ISSN 2398-2969      

Smoke inhalation

icanis
Contributor(s):

Penny Watson


Introduction

  • Combination of injuries to upper and lower airways produced by inhalation of smoke with consequent hypoxic, thermal and toxic damage.
  • Cause: inhalation of smoke usually in burning building.
  • Signs: cough, gagging, wheezing, changes in membrane color, external burns, CNS signs.
  • Diagnosis: history, clinical signs, blood gases, radiography.
  • Treatment: oxygen administration, maintenance of airways, fluids, bronchodilators, antibiotics.
  • Prognosis: depends on severity of damage: good to very guarded.

Pathogenesis

Etiology

  • Inhalation of smoke, usually in burning building.
  • Neurological effects of hypoxia reduce the will to escape so increasing smoke exposure.

Pathophysiology

  • Inhalation of smoke → combination of thermal injury to upper respiratory tract and toxic injury to lower respiratory tract.
  • Systemic effects of hypoxia and inhaled toxins contribute to syndrome.
  • Response to injury may be immediate or delayed from 6 hours to 2 days.
  • Exaggerated response if concurrent burns are present.
  • Inhalation of hot smoke→ immediate thermal injury to upper airways → laryngeal damage and spasm and inflammation and sloughing of upper tracheal mucosa → upper airway obstruction, dyspnea and cyanosis.
  • Inhalation of steam, but not dry smoke, will also → thermal injury to lower airways and lungs: steam has 4000 times the heat carrying capacity of dry air.
  • Reduction of available oxygen in the air (result of consumption in fire) combined with increased carbon monoxide → asphyxia and tissue hypoxia.
  • Inhalation of particulate matter→ damage to alveoli and poisoning of soot-laden pulmonary macrophages → predisposes to the late development of pneumonia.
  • Partial combustion of carbon-containing compounds → production of carbon monoxide which is inhaled → preferentially binds to hemoglobin rather than oxygen and shifts the oxyhemoglobin curve to the left and inhibits oxidative phosphorylation at the cellular level and is a direct myocardial depressant → profound hypoxemia and tissue hypoxia.
  • Hydrogen cyanide inhalation as a result of partial combustion of plastics → prevents oxygen use by mitochondria → tissue hypoxia and increased lactate production causing metabolic acidosis.
  • Acrolein inhalation as a result of combustion of wood and polypropylene → impaired ciliary and macrophage function and pulmonary edema → increased risk of pneumonia.
  • Injury to pulmonary tissue by inhaled chemicals and released oxygen free radicals → pulmonary edema which may → adult respiratory distress syndrome.
  • Concurrent external burns → hypermetabolism and skin damage → increased susceptibility to sepsis and development of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS).
  • Tissue hypoxia due to combined effects describes → cerebral hypoxia and myocardial hypoxia → behavioral changes, inco-ordination, collapse, convulsions and cerebral edema → respiratory and cardiac arrest and death.

Timecourse

  • Three distinct phases to smoke inhalation injury:
    • Early injury (1-12 hours): thermal injury to upper airway, chemical injury to lower airways with bronchospasm and early pulmonary edema, tissue hypoxia and impaired ciliary function.
    • Later injury (6-72 hours): pulmonary edema develops which may → ARDS → . Cerebral edema may develop as a result of hypoxic brain damage.
    • Delayed injury: development of secondary pneumonia, reduced lung compliance, atelectasis +/- systemic sepsis.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

Other sources of information

  • Faggella (1997) Electric cord and smoke inhalation injuries. Chapter 132 In: Handbook of Small Animal Practice. 3rd edn. Morgan (ed). W B Saunders.

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