Smoke inhalation injury is the damage to the body associated with breathing in superheated air or steam, other harmful gases, vapors, and particulate matter resulting from thermal combustion. Smoke inhalation injury can be associated with thermal injury, chemical injury, systemic toxicity, or any combination of these. This chapter does not cover toxicity of theatrical "smoke" machines that do not depend on pyrolysis (ie, that work by nebulization, fogging, or misting).
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.
The key points associated with managing a patient with potential smoke inhalation are:
A high degree of suspicion is required when assessing any patient with a thermal injury, particularly if a naked flame was involved.
The first treatment priority is the maintenance of the airway and administration of 100% oxygen. Early intubation should always be considered if the airway appears to be at risk in any way.
If concurrent cyanide poisoning is suspected, hydroxocobalamin should be administered as early as possible, without waiting for diagnostic confirmation.
Lung-protective ventilation strategies should be used.
Early airway washout using bronchoscopy should be performed.
Fluid resuscitation is important, but should be administered carefully to avoid over- or under-resuscitation.
The possibility of concurrent carbon monoxide poisoning should be considered. The mainstay of treatment is administration of 100% oxygen. The combination of severe burns plus severe carbon monoxide poisoning generally has a poor clinical outcome—consider early euthanasia in these cases.
The cornea and other ocular structures should be checked for the presence of injuries or ulceration, especially if the eyelashes or hair around the eyes have been burned or damaged.
Etiology of Smoke Inhalation Injury in Animals
Important agents involved in smoke inhalation include thermal injury, soot (inhalable and/or respirable carbon-cored particles that contain a variety of other pyrolysis products), carbon monoxide, cyanide gas, nitrogen, methane, oxides of nitrogen (NOx), zinc oxide, phosphorus, sulfur trioxide, titanium tetrachloride, oil fog, polytetrafluoroethylene particles and 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 hours 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 exchange capacity. 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 pyrolysis-derived 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 common with smoke inhalation. Essentially, pyrolysis of most nitrogen-containing materials (eg, nitrocellulose, nylon, wool, silk, asphalt, polyurethane, and many plastics) will produce cyanide. Cyanide is a rapidly acting, systemic, histotoxic agent that inhibits mitochondrial cytochrome c oxidase, resulting in the arrest of aerobic metabolism.
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, resulting in tissue hypoxia. A visible flame is not necessary for carbon monoxide poisoning, and ordinary domestic 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 reaction. Notably, tolerance to zinc oxide fumes develops rapidly but is also quickly lost.
Phosphorous, titanium tetrachloride, and sulfur trioxide fumes are also 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.
Inhalation of polytetrafluoroethylene 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 polytetrafluoroethylene cooking ware, polymer fume fever has been caused by burning of hair spray, dry lubricants, and water-proofing sprays.
Clinical Findings of Smoke Inhalation Injury in Animals
The most important aspects of the history sought for suspected smoke inhalation injury are the duration of exposure, the circumstances of exposure (eg, enclosed versus open spaces, amount of ventilation present), amount of smoke inhaled, severity of injury to other animals, whether loss of consciousness occurred, 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. Pre-existing respiratory diseases (eg, COPD) will likely increase the clinical manifestations of any injury.
Important clinical signs to check for include:
voice changes, hoarseness, and stridor (these are particularly concerning clinical signs because they suggest that edema of the larynx and upper airways may be present)
presence of coughing, because this may indicate damage to the trachea, bronchi, and other large airways
burns to the face, lips, tongue, mouth, pharynx, or nasal mucosa
burns to, or loss of, eye lashes, because this may suggest the presence of eye injuries
soot in the saliva or sputum and/or soot in the nose and mouth
signs of respiratory distress
changes to the level of consciousness
pulse oximeter readings suggestive of SPO2 of less than 94% in room air. However, clinicians should beware of inaccurate pulse oximetry findings if concurrent carbon monoxide poisoning is suspected. If carbon monoxide poisoning is suspected, use of pulse CO-oximetry is advised, if available. Because blood gas machines usually calculate oxygen saturation based on PaO2, this measurement will also be inaccurate if carbon monoxide poisoning is present
presence of cyanosis or muddy mucous membranes or any other evidence of carbon monoxide poisoning
Critical smoke inhalation injury often occurs in the absence of obvious external physical injury. Furthermore, both upper and lower respiratory injury may be relatively slow to develop and may peak 12–24 hours or even later after exposure. Thus, there is always a substantial risk of delayed airway obstruction secondary to upper airway edema for at least 24–48 hours 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, which is 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 when this occurs is generally poor.
The onset of zinc oxide fume fever is typically delayed by 4–8 hours 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 hours later.
Polymer 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.
Diagnosis of Smoke Inhalation Injury in Animals
The primary clinical survey is the key initial diagnostic step in smoke inhalation injury and should be done concurrently with, or as soon as possible after, administering 100% oxygen, assessment of airway patency, collecting the clinical history, and establishing intravenous access.
The primary clinical survey should consist of:
Assessment for the presence of upper airway burns, pending upper airway obstruction and the presence of smoke inhalation injury. Bronchoscopy and laryngoscopy are the gold-standard diagnostic methods. Bronchoscopy is the single most reliable method to establish a diagnosis and to establish the extent of injury. Both bronchoscopy and laryngoscopy are superior to and more reliable than other diagnostic methods (including clinical examination). Classic findings include severe subglottic injury, erythema, charring, deposition of soot, edema, and/or mucosal ulceration.
Bronchoscopic washout and clearance of particulate matter. Early clearance of particulate matter and airway washout are associated with improved outcomes.
Assessment of cardiac function and electrocardiography.
Blood carboxyhemoglobin measurement. 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 concentration and the ultimate neurologic outcome.
Assessment for the presence of metabolic acidosis and/or elevated anion gap acidosis. 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.
Although the initial assessment may be clinically reassuring, upper airway edema can develop fairly quickly and make subsequent intubation difficult. Some patients that require early intubation may not display clinical signs supportive of need for this urgent intervention. In unclear cases, it is useful to perform nasal fiberoptic endoscopy (or examination of the nasal cavity using a speculum) after administration of a nasal decongestant and local anaesthetic spray to check for soot in the nasal cavities. Soot in the oral cavity, intraoral burns and bleeding, facial and body burns, and laryngeal edema identified via laryngoscopy are strongly correlated with the need for early intubation.
Critically, diagnostic imaging changes can be slow to develop in smoke inhalation injury. 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. Pulmonary radiographic changes after smoke inhalation typically develop 24–36 hours after exposure. An initially normal chest radiograph does not exclude significant lung injury after smoke inhalation. Repeat imaging at 24–36 hours 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.
Hematologic changes are also often delayed. Clinically significant smoke inhalation is often associated with declines in hemoglobin concentration and PCV approximately 1 week after exposure.
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. Despite the limitations of PaO2 as a diagnostic indicator for carbon monoxide poisoning, the best predictor of longterm clinical outcome is the PaO2/FiO2 ratio.
Treatment, Control, and Prevention of Smoke Inhalation Injury in Animals
Initial basic treatment priorities for smoke inhalation injury consist of:
administration of 100% oxygen
immediate intubation with a low-pressure or uncuffed tube if there is impending airway obstruction, reduced level of consciousness, cardiac arrest or impending cardiac arrest, and/or hypoventilation; beware of repeated attempts to intubate because this will exacerbate any injury or edema present
a quick body examination for airway patency and the presence of any accompanying injuries (including trauma)
establishing IV access and starting fluid therapy if required but with careful and continued assessment. See table: The Parkland Formula
initial management of clinically significant burns
administration of cyanide antidotes if there is a strong index of suspicion of cyanide poisoning; hydroxocobalamin is regarded as the safest antidote for patients with concomitant smoke inhalation and burns. Human patients receive this routinely before arrival at the hospital.
Key aspects of ongoing treatment for smoke inhalation injury include:
Burn management
Respiratory support
Cardiovascular support
Respiratory support can include escharotomy if severe chest burns that restrict chest movement are present. If ventilation is used, tidal volume should be limited to 6 mL/kg predicted body weight. Positive end-expiratory pressure ventilation and permissive hypercapnia have been recommended. Administration of nebulized heparin and 20% acetylcysteine is recommended. Acetylcysteine is a mucolytic agent and thus should diminish airway cast formation. Heparin is a potent activator of antithrombin III and thus leads to thrombin inactivation and decreases airway casts. Heparin and acetylcysteine should be alternated so that patients receive treatment every 2 hours. Nebulized acetylcysteine can be irritating to the airway and should be discontinued if bronchospasm develops or worsens. Nebulized albuterol (salbutamol) 2–4 times hourly is recommended.
Chest coupage and regular respiratory tract clearing are essential. The use of steroids may have a limited role in reducing upper airway edema. Prophylactic antibiotics should not be used. Although patients with inhalation injury have increased risk for secondary bacterial infection, the use of prophylactic antibiotics promotes the emergence of resistant organisms.
Cardiovascular support should be provided initially in the form of fluid resuscitation and then by pharmacologic means as appropriate; the objective is to minimize tissue hypoxia.
Methemoglobinemia after smoke inhalation is uncommon and can be managed with methylene blue treatment if required.
Key Points
The first treatment priority for smoke inhalation is the maintenance of the airway and administration of 100% oxygen.
If concurrent cyanide poisoning is suspected, hydroxocobalamin should be administered as early as possible, without waiting for diagnostic confirmation.
The combination of severe burns with severe carbon monoxide poisoning generally has a poor clinical outcome—early euthanasia should be considered.
