C53-02 A Race Against Time: Acute Cyanide Poisoning Following Intentional Ingestion

Background Cyanide is a rapidly acting and highly lethal toxin that inhibits cellular respiration, leading to profound tissue hypoxia despite adequate oxygenation. Recognition is essential for intensivists, as delayed treatment can be fatal despite supportive measures. Case Presentation A 21-year-old male with major depressive disorder and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infection (PANDAS) presented to the emergency department after intentional ingestion of an unknown substance. Family later reported that he had purchased cyanide pills online and intercepted their delivery to a laboratory with premeditated suicidal intent. The amount ingested was unknown. On arrival, he was obtunded, tachypneic, and hypotensive, with bright red venous blood and severe lactic acidosis (lactate > 20 mmol/L). He was promptly intubated and treated with hydroxocobalamin, resulting in dark red/purple urine. Serial lactate and blood gas monitoring were used to assess tissue hypoxemia, with EKGs and chemistry panels were used to monitor for myocardial injury and end-organ damage. Aggressive fluid resuscitation led to rapid improvement in metabolic profile and mental status. He was extubated within 24 hours and transferred to psychiatric care. Discussion The combination of severe lactic acidosis, bright venous blood, and corroborating history quickly narrowed the differential toward cyanide toxicity. Cyanide binds to cytochrome oxidase a3 in the mitochondrial electron transport chain, halting oxidative phosphorylation and leading to anaerobic metabolism and lactic acidosis. Presentation may mimic other causes of shock or hypoxia, making diagnosis challenging when exposure is unclear. Rapid recognition depends on key clinical clues—severe lactic acidosis, bright venous blood, and a plausible source of exposure. Hydroxocobalamin is the preferred antidote given its safety and ease of administration, but efficacy is time dependent. Delayed recognition remains common due to the toxin’s rarity and nonspecific features, often leading to poor outcomes. The ease of online access to cyanide without safeguards also represents a growing public health concern. Conclusion Clinicians must maintain a high index of suspicion for cyanide toxicity in patients with unexplained cardiovascular collapse and lactic acidosis. Early empiric hydroxocobalamin administration is lifesaving and should not await confirmatory testing. Hospitals must ensure antidote readiness for rare but rapidly fatal toxic exposures.