{{More citations needed|date=March 2025}} {{Infobox medical condition | name = | synonyms = Cholinergic toxicity, cholinergic poisoning, SLUDGE syndrome | image = | width = | alt = | caption = | pronounce = | specialty = | symptoms = Hypersalivation, lacrimation, increased urination and defecation, vomiting, sweating, constricted pupils, spasms | complications = Respiratory failure, flaccid paralysis, death | onset = | duration = | types = | causes = Excess synaptic levels of acetylcholine | risks = | diagnosis = | differential = Myasthenia gravis | prevention = | treatment = | medication = Anticholinergics (atropine, diphenhydramine) | prognosis = | frequency = | deaths = }} A '''cholinergic crisis''' is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine,<ref>{{cite book| vauthors = Asensio JA, Trunkey DD |title=Current Therapy of Trauma and Surgical Critical Care E-Book|date=Apr 20, 2015|publisher=Elsevier Health Sciences|isbn=9780323079808|page=31|url=https://books.google.com/books?id=vkZ9CAAAQBAJ|access-date=2 October 2017}}</ref> as a result of the inactivity of the acetylcholinesterase enzyme, which normally breaks down acetylcholine.
== Signs and symptoms == As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of acetylcholine, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Cholinergic crisis is sometimes known by the mnemonic "SLUDGE syndrome" (salivation, lacrimation, urination, defecation, gastrointestinal distress, and emesis).<ref name="WagnerPromes2007">{{cite book |url=https://books.google.com/books?id=JAvX7hTta_wC |title=Last Minute Emergency Medicine : A Concise Review for the Specialty Boards |vauthors=Wagner MJ, Promes SB |date=1 January 2007 |publisher=McGraw Hill Professional |isbn=978-0-07-150975-6 |page=12}}</ref>
Some of the symptoms of increased cholinergic stimulation include: * Salivation: stimulation of the salivary glands * Lacrimation: stimulation of the lacrimal glands (tearing) * Urination: relaxation of the internal sphincter muscle of urethra, and contraction of the detrusor muscles * Defecation * Gastrointestinal distress: smooth muscle tone changes causing gastrointestinal problems, including cramping * Emesis: vomiting<ref>{{cite book | url=https://books.google.com/books?id=C7_NBQAAQBAJ&q=Killer+Bs+in+cholinergic%2C+bradycardia%2C+bronchorrhea%2C+bronchospasm&pg=PA129 | title=Lehne's Pharmacology for Nursing Care | vauthors = Burchum J | isbn=9780323340267 | date=2014-12-02 | publisher=Elsevier Health Sciences }}</ref> * Miosis:<ref>{{cite journal | vauthors = Reddy DS, Colman E | title = A Comparative Toxidrome Analysis of Human Organophosphate and Nerve Agent Poisonings Using Social Media | journal = Clinical and Translational Science | volume = 10 | issue = 3 | pages = 225–230 | date = May 2017 | pmid = 28238224 | pmc = 5421825 | doi = 10.1111/cts.12435 }}</ref> constriction of the pupils of the eye via stimulation of the pupillary constrictor muscles * Muscle spasm: stimulation of skeletal muscle (due to nicotinic acetylcholine receptor stimulation) * Diaphoresis: increased sweating * Bronchial secretions{{Citation needed|date=January 2025}}
==Causes== Cholinergic crisis can be a consequence of: * Contamination with – or excessive exposure to – certain chemicals including: **nerve agents, (e.g., sarin, VX, Novichok agents). **organophosphorus insecticides (e.g., parathion) *Ingestion of certain poisonous fungi (particularly the muscarine-containing members of the genera ''Inocybe'' and ''Clitocybe''). *Taking too high a dose of medications such as cholinesterase inhibitors, in patients with myasthenia gravis *Providing too high a dose of a cholinesterase inhibitor drug in order to reverse surgical muscle paralysis following general anaesthesia. Nicotine poisoning can also be thought of as a subset of cholinergic crisis, as it also involves excessive parasympathetic stimulation.<ref name="Schep">{{cite journal |vauthors=Schep LJ, Slaughter RJ, Beasley DM |date=September 2009 |title=Nicotinic plant poisoning |journal=Clinical Toxicology |volume=47 |issue=8 |pages=771–81 |doi=10.1080/15563650903252186 |pmid=19778187 |s2cid=28312730}}</ref>
== Treatment ==
Some elements of the cholinergic crisis can be reversed with antimuscarinic drugs like atropine or diphenhydramine, but the most dangerous effect — respiratory depression - cannot.<ref>{{Citation |last1=Lott |first1=Erica L. |title=Cholinergic Toxicity |date=2024 |work=StatPearls |url=https://www.ncbi.nlm.nih.gov/books/NBK539783/ |access-date=2024-02-01 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30969605 |last2=Jones |first2=Elizabeth B.}}</ref>
The neuromuscular junction, where the brain communicates with muscles (like the diaphragm, the main breathing muscle), works by acetylcholine activating nicotinic acetylcholine receptors and leading to muscle contraction. Atropine only blocks muscarinic acetylcholine receptors (a different receptor class than the nicotinic receptors at the neuromuscular junction), so it will not improve the muscle strength and ability to breathe in someone with cholinergic crisis. Such a patient will require neuromuscular-blocking drugs and mechanical ventilation until the crisis resolves on its own.{{Citation needed|date=January 2025}}
== See also == * Physostigmine * Edrophonium
== References == {{reflist}}
{{DEFAULTSORT:Cholinergic Crisis}} Category:Toxicology Category:Neurotransmitters Category:Parasympathomimetics Category:Medicinal chemistry Category:Medical mnemonics