Pediatric Terrorism and Disaster Preparedness: A ... - PHE Home

Clinical findings and diagnosis. Clinically, blast lung injury is evidenced by various
degrees of the following:
• Hemoptysis.
• Hypoxia.
• Hemothorax.
• Dyspnea.
• Tachypnea.
• Chest pain.
• Cough.
• Wheezing.
• Rales/crackles.
• Decreased breath sounds.
• Pneumothorax.
• Hypopharyngeal hemorrhage.
• Subcutaneous crepitus.
• Tracheal deviation.
Clinical findings range from contusion and ecchymosis to massive hemoptysis, severe
ventilation/perfusion mismatch, and air leak, leading rapidly to death. Most blast lung
injury develops early in the course of treatment, within 1–2 hours. Signs and symptoms
may progress within 24–48 hours to respiratory failure or acute respiratory distress
syndrome (ARDS), or both. Respiratory failure is often due to secondary additive effects
such as shock, organ failure, or inhalation of smoke and toxic substances.
The most important diagnostic test for blast lung injury is a chest radiograph. However,
in stable patients, CT scans provide important additional information. Pulmonary
hemorrhage is the most consistent microscopic finding in blast lung injury, and most
survivors of a blast will have infiltrates on a chest radiograph.
Treatment and complications. Blast lung injury is not universally fatal, given aggressive
and timely management. Initial management involves maximizing oxygenation and
minimizing additional barotrauma. Most important is maintaining a patent airway, free of
blood and secretions. Victims should be placed on oxygen to prevent hypoxia. Control of
massive hemoptysis involves tracheal intubation and, whenever possible, selective
ventilation of the contralateral lung. The source of bleeding in massive hemoptysis may
be from one or both lungs and is often difficult to determine. Having a high index of
suspicion for pneumothorax or tension pneumothorax cannot be overstated. The risk is so
great that prophylactic tube thoracostomy has been suggested.
The development of systemic air embolization from injured lung tissue is a grave
complication. The greater the degree of lung injury, the higher the risk of emboli
formation. Although the actual incidence is unknown and is probably underrecognized,
air embolization in blast injury is speculated to be the main cause of death within the first
hour after a blast. Air emboli in the vascular system carry a high mortality rate because
the air bubbles can potentially cause occlusion of the coronary arteries (myocardial
ischemia), cerebral vessels (stroke), or cardiac outflow tracts (shock). They cause
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