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Management of airway complications of burns in children
Insights
Children with smoke exposure or facial burns require immediate hospitalization. Prompt mechanical ventilation and supportive care are crucial to prevent delayed respiratory distress and complications like pulmonary edema.
Area of Science:
- Pediatric Critical Care
- Emergency Medicine
- Toxicology
Background:
- Smoke inhalation in children can lead to delayed respiratory distress.
- Facial burns or soot exposure indicate potential airway injury.
- Prompt medical intervention is critical for managing smoke inhalation injuries.
Observation:
- Children exposed to smoke in confined spaces or with facial soot/burns need hospital admission.
- Respiratory distress may manifest late but can progress rapidly.
- Progressive respiratory distress necessitates curarization, intubation, and mechanical ventilation.
Findings:
- Mechanical ventilation for at least 48 hours, followed by 24 hours of spontaneous breathing with positive airway pressure, is essential to prevent recurrence of stridor and pulmonary edema.
- Using an appropriately sized endotracheal tube prevents laryngeal damage and subglottic stenosis.
- High-humidity inspired gases maintain airway patency, while high oxygen concentrations support oxygenation.
Implications:
- Early and aggressive management of smoke inhalation in children can significantly improve outcomes.
- Careful airway management is vital to prevent long-term respiratory complications.
- Pharmacological interventions like dexamethasone and antibiotics play a role in managing associated cerebral edema and preventing infections.
Abstract:
Children who have been exposed to smoke in a confined space or who have soot or burns, however minimal, on the face should be admitted to hospital. Respiratory distress may be delayed, but if it is progressive the patient should be curarised, intubated, and mechanically ventilated. Unless ventilation continues for 48 hours, followed by 24 hours' spontaneous respiration against a positive airway pressure, stridor and pulmonary oedema may recur. An endotracheal tube small enough to allow a leak between it and the oedematous mucosa must be passed to prevent laryngeal damage and subsequent subglottic stenosis. High humidity of inspired gases keeps secretions fluid and the endotracheal tube patent. A high oxygen concentration compensates for deficient oxygen uptake and transport caused by pulmonary lesions and the presence of poisonous compounds interfering with oxygen transport. Dexamethasone to minimise cerebral oedema and antibiotics to reduce the incidence of chest infections should be given.