After major burns, about one-third of patients have pulmonary complications; these complications account for the majority of burn-related deaths. Smoke inhalation sufficient to cause respiratory injury may also occur without external burns.
Thermal injury to the lung is associated with four groups of complications:
- Immediate reaction-direct thermal injury to upper airways leading to upper airway obstruction
- Carbon monoxide and cyanide poisoning
- Acute respiratory distress syndrome (ARDS) developing 24 to 48 hours after the thermal injury
- Late-onset pulmonary complications, which include pneumonia, atelectasis, thromboembolism, and, in case of thoracic burns, chest wall restriction.
The constituents of smoke are by-products of pyrolysis and incomplete combustion. Many of these products are potent mucosal irritants and bronchoconstrictors and contribute to both upper and lower lung injury. Certain constituents of smoke have been identified consistently as contributors to respiratory injury. Smoke inhalation rarely causes thermal injury to the lung parenchyma; the large capacity of the upper airways to humidify and modify the temperatures of inhaled air protects the alveolar tissue from heat. Exceptions are steam burns and explosions in an enclosed space.
Symptoms of Smoke Inhalation
The initial signs and symptoms of smoke inhalation are tachypnea, cough, dyspnea, wheezing, cyanosis, hoarseness, and stridor (an ominous sign). Facial burns may ￼provide a clue to smoke inhalation and thermal injury to the upper airway. During the 12 to 48 hours after the injury, the patient can manifest increasing hypoxemia, and lung compliance may decrease owing to noncardiogenic pulmonary edema.
Roentgenograms of the chest may reveal a pattern of diffuse, patchy infiltrates. A major complication is infection, often caused by Pseudomonas aeruginosa or Staphylococcus aureus. The lung defenses against infection are compromised by thermal and chemical injury to the airway epithelium as well as by the presence of an endotracheal or tracheostomy tube. The pathway for infection is either by inhaling airborne organisms or by hematogenous spread from cutaneous burns.
ARDS may develop 24 to 48 hours after the initial injury. The causes of ARDS are controversial in burn patients, but possibilities include chemical pneumonitis from constituents in smoke, a circulating burn toxin, disseminated intravascular coagulation, microembolism, and neurogenic pulmonary edema. The extent of surface thermal injury does not correlate with the degree of respiratory distress that occurs subsequently.
Treatment of Smoke Inhalation
The most immediate life-threatening complications in the patient presenting with major burns or with a history of smoke inhalation are upper airway obstruction and carbon monoxide (CO) poisoning. The patient should be closely observed for evidence of these complications. Laryngeal and tracheobronchial inflammation may be detected by fiberoptic bronchoscopy. Arterial blood gases should be measured; prompt intubation or tracheostomy should be performed if there is evidence of significant airway obstruction. Corticosteroids may help treat edema of the upper airways, but they must be used with caution, because infection is a major concern for managing both skin and pulmonary injury. Prophylactic antibiotics are of no value in preventing pneumonia and may predispose to infection with resistant organisms. Careful pulmonary toilet, humidification, and sterile suctioning should be used to reduce the risk of pneumonia. Serial bronchoscopy may be necessary to remove mucus plugs and thereby prevent segmental atelectasis and postobstructive infection. Late-onset pulmonary burn complications include atelectasis, thromboembolism , and pneumonia.