Smoke inhalation

• often associated with carbon monoxide poisoning
• usually but not invariably associated with airway burn
• inhalation injuries to the respiratory tract depend not only on the dose of the offending agent but also on the particle size and solubility
• particles > 10 m m usually lodge in upper respiratory tract while those < 0.5 m m usually exhaled. Particles between these sizes are inhaled into the bronchi and if 0.5-3 m m into the alveoli
• highly soluble agents (eg hydrochloric acid, sulphur dioxide, ammonia and aldehydes) have an effect within minutes of exposure and cause damage to the conjunctivae, upper respiratory tract and bronchi
• low solubility agents (eg nitrogen dioxide, ozone and phosgene) have effects after hours-days and predominantly affect distal airways
• mechanisms of injury:
  • simple asphyxia
  • tissue asphyxia (eg cyanide, carbon monoxide)
  • direct mucosal injury (eg nitrogen dioxide, sulphur dioxide, ammonia)
  • hyperreactivity (eg sulphur dioxide)
• following injury to the mucosa vasoactive mediators are released which cause a tenfold increase in tracheobronchial blood flow resulting in increased airway oedema.
• necrotic cellular debris collects in airways as damaged respiratory epithelium sloughs causing airway obstruction (compounded by airway oedema). Results in:
  • increased airway resistance
  • post-obstructive atelectasis and emphysema
• 24-48 h after injury microvascular permeability is increased with resultant low pressure pulmonary oedema

Clinical features

Following should raise suspicion of inhalation injury

History

• burn in an enclosed space
• loss of consciousness
• impaired mental status
• associated drug or alcohol use
• concomitant head injury

Examination

Signs suggestive of an airway burn (eg burned nasal hairs, facial burns, soot in sputum) or airway obstruction

Investigations

• initial CXR usually normal
• bronchoscopy:
  • soot deposition in airway
  • airway oedema
  • mucosal erythema, haemorrhage and ulceration
  • may be relatively normal in initial stages before hyperaemia and oedema have developed
  • normal upper airway does not exclude distal injury

• supportive therapy
• intubate if there is any doubt regarding upper airway patency
• minimize ventilator-mediated lung injury
• ventilate all patients with respiratory symptoms on 100% oxygen until carboxyhaemoglobin < 5%