Smoke Inhalation Burns and smoke inhalation often occur together but may occur separately.

When smoke is inhaled, toxic products of combustion injure airway tissues. Hot smoke usually burns only the pharynx because the incoming gas cools quickly. A common 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) injure lower airways chemically. Some toxic products of combustion, such as carbon monoxide (see Poisoning: Carbon Monoxide Poisoning) or cyanide, impair cellular respiration systemically. Upper airway injury usually causes symptoms within minutes but occasionally over several hours; upper airway edema may cause stridor. Lower airway injury may also occur with upper airway injury and usually causes symptoms (eg, oxygenation problems highlighted by increasing O2 requirements or decreases in lung compliance) 24 h or later. 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. Diagnosis of upper airway injury is by endoscopy (laryngoscopy or bronchoscopy) that is adequate to see the upper airways and trachea fully and that shows edema or soot in the airways; however, injury occasionally develops after an early normal study. Endoscopy is done as soon as possible, usually with a flexible fiberoptic scope typically followed by endotracheal intubation in patients with significant findings. Diagnosis of lower airway injury is by chest xray and oximetry or ABGs, but abnormalities may develop only days later. Cyanide and carbon monoxide toxicity should be considered; carboxyhemoglobin levels are measured in patients with significant smoke inhalation. All patients at risk of smoke inhalation injury are given 100% O2 by face mask initially. Patients with airway obstruction or respiratory distress require endotracheal intubation or another artificial airway and mechanical ventilation (see Respiratory Failure and Mechanical Ventilation: Means and Modes of Mechanical Ventilation). Patients with edema or significant soot in the upper airways require intubation as soon as possible because intubation becomes more difficult as edema increases. Bronchoscopy is usually done at the same time as intubation. Patients with lower airway injury may require supplemental O2, bronchodilators, and other supportive measures. Radiation burns most commonly result from prolonged exposure to solar ultraviolet radiation (sunburnsee Reactions to Sunlight: Sunburn) but may result from prolonged or intense

exposure to other sources of ultraviolet radiation (eg, tanning beds) or from exposure to sources of x-ray or other nonsolar radiation (see Poisoning: Caustic Ingestion). Chemical burns may result from strong acids, strong alkalis (eg, lye, cement), phenols, cresols, mustard gas, phosphorus, and certain petroleum products (eg, gasoline, paint thinner). Skin and deeper tissue necrosis caused by these agents may progress over several hours. Electrical burns (see also Electrical and Lightning Injuries: Electrical Injuries) result from heat generation and electroporation of cell membranes associated with massive current of electrons. Electrical burns may cause extensive deep tissue damage to electrically conductive tissues, such as muscles and nerves, despite minimal apparent cutaneous injury. Events associated with a burn (eg, jumping from a burning building, being struck by debris, motor vehicle crash) may cause other injuries. Abuse should be considered in young children and elderly patients with burns. Pathophysiology Burns cause protein denaturation and thus coagulative necrosis. Around the coagulated tissue, platelets aggregate, vessels constrict, and marginally perfused tissue (known as the zone of stasis) can extend the injury. Around the zone of stasis, tissue is hyperemic and inflamed. Damage to the normal epidermal barrier allows bacterial invasion and external fluid loss; damaged tissues often become edematous, further enhancing volume loss. Heat loss can be significant because thermoregulation of the damaged dermis is absent, particularly in wounds that are exposed. Burn depth: First-degree burns are limited to the epidermis. Partial-thickness (also called 2nd-degree) burns involve part of the dermis and can be superficial or deep. Superficial partial-thickness burns involve the papillary (more superficial) dermis. These burns heal within 1 to 2 wk and rarely scar. Healing occurs from epidermal cells lining sweat gland ducts and hair follicles; these cells grow to the surface, then migrate across the surface to meet cells from neighboring glands and follicles. Deep partial-thickness burns involve the deeper dermis and take 2 wk to heal. Healing occurs only from hair follicles, and scarring is common and may be severe. Full-thickness (3rd-degree) burns extend through the entire dermis and into the underlying fat. Healing occurs only from the periphery; these burns, unless small, require excision and skin grafting. Complications

Burns cause both systemic and local complications. The major factors contributing to systemic complications are breakdown of skin integrity and fluid loss. Local complications include eschars and contractures and scarring.