Central Anticholinergic Syndrome following Reversal of Neuromuscular Blockade

Ko, Sun

doi:10.1177/0310057x9302100324

Cited by 7 publications

(3 citation statements)

References 5 publications

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“…Many different drugs have been implicated in the pathogenesis of central anticholinergic syndrome. Implicated drugs used in anaesthesia include anticholinergic agents such as atropine 5 and scopolamine 6 , promethazine, benzodiazepines 7 , opioids 8 , inhalational volatile anaesthetics such as halothane and isoflurane 7 and also ketamine 9 . The incidence of central anticholinergic syndrome following routine anaesthesia has been reported as 1.9% by Link and co-workers 7 .…”

Section: Discussionmentioning

confidence: 99%

Presumed Central Anticholinergic Syndrome from Inadvertent Intravenous Hyoscine Hydrobromide (Scopolamine) Injection

Wilden

Rapeport

2004

Anaesth Intensive Care

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We present a case of presumed central anticholinergic syndrome due to a drug administration error. A 35-year-old woman was slow to emerge from anaesthesia for laparoscopic biliary surgery. Postoperative neurological and metabolic abnormalities were later diagnosed as central anticholinergic syndrome. Only after resolution of the clinical problems did the drug error origin of the syndrome become apparent. It was realized that hyoscine hydrobromide (scopolamine) had been inadvertently administered intraoperatively for biliary relaxation, instead of hyoscine butylbromide. This case report describes central anticholinergic syndrome and highlights potential problems involved for anaesthetists administering drugs they do not commonly use.

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Section: Discussionmentioning

confidence: 99%

Presumed Central Anticholinergic Syndrome from Inadvertent Intravenous Hyoscine Hydrobromide (Scopolamine) Injection

Wilden

Rapeport

2004

Anaesth Intensive Care

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“…Atropine and scopolamine are tertiary amines that can cross the blood-brain barrier and are two of the most commonly reported perioperative medications known to cause CAS. CAS has been associated with the use of atropine and/or scopolamine as a premedicant, the use of atropine for reversing neuromuscular blockade, 11 and with the repeated administration of atropine. 12 There has been one case report in the literature of glycopyrrolate associated CAS.…”

Section: Central Anticholinergic Syndromementioning

confidence: 99%

Central Anticholinergic Syndrome: A Case Report

Moos¹

2007

Journal of PeriAnesthesia Nursing

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“…7 Opioid-induced respiratory depression (OIRD) causes brain hypoxia that contributes significantly to the lethality associated with fentanyl. 8,9 The region of the brain responsible for breathing, the medulla oblongata, has a high density of μ-opioid receptors 10 ; as fentanyl saturates receptors, respiration decreases, resulting in systemic hypoxia, particularly in the brain. 11 OIRD can typically be reversed with μ-receptor antagonists such as naloxone, if administered quickly.…”

mentioning

confidence: 99%

Fentanyl overdose: Temporal effects and prognostic factors in SKH1 mice

Newman,

Lynch,

Connery

et al. 2024

Basic Clin Pharma Tox

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Fentanyl exposure and overdose are growing concerns in public health and occupational safety. This study aimed to establish parameters of fentanyl lethality in SKH1 mice for future overdose research. Lethality was determined using the up‐down procedure, with subjects monitored post‐administration using pulse oximetry (5 min) and then whole‐body plethysmography (40 min). Following the determination of subcutaneous dose–response, [18F]Fluorodeoxyglucose positron emission tomography (18F‐FDG PET) was performed after LD10 fentanyl at 40 min, 6 h, 24 h or 7 days post‐dose. LD10 and LD50 were observed to be 110 and 135 mg/kg, respectively, and consistent with four‐parameter logistic fit values of 111.2 and 134.6 mg/kg (r2 = 0.9996). Overdose (LD10 or greater) yielded three distinct cardiovascular groups: survival, non‐survival with blood oxygen saturation (SpO2) minimum ≥37% and non‐survival with SpO2 <37%. Breaths per minute, minute volume and inspiratory quotient were significantly different between surviving and non‐surviving animals for up to 40 min post‐injection. 18F‐FDG PET revealed decreased glucose uptake in the heart, lungs and brain for up to 24 h. These findings provide critical insights into fentanyl lethality in SKH1 mice, including non‐invasive respiratory effects and organ‐specific impacts that are invaluable for future translational studies investigating the temporal effects of fentanyl overdose.

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Central Anticholinergic Syndrome following Reversal of Neuromuscular Blockade

Cited by 7 publications

References 5 publications

Presumed Central Anticholinergic Syndrome from Inadvertent Intravenous Hyoscine Hydrobromide (Scopolamine) Injection

Presumed Central Anticholinergic Syndrome from Inadvertent Intravenous Hyoscine Hydrobromide (Scopolamine) Injection

Central Anticholinergic Syndrome: A Case Report

Fentanyl overdose: Temporal effects and prognostic factors in SKH1 mice

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