A 27-year-old woman is brought to the emergency department by local paramedics. The patient was found unconscious at the scene of a house fire. On examination, she does not appear to have any burns. Black soot is present near the patient's nares and mouth. Her capillary refill time is 4 seconds. Blood pressure is 132/90 mm Hg, heart rate is 122/min and regular, and respirations are 24/min. Supplemental oxygen by a non-rebreather mask is administered. Laboratory results are as follows:
Which of the following should be empirically treated in this patient?

Question

A 27-year-old woman is brought to the emergency department by local paramedics.  The patient was found unconscious at the scene of a house fire.  On examination, she does not appear to have any burns.  Black soot is present near the patient's nares and mouth.  Her capillary refill time is 4 seconds.  Blood pressure is 132/90 mm Hg, heart rate is 122/min and regular, and respirations are 24/min.  Supplemental oxygen by a non-rebreather mask is administered.  Laboratory results are as follows:  
Which of the following should be empirically treated in this patient?

Quizplus · Accepted Answer

11ec25c8_d1d1_b147_bc81_d726bfa832da_MD0003_00 This patient is the victim of a house fire and most likely has a smoke inhalation injury; such injuries are estimated to cause 60%-80% of deaths during fire incidents. Smoke injury results in glottic edema from heat and airway irritation due to particulate matter found in smoke. Smoke also contains multiple toxins that are absorbed systemically. Hydrogen cyanide (HCN) and carbon monoxide (CO) are the 2 major products of combustion in closed spaces. HCN is produced from the combustion of nitrogen-containing synthetic polymers (eg, foam, cotton, paint, silk). HCN is a potent and fast-acting poison, and blood levels cannot be measured rapidly to confirm diagnosis prior to treatment. Toxic exposure can be inhalational, dermal, or intestinal. Exposure to moderate to high concentrations causes symptoms to develop within seconds to minutes. Early acute toxicity causes neurologic and cardiorespiratory stimulation, and patients develop headache, vertigo, dizziness, hyperventilation, tachycardia, nausea, and vomiting. Neurologic, respiratory, and cardiovascular depression eventually occurs and manifests as coma, seizures, bradycardia, hypotension, and cardiorespiratory arrest. HCN can also cause anoxic brain injury leading to permanent neurologic deficits. Cyanide toxicity can be treated with an antidote such as hydroxocobalamin or sodium thiosulfate, which directly binds cyanide molecules. An alternate treatment is induction of methemoglobinemia with nitrites to increase ferric iron (Fe3+) in circulating hemoglobin. Cyanide binds avidly to Fe3+, and so methemoglobinemia provides an alternate binding site. (Choice B) Methanol is found in antifreeze solutions (eg, windshield wiper fluid, fuels, solvents). Poisoning occurs after ingestion of such compounds. (Choice C) Methemoglobin is formed by the oxidation of ferrous (Fe2+) to ferric (Fe3+) iron in hemoglobin. Fe3+ is unable to bind oxygen, and it also increases the affinity of Fe2+ to oxygen, causing a left shift in the oxygen dissociation curve. The result is functional anemia due to reduced oxygen delivery to tissues. Methemoglobinemia occurs after exposure to oxidizing agents (eg, dapsone, nitrates, topical/local anesthetics). left shift (Choice D) Salicylate toxicity usually results from intentional or accidental ingestion of 10-30 g of salicylic acid in adults (3 g in children). Because levels can be readily measured, there is no need to treat salicylate toxicity empirically in this patient, who is more likely to have suffered HCN and CO poisoning. (Choice E) Antiepileptics may be needed if seizures or status epilepticus develops as a complication of cyanide toxicity. This patient has no symptoms of ongoing seizure activity. Early decontamination with an antidote is crucial in the prevention and treatment of this complication. Educational objective: To prevent cardiorespiratory arrest and permanent neurologic disability, victims of smoke inhalation injury should be treated empirically for cyanide toxicity with an antidote, such as hydroxocobalamin or sodium thiosulfate, or with nitrites to induce methemoglobinemia. References: Cyanide poisoning by fire smoke inhalation: a European expert consensus. (http://www.ncbi.nlm.nih.gov/pubmed/22828651)

A 27-Year-Old Woman Is Brought to the Emergency Department by Local