Blasts by Professor Michael Reade

Blast trauma
Michael Reade
MBBS MPH DPhil DMedSc AFRACMA FCCM FANZCA FCICM
Anaesthetist & Intensive Care Physician
ADF Professor of Military Medicine & Surgery
Brigadier. Assistant Surgeon General – Australian Army
Joint Capabilities Group │ Joint Health Command │ Defence Professor of Military Medicine and Surgery

22 March 2016
Airport:
3 bombs (2 functioned)
Railway station:
1 bomb
All blast (acetone/peroxide)-fragmentation devices
32 (+3) killed incl. 4 DoW
300 wounded
Relevance to civilians

Actual casualties: 3 dead, 264 wounded
Relevance to civilians

Blast wave

Blast wave: conventional vs. enhanced

Blast injury classification
Displacement
of the victim
Flying
debris
Pressure
wave
Crush, burn,
asphyxia, toxins
Courtesy
LTCOL
Anthony
Chambers
RAAMC

High explosive
• > 300 m/sec (or subsonic)
• detonation
• E.g. TNT, C4, dynamite, ammonium
nitrate fuel oil (ANFO) e.g. Oklahoma
City, Bali (Sari Club), Oslo and Marriott
Hotel (Jakarta)
Low explosive
• < 300 m/sec (or supersonic)
• Deflagration
• E.g. LPG bottle, gunpower
Blast injury classification

Blast trauma

Primary blast trauma
Mechanisms of tissue damage by a blast wave:
• Spalling: as the wave moves from a more to less dense medium, disrupting the interface
• Implosion: due to compression then expansion of gas in hollow organs
• Shearing: blast wave causes different density tissues to accelerate at different speeds

Pathophysiology of ballistic trauma
Michael C. Reade, MBBS MPH DPhil DIMCRCSEd DMCC FANZCA FCICM
Peter D. (Toby) Thomas, MBBS FRACP FANZCA FCICM

Secondary blast trauma

Secondary blast trauma
Ballistic trauma in blast injury
Pathophysiology of ballistic trauma
Michael C. Reade, MBBS MPH DPhil
DIMCRCSEd DMCC FANZCA FCICM
Peter D. (Toby) Thomas, MBBS FRACP
FANZCA FCICM
Up to 10% of survivors
have some eye injury
especially due to high
velocity perforations

Tertiary blast trauma

Quaternary blast trauma

Blast injury epidemiology
Open air
Enclosed
space
Structural
collapse
Under water

Blast injury epidemiology

Myths & facts

Myth: Survivors have critical injuries

Myth: Survivors will overwhelm surgical capacity

Myth: Traumatic amputation is common

Myth: The prehospital triage system will work
80% will arrive in first hour
Less severely injured patients
arrive first

Myth: blast wave injuries will be common amongst
survivors of civilian blast
Civilian low-explosive blast
• E.g. black powder, gunpowder,
petroleum-based liquids / gels.
Contained in e.g. pipe bombs,
Molotov Cocktails
• Almost never cause primary blast
injury

Myth: blast wave injuries will be common amongst
survivors of civilian blast
Enhanced blast in a civilian context:
• Combustion of air/dust mixtures in grain silos or coal stores
• Boiling liquid-expanding vapour explosions (BLEVEs) – when
gases stored as liquids under pressure at temperatures
above their boiling points (e.g. LPG bottles in a fire)

Myth: Significant blast trauma is always associated with tympanic
membrane perforation

Myth: Significant blast trauma is always associated with tympanic
membrane perforation
• No tympanic membrane perforation -> don’t be reassured
• Tympanic membrane perforation & everything else seems OK -> it
probably is
Direction of
blast

Myth: blast-fragmentation penetrating wounds are
usually ‘high energy’ transfer

Tips for hospital management
of blast trauma

Blast lung
• Pathogenesis: disruption of capillaries. Early deaths are due to arterial air emboli
(causing stroke and cardiac ischaemia).
• Develops over 24-72hrs and takes 7-10 days to resolve.
• Signs: hypoxaemia, frothy sputum, subcutaneous emphysema
• DDx pneumothorax, haemothorax, inhalation of toxic gases
Treatment: we have no idea!
• Extrapolate from ARDS principles (permissive hypercapnia, low tidal volume,
restrict fluid)
• Higher Ppeak = greater risk of air embolus (???)

Occult abdominal injury
• Uncommon
• Presents late (up to 14 days) with peritoneal irritation
from visceral rupture (esp. colon or multifocal)
• Requires conventional surgical management

A conventional organisational approach will not work
• Most patients will have >1
wound site, and so ideally
will require >1 operative
team.
• The median number of
surgical operations
required is 3.5

Triage is important but reverse triage is not
necessarily essential
London 2005
– 52 deaths (+4 bombers)
– 700+ wounded
– 350 hospitalised
– 100 admitted overnight
– No expectant category triage used

Two long term complications are particularly common
Incidence approx. 60% of
survivors from US military
in Iraq & Afghanistan
mTBI incidence 9% of 7909 US Marines
Main treatment is avoidance of repeat head trauma

Summary
• Asymmetric warfare arguably makes mass casualty blast events a legitimate tactic
• Low explosive blast (typical of civilian blast events) almost never causes blast wave injury
• High explosive primary blast injury is likely to be present only:
• If very close to the explosion (when mortality is very high);
• With enhanced blast;
• With underwater blast; or
• In a confined space
• Penetrating wounds due to blast are the commonest mechanism in survivors. They are
usually low-energy. Not all require surgical debridement.
• Most blast-related injuries should be managed according to conventional trauma principles.
• Treatment does not end with surviving the initial admission day

References

Blasts by Professor Michael Reade

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