Smoke Inhalation

Components of Smoke

(smoke has variable components -> these are dependent on oxygen availability and temperature of the smoke)

  • Acid Vapors and Aerosols
  • Aldehydes
    • Acetaldehyde
    • Formaldehyde (see Formaldehyde, [[Formaldehyde]])
      • Typical workplace exposure limit 1.0 ppm
    • Acrolein
      • The most severe aldehyde respiratory irritant found in smoke
      • Highly reactive chemical formed from pyrolysis of synthetic polymers (acrylic, etc) and natural polymers
      • Typical worplace exposure limit is 0.1 ppm
  • Ammonia (see Ammonia, [[Ammonia]])
  • Hydrogen Chloride Gas: results from pyrolysis of polyvinyl chloride (PVC, found in plastics)
  • Hydrogen Cyanide Gas (see Hydrogen Cyanide, [[Hydrogen Cyanide]])
  • Nitrogen Oxides (see Nitrogen Dioxide, [[Nitrogen Dioxide]])
  • Phosgene Gas (see Phosgene Gas, [[Phosgene Gas]])

Physiology

  • Products of Pyrolysis: smoke inhalation involves inhaled exposure to multiple products of pyrolysis
    • Generally, the chemical monomer is not major pyrolysis breakdown product of polymers (ex: in fire, polyvinyl chloride usually forms hydrogen chloride gas rather than vinyl chloride)
  • Determinants of Potential for Lung Damage: the potential for lung damage is related to size of particle, pH, chemical reactivity, and water solubility
    • Particles >10 µm will impact in upper airway
    • Particles <5 µm will impact in the lower airways and alveoli)
  • Mechanisms of Injury in Smoke Inhalation:
    • Thermal Injury to Airway: usually manifested in supraglottic airways within 24 hrs after exposure
      • Airway edema, mucosal injury, and sloughing with airway obstruction
    • Hypoxia: dependent on the fuel source for the fire
      • Potentiates toxicities of CO and cyanide
    • Systemic Toxicity
      • Hydrogen Cyanide Inhalation: hydrogen cynaide binds to iron-containing enzymes such as the cytochrome a-a3 complex, interfering with electron transport chain -> inducing anaerobic metabolism
      • Carboxyhemoglobinemia: causes 80% of smoke-inahlation-related deaths
    • Direct Bronchial Mucosal Toxicity
      • Formaldehyde/Chlorine/Phosgene Gas/Nitrogen Dioxide: produce cough/bronchorrhea/wheezing/dyspnea within 12-36 hrs after exposure
      • Acids: coagulate underlying tissue
      • Alkali (ammonia, etc): liquefact and penetrate mucosa
      • Soot: may serve as an absorbent career, allowing deeper penetration of toxic substances

Diagnosis

  • FOB: may be necessary to rule out upper airway thermal injury or chemical injury to airway
  • CXR/Chest CT: ranges from normal to acute lung injury pattern
  • Cyanide Level: while necessary to obtain, not rapid enough to be useful to guide therapy

Clinical Presentations

Upper Airway Manifestations

  • Thermal Injury to Upper Airway: typically laryngeal edema

Pulmonary Manifestations

  • Non-Specific Symptoms
    • Headache
    • Nausea
    • Malaise
    • Decreased Cognition
    • Seizures (see Seizures, [[Seizures]])
    • Chest Pain (see Chest Pain, [[Chest Pain]])
  • Carboxyhemoglobinemia (see Carboxyhemoglobinemia, [[Carboxyhemoglobinemia]])
    • Physiology: related to exposure levels of CO
    • Diagnosis
      • ABG Co-Oximetry: carboxyhemoglobinemia
    • Prognosis: there is no linear relationship between COHb level and the long-term neurologic outcome
  • Methemoglobinemia (see Methemoglobinemia, [[Methemoglobinemia]])
    • Physiology: related to exposure to oxidants
  • Acute Bronchospasm (see Obstructive Lung Disease, [[Obstructive Lung Disease]])
    • Epidemiology: may occur
  • Acute Lung Injury-ARDS (see Acute Lung Injury-ARDS, [[Acute Lung Injury-ARDS]])
    • Diagnosis
      • Pathology: diffuse alveolar damage
  • Reactive Airway Dysfunction Syndrome (see Reactive Airway Dysfunction Syndrome, [[Reactive Airway Dysfunction Syndrome]])
    • Clinical: increased non-specific airway responsiveness may occur after smoke exposure
  • Bronchiolitis Obliterans (see Bronchiolitis Obliterans, [[Bronchiolitis Obliterans]])
  • Bronchiectasis (see Bronchiectasis, [[Bronchiectasis]])

Treatment

  • Supportive Care
    • Mechanical Ventilation: if necessary
  • Treatment of Both Cyanide Toxicity and Carboxyhemoglobinemia
    • Administer 100% FiO2
      • The half-life of COHb: reduced from 240 min on RA -> 75-80 min on 100% FiO2
    • Hyperbaric Oxygen: hyperbaric oxygen at 2.0 atm decreases COHb half-life to approximately 20 min
      • However, the use of hyperbaric oxygen is controversial and is not recommended for COHb <25, nor for unstable patients who require continuous monitoring and therapy
    • Treatment of Cyanide Toxicity (if suspected)
      • Treatment utilizies induction of methemoglobinemia -> use of sulfur donors -> binding of cyanide
      • Cyanide antidote package
        • Amyl nitrite (twelve 0.3 mL ampules) for inhalation until IV access is established
        • Sodium nitrite (300 mg/10 mL) IV to induce methemoglobinemia
        • Sodium thiosulfate (12.5 g/50 mL) IV to act as a sulfur donor
      • Because hydrogen cyanide and CO are frequently encountered together in smoke inhalation, treatment with amyl nitrate or sodium nitrite is contraindicated with COHb >20
  • Steroids: not usually indicated

References

  • Smoke Inhalation Injury. New Horiz. 1993;1:422-434
  • Ellenhorn’s Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MA: Lippincott Williams & Wilkins; 1997
  • Clinical toxicology of cyanide. Ann Emerg Med. 1986;15:1067-1074
  • Principles of Critical Care. New York, NY: /McGraw-Hill; 1992
  • Inhalation injuries. Ann Emerg Med. 1988;17:1316-1320
  • Carbon monoxide poisoning–a public health perspective. Toxicology. 2000;145:1-14
  • Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest. 2000;117:801-808