The emergency clinician is occasionally called upon to treat smoke and burn injuries resulting from house fires or other sources
of thermal, chemical, or electrical injury. Most burn wounds seen in veterinary medicine are relatively minor, possibly because
animals with severe burns and smoke inhalation are less likely to be rescued from the scene of a house fire. However, life
threatening burns and inhalation injury are being seen with increasing frequency and the emergency clinician should therefore
be familiar with their pathophysiology and management.
Smoke Inhalation
Smoke inhalation can be associated with a variety of problems, including respiratory irritation or distress, neurologic effects,
and complicating factors such as the development of bacterial pneumonia.1 Additionally, the presence of toxic gases such as carbon monoxide, hydrogen cyanide, hydrogen sulfide and others may further
contribute to respiratory irritation and impaired oxygen delivery. The majority of fire-related deaths in animals result from
carbon monoxide poisoning rather than the fire itself.
Inhalation of superheated smoke particles has numerous adverse effects. Smoke is a potent respiratory irritant, resulting
in bronchoconstriction. The larynx and glottis can become edematous as a result of thermal burns, leading to upper airway
obstruction. Chemical and thermal damage to the cells lining the airways leads to sloughing of the tracheobronchial mucosa,
impairment of the mucociliary escalator, and formation of cellular casts that may obstruct the lower airways and promote bacterial
growth. Disruption of respiratory epithelium and vascular endothelium leads to exudation of proteinaceous fluid into the terminal
airways and further contributes to respiratory compromise, impaired surfactant production, and bacterial growth. Carbon monoxide poisoning frequently occurs in conjunction with inhalation injury. Carbon monoxide has approximately 200 times
the affinity for hemoglobin that oxygen does, allowing it to displace oxygen from the hemoglobin and form carboxyhemoglobin
instead. Oxygen delivery to the tissues is therefore decreased, and tissue hypoxia may occur, particularly to organs with
high oxygen demand, such as the brain and heart. Clinical findings include cherry-red mucous membranes, dyspnea, vomiting,
dizziness, headache, altered mentation, and loss of consciousness. Serious intoxications may lead to pulmonary edema, seizures,
coma, and death. Delayed neurologic sequellae have also been reported in dogs.
Burn Injury
Skin burns significantly affect patient outcome and increase morbidity and mortality. Animals that have been close enough
to the fire to sustain skin burns usually have the most severe pulmonary complications associated with smoke inhalation. Burns
are commonly classified according to the extent of body surface involved and the depth of injury to the skin. Extent of injury
is initially estimated in human burn patients using "the rule of nines". This rule divides the adult human body into areas
corresponding to 9% of the total body surface area, or multiples of 9%. For example, each forelimb comprises approximately
9% of total body surface area; each hind limb, 18%; head and neck, 9%; chest and abdomen, 18%; back, 18%; and perineum, 1%.
Body surface area percentages vary in children, and as such, the rule of nines is not typically used in children less than
10 years of age. Although the rule of nines has been cited in veterinary texts, it seems similarly unlikely that these percentages
accurately describe the majority of veterinary patients. Other methods of estimating extent of injury include serial halving
(Do burns cover more than half the patient's surface area? If not, do burns cover ¼- ½ the surface area? and so forth), or
measuring the burn area in centimeters and using a chart to calculate meters2 from the patient's body weight in kilograms.
