Hot as a hare
Red as a beet (hyperthermia)
Blind as a bat (Pupillary Dilation)
Dry as a bone
Mad as a hen (Delirium and Hallucinations)
(Morton HG: Atropine intoxication: Its manifestations in infants and children. J Pediatr 1939; 14:755-60)
Mouth of marbles voice very characteristic
Tachy, decreased bowel sounds, bladder distension, seizures, delirium
Belladonna, Jimson Weed, Henbane
Also seen in H1 blockers and TCAs (never give physostigmine)
Temp, Benzos for agitation,
Gastric Emptying even if greater than 2 hrs b/c of decreased gi motility then
can cause seizures and cholinergic syndrome, have atropine at bedside. That being said, it is probably quite safe. Small retrospective study confirms this (Ann Emerg Med 42:1, 14 2003)
1-2 mg over 5 minutes.
Can repeat .5 mg every 5 minutes until max of 2 mg reached.
Hits central and peripheral sites
Limitations to Physostigmine Reversal of delirium often temporary Dosing Recommendations Patient on cardiac monitor, continuous pulse oximetry Check EKG for ↑QRSd Atropine at bedside If severe bronchospasm or bradycardia occurs 0.5 mg IV aliquots Titrate to effect, ~q5 min Stop after 2.0 mg If it didnt work, its probably not anticholinergic toxidrome
From twin cities tox blog:
My general recommendation is that physostigmine should be used in cases of clear anticholinergic toxicity where the antidote would likely reduce morbidity or increase the efficient use of hospital resources. If intubation is likely in an anticholinergic patient due to combativeness or coma, it would be great to prevent the intubation if possible. If an ICU admission is needed, then reversing altered mental status or lowering the level of tachycardia might enable admitting the patient to a step-down unit or telemetry. We have experienced this reduced morbidity and cost in patients with ingestions of diphenhydramine, quetiapine, atropine, and anticholinergic botanicals.
Here are 7 articles to check out if you want a “complete” library of pro-physo and anti-physo literature:
- 1) Tong TG et al. Tricyclic Antidepressant Overdose. DICP 1976;10:712-3.
- 2) Pentel P et al. Asystole Complicating Physostigmine Treatment of Tricyclic Antidepressant Overdose. Ann Emerg Med 1980;9:588-90.
- 3) Shannon M. Toxicology Reviews: Physostigmine. Pediatr Emerg Care 1998;14:224-6.
- 4) Burns MJ et al. A Comparison of Physostigmine and Benzodiazepinesfor the Treatment of Anticholinergic Poisoning. Ann Emerg Med 2000;35:374-81.
- 5) Schneir AB et al. Complications of Diagnostic Physostigmine Administration o Emergency Department Patients. Ann Emerg Med 2003;2:14-19.
- 6) Suchard JR. Assessing Physostigmine’s Contraindication in Cyclic Antidepressant Ingestions. J Emerg Med 2003;25:185-191.
- 7) Rasimas JJ et al. A Review of Bedside Toxicologic Experience with Physostigmine and Flumzenil. Clin Toxicol 2010;48:48.
Tacrine to reverse altered mental status (30 mg IV)
Neostigmine can reverse ileus (Annals Emerg Med 38:6)
When giving physo, pts need to be on a monitor, with pulse oxymetry, and with frequent auscultations after each dosing listening for bronchospasm, while having atropine at your side.
Dilute the 1mg/mL of physo 1:10 so that you only give 0.1mg (1mL of the dilute sol.) at a time. This will prevent the possibility of acute seizures, bradycardia/ AV blocks or sialorrhea/ bronchospasm. If after 1mg of physo given the patient is still anticholinergic you’ve made a diagnosis of anticholinergic toxicity. They should have become cholinergic after that dose. You need to give more physo until the MS is OK/ or anticholinergic symptoms are gone. This depends on how much, and when the patient overdosed, etc. Titrating this takes time at the bedside and keen clinical observation. (Olmedo)
Other Drugs with Anticholinergic Effects
Antipsychotics, Antihistamines, TCAs, Parkinson’s Meds, Atropine Products
Jimson weed (Datura stramonium), grows along roadsides, in pastures and in vacant lots throughout Maryland. Other common names for jimson weed include devils weed, stinkweed, locoweed, thornapple, Angels trumpet, and Devils trumpet. The seeds and dried leaves of jimson weed are often ingested dry or in a tea, or smoked, to deliberately produce delirium and hallucinations. Jimson weed is primarily used by adolescents looking for a no-cost, easily accessible hallucinogenic high. Jimson weed can reach 3-5 feet in height, has purple or white trumpet- or funnelshaped flowers, and prickly seed pods which split along 4 seams to reveal numerous small black seeds. Poisonings from this plant are often seen in the Fall, when the plant reaches maturity. All parts of the plant contain atropine, hyoscyamine and scopolamine. Exposure to these alkaloids produces anticholinergic effects. Signs and symptoms include dilated pupils, diminished bowel sounds, urinary retention, dry mucus membranes, flushed skin, tachycardia, hypertension, hyperthermia, agitation, delirium, hallucinations and seizures. Most cases of jimson weed intoxication respond to basic supportive care. Activated charcoal can be given for recent ingestions if the patient is awake and able to protect their airway. Benzodiazepines may be used for agitation or seizures. Drugs with anticholinergic properties should be avoided (e.g., atropine, antihistamines, haloperidol). Physostigmine is a tertiary amine that rapidly traverses the blood brain barrier and inhibits cholinesterases resulting in reversal of anticholinergic effects. Long lasting reversal of signs and symptoms is generally not achieved because of the relatively short duration of action of physostigmine. The use of physostigmine should be limited to severely affected patients, and only with poison center consultation due to the risk of seizures, bradycardia and dysrhythmias. Call the Maryland Poison Center for assistance in managing suspected cases of jimson weed intoxication (From Toxtidbits Maryland Poisons/
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