Respiratory Complications of Burns and Smoke Inhalation (Respiratory Burns)
Marianna M. Sockrider
Respiratory complications are a major source of morbidity and mortality from fires. Overall, nearly one-third of all victims of major burns suffer from various degrees of smoke inhalation injury. Smoke inhalation is responsible for approximately 75% of deaths from structural fires in the United States. The mortality rate is greater among patients who have both cutaneous burns and inhalation injury. Severe injury to the respiratory tract can occur in the absence of surface burns. Several factors are associated with greater risk of incurring respiratory injury: trapping of victims in confined spaces, unconsciousness of victims, fires involving plastics or steam, and victims who are small children or elderly individuals. The likelihood of suffering asphyxia or respiratory inhalation injury is increased in the presence of cutaneous burns. Unconscious victims are at higher risk of incurring injury caused by loss of the protective mechanisms of holding one’s breath and laryngospasm. Injuries of the respiratory tract are distributed as follows: 60% upper airway, 30% major lower airway, and 10% parenchymal. Injuries may occur at several levels simultaneously.
The time course of clinical symptoms depends on the type and severity of injury. Carbon monoxide (CO) intoxication, upper airway tract injury, and tracheobronchial obstruction develop in the first 24 hours. Late pulmonary injury likely is attributable to metabolic, infectious, or circulatory derangements complicating the surface burns. During the next 2 to 5 days, noncardiogenic pulmonary edema may develop, particularly in the presence of superimposed sepsis. Nosocomial pneumonia and pulmonary embolism usually occur late, more than 5 days after the event.
TYPES OF DIRECT RESPIRATORY INJURIES
Direct respiratory injuries are classified as asphyxial, thermal, and chemical or toxic (Table 125.1).
Asphyxial Injuries
Hypoxemia may occur as a consequence of CO intoxication, low inspired oxygen tension at the fire site, or ventilation-perfusion mismatch as a result of airway obstruction, atelectasis, and/or fluid overload.
Thermal Injuries
Thermal injury may result from exposure to direct flames, inhalation of hot gases, or inhalation of steam. The normal function of the upper airway as a heat exchanger limits the exposure of the lower airway to thermal injury. Direct thermal damage, then, affects primarily the supraglottic airways. Immediate injury to the oropharyngeal area with edema, erythema, and ulceration may lead to life-threatening upper airway obstruction. Steam produces the most serious burns because of its higher heat-carrying capacity. Only with steam, which is a very unusual occurrence in most fires, or with prolonged exposure to high ambient temperatures does thermal injury occur to the intrathoracic airways.
Chemical/Toxic Injuries
Chemical or toxic injury occurs from exposure to a variety of noxious gases. Chemical injury occurs more frequently than does heat injury. The site of injury depends on the duration of exposure, the size of soot particles, and the solubility of the gases. Damage to the airways results mainly from chemicals that are present in smoke. Particulate matter carried in the smoke (soot) probably does not itself produce injury; toxic gases may be absorbed on the surface of the particles and
carried into the lungs. The soot particles may be responsible for inducing reflex bronchoconstriction. The inhaled gases may act as airway irritants, or they may be absorbed and become systemic toxins. Irritant gases, such as hydrogen chloride and oxides of nitrogen and sulfur, combine with water in the lung to form corrosive acids or alkalis. Aldehyde gases lead to the denaturation of surface proteins, resulting in pulmonary edema. The two principal systemic toxins are hydrogen cyanide and CO.
carried into the lungs. The soot particles may be responsible for inducing reflex bronchoconstriction. The inhaled gases may act as airway irritants, or they may be absorbed and become systemic toxins. Irritant gases, such as hydrogen chloride and oxides of nitrogen and sulfur, combine with water in the lung to form corrosive acids or alkalis. Aldehyde gases lead to the denaturation of surface proteins, resulting in pulmonary edema. The two principal systemic toxins are hydrogen cyanide and CO.
TABLE 125.1. TYPES OF RESPIRATORY INJURIES SEEN WITH FIRE OR SMOKE EXPOSURE (MAY BE CONCURRENT) | |||||||||||||||||||||||||||||||||
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Hydrogen Cyanide
Cyanide exposure resulting from the incomplete combustion of products such as plastics and acrylics may be a significant, often hidden, cause of comorbidity in smoke inhalation. Hydrogen cyanide gas causes systemic cyanide poisoning by inhibiting cellular oxidation. Studies of fire victims have revealed concentrations of toxic cyanide, with significantly higher levels found in those who die than in those who survive. Blood cyanide levels correlate with levels of CO. Plasma lactate levels are better correlated with cyanide levels, and a plasma lactate concentration greater than 10 mmol/L is a sensitive indicator of cyanide poisoning. All patients who are obtunded and have significant acidosis should have their levels of plasma lactate and cyanide measured.
Carbon Monoxide
CO is the gas most commonly produced in fire. CO intoxication and hypoxia may account for as many as 80% of smoke inhalation fatalities, particularly deaths that occur at the scene of the fire. CO produces its toxic effects by three mechanisms: