Cholinergic crisis

A cholinergic crisis is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine (ACh), as of a result of the inactivity (perhaps even cholinesterase inhibitor) of the AChE enzyme, which normally breaks down acetylcholine. A cholinergic crisis is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine (ACh), as of a result of the inactivity (perhaps even cholinesterase inhibitor) of the AChE enzyme, which normally breaks down acetylcholine. Cholinergic crisis, sometimes known by the mnemonic 'SLUDGE syndrome', can be a consequence of: As a result of cholinergic crisis, the muscles stop responding to the bombardment 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 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), which worsens the paralysis caused by cholinergic crisis, but strengthens the muscle in the case of myasthenia gravis. (Edrophonium is an cholinesterase inhibitor hence increases the concentration of acetylcholine present). It is useful to remember some of the symptoms of increased cholinergic stimulation that include: Some elements of the cholinergic crisis can be treated with antimuscarinic drugs like atropine or diphenhydramine, but the most important element, respiratory arrest, 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 blocks muscarinic acetylcholine receptors (a different subtype 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 support via endotracheal intubation until the crisis resolves on its own. The respiratory compromise from cholinergic crisis unfortunately has no less invasive intervention.