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
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
