Smoke inhalation (Proceedings)

August 1, 2011

Smoke inhalation injury represents a unique form of lung injury in dogs in cats. Despite the prevalence of house fires in the United States, smoke inhalation is uncommonly encountered in veterinary emergency practice.

Smoke inhalation injury represents a unique form of lung injury in dogs in cats. Despite the prevalence of house fires in the United States, smoke inhalation is uncommonly encountered in veterinary emergency practice. In people a large body of literature exists concerning smoke exposure, however reports of smoke inhalation in dogs and cats are sparse. The composition of items burned is an important consideration when faced with an animal that has been in a house fire. With progression away from wood and natural-based products and increasing predominance of synthetic materials, the speed of ignition, heat generated, and gases emitted also change.

Pathophysiology

Injuries associated with smoke inhalation include physical irritation of mucous membranes, impaired oxygen delivery secondary to toxic gases, neurologic dysfunction, and secondary pneumonia. A variety of toxic inhalants are produced in house fires, with the exact nature of the toxic chemical produced depending on the composition of items that have burned.

Common gases released in house fires include carbon monoxide and hydrogen cyanide. Carbon monoxide (CO) is a colorless, tasteless, odorless gas produced as a result of incomplete combustion of organic matter. Carbon monoxide, like oxygen, binds hemoglobin but with a much greater affinity for hemoglobin (roughly 200 times) than that of oxygen. In addition to displacing oxygen from hemoglobin, a left shift in the oxygen dissociation curve due to carboxyhemoglobinemia results in slower release of oxygen from hemoglobin thus worsening oxygen deprivation of tissues. Resulting tissue hypoxia can be severe and contribute to organ failure.

Hydrogen cyanide (HCN) is the gaseous form of cyanide and is released in many fires involving carbon containing substances such as wool, sick, cotton and paper, as well as nitrogen containing compounds such as nylon and plastics. Hydrogen cyanide, while non-irritating, interferes with oxidative phosphorylation leading to reduced ATP production, depletion of cellular energy stores, and increased lactic acid production. Clinical signs of hydrogen cyanide include weakness, vomiting, tachycardia, cardiac arrhythmias, and neurologic dysfunction ranging from seizures to coma.

In addition to the non-irritating gases described above, smoke inhalation may result in exposure to gases that contribute to physical irritation of mucous membranes. In particular, aldehydes can cause direct irritation of the pulmonary mucosa, and some are converted to acids that cause further erosion of the pulmonary mucosa.

The presence of particulates such as soot may contribute to the irritation in smoke inhalation. More importantly, these particulates can act as carriers to deliver the gases described above deep into the airways. Compounds such as ammonia can also be irritating both to the upper and lower airways, and may negatively impact both mucociliary clearance and macrophage function.

The upper airway is generally most severely affected by direct thermal injury. Laryngeal edema and laryngospasm can contribute to upper airway obstruction and a temporary tracheostomy may be required in severe cases.

Clinical signs

The most common clinical signs of smoke inhalation injury include coughing and respiratory distress. Inspiratory stridor may be noted in animals with severe upper airway swelling. Cherry red mucous membranes may be noted due to CO toxicity. Many animals smell of smoke, and have soot around the nose and mouth. Ocular irritation and mucosal erosions may be present. Neurologic signs may include agitation, ataxia, weakness, loss of consciousness, or in severe cases, seizures. Many of these signs are related to CO toxicity and will improve with oxygen supplementation. Some animals may present with concurrent burns which complicate therapy and lead to a more guarded prognosis.

The presence of carboxhemoglobinemia can complicate diagnostics, since pulse oximetry is unable to differentiate between oxyhemoglobin and carboxyhemoglobin. Carboxyhemoglobin levels can be detected using co-oximetry which may not be widely available at most practices, but can often be run at a human health facility. Thoracic radiographs typically show some abnormalities on admission and can be useful as a baseline.

Treatment

Treatment of animals suffering from smoke inhalation begins with assurance that the animal has a patent airway. Some degree of laryngeal swelling is to be expected, and excessive secretions can obstruct air flow. Suction of the oropharyngeal cavity can be helpful, and in rare cases of upper airway obstruction, intubation followed by a temporary tracheostomy may be required.

All animals suffering from smoke inhalation should receive supplemental oxygen. In addition to reversing hypoxia, an oxygen rich environment will reduce the binding of carbon monoxide to hemoglobin thus reversing carboxyhemoglobinemia. In practices without co-oximetry, oxygen supplementation should be continued despite improvement in respiratory signs for at least 6 hours.

Administration of bronchodilators can be helpful to reduce the brochospasm resulting from airway irritation. Despite the temptation to administer antibiotics to animals suffering from smoke exposure, antibiotics should not be administered prophylactically. Pronounced thermal injury is sure to lead to secondary infection, and prophylactic antibiotic administration will only lead to colonization with more resistant organisms. Instead, owners should be warned that the first phase of treatment consists of support through the irritation and swelling associated with smoke exposure, and that infection is likely 5-7 days post exposure. In general, the use of glucocorticoids is not recommended in animals with smoke inhalation injury.

Intravenous fluids are often warranted to maintain intravascular volume, despite concerns related to potential pulmonary parenchymal damage and potential for edema formation. In general, large volumes of rapidly administered fluids should be avoided. Instead, isotonic crystalloids can be administered at moderate rates to ensure proper organ perfusion.

Other injuries commonly associated with smoke exposure include corneal ulceration. A thorough ocular examination along with fluorescein staining should be performed, and prompt treatment of any erosion should be initiated to minimize the long term consequences severe ulceration.

Prognosis

Most animals presenting to the emergency room with smoke inhalation injury will recover with supportive care and time. Unfortunately losses sustained in house fires are often significant and the financial implications of emergent pet care can be difficult to assume. Studies show that animals with smoke inhalation injury were either discharged within 48 hours or were hospitalized for a week or more. Delayed neurological complications have been described, requiring additional supportive care.

References

Kent M, Creevy KE, deLahunta A. Clinical and neuropathological findings of acute carbon monoxide toxicity in Chihuahuas following smoke inhalation. J Am Anim Hosp Assoc 2010;46:259-264.

Fitzgerald KT and Flood AA. Smoke inhalation. Clin Tech Sm An Pract 2006;21:205-214.

Mariani CL. Full recovery following delayed neurologic signs after smoke inhalation in a dog. J Vet Emerg Crit Care 2003;13(4):235-239.

Drobatz KJ, Walker LM, Hendricks JC. Smoke exposure in dogs: 27 cases (1988-1997). J Am Vet Med Assoc 1999;215(9):1306-11.

Drobatz KJ, Walker LM, Hendricks JC. Smoke exposure in cats: 22 cases (1986-1997). J Am Vet Med Assoc 1999;215(9):1312-6.