The most feared consequence of physostigmine administration includes cardiovascular effects, especially sudden cardiac arrest. However, published reviews of these two cases subsequently suggested the associated fatalities were more likely due to the severe TCA toxicity rather than a consequence of physostigmine administration. 2 The medical community's reaction to these two cases published in Annals of Emergency Medicine in 1980 was dramatic and global, resulting in an almost immediate rejection of physostigmine and movement towards seemingly safer delirium treatment options such as benzodiazepines. 1 However, following a report of two deaths during the treatment of tricyclic antidepressant overdoses with physostigmine, opinions rapidly changed. 1 It was also during the 1970s that it was suggested as a potentially life-saving antidote in tricyclic antidepressant (TCA) toxicity. Physostigmine was used extensively in the 1960s and ’70s in the treatment of undifferentiated delirium. Consequently, physostigmine is effective in reversing the peripheral and central effects of anticholinergic toxicity. Physostigmine is a carbamate acetylcholinesterase inhibitor that is readily capable of crossing the blood-brain barrier due to its tertiary amine properties. Despite evidence that physostigmine is undeniably effective in treating the symptoms of confirmed anticholinergic poisoning, its use has plummeted since the early 1980s. Physostigmine became one of a handful of drugs that don’t get the respect they deserve. Yet a growing amount of more current evidence suggests the toxicity profile associated with physostigmine is misunderstood and occurs when used inappropriately. However, its effectiveness, safety profile, and dosing have been disputed in recent years, leading to a decline in its use. Physostigmine has long been recognized as an antidote to reverse antimuscarinic delirium.
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