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1
Question:

A 46-year-old woman with confusion and fever is brought to the emergency department.  She is disoriented, somnolent, and difficult to rouse.  A friend who accompanies the patient says, "She sounded really anxious when I talked to her on the phone so I decided to check in on her.  She was just lying on the couch and groaning when I got there.  I hope she didn't overdose again—she's tried to before."  On physical examination, the patient's skin is flushed, oral mucosa is dry, and pupils are dilated and poorly responsive to light.  Which of the following drugs, if taken in overdose, would most likely cause this clinical presentation?

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Explanation:

Anticholinergic toxicity

Symptom

Mechanism

"Hot as a hare"
↑ Body temperature

  • ↓ Sweating leads to ↓ heat dissipation

"Dry as a bone"
↓ Secretions (eg, mucous membranes, sweat glands)

  • ↓ Glandular secretion & smooth muscle contraction

"Red as a beet"
Flushed skin

  • Superficial vasodilation from ↑ body heat

"Blind as a bat"
Cycloplegia, mydriasis

  • Paralysis of ciliary muscle & iris sphincter

"Mad as a hatter"
Altered mental status

  • Permeates blood-brain barrier & affects CNS pathways

"Full as a flask"
Constipation,
urinary retention

  • ↓ Intestinal smooth muscle contraction
  • ↓ Detrusor contraction & ↓ internal urethral sphincter relaxation

"Fast as a fiddle"

Tachycardia

  • ↓ Vagal tone at the sinoatrial node

This patient exhibits signs and symptoms of anticholinergic toxicity, which results from the inhibition of cholinergic neurotransmission at muscarinic receptors.  Classic manifestations include fever, delirium, mucosal and axillary dryness, cutaneous flushing, nonreactive mydriasis, and urinary retention.  Tachycardia and decreased bowel sounds are other common signs.

Anticholinergic toxicity is associated with numerous over-the-counter (eg, antihistamines, sleep aids, cold preparations) and prescription medications.  Tricyclic antidepressants (TCAs) are commonly implicated, particularly ones with strong anticholinergic properties such as amitriptyline.  When taken in excess, TCAs can also increase QRS duration, cause arrhythmias, and precipitate seizures.

(Choice B)  Typical symptoms of benzodiazepine overdose include sedation, anterograde amnesia, and respiratory depression.

(Choice C)  Haloperidol is a high-potency, first-generation antipsychotic (FGA) that primarily causes neurological side effects due to potent D2 antagonism; anticholinergic effects are more common with low-potency FGAs (eg, chlorpromazine).

(Choice D)  Prazosin is an alpha-1 adrenergic blocker used to treat hypertension and urinary retention due to benign prostatic hyperplasia.  Its major adverse effect is hypotension (especially postural hypotension).

(Choice E)  Adverse effects associated with an overdose of a nonselective beta adrenergic blocker include bronchoconstriction, hypotension, and bradyarrhythmias.

(Choice F)  An overdose of a selective serotonin reuptake inhibitor (eg, sertraline) may result in serotonin syndrome, which is characterized by agitated delirium, autonomic instability, seizures, myoclonus, hyperreflexia, and diaphoresis (not anhidrosis as in anticholinergic overdose).

Educational objective:
Anticholinergic toxicity is characterized by fever; confusion; cutaneous flushing; dry oral mucosa; and dilated, poorly reactive pupils.  Tricyclic antidepressants, particularly amitriptyline, have strong anticholinergic effects.