Blast and crush injuries

Introduction

• Higher rates of immediate scene mortality, hospital mortality, need for surgical intervention, longer hospital stays and greater use of critical care than other trauma patients
• Pathophysiology
  • Blast = Instantaneous transformation of solid or liquid into gas with release of kinetic and heat energy
  • Blast wave loses energy over distance and time and is combination of:
    • Shock wave of high pressure followed by
    • Blast wind, air mass in motion

Blast injuries

• Primary blast injury
  • Due to direct effect of blasé wave overpressure on tissue
  • Mostly affects air-filled structures such as lungs, ears, GI tract by three main mechanisms:
    • Spalling: Displacement and fragmentation of a dense medium into a less dense medium (e.g. lung parenchyma exploding into alveolar space)
    • Shearing: Stress caused by blast wave travelling through different tissue densities at different velocities (e.g. pulmonary vessels and air spaces with ruptured vascular and bronchial pedicles)
    • Implosion: The opposite of spalling where less dense material is displaced into more dense material (e.g. flexible airways rebound to greater than original size, causing air embolism from alveoli into pulmonary vessels)

Blast injuries

• Secondary blast injuries
  • Collateral damage from flying objects and shrapnel
• Tertiary blast injuries
  • Result from victim being thrown into stationary objects
• Quaternary blast injuries
  • Burns, smoke inhalation and checmical agent release

Factors affecting blast injury

• Distance from explosion
  • Intensity of pressure wave declines with the cubed root of the distance
  • If 3m from explosion, experience 8x more overpressure than a person 6m away
  • Mainly affects primary blast injury
• Enclosed versus open space
  • If enclosed, much more severe with greater mortality. Higher risk of inhalational injury also
• Surrounding environment
  • Blast waves reflected by solid surfaces so primary blast injury can be increased if standing next to wall for instance

Factors affecting blast injury

• Quantity of explosive
• Type of explosive
  • Low-order: Burn rapidly and produce blast wave <1000m/s e.g. black powder
  • High-order: Detonate when shock wave passes through them, causing almost instantaneous transition from solid/liquid to gas in same amount of space under extremely high pressure. High pressure expands rapidly compressing the surrounding medium and produce a supersonic overpressure wave >4500m/s followed closely by a negative pressure wave
• Embedded shrapnel
  • Maximises number and severity of secondary injuries

Clinical features

• Cardiopulmonary
  • Pulmonary barotrauma is most common fatal primary blast injury
    • Haemorrhage, contusion, PTX, haemothorax, pneumomediastinum and subcutaneous emphysema
    • Air embolism is a likely cause of immediate cardiopulmonary collapse
      • Neurological symptoms need to be differentiated from direct CNS trauma
    • Pulmonary fat embolism can lead to ARDS in survivors
  • Manage as for ARDS
  • Limit Vt to 6-7mL/kg ideal body weight to minimise volu/barotrauma
  • Appropriate volume resuscitation
  • ECMO may become necessary within hours of injury
  • Asymptomatic patients with normal CXR and normal SpO2 may be considered for d/c after 4-6 hours of observation

Clinical features

• Ears
  • TM ruptures at 1-8 psi of overpressure
  • Dislodgement of ossicles
  • Using perforation of TM as indicator of primary blast injury misses 50% of primary blast injury to the lung
  • Limited observation is reasonable for patients with limited TM
• Abdomen
  • 1.3-33% incidence
  • Terminal ileum and caecum most commonly injured
  • Serial abdo examination, serial imaging and 24-48 hours of observation if any suspicion exists
  • If abdominal injury occurred as a result of blast wave (primary blast injury), they were likely situated near the explosive device (as air is a poor conductor of blast-wave energy

Clinical features

• CNS
  • Shrapnel may enter cranial vault with missed entry points under hair
  • Evidence for TBI may be masked by anaesthesia
  • Early CT is crucial
• Vascular injury
  • Small entry wounds of shrapnel may mask significant vascular injuries
  • Compartment syndrome may develop and be difficult to diagnose in the anaesthetised patient
  • Carefully assess and document pulses and perfusion in affected limbs
  • Measure compartment pressures if any suspicion exists
  • Early angiography and intervention are crucial if perfusion is lost

Clinical features

• External haemorrhage
  • Bleeding is the most commonly found life-threatening finding
  • Haemorrhage is the most common preventable death in penetrating trauma so control any external haemorrhage first
  • Tourniquets if direct pressure inadequate (up to 6 hours safely)
  • Angiographic vascular embolisation is attractive if available
• Ocular injuries
  • Shearing damage to orbit
  • Lid and brow lacerations, open globe injuries, orbital fractures, retinal detachment, retained intraocular foreign body, lens dislocation, vitreous haemorrhage and retinal tears

Investigations

• Need to sparingly use imaging and lab tests in mass casualty situation
• Use FAST liberally
• Plain CXR, USS and single plain radiography are rapidly available to guide therapy in this situation

Treatment

• Mass casualty details
  • Nature and location of blast
  • Size and type of charge
  • Open or closed space
  • Structural collapse
  • Fire/smoke
  • Toxic agent release
• Triage
  • Severely injured – Airway compromise, breathing difficulty, haemodynamic instability, ALOC, vascular trauma, extensive 2^nd/3rd degree burns
  • Lightly injured – Minor wounds, 1^st/2^nd degree burns, isolated trauma to limb, anxiety, most walking patients

Treatment

• Analgesia
  • Mild – Panadol/NSAID
  • Moderate – Ketorolac
  • Severe – Morphine
• Copiously irrigate and disinfect wounds urgently but leave debridement/closure until later
• Temporary splinting, traction and dressings are usually sufficient early on
• Prophylactic antibiotics for soiled wounds/penetrating thoraco-abdominal wounds and open fractures and in patients with diabetes or immunocompromise

Treatment

• Should perform secondary assessments of all patients prior to discharge given propensity to miss injuries in a mass casualty incident
• Return instructions

Pregnancy

• Direct injury to foetus is uncommon thanks to amniotic fluid
• Injuries to the placenta are common
• Admit 2^nd/3rd trimester patients for CTG for at least 4 hours
• Pelvic USS and obstetric consultation is required in all cases
• Consider anti-D

Children

• Sedation for imaging is often necessary
• High risk of tertiary blast trauma due to being thrown

Staff safety

• Possible infiltration of ED by perpetrators
• Unexploded explosives being brought into ED accidentally
• Transmissable disease risk e.g. needle stick
• Victim contamination with chemical/radiation/biologic hazards

Crush injury

• Crush injury that produces ongoing ischaemia of a fascial muscle compartment is termed compartment syndrome
• Crush syndrome is the systemic manifestation of muscle cell damage with or without compartment syndrome
• Normal compartment pressure <10mmHg
  • Crush injury leads to microcirculation trauma, oedema, interstitial bleeding, stasis, venous obstruction and loss of intracellular water
  • Oedema in a closed space leads to increased pressure, which further collapses the microcirculation and venous outflow
  • Pressure >30mmHg produce muscle ischaemia
  • Irreversible nerve and muscle damage occurs after 4-6 hours

Pathophysiology

• Rupture of sarcolemma leads to release of calcium stimulating proteolytic enzymes and oxygen free radicals
• This causes further myocyte destruction and release of potassium, phosphate, myoglobin, CK and uric acid into bloodstream
• Myoglobin then causes direct kidney injury (?)
• Myocyte and capillary endothelium damage leads to vascular leakage and hypovolaemia
• Hyperkalaemia and hypocalcaemia can cause arrhythmias
• Metabolic acidosis caused by hypovolaemia and shock aggravates arrhythmogenesis

Pathophysiology

• Renal failure is the most serious complication
  • Systemic hypoperfusion, renal vasoconstriction, direct myoglobin damage and uric acid/phosphate precipitation in distal tubules
  • Low urine pH and renal vasoconstriction promote precipitation of nephrotoxins
  • Myoglobin forms ferrihemate, which produces free hydroxyl radicals and lipid peroxidation
• Reperfusion syndrome
  • Oxidant release, complement activation and inflammatory response (local and systemic)
  • Can result in hypotension, vasodilation, hypovolaemia, myocardial depression, hyperkalaemia and acidosis

Clinical features

• Compartment syndrome (5P’s)
  • Pain
  • Pulseless
  • Pain with passive stretch
  • Paraesthesias
  • Pressure
• Pain described as diffuse and intense; exacerbated by movement, touch or pressure; and out of proportion to physical signs
• Pulselessness is a late sign
  • Microvasculature pathology so major vessels often NOT affected

Diagnosis

• Compartment pressure >30 = Positive test
• Labs
  • Serum CK may not predict severity but useful initial triage tool
  • Monitor Ca, K, Phos, pH, creatinine, Hb, coags and urine pH and electrolytes
  • Q2-4hourly planned blood and urine tests are best

Management

• 2xlarge-bore IVC
• 1-2L N/Saline bolus
• Avoid Hartmann’s (as contains potassium) as fatal hyperkalaemia may occur (even in absence of renal failure)
• Initial IV fluid rate 1000mL/hr for 2 hours
• Then reduce to 500mL/hr
• Target UO of 200-300mL/hr (5-7 litres every 24 hours) for an adult
• Admit to ICU for monitoring of electrolytes and fluid balance

Management

• Fasciotomy
  • Should not be performed routinely
  • Indications:
    • Absent distal pulses
    • Debridement of necrotic wounds required
    • Compartment pressure >30 within 6 hours of injury and difference between compartmental pressure and diastolic blood pressure >30mmHg
  • If initial compartment pressure is normal and subsequent develops, fasciotomy may be required but has a high infection rate and may result in profuse bleeding

Management

• Hyperbaric O2 therapy
  • 3 benefits
    • Enhanced oxygen at the tissue level
    • Increased oxygen delivery per unit blood flow
    • Oedema reduction
  • At 2atm, blood O2 content increased by 125% and oxygen tension in tissue fluid is increased 10-fold compared to room air
  • Oedema reduction due to oxygen-induced vasoconstriction is also of benefit
    • Reduces blood flow 10-20% with retained oxygen delivery
  • May see improved wound repair after fasciotomy, diminished infection rates and improved outcomes of skin grafts

Last Updated on October 9, 2020 by Andrew Crofton