Anticholinergic syndrome in the perioperative period (review). Part 1

Anticholinergic syndrome is a febrile toxidrome characterized by the suppression of cholinergic neurotransmission in muscarinic receptors. A prerequisite for its development is that pharmacological agents must be lipophilic and capable of crossing the blood-brain barrier to block muscarinic cholinergic receptors. Triggers of anticholinergic toxidrome include alkaloids from over 2,000 species of plants and fungi, antipsychotics, antidepressants, antiparkinsonian drugs, antispasmodics, ocular and antihistamine medications, general and local anesthetics, which are often prescribed in combinations, although these drugs vary significantly in their anticholinergic effects within classes. Overdose of anticholinergic compounds can be accidental or intentional. Contributing factors include old age, central nervous system diseases, vitamin B1 deficiency, genetic predisposition, and polypharmacy. The mechanism of action of anticholinergic compounds is based on the antagonism of the neurotransmitter acetylcholine and its deficiency in the synaptic cleft of muscarinic anticholinergic receptors, which can be due to various factors. Symptoms caused by acetylcholine deficiency can be divided into peripheral and central, depending on whether the triggering substance can cross the blood-brain barrier. In anticholinergic syndrome, rhabdomyolysis is usually not present due to the rare occurrence of severe muscle tone increase or rigidity. The cumulative effect from taking several anticholinergic drugs, known as anticholinergic load, can negatively affect cognitive and physical functions and increase the risk of mortality.