# Survival After Massive Potassium Cyanide Ingestion Without Antidote in a Tertiary Care Setting

## TL;DR

A man survived a large potassium cyanide poisoning without antidotes through intensive supportive care, highlighting the importance of rapid diagnosis and treatment.

## Contribution

This case reports survival from massive potassium cyanide ingestion without antidotes, emphasizing supportive care and systemic issues in antidote access.

## Key findings

- The patient survived massive potassium cyanide ingestion with supportive care but no antidotes.
- He developed severe liver injury but recovered with N-acetylcysteine and hepatoprotective agents.
- Urine tests for cyanide were negative due to delayed sampling, showing limitations in toxicology testing.

## Abstract

Cyanide is a rapidly acting cellular toxin that blocks mitochondrial oxidative phosphorylation, causing abrupt lactic acidosis, cardiovascular collapse, and death within minutes if untreated. Survival after massive oral ingestion is rare, and published cases almost always involve the use of specific antidotes such as hydroxocobalamin or sodium nitrite with sodium thiosulfate. A 29-year-old man with emotionally unstable personality disorder/bipolar disorder, on regular psychotropic medication, ingested approximately 8 g of potassium cyanide dissolved in water in an impulsive act of self-harm. He rapidly developed multiple episodes of green, non-bloody vomiting and loose stools and was taken to a local hospital, where he was found to have elevated lactate and creatinine. In the absence of a cyanide antidote, he was started on high-flow oxygen via a non-rebreathing mask and noradrenaline and referred to a tertiary center. On arrival, he was anxious but fully conscious, with stable oxygenation, tachycardia, and mild hypotension under vasopressor support. Arterial blood gas (ABG) showed mixed respiratory alkalosis and metabolic acidosis with hyperlactatemia, hypokalemia, and hyperglycemia. Intensive supportive care included invasive hemodynamic monitoring, aggressive crystalloid resuscitation, titrated noradrenaline, broad-spectrum antibiotics, careful renal protection, correction of electrolytes, and serial blood gas monitoring. He subsequently developed marked hepatocellular injury (peak aspartate aminotransferase: 490.5 IU/L and alanine aminotransferase: 1069.4 IU/L) with preserved bilirubin and coagulation profile, for which N-acetylcysteine infusion and hepatoprotective agents were administered, with excellent response. Urine toxicology performed later in the course was negative for cyanide and thiocyanate, likely due to delayed sampling of approximately 11 hours. He was discharged on Day 13 in a stable condition with improving liver enzymes and arranged follow-up with hepatology and psychiatry. This case demonstrates that survival is possible after apparently massive potassium cyanide ingestion, even without antidote availability, when clinicians rapidly recognize the diagnosis and provide meticulous supportive care. It also highlights critical gaps in antidote access and underscores the need for integrated psychiatric follow-up and tighter control of online cyanide sales, particularly in low-resource settings.