Blast
injuries
Mechanism
of explosive blast injury
The explosive pressure that accompanies the bursting of bombs or shells
ruptures their casing and imparts a high velocity to the resulting fragments.
These fragments have the potential to cause even more devastating injury to the
tissues than bullets. They are unstable in flight and may tear through tissue at
high speed in a tumbling fashion. These statements are particularly true of old
artillery shells and terrorist bombs where the casing fragments naturally into
pieces of variable size. However, the trend in conventional war is towards
carefully
engineered weapons which carry preformed munitions, such as notched wire or ball
bearings, or have their casing etched to allow predictable fragmentation
patterns resulting in a multitude of small, relatively low-energy fragments (Fig.
19.2). The aim is to incapacitate, not kill, by inflicting multiple
low-energy transfer wounds to two or more body systems.
In
addition, all explosives are accompanied by a complex blast wave. The two main
components of this wave are a blast pressure wave (known as dynamic
overpressure), with a positive and negative phase, and the mass movement of air
(known as blast wind) (Fig. 19.7).
The
positive pressure phase of the blast wave lasts for only a few milliseconds, but
close to an explosion it may rise to over 7000 kN/m2. As the healthy
tympanic membrane ruptures at about 150 kN/m2, it is evident that
the effects on the human body of such an explosion can be devastating, especially
in confined areas. Like sound waves, the blast pressure waves flow over and
around an obstruction and affect anyone sheltering behind a wall or in a trench.
The pressure affecting such a person is known as the incident pressure (defined
as the pressure level at 900 to the direction of travel of the blast shock
front). Also, any person standing in front of a wall or other vertical surface
facing an explosion is subjected to the added effect of a reflected pressure.
The negative effect of a pressure wave is of low amplitude, lasts longer
than the positive wave and is of doubtful clinical significance.
A
mass movement of air or dynamic pressure results from the rapidly expanding
gases at the centre of the explosion which displaces air at supersonic (greater
than the speed of sound in air) speed. This has been described by an eminent
blast scientist as ‘fresh air moving very fast’. The mass movement of air
results in what is colloquially known as blast wind and disrupts the
environment, hurling debris and people. This phenomenon results in injury
patterns ranging from traumatic amputation to total body disruption. The mass
movement of air may disrupt buildings, causing entrapment and crush injuries.
Blast
pressure waves travel at the speed of sound in the medium being traversed. In
water, velocity and distance are greater and injuries tend to be more complex
and severe. For example, blast pressure waves in air rarely affect the gastrointestinal
tract to any clinically significant extent in survivors; however, in water, the
blast wave exerts a ‘water hammer’ effect with significant rates of
gastrointestinal perforation.
When
the body is impacted by a blast pressure wave, it couples into the body
and sets up a series of stress waves which are capable of injury, particularly
at air—fluid interfaces. Thus, injury to the ear, lungs, heart and, to a
lesser extent, the gastrointestinal tract (see above) is notable. The exact
mechanisms of injury at each specific tissue are still the subject of
controversy but need not unduly worry readers as this topic is debated well by
Cripps and Guy in Trauma and by Ryan et al. in Ballistic
Trauma, as listed in the ‘Further reading’ section of this chapter.
General
management of blast injuries
The structures injured by the primary blast wave, in order of
prevalence, are the middle ear, the lungs and the bowel. However, the most
common urgent clinical problem in survivors is usually penetrating injury caused
by blast-energised debris and fragments from the casing of the exploding device
(see below). Many of those exposed will have blunt, blast and thermal injuries
in addition to more obvious penetrating wounds (the clinical picture is usually
referred to as combined injury). The deafness of the victims of blast,
due to disruption of the tympanic membrane, makes communication with them
difficult and may complicate early assessment and management. Here, the primary
survey and resuscitation phases of a system such as ATLS are particularly apt.
The management of penetrating wounds differs little from that of missile wounds
referred to earlier. The soft-tissue wounds are usually heavily contaminated
with dirt, clothing and secondary missiles such as wood, masonry and other
materials from the environment. Such contaminants may be driven deeply into
adjacent tissue planes opened up by the force of the explosion. The propensity
for wound infection in these cases is considerable and is often underestimated.
Some cases are associated with multiple wounds of varying severity affecting a
limb (Fig. 19.8).
It
may not always be practical to explore every wound at first surgery. The larger
and deeper wounds should have priority of management due to the more serious
consequences of infection. In many blast injuries one cannot be sure of complete
wound excision and, therefore, it is imperative that all blast wounds should be
left open at the end of the initial operation and delayed primary closure
performed 4—6 days later.
Regional
management of blast injuries
Here one is particularly concerned with identifying specific injuries
caused by the primary blast wave.
Auditory
system
Blast damages the hearing in three ways. There may be rupture of the
tympanic membrane, dislocation of the ossicles or widespread disruption of the
inner ear. The latter is sometimes accompanied by permanent deafness. It should
be remembered that the likelihood of ear damage depends on the angle between the
incident blast wave and the external auditory meatus. Although deafness is a
certain indicator of exposure to significant blast loading, its absence does not
imply the absence of blast injury to other systems.
Respiratory
system
Injury to the lung parenchyma is complex and the exact mechanisms are
still the subject of debate. Undoubtedly, the impacting primary blast wave may
cause a rapid inward movement of the chest wall and result in underlying
pulmonary
contusion, but this is not the principal mechanism in the severe and progressive
acute lung injury picture seen in small numbers of survivors. In these
casualties it is probable that the initial blast wave couples into the chest
resulting in stress waves which spread out, reflect and reinforce at tissue
interfaces. At air—fluid interfaces they may result in considerable
disruption. This is particularly notable at the alveolar—capillary membrane
and leads to capillary leakage resulting in a spreading haemorrhagic alveolar
contamination (Fig. 19.9).
An
inflammatory cascade now ensues resulting in a post-blast respiratory
insufficiency (PBRI), which is virtually indistinguishable from adult
respiratory distress syndrome (ARDS) following generalised sepsis or fat
embolism syndrome (FES), and posing a difficult clinical problem in critical care
units. PBRI varies from a mild and localised area of pulmonary contusion injury
to a fulminating and rapidly fatal condition involving both lungs. This rapid
and progressive condition is relatively rare, as casualties sufficiently close
to suffer extreme blast loading to the chest wall are usually killed by multiple
penetrating wounds or are dismembered by blast winds. In severe cases,
respiratory insufficiency may
Specific
clinical management of an established case remains controversial. There is still
little hard evidence to guide clinicians. However, most agree with the
guidelines listed in below
Postblast respiratory insufficiency (PBRI) — clinical guidelines
• Work within the ABCDE system of the ATLS system
• Avoid overhydration while maintaining vital organ perfusion
• Administer high-flow oxygen (12 litres/minute) with mask and
rebreathing bag
• Carry out arterial blood analysis to assess need for further measures
• Resort to mechanical ventilation early to ensure adequate oxygenation
• Use positive end-expiratory pressure (PEEP) carefully while avoiding
excessive peak and plateau pressures
• Corticosteroids should be avoided
Gastrointestinal
tract
The
eye
The eye should be examined in both the primary and secondary surveys,
yet injury is easily missed. Conjunctival haemorrhage following blast exposure
may herald a more serious underlying problem of penetration of the globe by
blast-energised debris or fragments. The pupil must be carefully examined and
any abnormality, distortion of the iris or the presence of a hyphema, for
example, should be investigated by an ophthalmologist.
Other
factors
Factors
that increase the morbidity and mortality following bomb blast injuries are
associated chemical and thermal burns, and the inhalation of toxic gases and
smoke.