Cholinergic crisis

A cholinergic crisis is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine (ACh),[1] as a result of the inactivity of the AChE enzyme, which normally breaks down acetylcholine.

Cholinergic crisis
Other namesCholinergic toxicity, cholinergic poisoning, SLUDGE syndrome

Symptoms and diagnosisEdit

As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of ACh, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis (constricted pupils).

This crisis may be masked by the concomitant use of atropine along with cholinesterase inhibitor medication in order to prevent side effects. Flaccid paralysis resulting from cholinergic crisis can be distinguished from myasthenia gravis by the use of the drug edrophonium (Tensilon), as it only worsens the paralysis caused by cholinergic crisis but strengthens the muscle response in the case of myasthenia gravis. (Edrophonium is a cholinesterase inhibitor, hence increases the concentration of acetylcholine present).

Some of the symptoms of increased cholinergic stimulation include:

CauseEdit

Cholinergic crisis, sometimes known by the mnemonic "SLUDGE syndrome" ( Salivation, Lacrimation, Urination, Defecation, Gastrointestinal distress and Emesis),[4] can be a consequence of:

TreatmentEdit

Some elements of the cholinergic crisis can be reversed with antimuscarinic drugs like atropine or diphenhydramine, but the most dangerous effect - respiratory depression, cannot.

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 atropine 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.

See alsoEdit

ReferencesEdit

  1. ^ Asensio JA, Trunkey DD (Apr 20, 2015). Current Therapy of Trauma and Surgical Critical Care E-Book. Elsevier Health Sciences. p. 31. ISBN 9780323079808. Retrieved 2 October 2017.
  2. ^ Burchum J (2014-12-02). Lehne's Pharmacology for Nursing Care. ISBN 9780323340267.
  3. ^ Reddy DS, Colman E (May 2017). "A Comparative Toxidrome Analysis of Human Organophosphate and Nerve Agent Poisonings Using Social Media". Clinical and Translational Science. 10 (3): 225–230. doi:10.1111/cts.12435. PMC 5421825. PMID 28238224.
  4. ^ Wagner MJ, Promes SB (1 January 2007). Last Minute Emergency Medicine : A Concise Review for the Specialty Boards. McGraw Hill Professional. p. 12. ISBN 978-0-07-150975-6.
  5. ^ Schep LJ, Slaughter RJ, Beasley DM (September 2009). "Nicotinic plant poisoning". Clinical Toxicology. 47 (8): 771–81. doi:10.1080/15563650903252186. PMID 19778187. S2CID 28312730.