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Chapter: Clinical Anesthesiology: Perioperative & Critical Care Medicine: Critical Care

Critical Care: Smoke Inhalation

Smoke inhalation is the leading cause of death from fires. Affected persons may or may not have sustained a burn.



Smoke inhalation is the leading cause of death from fires. Affected persons may or may not have sus-tained a burn. Burn victims who suffer from smoke inhalation have a mortality rate significantly greater than other comparably burned patients without smoke inhalation. Any exposure to smoke in a fire requires a presumptive diagnosis of smoke inhala-tion until proved otherwise. A suggestive history might include loss of consciousness or disorienta-tion in a patient exposed to a fire, or a burn acquired in a closed space.



The consequences of smoke inhalation are complex because they can involve three types of injuries: heat injury to the airways, exposure to toxic gases, and a chemical burn with deposition of carbonaceous particulates in the lower airways. The pulmonary response to smoke inhalation is equally complex and depends on the duration of the exposure, com-position of the material that burned, and presence of any underlying lung disease. Combustion of many synthetic materials produces toxic gases such as car-bon monoxide, hydrogen cyanide, hydrogen sulfide, hydrogen chloride, ammonia, chlorine, benzene, and aldehydes. When these gases react with water in the airways, they can produce hydrochloric, acetic, formic, and sulfuric acids. Carbon monoxide and cyanide poisoning are common.

After smoke inhalation direct mucosal injury may result in edema, inflammation, and slough-ing. Loss of ciliary activity impairs the clearance of mucus and bacteria. Manifestations of acute lung injury and ARDS typically appear 2–3 days after the injury and seem related to the delayed develop-ment of SIRS rather than the acute smoke inhala-tion itself.

Clinical Manifestations


Patients may initially have few if any symptoms after smoke inhalation. Suggestive physical find-ings include facial or intraoral burns, singed nasal hairs, cough, carbonaceous sputum, and wheez-ing. The diagnosis usually can be confirmed when flexible bronchoscopy of the upper airway and the tracheobronchial tree reveals erythema, edema, mucosal ulcerations, and carbonaceous depos-its. Arterial blood gases initially may be normal or reveal only mild hypoxemia and metabolic acidosis due to carbon monoxide. The chest radiograph is often normal on presentation.


Heat injury to the airways is usually confined to supraglottic structures in the absence of pro-longed exposure to steam. Progressive hoarseness and stridor are ominous signs of impending air-way obstruction, which may develop over 12–18 h. Fluid resuscitation of any burn injury will frequently aggravate the edema.


Carbon monoxide poisoning is usually defined as greater than 15% carboxyhemoglobin in the blood. The diagnosis is made by cooximetric mea-surements of arterial blood. Carbon monoxide has 200–300 times the affinity of oxygen for hemoglo-bin. When a CO molecule combines with hemo-globin to form carboxyhemoglobin, it decreases the affinity of the other binding sites for oxygen, shift-ing the hemoglobin dissociation curve to the right. The net result is a marked reduction in the oxygen-carrying capacity of blood.


Carbon monoxide dissociates very slowly from hemoglobin with a half-life of approximately 2–4 h. Clinical manifestations result from tissue hypoxia from impaired oxygen delivery. Levels greater than 20–40% carboxyhemoglobin are associated with neurological impairment, nausea, fatigue, disorien-tation, and shock. Lower levels may also produce symptoms because carbon monoxide also binds cytochrome c and myoglobin. Compensatory mech-anisms include increased cardiac output and periph-eral vasodilation.


Cyanide toxicity may occur in patients exposed to fumes from fires that contain synthetic materi-als, particularly those containing polyurethane. The cyanide, which may be inhaled or absorbed through mucosal surfaces and skin, binds the cytochrome system of enzymes and inhibits cellular production of adenosine triphosphate (ATP). Patients present with neurological impairment and lactic acidosis; they typically have arrhythmias, increased cardiac output, and marked vasodilation.


A chemical burn of the respiratory mucosa follows inhalation of large amounts of carbona-ceous material, particularly when combined with toxic fumes. Inflammation of the airways results in bronchorrhea and wheezing. Bronchial edema and sloughing of the mucosa lead to obstruction of the lower airways and atelectasis. Progressive ventilation/perfusion mismatching can lead to marked hypoxemia over the course of 24–48 h. Development of the systemic inflammatory response syndrome can lead to acute lung injury or ARDS.



Fiberoptic bronchoscopy usually establishes the diagnosis of an inhalation injury. Bronchoscopy is usually carried out with a tracheal tube loaded over the bronchoscope so that intubation can quickly be performed if edema threatens the patency of the airway. Early elective tracheal intubation is advis-able when there are obvious signs of heatinjury to the airway. Patients with hoarseness and stridor require immediate intubation; emergency cricothyrotomy or tracheostomy is necessary if oral or nasal intubation is unsuccessful.


The presence of clinically important carbon monoxide or cyanide poisoning, as evidenced by obtundation or coma, also requires prompt tracheal intubation and ventilation with oxygen. The diag-nosis of carbon monoxide poisoning requires coox-imetry: pulse oximeters cannot reliably differentiate between carboxyhemoglobin and oxyhemoglobin. The half-life of carboxyhemoglobin is reduced to 1 h with 100% oxygen; some clinicians advocate hyper-baric oxygen therapy if the patient does not respond to 100% oxygen. The diagnosis of cyanide poison-ing is difficult because reliable measurements of cyanide are not readily available (normal levels are <0.1 mg/L). The enzyme rhodanase normally con-verts cyanide to thiocyanate, which is subsequently eliminated by the kidneys. Treatment for severe cyanide toxicity consists of administering sodium nitrite, 300 mg intravenously as a 3% solution over 3–5 min, followed by sodium thiosulfate, 12.5 g intravenously in the form of a 25% solution over 1–2 min. Sodium nitrite converts hemoglobin to methemoglobin, which has a higher affinity for cya-nide than cytochrome oxidase; the cyanide, which is slowly released from cyanomethemoglobin, is con-verted by rhodanase to the less toxic thiocyanate.


Marked hypoxemia due to intrapulmonary shunting should be managed with tracheal intuba-tion, oxygen therapy, bronchodilators, positive-pressure ventilation, and PEEP. Corticosteroids are ineffective and increase the rate of infections. As with other forms of acute lung injury, nosocomial infectious pneumonias are common.

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