# Fatal nicotine poisoning with an extremely high first available serum nicotine concentration and serial nicotine/cotinine measurements: A case report

## TL;DR

A woman died from fatal nicotine poisoning with an extremely high serum nicotine concentration, providing insights into nicotine's toxic effects and metabolism.

## Contribution

This case report provides detailed serial nicotine and cotinine measurements and clinical findings in a fatal nicotine poisoning case.

## Key findings

- First available serum nicotine concentration was 6569.1 ng/mL.
- Serial measurements showed nicotine decline with rising cotinine.
- Neurological injury was consistent with post–cardiac arrest hypoxic–ischemic brain injury.

## Abstract

Human toxicokinetic data after massive nicotine exposure are scarce, and the relationship between circulating nicotine kinetics and organ-specific pathophysiology remains poorly understood, particularly in the post–cardiac arrest setting. We report a fatal case of a 36-year-old woman found collapsed with an empty 100-mL nicotine e-liquid bottle labeled 100 mg/mL (propylene glycol solvent) at the scene; the ingested volume and emesis were unknown. She was in asystolic cardiac arrest on emergency medical services arrival and achieved sustained return of spontaneous circulation after prolonged resuscitation. The first available serum nicotine concentration obtained on emergency department presentation was extremely high (6569.1 ng/mL). Serial measurements showed a marked decline in nicotine with rising cotinine, consistent with substantial metabolic conversion; however, toxicokinetic interpretation is constrained by sparse sampling under post–cardiac arrest physiology and potential hemodilution secondary to resuscitation. Early non-contrast head CT demonstrated diffuse cerebral edema, consistent with severe global hypoxic–ischemic injury; no nicotine-specific attribution for neurological outcome can be made in the absence of supportive biomarkers, electrophysiology, or neuropathology and given uncertainty in exposure timing. Endoscopy demonstrated acute gastric erosions without evidence of corrosive injury and with rapid healing. This case provides a detailed clinical and toxicological record of suspected massive nicotine exposure in a complex post–cardiac arrest setting, including serial nicotine/cotinine profiles and early organ-specific findings, with subsequent organ donation.

•First available serum nicotine concentration was 6569.1 ng/mL.•Serial measurements showed nicotine decline with rising cotinine.•Neurological injury was most consistent with severe post–cardiac arrest hypoxic–ischemic brain injury.•Endoscopy revealed acute gastric erosions with rapid healing.•The case illustrates major evidentiary limitations at extreme nicotine concentrations (semi-quantitative interpretation).

First available serum nicotine concentration was 6569.1 ng/mL.

Serial measurements showed nicotine decline with rising cotinine.

Neurological injury was most consistent with severe post–cardiac arrest hypoxic–ischemic brain injury.

Endoscopy revealed acute gastric erosions with rapid healing.

The case illustrates major evidentiary limitations at extreme nicotine concentrations (semi-quantitative interpretation).