Smoke inhalation (Proceedings) - Veterinary Healthcare
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Smoke inhalation (Proceedings)


CVC IN KANSAS CITY PROCEEDINGS


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.


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