Physostigmine for gamma-hydroxybutyrate coma: Inefficacy, adverse events, and review

Zvosec, Deborah L.; Smith, Stephen W.; Litonjua, Regina; Westfal, Richard E.

doi:10.1080/15563650601072159

Cited by 27 publications

(15 citation statements)

References 36 publications

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“…17 Rohm et al found that physostigmine does not accelerate emergence after desflurane anesthesia, 18 and Zvosec et al reported that physostigmine is not effective for treating gamma-hydroxybutyrate intoxication. 39 …”

Section: Discussionmentioning

confidence: 99%

Physostigmine and Methylphenidate Induce Distinct Arousal States During Isoflurane General Anesthesia in Rats

Kenny

Chemali

Cotten

et al. 2016

Anesthesia &Amp; Analgesia

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Background Although emergence from general anesthesia is clinically treated as a passive process driven by the pharmacokinetics of drug clearance, agents that hasten recovery from general anesthesia may be useful for treating delayed emergence, emergence delirium, and post-operative cognitive dysfunction. Activation of central monoaminergic neurotransmission with methylphenidate has been shown to induce reanimation (active emergence) from general anesthesia. Cholinergic neurons in the brainstem and basal forebrain are also known to promote arousal. The objective of this study was to test the hypothesis that physostigmine, a centrally acting cholinesterase inhibitor, induces reanimation from isoflurane anesthesia in adult rats. Methods The dose-dependent effects of physostigmine on time to emergence from a standardized isoflurane general anesthetic were tested. It was then determined whether physostigmine restores righting during continuous isoflurane anesthesia. In a separate group of rats with implanted extradural electrodes, physostigmine was administered during continuous inhalation of 1.0% isoflurane, and the electroencephalogram changes were recorded. Finally, 2.0% isoflurane was used to induce burst suppression, and the effects of physostigmine and methylphenidate on burst suppression probability (BSP) were tested. Results Physostigmine delayed time to emergence from isoflurane anesthesia at doses ≥0.2 mg/kg (n=9). During continuous isoflurane anesthesia (0.9% ± 0.1%), physostigmine did not restore righting (n=9). Blocking the peripheral side effects of physostigmine with the co-administration of glycopyrrolate (a muscarinic antagonist that does not cross the blood-brain barrier) produced similar results (n=9 each). However, during inhalation of 1.0% isoflurane, physostigmine shifted peak electroencephalogram power from δ (<4 Hz) to θ (4-8 Hz) in 6/6 rats. During continuous 2.0% isoflurane anesthesia, physostigmine induced large, statistically significant decreases in BSP in 6/6 rats, whereas methylphenidate did not. Conclusions Unlike methylphenidate, physostigmine does not accelerate time to emergence from isoflurane anesthesia, and does not restore righting during continuous isoflurane anesthesia. However, physostigmine consistently decreases BSP during deep isoflurane anesthesia, whereas methylphenidate does not. These findings suggest that activation of cholinergic neurotransmission during isoflurane anesthesia produces arousal states that are distinct from those induced by monoaminergic activation.

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Section: Discussionmentioning

confidence: 99%

Physostigmine and Methylphenidate Induce Distinct Arousal States During Isoflurane General Anesthesia in Rats

Kenny

Chemali

Cotten

et al. 2016

Anesthesia &Amp; Analgesia

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“…The use of physostigmine is controversial, but most reports have found that it provides no clinical benefit 17–19. In addition, it reduces the convulsive threshold and may cause heart block 18. After recovery from coma, amnesia with respect to the preceding events is common 20…”

Section: Discussionmentioning

confidence: 99%

Liquid ecstasy intoxication: clinical features of 505 consecutive emergency department patients

Galícia

Nogué

Miró

2011

Emergency Medicine Journal

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“…Management is supportive, with intubation only required for prolonged coma, airway security or other complications 43–45 . Antidotes such as physostigmine are not beneficial 46 …”

Section: Discussionmentioning

confidence: 99%

Teenage toxins: Recreational poisoning in the adolescent

Gunja

2011

J Paediatrics Child Health

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Adolescents are experimenting with recreational drugs on a regular basis, particularly at social gatherings such as parties, raves and mass events. A combination of reduced fluid intake, physical activity and drug-induced hyperthermia leads to complications such as heat stroke, delirium and potentially death. The clinician needs to be aware of the variety of pharmacologically active substances available in the recreational marketplace in order to diagnose and manage these patients. Recreational misadventure, because of incorrect dosage or mixing multiple substances, is a common reason for teenagers presenting to hospital with toxidromes. Death from club drug overdose is more likely to be associated with suicidal intent, related risky behaviour and trauma, as well as the inherent toxicity of the drug itself. Although many teenagers are concerned about 'drink spiking' with club drugs, the most common agent causing drink spiking incidents is ethanol.

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Physostigmine for gamma-hydroxybutyrate coma: Inefficacy, adverse events, and review

Cited by 27 publications

References 36 publications

Physostigmine and Methylphenidate Induce Distinct Arousal States During Isoflurane General Anesthesia in Rats

Physostigmine and Methylphenidate Induce Distinct Arousal States During Isoflurane General Anesthesia in Rats

Liquid ecstasy intoxication: clinical features of 505 consecutive emergency department patients

Teenage toxins: Recreational poisoning in the adolescent

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