Cholinergic Crisis

Reversal is our own trigger - Neostigmine inhibits acetylcholinesterase, and bronchospasm, miosis, increased peristalsis, and heavy secretions are the muscarinic tell after reversal. Per the ASA 2023 neuromuscular blockade guideline, neostigmine is co-administered with an anticholinergic — glycopyrrolate or atropine — to mitigate muscarinic effects including bradycardia. Where the relaxant allows it, sugammadex sidesteps the problem entirely: it antagonizes rocuronium and vecuronium without touching acetylcholinesterase.

Distinguish it from myasthenic crisis - Both present as weakness and the clinical pictures overlap closely. Edrophonium 2 mg IV is the discriminator: symptoms improve in myasthenic crisis and worsen in cholinergic crisis.

Airway first, regardless of cause - Progressive respiratory failure is the most common cause of death. Secure the airway when there is any concern for compromise, and expect that bronchorrhea and bronchospasm make oxygenation worse than the weakness alone would predict.

Read the toxidrome - SLUDGEM (salivation, lacrimation, urinary frequency, diarrhea, GI cramping, emesis, miosis) or DUMBELS (diaphoresis and diarrhea, urinary frequency, miosis, bronchospasm and bronchorrhea, emesis, lacrimation, salivation) is how you tag the muscarinic half at the bedside.

Atropine covers the muscarinic half only - It competitively blocks the postsynaptic muscarinic receptor. Roughly 2 mg for an adult, 0.03 to 0.05 mg/kg pediatric, repeated until signs of atropinization appear. It has no effect on nicotinic receptors, so weakness will not resolve on atropine alone.

Pralidoxime covers the nicotinic half - It separates the organophosphate from acetylcholinesterase, so it is the agent for respiratory or generalized muscle weakness after organophosphate exposure. Give it inside the window before the enzyme 'ages' — aging half-life runs from two minutes for soman to several hours for sarin, with a 48-hour outer window. It does not cross the blood-brain barrier, so CNS effects still need atropine.

Succinylcholine in organophosphate exposure - Avoid it. It sits on the list of agents that worsen toxicity, along with loop diuretics, theophylline, and caffeine.

Seizures and agitation - Treat with a benzodiazepine — midazolam or lorazepam.

Decontaminate before anything else - With organophosphate or nerve agent exposure, remove all clothing to stop ongoing absorption and to keep the crisis from spreading to the team.

Expect a wet airway - Salivation, lacrimation, and bronchorrhea flood the field. Have suction running, plan for a soiled laryngoscopic view, and keep suctioning after the tube is in.

Disposition is the ICU - These patients need continued cardiopulmonary support and monitoring after stabilization, not a floor bed.

Cholinergic crisis is what follows when acetylcholinesterase is inhibited or inactivated, acetylcholine accumulates at the neuromuscular junction and synapses, and both nicotinic and muscarinic receptors are overstimulated at once.

Three routes lead there. Overmedication with an acetylcholinesterase inhibitor such as pyridostigmine in a patient being treated for myasthenia gravis (MG). Exposure to organophosphates — pesticides, insecticides, and nerve agents — by inhalation, ingestion, or skin contact. And the one that belongs to the anesthesia provider: neostigmine or pyridostigmine given to reverse a nondepolarizing block.

Muscarinic overload produces salivation, lacrimation, urinary frequency, diarrhea, GI cramping, emesis, miosis, bronchospasm, and bronchorrhea. Nicotinic overload produces fasciculations, weakness, and flaccid paralysis. Mortality runs 3% to 25%, and the usual cause of death is progressive respiratory failure.