Poison Hemlock

Poison hemlock is an herbaceous plant that is often confused with the edible Queen Anne's lace, as well as with wild carrot. It is easily found in woodlands all over the world, and is distinguished from the water hemlock by its purple speckles and pungent musk.

All parts of the poison hemlock contain numerous piperidine alkaloids, with coniine being the most toxicologically-relevant. It primarily acts on nicotinic receptors in the neuromuscular junction.

Presentation:

The ingested alkaloid cocktail causes a nicotinic "toxidrome" — tremor, anxiety, mydriasis, salivation, urinary frequency, and nausea; as well as direct rhabdomyolysis and subsequent myoglobin-induced acute tubular necrosis.

Much like succinylcholine, coniine causes persistent NMJ depolarization, leading to brief muscular spasm followed by flaccid paralysis. Unlike succinylcholine, it has a sluggish onset and a long duration of effect. It manifests as an ascending paralysis, affecting first the lower extremities and then the upper extremities and bulbar muscles.

Like its etymological cousin, the mechanism of death for patients who have ingested poison hemlock is typically respiratory paralysis.

Management:

There are tests that can detect the metabolite of coniine, γ-coniceine, but these are not part of typical ED toxicological panels and may not be available in your locale.

Decontamination with activated charcoal or gastrointestinal lavage is possible if the ingestion occurred within 1-2 hours, though cases where delayed decontamination was still efficacious have been described.

Treatment is otherwise supportive: if respirations are compromised, intubation and mechanical ventilation can keep the patient alive until the effects of NMJ blockade resolve; for the rhabdomyolysis, aggressive fluid resuscitation, bicarbonate, electrolyte correction, and even hemodialysis may be warranted depending on severity.