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Blast Injury
Surg Cdr Jane Risdall Royal NavyConsultant Neuroanaesthetist/Intensivist
Senior Lecturer, Academic Dept Military Anaesthesia and Critical Care
Visiting Research Fellow, University of Cambridge
Cambridge Trauma Conference 24 April 2014
The Problem
• Blast injuries are a current and increasing problem (Champion HR J Trauma 2009, Nelson TJ J Am Coll Surg 2006)
• 46% casualties treated by US Forward Surgical Teams suffered injuries from blast (Rush RM Am J Surg 2005)
• More blast casualties are likely if enhanced blast weapons are used (Dearden P JRAMC 2001)
Detonation of bare explosive
• Blast wave– Shock wave– Dynamic
overpressure
• Heat from explosive products– Radiant– Convective
Shock front
Edge of explosive products
Blast Injuries• Primary
–Rapid acceleration of body wall by blast wave : generation of pressure wave eg. lung damage (blast lung)
• Secondary–Fragments and debris : penetrating injuries eg.
damage to major blood vessels, haemorrhage
• Tertiary–Gross body displacement : limb avulsions eg.
blunt injuries including musculo-skeletal
Blast (explosive) Injuries• Primary (shock
wave)– Rapid displacement
of body wall by shock wave
– Generation of pressure wave: damage to gas filled organs & at fluid gas interfaces
– BLAST LUNG
Blast (explosive) Injuries 2
• Secondary (fragments and debris)– Penetrating injuries– Soft tissue injuries– Contamination– TISSUE VIABILITY
and HAEMORRHAGE
Blast (explosive) Injuries 3
• Tertiary (translational, blast wind)– Gross body
displacement– Limb avulsions– TRAUMATIC
AMPUTATIONS and BLUNT TRAUMA
Blast: multiple mechanisms of injury
• Pressure (shock wave)• Energised fragments and debris• Blast winds
– Throwing things against the body– Throwing the body against things
• Heat– Convection– Radiation
Unique features of blast exposure
• Blast wave– Shock wave– Dynamic overpressure
• Confounder– Location of explosion
Blast overpressure/time profiles
Idealised blast wavein free space
Blast in a room/tunnel/enclosed vehicle
Primary Blast Injury
• Effects of shock wave:–Rapid displacement of body wall–Coupling of shock wave to generate
pressure wave which damages gas filled organs in particular
Primary blast injury to the thorax
• Pulmonary contusion and oedema Hunter Proc Royal Soc Med 1941, Zuckerman Lancet 1940
• Reduced gas transfer Damon et al Aerospace Med 1993
• Vagal driven cardiorespiratory response– Bradycardia– Hypotension– Apnoea/rapid shallow breathing– Rapid onset (2-5 secs)
Krohn et al Lancet 1942, Guy et al J Trauma 1998, Ohnishi et al Exp Physiol 2001
•
Primary blast lung
• Acute pulmonary oedema• Alveolar haemorrhage with
consolidation• Pneumothorax/
haemopneumothorax• Thrombo-embolic
phenomena• Release of pulmonary
inflammatory mediators• Systemic Inflammatory
Response Syndrome (SIRS)
Clinically
• Oxygenation is likely to be very difficult, may require ECMO
• ARDS picture is universal
• However, this is compounded by the effects on other systems…
Acute cardiovascular response to thoracic blast
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Time(bar = 10 s)Blast
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Time(bar = 10 s)Blast
Kirkman et al Philos Trans R Soc Lond Biol Sci 2011
Effects of blast on the response to haemorrhage
Sawdon et al Exp Physiol 2002
Sham blast
Blast
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Mild Blast Brain Injury• Circumstantial evidence of neuropsychological
problems after blast exposure – Okie NEJM 2005 – Belanger et al J Rehabil Res Dev 2005 – Lew J Rehabil Res Dev 2005
• Evidence of neuronal injury but mechanism unclear
– Cernak et al Brain Inj 2001– Cernak et al J Trauma 2001 – Moochhala et al J Trauma 2004
• Unknown: whether neuropsychological symptoms caused by blast
Thoracic protection attenuates neuronal injury
• Anaesthetised rats exposed to 126-147 kPa overpressure (whole body)
• ± thoracic protection (Kevlar® vest)
• Vest attenuated – Cardiovascular response to
blast– Neuronal injury
Long et al J Neurotrauma 2009
Significant Blast Brain Injury
• Blast-exposed casualties show increased incidence and severity of brain oedemaArmonda et al Neurosurgery 2006
– Can be serious and life-threatening– May require hemicraniectomy to decompress– Mechanism and specific treatment unknown
Bauman et al J Neurotrauma 2009
Mechanisms
• Physical– Shear forces within the brain– Vascular stretch– Bulk acceleration of the head
• Molecular– Unknown– Evidence for inflammatory mediators
• Local• Systemic
Although these animals received a significant cranial blast exposure (that would have been fatal if directed at the thorax) there was no evidence of histological damage (haemorrhage, oedema, leucocyte infiltration) in brain sections taken eight hours post exposure.
Elevation in endogenous Epo and pro-inflammatory
cytokines
MIP1α, IL6, IL1α and IL1β were also detectable but at levels below those permitting quantification. The trend was suggestive of an increase in the blast exposed group.
qRT-PCR array of inflammatory genes
• 87 genes involved in inflammation analysed (qRT-PCR array)
• Data presented as fold change (Blast vs control)
• Biologically relevant changes in genes if:– >2 fold change and – p-value <0.05
Summary• Blast injuries are multimodal
– Pressure wave– Penetrating trauma– Blunt trauma
• Each injury should be managed initially in accordance with standard algorithms
• Multiple systems will be affected• Inflammation will play a significant role in
the subsequent clinical course
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