Smoke Inhalation

Chapter 28 Smoke Inhalation



Shailen Jasani, MA, VetMB, MRCVS, Dez Hughes, BVSc, MRCVS, DACVECC



KEY POINTS



• The lack of clinical veterinary information on smoke inhalation likely reflects a very high incidence of preadmission mortality. Hypoxia from carbon monoxide poisoning is presumed to be the most common cause of acute death.

• Direct thermal injury to the upper respiratory tract can cause laryngeal obstruction. Lower respiratory tract injury from irritant gases and superheated particulate matter can result in atelectasis, pulmonary edema, decreased lung compliance, and acute respiratory distress syndrome.

• Bacterial bronchopneumonia typically occurs later in the course of the condition and is usually secondary to therapeutic interventions or sepsis.

• Acute neurologic dysfunction may be seen initially or as a delayed syndrome.

• Significant dermal burn injury exacerbates morbidity and mortality.

• Aggressive oxygen supplementation is the immediate priority to hasten carbon monoxide elimination. Supportive measures for respiratory and neurologic complications follow.

• If carbon monoxide poisoning resolves, the prognosis is good in the absence of significant dermal burn injury, bronchopneumonia, or acute neurologic signs.


INTRODUCTION


A significant number of dogs and cats are likely to be involved in residential fires each year, yet there is very little information available regarding clinical cases. Most information is derived from experimental animal studies or extrapolated from the human literature. This dearth of clinical veterinary information is most likely due to a very high incidence of preadmission mortality.



PATHOPHYSIOLOGY



Carbon Monoxide


Carbon monoxide (see Chapter 87, Carbon Monoxide) is a nonirritant gas that competitively and reversibly binds to hemoglobin at the same sites as oxygen, with an affinity that is 230 to 270 times greater and results in marked anemic hypoxia.1,2 It is produced by incomplete combustion of carbon-containing materials and is therefore most significant in enclosed fires as there is increasingly less oxygen available.3 The resultant carboxyhemoglobin (COHb) also shifts the oxygen-hemoglobin dissociation curve to the left, resulting in less offloading at the tissue level.1 There are three possible outcomes in pure, uncomplicated carbon monoxide poisoning: (1) complete recovery with possible transient hearing loss but no permanent effects, (2) recovery with permanent central nervous system abnormalities, and (3) death.1,4-8 Carbon monoxide poisoning is the main cause of acute death from smoke inhalation in humans, and death is due to cerebral and myocardial hypoxia.5,6



Hydrogen Cyanide


Hydrogen cyanide (HCN) (see Chapter 86, Cyanide) is most prevalent in fires involving wools, silks, and synthetic nitrogen–containing polymers (e.g., urethanes, nylon). It is a nonirritant gas that interferes with the utilization of oxygen by cellular cytochrome oxidase, thereby causing histotoxic hypoxia.2,5 The incidence and significance of cyanide toxicity in veterinary smoke inhalation victims remain undefined.3,9



Thermal Injury


Direct thermal injury involving hot, dry air is highly unusual distal to the larynx because heat is dissipated effectively by the thermal regulatory system of the nasal and oropharyngeal areas.10,11 Thermal injury can manifest as mucosal edema, erosions, and ulceration. Of greatest concern is the potential for laryngeal edema that may result in fatal upper respiratory tract obstruction. Although these changes may not be apparent initially, they can be progressive. In one study, a tracheostomy was required for laryngeal obstruction in 2 of 27 dogs and was performed 24 and 72 hours after admission.7 Steam has a much greater heat capacity than dry air and is therefore liable to produce more extensive injury throughout the respiratory tract.10 Inhalation of superheated particulate matter (mainly soot) can result in thermal injury to the trachea and lower respiratory tract.



Irritant Gases and Superheated Particulate Matter


A variety of irritant noxious gases can be inhaled during a fire, depending on the nature of the materials undergoing combustion. These include short-chain aldehydes, gases that are converted into acids in the respiratory tract (e.g., oxides of sulfur and nitrogen), highly water-soluble gases (e.g., ammonia, hydrogen chloride), and benzene (from plastics).5,11 Particulate matter acts as a vehicle by which these gases can be carried deep into the respiratory tract. The pathophysiology that results depends on the types of gases and particulate matter inhaled, the duration of exposure, and underlying host characteristics.10,12



Reduced Lung Compliance


Lung compliance may be markedly reduced as a result of alveolar atelectasis and pulmonary edema. Alveolar atelectasis can occur within seconds of injury due to impaired pulmonary surfactant activity (see Chapter 29, Atelectasis).2,13,14 Pulmonary edema results from increased permeability of the microvasculature, possibly associated with sequestered leukocytes (see Chapter 21, Pulmonary Edema).14,15 Alveolar edema is exacerbated by a concurrent increase in epithelial permeability.15 Pulmonary edema can occur within minutes of smoke inhalation, although it typically develops over a period of up to 24 hours.10 Ventilation-perfusion alterations also occur, and acute lung injury and acute respiratory distress syndrome are potential sequelae (see Chapter 24, Acute Lung Injury and Acute Respiratory Distress Syndrome).



Airway Damage and Obstruction


The mucociliary escalator is significantly impaired following smoke inhalation. Progressive mucosal edema may be accompanied by mucosal sloughing over several hours and the damaged epithelium gives rise to pseudomembranous casts.10,14 Marked tracheobronchitis, necrotizing bronchiolitis, alveolar hyaline membrane formation, and intraalveolar hemorrhage may all follow.10,14 Smoke inhalation induces a reflex bronchoconstriction, and airway obstruction is exacerbated by the copious secretions and edema fluid.10



Bacterial Pneumonia


Smoke inhalation may increase the likelihood of bacterial pneumonia by impairment of alveolar macrophage function. In addition, the stagnant luminal contents create a milieu conducive to bacterial colonization. Nevertheless, bacterial pneumonia is thought to typically occur as a secondary phenomenon following therapeutic interventions such as endotracheal intubation and tracheostomy, or due to sepsis associated with dermal burn injuries.12,16 Infection usually is not seen for at least 12 to 24 hours and is associated with a higher incidence of respiratory failure. 10,12,16Pseudomonas aeruginosa, Staphylococcus spp, and Streptococcus spp are most commonly involved in humans, but it is unknown if the same is true of dogs and cats.



Dermal Burn Injury


The morbidity and mortality associated with smoke inhalation are much greater when significant concurrent dermal burn injury is present.7,9,11 This is due to both the pulmonary pathophysiology (pulmonary edema, bacterial pneumonia, acute lung injury, and acute respiratory distress syndrome) associated with dermal burns and their management requirements, including more aggressive fluid therapy and repeated general anesthesia (see Chapter 158, Thermal Burn Injury).9,11



HISTORY


If owner contact is possible, a full medical history should be obtained at the appropriate time. The history of current illness is usually related to being involved in an enclosed-space fire, and the duration of exposure and types of items involved should be ascertained. The patient’s neurologic status at the scene predominantly reflects the degree of carbon monoxide poisoning. Paroxysmal or intractable coughing may suggest the inhalation of more irritating gases.

Related posts:

  1. Deteriorating Mental Status
  2. Hyperthermia and Fever
  3. Thoracentesis
  4. Pulmonary Contusions and Hemorrhage

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Smoke Inhalation

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