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Clinical Summary

Acetylcholine (Ach) is a neurotransmitter of both the central and peripheral nervous system. It is the neurotransmitter for both muscarinic and nicotinic receptors. Inhibition of acetylcholinesterase increases Ach in the synapse. This results in the clinical syndrome of both muscarinic and nicotinic effects. One mnemonic for the muscarinic effects is DUMBBEL(L)S: diarrhea, urination, miosis, bronchorrhea, bradycardia, emesis, lacrimation, and salivation. Nicotinic effects include the fasciculations, paralysis, and occasional sympathomimetic effects of mydriasis and tachycardia.

The most common cholinergic poisoning occurs after exposure to anticholinesterase insecticides. These include organic phosphorus (OP) compounds and carbamates. OP compounds bind to acetylcholinesterase, and after a period of time, this bond “ages” and becomes permanent. Carbamates are reversible binders of acetylcholinesterase and tend not to cross the blood-brain barrier.

Management and Disposition

The initial management of patients with acute cholinergic poisoning includes decontamination of their clothing and skin. The airway should be secured early in the resuscitation because most patients have difficulty oxygenating and ventilating due to bronchorrhea and the muscle weakness; however, succinylcholine should be avoided as a paralytic agent because succinylcholine requires acetylcholinesterase for its metabolism. Atropine is the initial therapeutic agent, and dosing is doubled until the pulmonary secretions are dried. Pralidoxime is administered as early as possible for patients with acute OP poisoning but would not be of benefit to patients who have known carbamate poisoning. Seizures should be aggressively treated with benzodiazepines.

Pearls

  1. Atropine is the first-line agent to dry the secretions from cholinergic poisoning. Glycopyrrolate may be used if there is a limited amount of atropine available; however, glycopyrrolate does not cross the blood-brain barrier and thus would not treat the central cholinergic effects.

  2. The nicotinic clinical findings can be remembered by the days of the week: MTWtHF: mydriasis, tachycardia, weakness, hypertension, and fasciculations.

  3. Nerve agents such as sarin, tabun, and soman are OP compounds and are readily absorbed through inhalational routes.

  4. The pharmaceutical agents physostigmine, neostigmine, and pyridostigmine are carbamates; only physostigmine crosses the blood-brain barrier.

FIGURE 17.22

Cholinergic Miosis. Significant miosis seen in a patient with acute cholinergic poisoning from a pesticide. (Photo contributor: Shannon Langston, MD.)

FIGURE 17.23

Cholinergic Toxidrome. This patient is manifesting profound muscarinic effects from acute cholinergic poisoning and has intractable vomiting and diarrhea. (Photo contributor: Shannon Langston, MD.)

FIGURE 17.24

Atropine Therapy. This picture demonstrates the use of multiple vials of atropine required to dry the secretions of a patient with acute cholinergic poisoning. (Photo contributor: Shannon Langston, MD.)

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