The dose required to produce toxicity is dependent on formulation, duration, and route of exposure.
This is because in 1982, someone in Chicago laced Tylenol capsules with potassium cyanide and killed 7 people.Ĭyanide toxicity occurs through inhalation or ingestion as well as through the dermal and parenteral routes. We also have cyanide to thank for the tamper-evident packaging for over-the-counter medications. In 1978, over 900 members of the People’s Temple cult died after they “drank the Kool-Aid” which contained cyanide and other drugs. In the 1940s it was used in German concentration camps, and cyanide pills were used in the suicides of Erwin Rommel, Eva Braun, and Heinrich Himmler. This is one of the reasons we try not to use this agent anymore.Ĭyanide has a very ominous history. Each nitroprusside molecule contains 5 cyanide molecules, and if sulfate stores are depleted (as they may be in malnourished patients or those with liver disease) cyanide may accumulate and cause toxicity. Remember that cyanide is also found in nitroprusside.
Also, the pits of fruits such as apricots, peaches, and cherries contain amygdalin, which when ingested is transformed to glucose, aldehyde, and cyanide-but don’t worry, you would have to eat hundreds of seeds to see any toxicity, and usually they are non-toxic if swallowed whole. Note that only 60% of the population has the gene to detect this odor.Ĭyanide is found naturally in a number of plants. Sodium salts react with water to form hydrogen cyanide (HCN), which is a colorless gas with a “bitter almond” odor. Cyanide exists as an inorganic salt (CN-) and also commonly as sodium cyanide (NaCN) and potassium cyanide (KCN). This week, we have our first toxicology-related discussion and we will take a few minutes to discuss what cyanide does and which antidotes are available for patient management.Ĭyanide toxicity is most commonly associated with smoke inhalation, but it can also occur in laboratory accidents, suicide attempts, and criminal activity. Hello and welcome to Episode 20 of ER-Rx. You can repeat ½ of the dose after 30 min if needed The dose is 12.5 g IV over 10 min in adults or 400 mg/kg (with a max of 12.5 g) in peds. However, it has a slow onset of action of up to 1 hour. – The other component of this kit was sodium thiosulfate, which works by donating the sulfur necessary for the rhodanese enzyme. The adverse effects of methemoglobinemia, hypotension, and bradycardia led to this kit becoming a less favorable option, especially in patients who also have possible carbon monoxide exposure Nitrites work by generating methemoglobin, as CN has a higher affinity for methemoglobin than for cytochrome oxidase. This kit continued amyl nitrite, sodium nitrite, and sodium thiosulfate. – Historically, the Cyanide Antidote Kit was available, but it is no longer manufactured. Adverse effects include hypotension, allergic reactions, and red discoloration of skin, mucous membranes, and urine The dose is 5g IV over 15 minutes in adults and 70 mg/kg (max of 5 g) over 30 minutes in peds, with a repeat dose in 1-2 hours if needed.
– For antidotes, the first-line agent is Cyanokit (hydroxocobalamin) which binds CN to form cyanocobalamin (vitamin B12). Labs should include an ABG, BMP, lactate, whole blood CN level, CBC, blood gases, and carbon monoxide levels – Management consists of supportive care initially. – In smoke inhalation victims, the presence of soot in the mouth or nose, altered mental status, and an elevated lactate can be signs of CN exposure
A lactate > 8 mmol/L has a PPV of 64% and a NPV of 98% for CN concentrations above 1 mcg/mL – A good surrogate measure of CN concentrations is lactate. – CN levels are not readily available, but levels > 3 mcg/mL lead to death and lower levels can cause a spectrum of coma, reduced consciousness, and/ or tachycardia – Sign/symptoms include agitation, confusion, seizures, coma, and respiratory/ cardiovascular collapse – CN acts as a “chemical asphyxiant” by inhibiting cytochrome oxidase, which is essential for aerobic energy production. In acute poisoning the rate-limiting step of rhodanese is the availability of sulfur donors – CN is typically eliminated through the conversion to thiocyanate by the rhodanese enzyme. – Cyanide (CN) toxicity is most commonly associated with smoke inhalation
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