Hypersensitivity. Congenital or idiopathic methaemoglobinaemia, serious cardiac conduction problem, severe anaemia, cardiogenic and hypovolemic shock. Sepsis in administration site. Children <6 months (as 2% solution).
Patient with anaemia, CV disorders (e.g. arteriosclerosis, hypo-/hypertension, bradycardia, cardiac impairment or block), neurological or neuromuscular disorders (e.g. multiple sclerosis, hemiplegia, paraplegia), diabetes mellitus, respiratory impairment, familial malignant hyperthermia, G6PD, porphyria; debilitations. Renal and hepatic impairment. Elderly, children. Pregnancy and lactation. Not intended for paracervical and pudendal blocks in an obstetric patient; post-operative intra-articular continuous infusion.
This drug may impair locomotion and alertness, if affected, do not drive or operate machinery.
Symptoms: CNS toxicity including paraesthesia in the areas of the mouth and tongue, light-headedness, hearing problems (e.g. tinnitus), visual problems, abnormal muscular contractions, unconsciousness, generalised convulsions, hypoxia, hypercapnia; CV toxicity including hypotension, bradycardia, arrhythmia, cardiac arrest; methaemoglobinaemia. Management: Provide respiratory support (e.g. oxygenation, ventilation). Manage generalised convulsions with an anticonvulsant agent; cardiac arrest by cardiopulmonary resuscitation and provision of circulatory support; CV depression (manifested by hypotension, bradycardia) with IV fluids and vasopressor, chronotropic and/or inotropic agents; methaemoglobinaemia with IV 1% methylene blue.
Increased cardiac related reactions with antiarrhythmic agents (e.g. amiodarone). Increased risk of methaemoglobinaemia with sulfonamides, antimalarials (e.g. chloroquine), certain nitric compounds (e.g. sodium nitroprussiate).
Description: Mechanism of Action: Prilocaine is an amide type local anaesthetic. It selectively binds to the intracellular surface of Na channels and reversibly inhibits influx of Na along nerve fibres thereby, preventing depolarization and conduction of nerve impulses. As a result, it decreases perception of pain, cold, heat, pressure and touch. Onset: As 4% solution: Infiltration: <2 minutes. Inferior alveolar nerve block: <3 minutes. Duration: As 2% solution: Peripheral nerve block: Up to 4 hours. Epidural block: 1.5-2 hours. As 4% solution: Infiltration: Approx 20 minutes. Inferior alveolar nerve block: Approx 2.5 hours. Pharmacokinetics: Distribution: Crosses the placenta and the blood-brain barrier; enters breast milk. Apparent volume of distribution: 190-260 L. Plasma protein binding: 40-55% to α1 acid glycoprotein. Metabolism: Metabolised in the liver and to a lesser extent, in the kidney by amidases via amide hydrolysis into O-toluidine and N-propylalanine; may be further metabolised via ring hydroxylation (e.g. O-toluidine into 2-amino-3-hydroxytoluene and 2-amino-5-hydroxytoluene). Excretion: Via urine (as O-toluidine metabolite; <5% as unchanged drug). Terminal elimination half-life: 1.6 hours.