Module 26.3 - Cyanide - Lecture

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Cyanide poisoning is a severe, rapidly progressing toxicological emergency that demands prompt recognition for life-saving intervention. In this educational module, we equip clinicians to tackle this critical challenge by mastering its core principles.
We trace cyanide’s tragic history—from its early isolation in 1782 to its use in warfare and contemporary sources like industrial settings (metallurgy, mining), fire smoke inhalation, and natural cyanogenic glycosides found in plants like cassava and apricots. Crucially, we detail the core pathophysiology: cyanide disrupts cellular respiration by binding to mitochondrial cytochrome oxidase, causing profound cellular hypoxia and leading to a rapid spike in lactate and severe anion gap metabolic acidosis.
Diagnosis is often challenging because symptoms are non-specific (CNS and CV dysfunction). We emphasize why relying on the alleged "bitter almond odor" is a critical error, as approximately 20% of the population cannot detect it. Instead, clinicians must utilize suggestive lab findings such as an increased anion gap metabolic acidosis, elevated lactate concentration, and elevated venous oxygen saturation (reflecting decreased tissue oxygen use).
Given the rapid lethality, immediate empirical antidotal therapy is essential. We differentiate the two primary antidotal strategies:
Hydroxocobalamin (Preferred): This agent directly binds cyanide and is favored in smoke inhalation or severe anemia because it does not induce methemoglobinemia.
Sodium Nitrite and Sodium Thiosulfate: Nitrite creates a methemoglobin sink, while thiosulfate provides the sulfur donor necessary for the natural detoxification pathway catalyzed by rhodanese.
Understanding high-risk contexts and prioritizing aggressive supportive care alongside rapid antidote administration are the cornerstones of effective management for this high-acuity toxicologic scenario.