Quick Recap
This completes the Toxicology System - all 8 protocols now have Quick Recap sections.
Toxicology System, Protocol 8/8 — completing the Toxicology System. Full management detail already covered in the Smoke/Inhalational Injury protocol (Respiratory System, Section 10), since cyanide poisoning most commonly presents in the context of fire/smoke exposure. This protocol covers ISOLATED cyanide exposure and cross-references the shared antidotal management framework.
1. Isolated (Non-Fire) Cyanide Exposure Sources
Industrial exposure (electroplating, mining, chemical manufacturing), certain pesticides/fumigants, laboratory exposure, deliberate ingestion (cyanide salts), and iatrogenic exposure from prolonged/high-dose sodium NITROPRUSSIDE infusion — nitroprusside is metabolized to cyanide, and prolonged infusions >24-48 hours or high-dose infusions carry a real accumulation risk, particularly in renal or hepatic impairment (impaired thiocyanate clearance) — actively consider this iatrogenic source in any ICU patient on a nitroprusside infusion who develops unexplained lactic acidosis, altered mental status, or hemodynamic instability.
2. Mechanism (Shared with Smoke Inhalation Protocol)
Cyanide inhibits cytochrome c oxidase, blocking oxidative phosphorylation -> cellular/cytopathic hypoxia and a shift to anaerobic metabolism (lactic acidosis) DESPITE adequate oxygen delivery — tissue hypoxia occurs at the cellular respiratory chain level, not from impaired oxygen-carrying capacity or delivery.
3. Diagnostic Principle
Maintain a low threshold to treat empirically in any patient with unexplained lactic acidosis, altered mental status, or hemodynamic instability in a compatible exposure context (industrial, occupational, nitroprusside infusion) — cyanide levels are not rapidly available in most clinical settings, so treatment decisions must be made on clinical suspicion, not confirmatory testing. Oxygen saturation gap concept (see Smoke/Inhalational Injury protocol) can support the diagnosis if methemoglobinemia is also present/relevant, though cyanide toxicity itself does not directly cause an oximetry-COoximetry discrepancy the way CO does.
4. Management (Full Detail in Smoke/Inhalational Injury Protocol)
First-line: hydroxocobalamin + sodium thiosulfate — hydroxocobalamin does NOT induce methemoglobinemia (a key advantage, particularly relevant in fire settings with possible concurrent CO exposure, though less critical in isolated cyanide exposure without CO co-poisoning).
Alternative (traditional cyanide antidote kit): amyl nitrite + sodium nitrite + sodium thiosulfate — nitrites induce methemoglobinemia (which binds cyanide), a reasonable approach when CO co-exposure is NOT a concern (i.e., more appropriate for isolated cyanide exposure than for fire-associated combined exposure, where hydroxocobalamin is generally preferred).
See the Smoke/Inhalational Injury protocol (Respiratory System, Section 10) for full dosing detail on both antidotal approaches.
5. Nitroprusside-Associated Cyanide Toxicity — A Distinct ICU-Relevant Scenario
Risk factors: infusion duration >24-48 hours, high infusion rates, renal or hepatic impairment (impaired clearance of thiocyanate, the downstream detoxification product).
Presentation: unexplained/worsening lactic acidosis, altered mental status, tachyphylaxis to the nitroprusside's hypotensive effect (a subtle early clue — rising BP despite unchanged/increasing infusion rate can reflect evolving cyanide-mediated cytopathic dysfunction rather than simple tolerance), and eventually hemodynamic instability.
Management: discontinue or reduce the nitroprusside infusion; administer sodium thiosulfate (co-infusion with nitroprusside has been used prophylactically in some high-risk/prolonged-infusion scenarios per institutional protocol); hydroxocobalamin if significant toxicity is suspected; monitor thiocyanate levels if available and renal function closely during any prolonged nitroprusside use.
This risk is directly relevant given nitroprusside's use elsewhere in this protocol library — see the Hypertensive Emergencies and Acute Aortic Syndromes protocols (Cardiovascular System), both of which reference nitroprusside as a treatment option and note the cyanide/thiocyanate toxicity caution, particularly with prolonged or high-dose use.
6. Investigations
Lactate (a key clinical clue — elevated out of proportion to apparent shock severity or oxygen delivery status), ABG, cyanide level if available (not treatment-gating given turnaround delay), thiocyanate level if nitroprusside-associated toxicity suspected, renal/hepatic function (clearance assessment), EtCO2 (a compensatory drop can accompany cyanide-induced lactic acidosis).
7. Organ Support
Hydroxocobalamin + sodium thiosulfate (or the nitrite-based alternative if appropriate for the exposure context) as the primary antidotal therapy; discontinuation of the causative infusion if iatrogenic; standard ICU supportive care for the resulting shock/acidosis/altered mental status.
See the Smoke/Inhalational Injury protocol (Respiratory System) for the complete pathophysiology, full antidotal dosing tables, and the CO/cyanide co-exposure management nuance; see the Hypertensive Emergencies and Acute Aortic Syndromes protocols (Cardiovascular System) for the nitroprusside-specific toxicity caution in its therapeutic context.
This completes the Toxicology System (8/8 protocols).