Snapshot A 45-year-old woman presents to the emergency room after ingesting an unknown substance in a suicide attempt. She is confused and reports having a headache, nausea, and vomiting. Beside her was a bottle of powder labeled “potassium sodium cyanide.” On physical exam, she is hypoxic and tachycardic. She has a unique almond-odor and her cheeks are flushed. She is given activated charcoal and a toxicology panel is sent to the laboratory. Oxygen supplementation does not improve her hypoxia and she is started empirically on nitrate and thiosulfate for cyanide poisoning, as this hospital does not carry hydroxocobalamin. Introduction Clinical definition cyanide is a lethal poison that can act rapidly and fatally Etiology cyanide poisoning can occur from many exposures, including inhalation, ingestion, or direct contact fires especially with burning carpets and textiles occupational plastic and rubber industry, rodent pesticides, etc. medical sodium nitroprusside, which contains 5 cyanide groups per molecule add sodium thiosulfate to nitroprusside solution to prevent cyanide poisoning diet stone fruits (apricots, plums, peaches, etc.) and apples contain cyanide compounds in their stones/seeds ingestion of cyanide salts suicidal or homicidal acts Pathogenesis mechanism of cyanide poisoning cyanide binds ferric ion (Fe3+) in the mitochondrial cytochrome complex IV, which inhibits oxidative phosphorylation this causes the cell to convert to anaerobic metabolism, causing accumulation of lactic acid and a metabolic acidosis results in functional hypoxia, as cells, cannot use oxygen Prognosis can be rapidly fatal if untreated Presentation Symptoms hypoxia not responsive to supplemental O2 central nervous system headaches confusion vertigo Physical exam cardiovascular initially tachycardic and hypertensive then bradycardic and hypotensive almond breath odor pulmonary edema flushing “cherry-red” skin due to high venous oxyhemoglobin concentration cyanosis irritant dermatitis if skin is exposed to cyanide nausea and vomiting if cyanide is ingested Studies Labs ↑ lactic acid arterial blood gas metabolic acidosis with anion gap carboxyhemoglobin and methemoglobin if concern for concomitant carbon monoxide poisoning cyanide concentration results are typically not available in time Making the diagnosis most cases are clinically diagnosed Differential Carbon monoxide poisoning distinguishing factor often presents with cyanide poisoning improvement with 100% oxygen Treatment Management approach supplemental oxygen is not useful in this case all contaminated clothes should be removed all wounds from cyanide exposure should be cleaned Medical hydroxocobalamin first-line mechanism hydroxocobalamin combines with cyanide to form cyanocobalamin, which is renally excreted sodium thiosulfate first-line mechanism thiosulfates convert cyanide to thiocyanide, which can be renally excreted nitrates second-line mechanism nitrates convert hemoglobin to methemoglobin, which will bind to cyanide contraindicated concomitant carbon monoxide toxicity activated charcoal indication if cyanide is ingested Complications Parkinsonism basal ganglia is susceptible to cyanide toxicity via hypoxic effects or direct cellular injury