Smoke inhalation caused by fires is a major cause of fatalities in animals. It usually involves inhalation of a complex mixture of toxicologic agents and pyrolysis products. Injury typically results from a combination of thermal injury to the upper airways, oxygen deprivation, and toxicity from inhaled materials. Smaller animals and in particular birds are usually more susceptible to inhaled toxicants because of their greater respiratory minute volume per unit mass and relatively larger respiratory surface area per unit mass.
Important agents involved in smoke inhalation include thermal injury, soot, carbon monoxide, cyanide gas, nitrogen, methane, oxides of nitrogen (NOx), zinc oxide, phosphorus, sulfur trioxide, titanium tetrachloride, oil fog, Teflon® particles, and Teflon® pyrolysis products (polymer fume fever). Nitrogen and methane are not especially toxic; however, they are important in fires because they dilute oxygen in the breathable atmosphere.
Inhalation thermal injury can occur without obvious external injuries and be relatively slow to manifest, so it is often clinically underestimated. Airway compromise generally peaks 12–24 hr after initial injury. Except for steam inhalation and possibly inhalation of particles with continuing pyrolysis, inhalation thermal injuries are usually confined to the upper airways because of their large heat capacitance. Burns of the upper airway typically induce upper airway edema. Loss of oncotic pressure and fluid resuscitation can exacerbate these effects. Inhalation of steam typically produces severe lung injuries.
Carbonaceous soot particles are not especially toxic in themselves. However, they act as carriers of other toxicants adsorbed onto the surfaces of soot particles. This results in increased toxicant exposure and, depending on particle size, deeper penetration of toxicants into the respiratory system. The degree and site of damage depends on particle size, particle surface area, solubility, concentration, duration of exposure, and rate of particle clearance. Large, chemically reactive and irritating particles tend to affect the upper airways and are cleared quickly, whereas smaller, low-solubility particles tend to affect the deeper respiratory structures and are cleared more slowly.
Important inhaled blood agents/asphyxiants that disrupt tissue oxygen delivery or utilization include cyanide, carbon monoxide, nitrogen, and methane. Cyanide inhalation is extremely common with smoke inhalation. Essentially, pyrolysis of most nitrogen-containing materials (eg, nitrocellulose, nylon, wool, silk, asphalt, polyurethane, and many plastics) will liberate cyanide. Cyanide is a rapidly acting histotoxic agent that inhibits mitochondrial cytochrome c oxidase, resulting in the arrest of aerobic metabolism. (Also see Cyanide Poisoning Cyanide Poisoning read more .)
Carbon monoxide poisoning is ubiquitous after smoke inhalation. Carbon monoxide is produced by the incomplete combustion of any organic material. Carbon monoxide binds to hemoglobin to form carboxyhemoglobin, which cannot carry oxygen and, therefore, results in tissue hypoxia. A visible flame is not necessary for carbon monoxide poisoning, and gas appliances can liberate large amounts of it. Epizootics of fatal carbon monoxide poisoning classically occur during periods of cold weather, particularly after an electrical outage.
NOX have low water solubility, and low concentrations generally cause delayed pulmonary irritation. Also, compared with other agents, the NO2 present in NOX reacts relatively slowly with respiratory secretions, forming nitrous (HNO2) and nitric (HNO3) acid. The end result is delayed chemical pneumonitis and pulmonary edema. These features often result in delayed clinical recognition of NOX injuries.
Zinc oxide fumes are a classical cause of metal fume fever and are formed when zinc or zinc alloys (eg, galvanized metals, brass) are heated. Metal fume fever is a classical cytokine cascade acute phase–like response. Notably, tolerance to zinc oxide fumes develops rapidly but is also quickly lost.
Phosphorous, titanium tetrachloride, and sulfur trioxide fumes are notoriously irritating. Titanium tetrachloride releases hydrochloric acid in contact with water in respiratory secretions. Inhaled sulfur trioxide forms sulfuric acid when it contacts respiratory secretions. Smoke machines that atomize mineral oils can produce an oil mist that is mildly irritating to the respiratory system and may trigger underlying respiratory conditions.
Inhalation of PTFE (Teflon®) fumes triggers acute malaise, fever, and respiratory irritation (polymer fume fever). It can result in severe chemical pneumonitis and is notoriously lethal for caged birds. In addition to overheated cooking ware, Teflon® fume fever has been caused by burning of hair spray, dry lubricants, and water-proofing sprays.
The most important aspects of the history are duration of exposure, the circumstances of exposure (eg, enclosed versus open spaces), amount of smoke inhaled, severity of injury to other animals, and the sources of the smoke (ie, what toxicants are likely to have been present in the smoke). Unfortunately, this type of information is rarely available. Exposure to smoke in an enclosed space, prolonged entrapment, carbonaceous oculonasal discharges, a history of resuscitation, evidence of respiratory distress, and altered consciousness all indicate a higher risk of serious lung damage. Preexisting respiratory diseases (eg, COPD) will likely increase the severity of injury.
Clinically serious smoke inhalation often occurs in the absence of obvious external physical injury. However, facial burns, oropharyngeal blistering and/or edema, changed voice, stridor, coughing, upper airway mucosal lesions, and carbonaceous discharges may be present. Evidence of lower respiratory tract injury such as tachypnea, dyspnea, cough, decreased breath sounds, wheezing, rales, rhonchi, and retractions may be present. Both upper and lower respiratory injury may be relatively slow to develop and may peak 12–24 hr or even later after exposure. There is always a substantial risk of delayed airway obstruction secondary to upper airway edema for at least 24–48 hr after initial injury. Lack of apparent injury immediately after smoke inhalation should not reduce the level of clinical suspicion.
In general, evidence of asphyxiant exposure commonly includes CNS depression, changes in affect, lethargy, generalized muscle weakness, and obtundation. Neurologic injury secondary to hypoxia, often permanent, is common under these circumstances. Coma after smoke inhalation is most commonly caused by severe carbon monoxide poisoning and the ensuing hypoxia. The prognosis is poor.
The onset of zinc oxide fume fever is typically delayed by 4–8 hr after exposure. Common clinical signs include general malaise, cough, sternal pain, voice changes, and fever. Typically, these signs are self-limiting, and recovery is rapid unless high levels of exposure have occurred. In these cases, there is often an apparent period of recovery followed by onset of dyspnea and respiratory distress 24–36 hr later.
Polymer (Teflon®) fume fever typically presents as general malaise, cough, sternal pain, voice changes, and fever. Severe lung injuries are common in birds, and sudden death is a common outcome.
Important diagnostic techniques include laryngoscopy/bronchoscopy, pulse oximetry/co-oximetry, arterial blood gases, carboxyhemoglobin level determination, lactate level determination, CBCs, chest imaging, electrocardiography, and pulmonary function testing.
Bronchoscopy and laryngoscopy are the gold standard methods to diagnose and assess smoke inhalation. Bronchoscopy is the single most reliable method to establish the diagnosis and extent/severity of injury. It is generally superior to and more accurate than other diagnostic methods (including clinical examination). Classic findings include severe subglottic injury, erythema, charring, deposition of soot, edema, and/or mucosal ulceration.
Ordinary pulse oximetry (two wavelengths) is inaccurate when carboxyhemoglobin and/or methemoglobin are present. Both situations will generate falsely high pulse oximetry readings that are not reflective of the degree of underlying disease. Pulse co-oximetry (four or five wavelengths) is more reliable in these situations.
PaO2 is a poor indicator of carbon monoxide poisoning and/or cellular hypoxia, because it reflects the amount of oxygen dissolved in blood. This is not altered in carbon monoxide poisoning, because the dissolved oxygen is a small fraction of total arterial blood oxygen content. Because blood gas machines usually calculate oxygen saturation based on PaO2, this measurement will also be inaccurate.
Blood carboxyhemoglobin measurements may underestimate the actual level of exposure if oxygen has been administered before sample collection. Additionally, there is a poor correlation between carboxyhemoglobin level and the ultimate neurologic outcome in cases of significant poisoning.
Metabolic acidosis and increased lactate is common when hypoxia, carboxyhemoglobin, cyanide poisoning, methemoglobinemia, and trauma are present. Very high blood lactate levels are typical in acute cyanide poisoning. Given the usually slow turnaround time associated with cyanide measurements, high levels of blood lactate combined with a history of smoke inhalation provide a strong index of suspicion of cyanide poisoning. Cyanide measurements are strongly correlated with exposure and toxicity levels.
Clinically significant smoke inhalation is often associated with declines in hemoglobin and PCV approximately 1 wk after exposure.
Pulmonary radiographic changes after smoke inhalation typically develop 24–36 hr after exposure. An initially clear chest radiograph does not exclude significant lung injury after smoke inhalation. Repeat imaging at 24–36 hr after exposure typically demonstrates radiographic signs consistent with atelectasis, pulmonary edema, and hyperinflation. Depending on the agents involved, late radiographic changes may reflect fibrosis and bronchiolitis obliterans.
CT changes typically develop earlier than chest radiographic changes and classically consist of peribronchial ground-glass opacities and peribronchial consolidations. Brain CT findings may demonstrate cerebral hypoxia–associated ischemia and injuries to the globus pallidus, which are nearly pathognomonic for carbon monoxide poisoning.
Treatment involves maintenance of the airway, aggressive management of acute respiratory distress, antidote treatment if warranted, suppression of inflammation, and prevention of secondary infections with broad spectrum antibiotics. Severe carbon monoxide poisoning combined with significant smoke inhalation is almost uniformly fatal in people; thus, euthanasia should be considered early in the treatment and assessment processes.
Maintenance of the airway either by endotracheal intubation or tracheostomy is often critical given that severe upper airway edema may occur. It is often better to intubate earlier in the disease progression, because delayed airway edema may subsequently make intubation difficult or impossible.
Carbon monoxide poisoning should always be assumed to have occurred in all individuals with smoke inhalation. The mainstay of treatment is oxygen supplementation.
Some degree of cyanide poisoning should also be assumed in almost all cases of smoke inhalation. Induction of methemoglobinemia is not recommended in cases of smoke inhalation because of the risk of further reducing oxygen-carrying capacity of the blood in the presence of carboxyhemoglobinemia. Because of its efficacy, ease of administration, and low toxicity, hydroxocobalamin administration is currently recommended in cases of smoke inhalation. Hydroxocobalamin can be combined with thiosulfate administration. Data are limited on the effectiveness of thiosulfate alone; however, it is useful in cyanide poisoning and will not compromise oxygen-carrying capacity of the blood (ie, unlikely to cause harm and may be beneficial).
Methemoglobinemia after smoke inhalation is uncommon and can be managed with methylene blue treatment if required.
Notably, N-acetylcysteine has been effective for the treatment of polymer fume fever. Chest physiotherapy is regarded as being beneficial. Low tidal volume positive-pressure ventilation (PEEP) and high-frequency percussive ventilation (HFPV) have been demonstrated to increase short-term survival in people but are rarely available in veterinary practice.
Bronchodilation with a β2-agonist (eg, albuterol, terbutaline, epinephrine) is an important aspect of treatment, because smoke induces bronchospasm and bronchoconstriction. When combined with airway edema, these effects contribute to airway obstruction.
The effectiveness of corticosteroids after smoke inhalation is contentious. Corticosteroids are notably beneficial in cases of metal fume fever.
Control and prevention of smoke inhalation involves avoidance of exposure, adequate ventilation if smoke is likely to be present, and use of smoke detection systems.