Photo credit: Russ Kerns, MD, Emergency Medicine Attending and Medical Toxicologist, Atrium Health’s Carolinas Medical Center. While this was performed, intravenous access would be established to administer the sodium nitrite and sodium thiosulfate.Ĭyanide antidote kit. The amyl nitrite was prepared in small glass ampules that, when cracked, would release vapors to be sniffed by the patient. While no longer available in the United States, the Lilly Cyanide Antidote kit (Eli Lilly & Co) was the only antidote kit available for many years, consisting of amyl nitrite, sodium nitrite, and sodium thiosulfate. The vast majority of CN-poisoned patients encountered in the ED are victims of fire, inhaling significant quantities of hydrogen cyanide (HCN) gas from the combustion of textiles and synthetic materials. Treatment Options: Nitrates & Sodium Thiosulfate So, once the diagnosis of cyanide poisoning is suspected, what are the treatment options? In this context, a serum lactate concentration greater than 10mmol/L was found to be 87% sensitive and 94% specific for cyanide poisoning, with a positive predictive value of 95%. In fire victims, for example, serum lactate levels rise alongside serum CN levels. For this reason, serum lactate levels can be a useful, albeit nonspecific, marker of CN poisoning. This produces, as a byproduct, a buildup of lactate. In CN-poisoned patients, this reaction is rapidly trying to regenerate enough NAD + to power the anaerobic production of ATP. Without the electron transport chain, however, the only way to convert NAD + to NADH is through the breakdown of pyruvate: When oxidative phosphorylation is occurring, NADH will donate electrons to the electron transport chain and convert back to NAD +. Doing this requires the regeneration of ample NAD + which is converted to NADH during glycolysis. This forces the body to rely on anaerobic metabolism to produce ATP. Still, while not diagnostic, there is a laboratory test that can be helpful.Īs previously discussed, CN produces its deadly effects by inhibiting oxidative phosphorylation. A CN level can be measured, but will typically take a day or so to come back, rendering it useless in the initial treatment of the unstable patient. In a review of 102 patients, only 11% had skin changes and 15% had an odor present.Ĭomplicating the diagnosis is the lack of timely and definitive laboratory testing. How about abnormalities on the skin exam? Or that bitter almond smell? Unfortunately, these board exam giveaways are rare in actual patients. In severe toxicity, you might also see patients present with dyspnea and tachypnea. Tachycardia can result from an initial catecholamine surge but may quickly devolve into bradycardia and, ultimately, cardiac arrest. However, neurologic signs of toxicity can start with dizziness and generalized headache before progressing to decreased consciousness, seizures, or coma. In severe CN toxicities, unresponsiveness is the most common presentation. Still, it is important to be familiar with the typical, presenting symptoms. Often, it will take a reported exposure (or signs of exposure such as soot to the face after a fire) to clue you into its presence. The symptoms of CN poisoning are fairly non-specific. Want more details on its mechanism? Check out Tox and the Hound (image from Tox and the Hound) Its resulting toxicity is one that we are likely to treat as Emergency Medicine providers – most commonly in victims of fires (though we should be prepared for the other nefarious presentations as well).Ĭyanide (CN) is a rapidly lethal toxin, producing damage to highly ATP-dependent organs like the brain and heart by inhibiting oxidative phosphorylation, thereby decreasing ATP production.Ĭyanide inhibits oxidative phosphorylation by binding cytochrome a3 (a part of Complex IV of the electron transport chain). Peer reviewers: Nic Anthony, MD Wesley Chan, MDįrom apple seeds to false teeth, Tylenol, and cigarettes, salad bars to kool-aid, cyanide is among the most ubiquitous deadly poisons discussed in popular culture and news outlets. PART I – Cyanide Poisoning (aka “Doc, it hurts right here” *points to mitochondria*)Īuthors: Trevor Cerbini, MD Alec Feuerbach, MD,
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