Inhalation of the thermal, gaseous, or particulate products of combustion
Pulmonary injury due to inhalation of the thermal, gaseous, or particulate products of combustion is the most common cause of death in fire injury victims. Two major types of lung injury are observed: thermal injury of the airways and inhalation of gaseous or particulate matter.
Thermal injury is usually limited to structures above the vocal cords because the airways possess a very efficient cooling system. Combustion (flame) and pyrolysis (smolder) of materials release a complex array of organic acids, aldehydes, and gases that may induce a chemical injury of the airway mucosa with resultant peribronchial edema and bronchoconstriction. Asphyxia may also occur, since the ambient Flo2 in the area of a ﬁre usually falls to about 0.10 because combustion uses O2. Impairment of mucociliary and phagocytic function predisposes to subsequent lung infection, and alveolar damage may result in ARDS. The presence of a body burn markedly aggravates the lung injury. ARDS is uncommon, possibly because the degree of exposure required for its development is likely to result in fatal carbon monoxide poisoning. Carbon monoxide is an odorless, tasteless, and colorless gas; that does not produce lung injury but has a dual effect l on tissue oxygenation. Its marked affinity for hemoglobin (Hb) (210 times that of O2) limits the O2 carrying capacity of blood. In addition, it shifts the O2 dissociation curve to the left, which impairs O2 release to the tissues.
The clinical presentation depends on the predominant form of injury. Facial burns and singed nasal hairs should arouse suspicion of lung injury, although pulmonary involvement occurs in only a small proportion of such patients. Thermal injury may produce upper airway obstruction with stridor, hoarseness, and phonation difficulties, necessitating further evaluation (with possible bronchoscopy) and intubation to maintain a patent airway. Lower airway involvement may be associated with the production of carbonaceous sputum, wheezes, and crackles. The chest x-ray is insensitive in the early stages, although pulmonary infiltrates or edema may subsequently develop. Features associated with carbon monoxide intoxication include; headache, nausea, fatigue, behavioral change, ataxia, and hypoxic damage of the heart or brain. Cherry-red coloration of the lips is usually absent unless the carboxyhemoglobin (COHb) concentration is above 40 per cent. An intoxicated patient displays a normal Pao2 and calculated O2 saturation, but there is a severe reduction in measured O2 saturation. Despite the severe O2 desaturation, minute ventilation is not increased in carbon monoxide intoxication, since the carotid body responds to Pam. Conﬁrmation is made by measurement of blood COHb: less than 2% in healthy subjects, 5 to 10% in cigarette smokers, and 30 to 50% in ﬁre injury victims.
Management includes removing the victim from exposure, checking vital signs, and establishing a patent airway. Administration of supplemental O2 relieves hypoxemia and enhances the dissociation of carbon monoxide from Hb, decreasing the half-time for elimination from 300 min on room air, to 60 min, with an FIO2 of 1.0. In order to achieve an adequate FIO2, intubation and mechanical ventilation may be required. The use of hyperbaric O; has been suggested for patients with severe CO intoxication, although its advantage over breathing 100 per cent O2 is unproven. Bronchospasm usually responds to bronchodilators. Corticosteroids are no longer recommended in the management of smoke-inhalation injury. Antibiotics should be prescribed only if there is evidence of infection. Patients surviving the acute clinical course usually recover completely. Long-term complications of tracheal stenosis, bronchiolitis obliterans, or bronchiectasis are rare.
Exposure to toxic gases and fumes is an increasing problem in modern industrial society and may cause harm by four basic mechanisms (Table 1). Asphyxia occurs when the O2 in inspired air is displaced by another gas. The most common mechanism of injury is local irritation, the form and extent of which depend on the concentration, solubility, and duration of exposure to the toxic gas. Highly soluble gases, such as ammonia, rapidly injure the mucous membranes of the eye and upper airway, causing an intense burning pain in the eyes, nose, and throat with lacrimation, rhinorrhoea, and a sense of suffocation.
Table 1. Toxic gases and fumes
Dr. Afsaneh Jeddi