SMOKE INHALATION



Pulmonary injury due to inhalation of the ther­mal, gaseous, or particulate products of combustion is the commonest 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, as the ambient Fto2 in the area of a fire usually falls to about 0.10 because combustion uses 02. Impairment of mucociliary and phago­cytic function predisposes to subsequent lung in­fection. Alveolar damage may result in ARDS but this is uncommon, possibly because the degree of exposure required for ARDS 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 on tissue oxygenation. Its marked affinity for hemoglobin (210 times that of 02) limits the 02-carrying capacity of blood. In addition, it shifts the 02 dissociation curve to the left, which im­pairs 02 release to the tissues.

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 to 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 02 saturation, but there is a severe re­duction in 02 saturation when it is measured. De­spite the severe 02 desaturation, minute ventila­tion is not increased in carbon monoxide intoxication, as the cartoid body responds to Pao2. Confirmation is made by measurement of blood COHb: below 2 per cent in healthy subjects, 5 to 10 per cent in cigarette smokers, and 30 to 50 per cent in fire injury victims.

Management includes removing the victim from exposure,’checking vital signs, and estab­lishing a patent airway. Administration of sup­plemental 02 relieves hypoxemia and enhances the dissociation of carbon monoxide from he­moglobin, decreasing the half-time for elimina­tion from 300 minutes on room air to 60 minutes with an Fi02 of 1.0. In order to achieve an adequate FrO;,, intubation and mechanical ventilation may be required. The use of hyperbaric 02 has been suggested for patients with severe CO intoxica­tion, although its advantage over breathing 100 per cent 02 is unproven. Bronchospasm usually responds to bronchodilators, but corticosteroids may be required if it is severe and unresponsive or severe upper airway obstruction is present. An­tibiotics should be prescribed only if there is ev­idence of infection. In the rare cases in which ARDS supervenes, the management is identical to that described in Chapter 22. Patients surviving the acute clinical course usually recover com­pletely. Long-term complications of tracheal sten­osis, bronchiolitis obliterans, or bronchiectasis