tissue subjected to
impact load. J Biomechanical Engineering 1988; 110:
50-56.
Gotts PL.Thoracic response to defeated body armour.
In ‘Rear effects of protection’ NATO Technical Report
AC/243(panel 8)TR/23 (Unclassified) 26 Feb 1998a.
L Cannon 95
96 Behind Armour Blunt Trauma
Gotts PL. Personal armour against small arms
ammunition: UK MOD solutions. In proceedings of
the XIIth European Small Arms and Cannon
Symposium (Unclassified). Shrivenham. Aug 1998b.
Haley JL, Alem NM, McEntire JB, Lewis JA. Force
transmission through chest Armour during the defeat
of a .50 calibre round. US Army Aeromedical Research
Laboratory, Fort Rucker, Alabama. Report No. 96-14,
Feb 1996.
Healey MA, Brown R, Fleiszer D. Blunt cardiac injury:
Is this diagnosis necessary? J Trauma 1990; 30(2):137-
146.
Jane’s Ammunition Handbook. Jane’s Information
Group Ltd, Surrey, UK.1999.
Jane’s Infantry Weapons. Jane’s Information Group
Ltd, Surrey, UK.1999.
Jonsson A, Arvebo E, Scantz B. Intrathoracic pressure
variations in an anthropomorphic dummy exposed to
air blast, blunt impact and missiles. J Trauma 1988;
29(1) Suppl: S125-131.
Jourdan PH Behind Body armour effect. Case Report.
Defence Research Group Panel 8 STBA Collaborate
10-12 Oct 95.
King JD, Curtis GM. Lung injury due to the
detonation of high explosives. Surg Gynecol Obste1942;
74: 53-62.
Knudsen PJT. In proceedings of the 3rd Meeting of the
Specialist Team on Body Armour. Conclusions of
STBA. NATO Unclassified. San Diego, USA, 23-25
April 1996.
Knudsen PJT. Preface. In ‘Rear effects of protection’
NATO Technical Report AC/243(panel 8)TR/23
(Unclassified) 26 Feb 1998.
Kroell CK, Pope ME,Viano DC et al. Interrelationship
of velocity and chest compression in blunt thoracic
impact to swine. In proceedings of the 25th Stapp Car
Crash Conference. Warrendale, PA: Society of
Automotive Engineers. Paper No. 811016 p549-582
1981.
Kroell CK.Thoracic response to blunt frontal loading.
The Human Thorax - Anantomy, Injury and
Biomechanics. Society of Automotive Engineers.
Warrendale, PA. Paper No 67 p 49-78 1976.
Lau IV, Horsch JD, Viano DC, Andrzejak DV.
Mechanism of injury from air bag deployment loads.
Accid Anal Prev 1993; 25(1): 29-45.
Link MS,Wang PJ, Pandian NG et al. An experimental
model of sudden death due to low-energy chest-wall
impact (commotio cordis). N Engl J Med 1998;
338(25): 1805-11.
Mehran R, Connely P, Boucher P, Berthiume E.
Modern war surgery: the experience of Bosnia 2: the
clinical experience. Can J Surg 1995; 38(3): 338-346.
Mirvis SE, Shanmuganathan K, Buel J, Rodriguez A.
Use of spiral computed tomography for the assessment
of blunt trauma patients with potential aortic injury. J
Trauma 1998; 45(5): 922-930.
Nahum AM, Schneider DC, Kroell CK. Cadaver
skeletal response to blunt thoracic impact. In
proceedings of the 19th Stapp Car Crash Conference.
Society of Automotive Engineers. Paper No. 751150
p259-293 1975.
National Institute of Justice. Ballistic Resistance of
Body Armour – NIJ Standard 0101.03. April 1987
Parmley L, Manion WC, Mattingly TW.
Nonpenetrating traumatic injury of the heart.
Circulation 1958; 18: 371.
Pearce W, Blair E. Significance of the
electrocardiogram in heart contusion due to blunt
trauma. J Trauma 1976; 16: 136.
Pepe PE. Acute post-traumatic respiratory physiology
and insufficiency. Surg Clin North Am 1989; 69: 157-
173.
Peterson HL. Body armor in Civil War. Ordnance 34:
432-433 1950.
Pretre R, Chilcott M. Blunt trauma to the heart and
great vessels. NEJM 1997; 336 (9): 626-632
Richardson JD, Woods D, Johanson WG et al. Lung
bacterial clearance following pulmonary contusion.
Surgery 1979; 86: 730.
Ross JM. Haemorrhage into the lungs in cases of death
due to trauma. Br Med J 1941; 1: 79-80.
Schild HH, Strunk H, Weber W et al. Pulmonary
contusions: CT vs plain radiograms. J Comput Assist
Tomogr 1989;13: 417.
Shepard GH, Ferguson JL, Foster JH. Pulmonary
contusion. Ann Thorac Surg 1969; 7(2): 110-119.
Tam W. Development of a behind armour injury
simulator. In proceedings of the 3rd meeting of the
Task Group on Behind Armour Blunt Trauma. NATO
Unclassified. Washington, USA. 20-23 April 1999.
The Sunday Times. 7 May, page 3. 2000.
Thomas GE. Fatal .45-70 rifle wounding of a
policeman wearing a bullet-proof vest. Journal of
Forensic Sciences 1982; 27(2): 445-449.
Unkle DW, Smejkal R, O’Malley KF. Myocardial
contusion without creatine kinase-MB elevation. Heart
Lung 1989; 18: 539-541.
Van Bree JLMJ, van der Heiden N. Behind armour
pressure profiles in tissue simulant. In Proccedings of
the Personal Armour Systems Symposium 1996.
Colchester UK. 3-6 Sep 1996.
Viano DC, Artinan CG. Myocardial conducting
system dysfunction from thoracic impact. J Trauma
1978; 18(6): 452-459.
Viano DC, Lau IV. A viscous tolerance criterion for
soft tissue injury assessment. J Biomechanics 1988;
21(5): 387-399.
Viano DC, Lau VK. Role of impact velocity and chest
compression in thoracic injury. Aviat Space Envir Med
1983; 54: 16-21.
Wagner RB, Crawford WO, Schimpf PP. Classification
of parenchymal injuries of the lung. Radiology 1988;
167: 77-82.
Wall SD, Federle MP, Jeffrey RB, Brett CM. CT
diagnosis of unsuspected pneumothorax after blunt
abdominal trauma. American J of Roentgenology 1983;
141: 919-921.
Wicky S, Capasso P, Meuli R et al. Spiral CT
aortography: an efficient technique for the diagnosis of
traumatic aortic injury. Eur Radiol 1998; 8(5): 825-
833.
