6,8-11 Overall, the use of physostigmine in anticholinergic toxicity has been associated with better delirium control, fewer intubations, and a remarkably low rate of bradycardia, seizures, and cholinergic excess. In the intervening years, several authors have reassessed the concern and published various studies investigating not only the efficacy, but also the side effect concerns. 6 Although the concern arose from TCA overdose, emergency department providers have become hesitant to use physostigmine for delirium and agitation caused by other anticholinergic medications like diphenhydramine. Since the publication of this case series, the use of physostigmine has been largely avoided because of the fear of causing cholinergic excess (bradycardia, seizure, and bronchorrhea). 7 Based on this temporal relationship alone, the authors concluded that the “use of physostigmine in patients who have ingested an overdose of TCAs carries the risk of life-threatening bradyarrhythmias.” In retrospect, it is clear these patients had clear contraindications to physostigmine and had received inadequate sodium bicarbonate to treat their life-threatening sodium channel blockade prior to their cardiac arrest.
3,6 These two patients were both in the final throes of severe TCA overdose –both with a widened QRS, one already hypotensive and seizing – who were given a dose of physostigmine and then developed bradycardia and asystole.
MAD AS A HATTER SERIES
Physostigmine is a centrally-acting acetylcholinesterase inhibitor that has fallen out of favor since the publication of two patient case series in 1980. 5įortunately, there is a better approach: delirium reversal with physostigmine. In severe circumstances, patients may require intubation and ICU placement - two interventions with significant associated morbidity and mortality. 4 Often this leads to an admission to a monitored floor until the medication wears off. Therefore, delirium can be completely refractory to repeated doses of benzodiazepines and may actually be worsened by the use of some antipsychotics that have anticholinergic properties. 3 This is because the delirium is caused by blockade of muscarinic receptors in the brain. Unfortunately, these interventions do not reverse the effects of anticholinergic delirium caused by diphenhydramine overdose. 1,2 When presented with this type of patient, many providers would consider treatment with benzodiazepines, antipsychotics, physical restraints, or all of the above. Diphenhydramine toxicity is especially common because of its easy access as an over-the-counter therapeutic as well as its abuse potential. This presentation is one that every emergency physician will confront during their career. Nurses are having a difficult time obtaining blood and an ECG, and several security guards are at the bedside attempting to control the patient. She is attempting to climb out of her hospital bed, reaching out at objects that are not there, and exhibits a mumbled speech pattern. Pertinent exam findings include dry mucous membranes, dilated pupils, normal muscle tone, and normal reflexes. Paramedics at the scene find no medications other than the diphenhydramine. Family found the patient moaning on the floor and called 911. A 34-year-old female with a history of bipolar disorder, depression, and multiple previous suicide attempts is brought into the emergency room after ingesting “an entire bottle” of diphenhydramine in a suicidal gesture.
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