Anticholinergic Plant Poisoning (Jimsonweed): An ICU Nurse's Guide

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Updated July 2026  |  More ICU nursing guides →

"Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter." The old mnemonic for the anticholinergic toxidrome is still the fastest way to recognize a patient poisoned by jimsonweed (Datura stramonium), deadly nightshade, angel's trumpet, or the many pharmaceuticals with anticholinergic activity. Teenagers seeking a cheap hallucinogen and foragers who mistake the plant for something edible are the classic ICU stories. The ICU nurse who recognizes the toxidrome can anticipate the agitated delirium, the tachycardia, the retained urine, and the hyperthermia — and knows why cooling, sedation, and sometimes a specific antidote matter.

The toxidrome, feature by feature

Anticholinergic plants block muscarinic acetylcholine receptors, shutting down the "rest and digest" side of the nervous system. The result is a recognizable cluster:

The distinguishing detail

The dry skin is what separates the anticholinergic toxidrome from the sympathomimetic one (cocaine, amphetamines), where the patient is also hot, tachycardic, and agitated but is drenched in sweat. That single observation — a hot, red, dry, delirious patient — often makes the diagnosis at the bedside.

The agitated delirium and the airway

Jimsonweed delirium can be prolonged and dangerous: patients pick at the air, cannot follow commands, and may injure themselves. First-line control is benzodiazepines, which sedate without adding to the anticholinergic burden. Antipsychotics with anticholinergic activity can worsen the picture and are generally avoided. Physical restraint alone risks hyperthermia and rhabdomyolysis from continued struggling, so chemical sedation, cooling, and IV fluids go together.

Supportive care that carries the patient

Most patients recover with time and good supportive care: benzodiazepines for agitation, active cooling for hyperthermia, IV fluids, continuous cardiac monitoring for the tachycardia and any QRS/QT changes, and a bladder scan or catheter for the retained urine that anticholinergic patients cannot void. An ECG matters because many anticholinergic agents — and the drugs people co-ingest — affect cardiac conduction. Because gut motility is slowed, the toxidrome can be prolonged, so plan for hours of monitoring, not minutes.

Related guides

For the opposite (cholinergic) toxidrome and other toxic exposures, see organophosphate poisoning, non-amatoxin mushroom toxidromes, water hemlock (cicutoxin) poisoning, and cardiac glycoside plant poisoning.