When smoke is inhaled, toxic products of combustion injure airway tissues and/or cause metabolic effects. Hot smoke usually burns only the pharynx because the incoming gas cools quickly. An exception is steam, which carries much more heat energy than smoke and thus can also burn the lower airways (below the glottis). Many toxic chemicals produced in routine house fires (eg, hydrogen chloride, phosgene, sulfur dioxide, toxic aldehydes, ammonia) cause chemical burns. Some toxic products of combustion, such as carbon monoxide or cyanide, impair cellular respiration systemically.
Burns and smoke inhalation often occur together but may occur separately.
Upper airway injury usually causes symptoms within minutes but occasionally over several hours; upper airway edema may cause stridor. Significant orofacial burns can cause edema that significantly compounds the upper airway problems created by smoke inhalation.
Lower airway injury may also occur with upper airway injury and usually causes delayed symptoms (eg, oxygenation problems highlighted by increasing oxygen requirements or decreases in lung compliance 24 hours or later).
Symptoms of smoke inhalation include
Local irritant phenomena: Cough, wheezing, stridor
Hypoxic manifestations: Confusion, lethargy, coma, tachycardia, tachypnea
Carbon monoxide poisoning: Headache, nausea, weakness, confusion, coma
Diagnosis of Smoke Inhalation
Carboxyhemoglobin (COHb) levels
Bronchoscopy
Chest x-ray
Smoke inhalation is suspected in patients with respiratory symptoms, a history of confinement in a burning environment, or carbonaceous sputum. Perioral burns and singed nasal hair may also be clues. Examination of the oropharynx, focused on the posterior pharynx, can identify edema that would prompt early prophylactic intubation. In the absence of posterior pharyngeal swelling 2 to 6 hours after the injury, significant upper airway injury is unlikely.
Diagnosis of upper airway injury is by endoscopy (laryngoscopy or bronchoscopy) that is adequate to see the upper airways and trachea and shows edema, tissue damage, or soot in the airways; however, injury occasionally develops after an initial normal study. Endoscopy is done as soon as possible, usually with a flexible fiberoptic scope, typically simultaneously with or after endotracheal intubation in patients with significant findings.
Diagnosis of lower airway injury is by chest x-ray and oximetry or arterial blood gases; abnormalities may develop early or only days later. Cyanide and carbon monoxide toxicity should be considered; COHb levels are measured in patients with significant smoke inhalation.
Toxic products of combustion other than carbon monoxide may not initially be suspected, particularly in patients with dramatic burns and obvious airway involvement. Cyanide may be suspected in patients who seem more obtunded than expected for their COHb level or who fail to respond quickly to treatment with oxygen; helpful tests include finding a decreased arteriovenous oxygen difference (due to higher-than-usual venous oxygen content) and high anion gap acidosis with increased lactate.
Treatment of Smoke Inhalation
Oxygen
Sometimes endotracheal intubation
All patients at risk of smoke inhalation injury are given 100% oxygen by face mask initially. Oxygen is a specific remedy for carbon monoxide poisoning; hyperbaric oxygen remains somewhat controversial but may be helpful for serious cardiopulmonary complications, pregnancy, coma/obtundation, and high ( > 25%) COHb levels.
Endotracheal intubation and mechanical ventilation is required for patients with
Impaired consciousness
Direct airway injury
Airway edema caused by fluid resuscitation
Respiratory distress
Patients with edema or significant soot in the upper airways (particularly in the posterior pharynx) require intubation as soon as possible because the airway becomes more difficult to intubate as edema increases. Bronchoscopy is usually done at the same time as intubation.
Patients with lower airway injury may require supplemental oxygen, bronchodilators, and other supportive measures.
Patients suspected of having cyanide poisoning should be given cyanide antidotes, which may be used presumptively in those with cardiovascular complications, coma or significant high anion gap acidosis.
