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Smoke inhalation

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Smoke inhalation

Pathophysiology and pathogenesis

  • 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

Management

  • 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%

Further reading

Ramzy PI, Barret JP, HerndonDN. Thermal injury. Crit Care Clinics. 15(2):333-52, 1999


ęCharles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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