Which clinical history findings are characteristic of patients affected by smoke inhalation?

Updated: Oct 15, 2021
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
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Answer

In patients exposed to smoke, details of the exposure—the duration, the amount of smoke inhaled, and the toxins contained in the smoke--can help determine the risk for inhalation injury. Unfortunately, these details are often not known, although some information can often be garnered from rescuers and other observers present at the scene.

Critical information regarding the scene includes the severity of injury to other victims, especially loss of consciousness or death. In addition, exposure to fire in a closed space, prolonged duration of entrapment, evidence of carbonaceous sputum, the requirement for cardiopulmonary resuscitation (CPR) at the scene, the presence of respiratory distress, and obtundation all increase the risk for significant pulmonary disease and hypoxic injury.

Simple carbon soot is not particularly toxic, although it may carry and deposit other toxins directly onto the airway surfaces, thereby increasing exposure. Significant toxicity occurs with the inhalation of asphyxiants, including carbon monoxide (CO), nitrogen, and methane. These asphyxiants cause injury by interrupting the delivery of oxygen to the tissues. Asphyxiants either displace oxygen from the air or interfere with tissue oxygen delivery by blocking the action of hemoglobin or cytochrome oxidase (eg, CO, cyanide [CN]).

CO poisoning must be considered in any person injured in a fire. CO is a major component of smoke produced in most open fires, particularly those involving wood, coal, gasoline, and other organic substances. In addition, significant CO exposure can occur in the absence of open flames, as a result of malfunctioning domestic equipment (eg, poorly ventilated space heaters, cooking gas) or exposure to automobile exhaust fumes either from a suicide attempt or accidentally from poor ventilation.

Hydrogen CN is an asphyxiant that is released during the incomplete combustion of products such as cellulose, nylon, wool, silk, asphalt, polyurethane, and plastics. CN has a characteristic almondlike odor. Hydrogen CN is absorbed rapidly, producing an almost immediate effect if exposure is by inhalation. In contrast, CN salts (eg, potassium, sodium CN, and, particularly, silver and copper CN), which are typically ingested, must be converted to hydrogen CN and are absorbed more slowly.

Damage varies with the chemical activity of the particular inhalants, their size, solubility, and the duration and concentration of exposure. Upper airway injuries tend to be caused by the more irritating, water-soluble, larger particles. Substances of smaller size and lower water solubility cause alveolar and parenchymal injury.

A history of respiratory illnesses, such as asthma or chronic obstructive pulmonary disease (COPD), predisposes patients to respiratory insufficiency.

The extent of illness from smoke inhalation can be notably different between children and adults, despite similar exposures. Children frequently become disoriented at fire scenes and may attempt to hide from flames and smoke, thereby prolonging their exposure to toxic inhalants. In addition, children have greater minute ventilation relative to body size than do adults, further increasing their exposure to toxic inhalants.

Inhalation injuries occur without skin burns or other obvious external injury; hence, a high degree of suspicion must be maintained. A retrospective review of 4,451 children with thermal injuries over 10 years demonstrated that inhalation injury was often not recognized, manifested late, and usually had significant consequences, including parenchymal injury and secondary pneumonia. [38]

Thermal injury is generally confined to the upper airway, because of its vast heat capacitance. Inhalation of steam is a notable exception, in which lower airway and pulmonary parenchymal thermal injury are common. Theoretically, continued combustion of inhaled particulate matter could possibly produce more distal airway injury.

Thermal injury to the mucosa produces burns and edema of the nose, mouth, pharynx, and larynx. The loose tissues of the upper airway swell readily in response to injury. Loss of colloid oncotic pressure can result in obstruction of the airway, particularly in patients receiving fluid resuscitation.

The full extent of airway compromise may not be evident until 12-24 hours after the initial injury. For patients with extensive surface burns, chest wall restriction may occur because of eschar formation, necessitating emergent escharotomy.


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