OshudPancuronium Bromide
Non depolarizing muscle relaxants
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📋 Indications & Uses Dosage & Administration⚠️ Contraindications⚡ Side Effects & Adverse Reactions🛡️ Warnings & Precautions🔬 Pharmacology & Mechanism
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📖 Official Clinical Monograph
DGDA Approved Prescribing GuidelinesPanalon is indicated as an adjunct to general anesthesia, to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgical procedure of medium and long duration.
Dosage & AdministrationFacilitate endotracheal intubation, Muscle relaxant in general anaesthesia:
Adult:
Initially, 50-100 mcg/kg by inj, may reduce to 20-60 mcg/kg if given after suxamethonium. Maintenance: 10-20 mcg/kg.
Child:
0-30 days Initially, 30-40 mcg/kg. Maintenance: 10-20 mcg/kg; >1 mth Same as adult dose.
Facilitate mechanical ventilation in intensive care:
Adult:
60 mcg/kg every 1-1.5 hr or less frequently.
Pancuronium must not be administered to patients with know hypersensitivity to puncuronium of the bromide ion.
Tachycardia, HTN, bradycardia, bronchospasm, hypotension, CV collapse, excessive salivation; pain or local skin reactions at inj site. Rarely, hypersensitivity reactions.
Patient with burn injury, biliary tract disease, pulmonary disease, muscular dystrophies, myasthenia gravis, myasthenic syndrome, electrolyte disturbance, altered pH, dehydration, CV disease, oedema, raised catecholamine concentration and those at risk of HTN. Renal and hepatic impairment. Childn. Pregnancy and lactation.
Pancuronium is a typical non-depolarising curare-mimetic muscle relaxant. It acts as a competitive acetylcholine antagonist on neuromuscular junctions, displacing acetylcholine (hence competitive) from its post-synaptic nicotinic acetylcholine receptors. It is, unlike suxamethonium, a non-depolarising agent, which means, that it causes no spontaneous depolarisations upon association with the nicotinic receptor in neuromuscular junction, thus producing no muscle fasciculations upon administration. Pancuronium has no hormonal activity. It exerts slight vagolytic activity (i.e. diminishing activity of the vagus nerve) and no ganglioplegic (i.e., blocking ganglions) activity.
Nondepolarizing neuromuscular blocking agents inhibit neuromuscular transmission by competing with acetylcholine for the cholinergic receptors of the motor end plate, thereby reducing the response of the end plate to acetylcholine. This type of neuromuscular block is usually antagonized by anticholinesterase agents.