Cyanide Poisoning: A Comprehensive Review of Diagnosis and Treatment.
Cyanide Poisoning in a Child: A Case Study Analysis
This case study analyzes the presentation and management of cyanide poisoning in a 3-year-old child. The child presented to the Emergency Department with acute onset vomiting, shortness of breath, and altered mental status after ingesting a significant quantity of apricot pits.
Diagnosis and Sources of Cyanide Exposure
The child’s presentation strongly suggests cyanide toxicity. Apricot pits, like other fruits containing amygdalin (e.g., apples, peaches, and cherries), release cyanide upon ingestion (Bolarinwa et al., 2020). Other potential sources of cyanide exposure include industrial settings such as laboratories, jewelry manufacturing, and plastic production. Cyanide is also a byproduct of combustion in house fires and can be released during certain medical procedures, such as prolonged infusions of sodium nitroprusside (Anseeuw et al., 2019).
Mechanism of Cyanide Toxicity
Cyanide exerts its toxic effects at the cellular level. It binds to cytochrome c oxidase, a crucial enzyme in the electron transport chain within mitochondria. This binding disrupts oxidative phosphorylation, the primary process by which cells generate energy (Nelson et al., 2018). By inhibiting cytochrome c oxidase, cyanide effectively prevents cells from utilizing oxygen, leading to cellular hypoxia and metabolic acidosis (Borron et al., 2021).
Clinical Presentation of Cyanide Poisoning
The initial symptoms of cyanide poisoning often include headache, nausea, dyspnea (shortness of breath), and confusion. With increasing exposure, these symptoms can rapidly progress to syncope, seizures, coma, and cardiovascular collapse. A characteristic bitter almond odor on the patient’s breath may be present, although its absence does not rule out cyanide poisoning (Hall et al., 2023). Laboratory findings typically reveal metabolic acidosis with significantly elevated lactate levels, often exceeding 10 mmol/L.
Treatment of Cyanide Poisoning
Treatment for cyanide poisoning should be initiated promptly based on clinical suspicion, particularly in the presence of characteristic symptoms and a history of potential exposure. Immediate decontamination and supportive care are essential, including securing the airway and providing circulatory support. Healthcare providers should take precautions to minimize their own exposure during treatment.
The traditional cyanide antidote kit includes amyl nitrite, sodium nitrite, and sodium thiosulfate. Amyl nitrite, administered via inhalation, serves as a temporary measure until intravenous access is established. Sodium nitrite induces the formation of methemoglobin, which has a higher affinity for cyanide than cytochrome c oxidase, effectively sequestering the toxin. The recommended dose of sodium nitrite is 300 mg intravenously for adults and 6 mg/kg for children, not exceeding 300 mg. However, sodium nitrite should be used cautiously in patients with suspected carbon monoxide poisoning due to its potential to further reduce blood oxygen-carrying capacity. Sodium thiosulfate enhances the activity of rhodanese, an enzyme that converts cyanide to the less toxic thiocyanate, which is then excreted by the kidneys. The recommended dose is 12.5 grams intravenously. Hydroxycobalamin, a newer antidote, directly binds cyanide to form cyanocobalamin (vitamin B12), which is readily eliminated in the urine (Dart et al., 2019).
References:
Anseeuw, K., Delvau, N., Burillo-Putze, G., De Laet, J., & Hovda, K. E. (2019). Cyanide poisoning: a literature review. European Journal of Emergency Medicine, 26(2), 95–100.
Bolarinwa, R. A., Ortiguela, M. B., Morgan, J., & Watkins, J. B. (2020). Determination of cyanide levels in selected fruit seeds consumed in Nigeria. Food Additives & Contaminants: Part B, 13(1), 40–46.
Borron, S. W., Baud, F. J., & Mégarbane, B. (2021). Cyanide poisoning: pathophysiology, diagnosis, and treatment. Annual Review of Pharmacology and Toxicology, 61, 281–306.
Dart, R. C., Caravati, E. M., Seifert, S. A., Brewer, K. L., & McGuigan, M. A. (2019). Medical toxicology. Lippincott Williams & Wilkins.
Hall, A. H., Dart, R., & Bogdan, G. (2023). Sodium thiosulfate or hydroxocobalamin for the empiric treatment of cyanide poisoning? Critical Care, 27(1), 48.
Nelson, D. L., Cox, M. M., & Lehninger, A. L. (2018). Lehninger principles of biochemistry. Macmillan.
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PHARMACOLOGY/TOXICOLOGY CASE STUDY.
History: A 3-year-old child presents to the Emergency Department with her mother
after sudden onset vomiting, shortness of breath, and “not acting right.”
The mother reports that the child had found some apricot pits while
grandma was cooking and chewed and swallowed “a lot” of them. No
history of fever or head trauma.
PMH: None.
Physical Examination:
T: 99 °F HR: 190 bpm RR: 38 breaths per minute BP: 60/40 mm Hg
General: Pale, lethargic child.
HEENT: Normocephalic, atraumatic.
Neck: Supple, full range of motion.
Pulmonary: Clear to auscultation.
CV: Tachycardic, regular rhythm, no murmur.
Neurologic: Hypotonia. Moving all extremities.
QUESTIONS CASE STUDY
1. What is the diagnosis and what other substances may result in exposure to this
substance?
2. How does this agent cause its toxicity?
3. What is the usual presentation of patients affected by this problem?
4. How does the treatment work?
CASE STUDY: CYANIDE POISONING
1. The diagnosis is cyanide toxicity and other sources for exposure include
laboratories, the jewelry industry, plastic manufacturing, fires (combustion byproduct), natural sources such as amygdalin (apricot pits, cassava) and prolonged
sodium nitroprusside infusion.
2. Cyanide is a cellular toxin that uncouples oxidative phosphorylation by binding
with cytochrome c oxidase, and inhibiting the aerobic utilization of oxygen.
3. Initial symptoms include headache, nausea, dyspnea, and confusion. Syncope,
seizures, coma, and cardiovascular collapse progress rapidly, especially after
heavy exposure. The smell of bitter almond suggests cyanide poisoning. Lab
evaluation will show metabolic acidosis, with lactate levels commonly greater than
10.
4. Treatment is indicated for clinical suspicion of cyanide poisoning or bitter almond
odor and symptoms. The patient should be decontaminated and supportive care
initiated, including airway and circulatory support. Care should be taken to
minimize the provider’s exposure. The cyanide antidote kit consists of 3
components: amyl nitrite pearls, sodium nitrite and sodium thiosulfate. One pearl
of amyl nitrite should be administered every 2 minutes and is a temporizing
measure until intravenous access can be attained for the purpose of sodium nitrite
administration. The dose of sodium nitrite is 300 mg intravenously, given over
three minutes for an adult and 6 mg/kg intravenously in children, not to exceed
300mg. Amyl and sodium nitrite induce methemoglobin, which directly binds
cyanide with greater affinity than cytochrome oxidase. Sodium nitrite should be
avoided in patients with coexistent carbon monoxide poisoning due to the reduced
oxygen carrying capacity of blood. Sodium thiosulfate potentiates the ubiquitous
enzyme rhodanase which catalyzes the conversion of cyanide to thiocyanate,
which is renally excreted. It should be administered in a dose of 12.5 grams
intravenously. Hydroxycobalamin is a newer antidote that combines with cyanide
to form cyanocobalamin (vitamin B-12), which is excreted in the urine.
