Common - Very common

Transient bradycardia

Not known

Respiratory, thoracic and mediastinal disorders

Bronchial secretion retention

Not known

Skin and subcutaneous tissue disorders

Flushing

Dry skin

Anhidrosis

Not known

** particularly in the elderly

Reporting of suspected adverse reactions

Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard.

4.9 Overdose

Symptoms

Since glycopyrronium is a quaternary ammonium agent, symptoms of overdosage are peripheral rather than central in nature.

Treatment

To combat the peripheral anticholinergic effects of glycopyrronium a quaternary ammonium anticholinesterase such as neostigmine methylsulphate may be given in a dose of 1000 micrograms (1.0mg) for each 1000 micrograms (1.0mg) of Glycopyrronium Bromide known to have been administered by the parenteral route.

5. Pharmacological properties

5.1 Pharmacodynamic properties

Glycopyrronium bromide (ATC Code: A03AB02) is a quaternary ammonium antimuscarinic with peripheral effects similar to those of atropine. It is used similarly to atropine in anaesthetic practice. Given as a premedicant before general anaesthesia, it diminishes the risk of vagal inhibition of the heart and reduces salivary and bronchial secretions. Intra-operatively, it may be given to reduce bradycardia and hypotension induced by drugs such as suxamethonium, halothane or propofol. Glycopyrronium bromide may be used before, or with, anticholinesterases such as neostigmine to prevent their muscarinic adverse effects.

Antimuscarinic drugs are competitive inhibitors of the actions of acetylcholine at the muscarinic receptors of autonomic effector sites innervated by parasympathetic (cholinergic postganglionic) nerves, as well as being inhibitors of the action of acetylcholine on smooth muscle lacking cholinergic innervation.

Peripheral antimuscarinic effects that are produced as the dose increases are: decreased production of secretions from the salivary, bronchial and sweat glands; dilatation of the pupils (mydriasis) and paralysis of accommodation (cycloplegia); increased heart rate; inhibition of micturition and reduction in gastrointestinal tone; inhibition of gastric acid secretion.

Quaternary ammonium compounds are sparingly lipid soluble and do not readily pass lipid membranes such as the blood-brain barrier. Central effects are negligible.

5.2 Pharmacokinetic properties

Absorption

Following intravenous administration, onset of action occurs within one minute, with peak activity at around 5 minutes.

Following intramuscular injection, maximum plasma concentration and onset of action of Glycopyrronium Bromide is achieved within 30 minutes. Peak effects occur after approximately 30 - 45 minutes; vagal blocking effects last for 2 – 3 hours and antisialagogue effects persist for 7 - 8 hours. There is a faster absorption rate when Glycopyrronium Bromide is injected into the deltoid muscle rather than into the gluteal or vastus lateralis muscles.

Distribution