Treatment of smoke inhalation in dogs and cats | VETgirl Veterinary CE Videos
Smoke inhalation can result in pulmonary injury secondary to non-irritant gases [carbon monoxide (CO), cyanide, carbon dioxide] and thermal injury. There are three primary gases in house fires: carbon monoxide (CO), cyanide, and carbon dioxide (CO2). It is the carbon monoxide that this considered the most common cause of death. Carbon monoxide occurs when there is inefficient combustion or burning of carbon-based products like coal, petroleum, wood, natural gas, etc. Unfortunately, this odorless gas is toxic to all species, and can easily accumulate in closed spaces (e.g., trailers, garages, sheds, etc.). CO competitively binds to hemoglobin at a much greater affinity (e.g., 240X) than oxygen, resulting in the production of carboxyhemoglobin (COHb). CO is readily absorbed across the alveolar membrane, and displaces oxygen resulting in cellular hypoxia. COHb also shifts the oxyhemoglobin saturation curve to the left, resulting in impaired oxygen release at the tissue level.
Clinical signs specifically for carbon monoxide toxicosis include lethargy, respiratory depression, hypoxemia, stupor, coma, secondary delayed neurologic sequelae, and death. While carboxyhemoglobin levels can be easily detected in blood, this test is not readily available in veterinary diagnostic laboratories. Treatment includes oxygen therapy or hyperbaric oxygen (to drive CO from Hb binding sites) and supportive care.
While this patient was given 100% oxygen on initial presentation, we don’t know for how long. That said, the use of 100% oxygen (ideally for less than 8 hours to prevent oxygen toxicity) is extremely beneficial, as the half-life of carbon monoxide can be reduced by nearly half (to about 150 minutes). A hyperbaric oxygen chamber, if available, can reduce this even further.
Secondary damage occurs from smoke inhalation due to the inhalation of particulate matter and gases along with secondary thermal injury; these critically ill patients should be evaluated for burns to the fur or skin, corneal ulceration, upper airway inflammation (with secondary edema, laryngospasm, and potential obstruction as a result of heat injury to the air passages), and increased risk for pneumonia (due to reduced mucociliary transport).
Treatment should include oxygen therapy, judicious IV fluids (to maintain hydration), ophthalmic medications (as needed), bronchodilators (such as inhaled albuterol or parenteral terbutaline or aminophylline), nebulization, analgesia (if burns are present), and symptomatic supportive care. Rarely, complete upper airway obstruction can occur and a temporary tracheostomy may be necessary. The use of steroids typically are not recommended unless there is upper airway edema present (if you do use steroids, use an appropriate anti-inflammatory dose of dexamethasone like 0.1-0.15 mg/kg IV).
Diagnotics for smoke inhalation may include radiographs to evaluate the severity of pulmonary parenchymal injury; in this dog, a mild diffuse bronchointerstitial pattern was seen. Other diagnostics may include arterial blood gas (ABG) monitoring to evaluate oxygenation and ventilation. Rarely, positive pressure ventilation (PPV) may be necessary. With smoke inhalation, a pulse oximetry is not very useful, as the SpO2 will be artificially elevated as most pulse oximeters cannot differentiate between carboxyhemoglobin and oxyhemoglobin.
In general, the overall prognosis for smoke inhalation is fair to good, depending on the severity of lung injury; however, in those patients that fail to respond to supportive care and oxygen – or in those who clinically worsen within the first few days – have a much higher morbidity rate. Unfortunately, while we’d love to give you a good outcome with this VETgirl video, this dog deteriorated and continued to have severe hypoxemia and was humanely euthanized.