A 27-year-old woman was found alone and unconscious at the scene of a house fire. The patient was placed on oxygen and transported to the emergency department. Medical history is unknown. On arrival, she is unresponsive. Black soot is present near the patient's nares and mouth. The lungs are clear to auscultation bilaterally. Her skin is reddish in color and capillary refill time is 4 seconds. There is no evidence of cutaneous burns. Temperature is 37.2 C (98.9 F), blood pressure is 98/60 mm Hg, heart rate is 140/min and regular, and respirations are 28/min. Pulse oximetry is 100% on a nonrebreather mask. Laboratory results are as follows:
| Arterial blood gases | |
| pH | 7.15 |
| PaO2 | 114 mm Hg |
| PaCO2 | 33 mm Hg |
| Carboxyhemoglobin level | 10% |
| Blood, plasma, and serum | |
| Bicarbonate | 12 mEq/L |
| Lactic acid, venous | 25 mg/dL |
Which of the following should be empirically treated in this patient?
Cyanide poisoning | |
Common etiologies |
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Pathophysiology |
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Clinical features |
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Management |
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*Sodium nitrite + sodium thiosulfate is an alternate treatment but is contraindicated in carbon monoxide poisoning. | |
This patient with prolonged house fire exposure likely has cyanide poisoning. Cyanide is a toxin released during the combustion of common household items (eg, plastics, polyurethane mattresses) that contain both carbon and nitrogen. Cyanide inhibits oxidative phosphorylation, halting aerobic metabolism and forcing a switch to anaerobic metabolism that results in lactic acidosis (eg, pH 7.15, lactic acid 25). Because tissues cannot effectively use oxygen, venous blood remains saturated with oxygen and appears bright red (causing reddish-colored skin). Early acute toxicity causes cardiorespiratory stimulation (eg, tachypnea, tachycardia), but cardiovascular collapse rapidly occurs unless treatment is administered.
Cyanide poisoning must be empirically treated because serum cyanide levels cannot be measured quickly. Hydroxocobalamin, the preferred treatment, binds to intracellular cyanide and forms cyanocobalamin, which can be renally excreted. Sodium thiosulfate, which acts as a sulfur donor that detoxifies cyanide to thiocyanate, is sometimes administered with hydroxocobalamin. In addition, treatment with 100% oxygen is continued to maximize oxygen delivery to tissues and to treat concomitant carbon monoxide poisoning, a common result of house fire exposure (typically associated with elevated carboxyhemoglobin levels).
(Choice B) Methamphetamine, which acts as an indirect neurotransmitter to produce an adrenergic surge, can cause tachycardia and tachypnea. However, hyperthermia, hypertension, and agitation or excited delirium (vs depressed consciousness) are also usually present.
(Choice C) Methemoglobinemia, which alters hemoglobin and decreases its capacity to deliver oxygen to peripheral tissues, can present with coma and metabolic acidosis. However, cyanosis (vs reddish skin) and decreased pulse oximetry reading that does not resolve with supplemental oxygen (due to methemoglobin light absorption) are also typically present. In addition, methemoglobinemia is usually associated with exposure to oxidizing agents (eg, dapsone, nitrates, topical/local anesthetics).
(Choice D) Opioid stimulation of central receptors (eg, mu receptors) in the brain can cause depressed mental status but would also be expected to cause bradypnea (vs tachypnea) and bradycardia (vs tachycardia).
(Choice E) Salicylate toxicity commonly causes tachypnea (due to activation of the medullary respiratory center) and altered mental status, but not reddish skin. In addition, empiric treatment of salicylate toxicity is typically not performed because salicylate levels can be readily measured and the condition is rarely rapidly fatal.
Educational objective:
Cyanide is a rapidly lethal toxin that may be produced in house fires. Patients with clinical features concerning for cyanide poisoning (eg, reddish skin, lactic acidosis) should be treated empirically with hydroxocobalamin.