Physostigmine reversal of baclofen? Inadvertent administration of intrathecal physostigmine [abstract] Abstract uri icon
  • Background: Physostigmine salicylate is a carbamate with a tertiary amine structure used to reverse anticholinergic delirium. Case reports also describe its use in the reversal of respiratory depression caused by baclofen overdose. We describe the case of a patient inadvertently administered intrathecal physostigmine while initiating baclofen therapy. Case Report: A 62-year-old woman presented to a health care facility early in the day to continue an early trial of intrathecal baclofen therapy. She was naive to baclofen, and physostigmine was readied by providers in the event of baclofen-induced respiratory depression. A trial of baclofen on the day before had been successful, however no intrathecal pump had yet been installed. Once the thecal sac had been accessed, 2 mg of physostigmine was inadvertently instilled instead of baclofen. Shortly after administration, the patient reported profound nausea without emesis. Vitals were notable for a heart rate of 77 beats per minute and a blood pressure of 150/84 mmHg. Expectant management of seizures with benzodiazepine therapy was recommended, and the patient was admitted to a monitored bed awake, alert, and talking. The patient experienced no vomiting despite her initially forceful nausea. Her vital signs remained normal, and she developed no seizures, bradycardia or other evidence of cholinergic excess. She required no therapies over her stay, and was discharged the following day. Case Discussion: The structure of physostigmine salicylate allows it to penetrate the blood:brain barrier, unlike quaternary amines (i.e. neostigmine), however direct intrathecal instillation has been reported only rarely. Notably feared complications of physostigmine administration include seizures, bradyasystole, increased oropharyngeal and upper respiratory secretions, and bronchospasm. Historically, cases of anejaculation were treated with intrathecal administration of neostigmine (Chapelle et al 1976), but only vague references to direct intrathecal administration of physostigmine. Both the paucity of cholinergic excess - apart from transient nausea - and the absence of ensuing seizure activity precipitated by intrathecal injection of physostigmine administration are particularly noteworthy. Conclusion: Current recommendations for the administration of physostigmine emphasize the slow administration to avoid side effects of seizure and bradydysrhythmia. This case demonstrates a lack of significant side effects following the direct instillation of 2 mg of physostigmine into the cerebrospinal fluid (CSF), suggesting low risk of seizure with transiently elevated CSF physostigmine concentration.

  • publication date
  • 2015
  • Research
  • Drugs and Drug Therapy
  • Emergency Medicine
  • Poisoning
  • Additional Document Info
  • 53
  • issue
  • 7