Etiology

• Smoke inhalation and thermal exposure from a fire event; commonly from a bush or grass fire or a barn fire.

Pathophysiology

• Smoke inhalation injury is a result of a combination of thermal injury to airways, carbon monoxide poisoning, and chemical injury to the airways.

Thermal injury to the airways

• The heat from the fire event causes direct injury to the upper airways which results in edema and obstruction.

Carbon monoxide poisoning

• Carbon monoxide poisoning affects oxygen exchange at the level of the hemoglobin (Hb) molecule. Carbon monoxide (CO) has a far greater affinity for hemoglobin than does oxygen. Therefore, it effectively out-competes the oxygen molecules for the hemoglobin binding sites, resulting in the formation of carboxyhemoglobin and reduced oxygen carrying capacity of the hemoglobin molecules.
• CO binding to Hb also changes the stability of the hemoglobin molecule (known as the R-state). This change increases the affinity for oxygen of other sites within the Hb tetramer, which further reduces the ability of the hemoglobin molecule to release and deliver oxygen to tissues.
• In human and canine studies, neither the clinical severity nor the clinical improvement of CO-poisoned patients directly correlates with the blood COHb level or COHb clearance.
• In addition to Hb, CO binds to other heme-containing proteins, including myoglobin in heart and skeletal muscle.
• CO also affects mitochondria and results in decreased ATP production in tissues such as the brain and heart.
• Neurological signs, such as ataxia can develop secondary to hypoxia Hypoxia.

Chemical injury to the airways

• Inhalation of chemicals, especially combustion products (such as hydrochloric acid, hydrogen cyanide, aldehydes, and sulfuric acid) can cause a pulmonary ventilation/perfusion mismatch. This occurs through the direct chemical injury to the airways causing severe tracheobronchitis, edema of the epithelial mucosa, mucosal sloughing, bronchoconstriction, decreased mucociliary transport, and altered surfactant action.
• Particulate matter (such as soot) that is inhaled can line the upper and lower respiratory tract.

Time course

• The time course can be influenced by the duration of exposure and chemicals within the smoke inhaled:
  • Initially upper airways damage and bronchoconstriction occurs within 6 h of exposure.
  • Development of pulmonary edema in 12-72 h post-exposure.
  • Development of bronchopneumonia in 24 h to 3 weeks post-exposure.

Epidemiology

• Large numbers of animals can be affected during a fire event, particularly bush fire, grass fire and farm building fires.