Anticholinergic toxicity
(Redirected from Anticholinergic)
Background
Anticholinergic toxicity Causes
- Medications[1]
- Atropine
- Antihistamines
- Antidepressants
- Antipsychotics
- Muscle relaxants
- Anti-Parkinsonians
- Plants
- Jimson weed (Devil's trumpet)
- Amanita mushroom
Clinical Features
- Red as a beet: cutaneous vasodilation
- Blind as a bat: nonreactive mydriasis (often delayed 12-24hr)
- Mad as a hatter: delirium; attention deficit; hallucinations; dysarthria; lethargy
- Full as a flask: urinary retention
- Hot as a hare: anhydrotic hyperthermia (may become severe w/ agitation)
- Dry as a bone: anhidrosis (esp axillae, mouth)
- And the heart runs alone: Tachycardia (HR 120-160) and decreased/absent bowel sounds
- ECG
- Sinus tachycardia
- QRS widening in some cases
Differential Diagnosis
- Sympathomimetic toxicity
- Red, dry skin and absent bowel sounds favors anticholinergic toxicity
- Encephalitis
- Head trauma
- ETOH/sedative withdrawal
- Neuroleptic Malignant Syndrome (NMS)
- Acute psychotic disorder
- Hypoglycemia
Toxidrome Chart
Finding | Cholinergic | Anticholinergic | Sympathomimetic | Sympatholytic^ | Sedative/Hypnotic |
Example | Organophosphates | TCAs | Cocaine | Clonidine | ETOH |
Temp | Nl | Nl / ↑ | Nl / ↑ | Nl / ↓ | Nl / ↓ |
RR | Variable | Nl / ↓ | Variable | Nl / ↓ | Nl / ↓ |
HR | Variable | ↑ | ↑ (sig) | Nl / ↓ | Nl / ↓ |
BP | ↑ | ↑ | ↑ | Nl / ↓ | Nl / ↓ |
LOC | Nl / Lethargic | Nl, agitated, psychotic, comatose | Nl, agitated, psychotic | Nl, Lethargic, or Comatose | Nl, Lethargic, or Comatose |
Pupils | Variable | Mydriatic | Mydriatic | Nl / Miotic | |
Motor | Fasciculations, Flacid Paralysis | Nl | Nl / Agitated | Nl | |
Skin | Sweating (sig) | Hot, dry | Sweating | Dry | |
Lungs | Bronchospasm / rhinorrhea | Nl | Nl | Nl | |
Bowel Sounds | Hyperactive (SLUDGE) | ↓ / Absent | Nl / ↓ | Nl / ↓ |
- ^Consider Sympatholytic when looking at Sedative OD or someone who doesn't respond to Narcan
- Withdrawal from substances have the opposite effect
Altered mental status and fever
- Infectious
- Sepsis
- Meningitis
- Encephalitis
- Cerebral malaria
- Brain abscess
- Other
Treatment
- Consider GI decon with Activated Charcoal if patient presents <2 hours after ingestion and remains cooperative
Sedation
- Decreases the risk of hyperthermia, rhabdo, traumatic injuries
- Benzos are agents of choice especially increase seizure threshold[2]
- Repeat boluses every 5-15 minutes as needed to halt seizures and provide adequate sedation
- Goal: QRS duration < 110 msec
Cholinesterase inhibition
- Indicated for severe agitation or delirium (esp if unresponsive to benzos)
- Contraindicated in QRS>100 or Na blockade signs (R' in aVR) and in narrow angle glaucoma
- Relatively contraindicated in asthma or ileus
- Physostigmine - strongly consider poison control consult before giving
- Crosses blood brain barrier, can be used to help make dx
- Dosing: 0.5mg-1mg IV over 5min (repeat dosing up to 2mg in first hour)[3]
- Onset of action: 5-10min
- If partial response, repeat x3
- If 3 or more administrations are needed over a 6-hour period, start IV infusion (bolus 1-2 mg followed by 1 mg/hour)
- Stop infusion every 12 hours to determine resolution of the toxidrome
- Side effects: bradycardia, dysrhythmias, cholinergic excess[4]
- Always have atropine at the bedside for bradycardia or cholinergic excess</ref>[5]
- Contraindicated in TCA toxicity (associated with cardiac arrest) and in the presence of bradycardia or AV block
Other therapies
- Sodium bicarbonate for conduction abnormalities (QRS prolongation)
- 2 mEq/kg bolus (typically 2-3 amps of bicarb)
- Begin continuous NaCO3 infusion at 250mL/hr if bolus effective
- Solution preparation = 1L D5W mixed with 3 ampules NaHCO3
Disposition
- Consider discharge for patients with mild symptoms after 6hr obs if their symptoms resolve
- Long-acting agents, plant seeds and large ingestions should have extended observation up to 24-48 hours even if asymptomatic due to decreased gastrointestinal motility
- Admit if physostigmine was given (half-life of physo is often shorter than the ingested drug)
- Patients may be cleared if symptoms do not recur within 6 hours of the last antidote dose
See Also
References
- ↑ Dawson AH, Buckley NA. Pharmacological management of anticholinergic delirium – theory, evidence and practice. Br J Clin Pharmacol. 2015;81(3):516-24.
- ↑ Burns MJ, et al. A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med. 2000:35(4):374-381.
- ↑ Rosenbaum C and Bird SB. Timing and frequency for physostigmine redosing for antimuscarininc toxicity. J Med Toxicol. 2010;6:386-92.
- ↑ Pentel P and Peterson CD. Aystole complicating physostigmine treatment of tricyclic antidepressant overdose. Ann Emerg Med. 1980 Nov;9(11):588-90.
- ↑ Nguyen TT, et al. Adverse events from physostigmine: an observational study. Am J Emerg Med. 2018;36:141-2.