BARITEKAL

Indications

• Local anesthesia for surgical procedures
• Dental anesthesia
• Regional anesthesia techniques

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in pediatric patients.

Adults: Refer to the BNF for specific dosing information as it may vary depending on the procedure and individual patient factors.

Mechanism of action

Prilocaine acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. It blocks conduction in nerves by preventing the large transient increase in permeability of excitable membranes to sodium ions, which is normally triggered by slight depolarization. This action results in reversible inhibition of action potential propagation and nerve function.

Pharmacodynamics

Prilocaine binds to the intracellular surface of sodium channels, effectively blocking the influx of sodium ions into the neuron. This inhibition of sodium channel function prevents the generation and conduction of nerve impulses, leading to a loss of sensation in the targeted area. The effects of prilocaine are dose-dependent and reversible, allowing for restoration of nerve function once the drug is eliminated from the site of action.

Pharmacokinetics

Prilocaine is metabolized primarily in the liver by cytochrome P450 enzymes, with a half-life of approximately 1.5 to 2.5 hours. Its onset of action is typically rapid, occurring within a few minutes when administered via injection. The duration of action can vary based on the specific formulation and site of administration, generally lasting 1 to 2 hours. Excretion occurs mainly via the kidneys, with metabolites being eliminated in urine.

Contra-indications

• Hypersensitivity to prilocaine or any of its components
• Severe liver disease
• History of methaemoglobinaemia

Adverse effects

• Methaemoglobinaemia
• Hypotension
• Cardiovascular collapse
• Respiratory depression
• Nerve damage
• Allergic reactions

Interactions

• metoclopramide: Severe (increases risk of methaemoglobinaemia)
• nitrates: Severe (increases risk of methaemoglobinaemia)
• aminosalicylic acid: Moderate (increases risk of methaemoglobinaemia)
• antiepileptics (fosphenytoin, phenobarbital, phenytoin, primidone): Moderate (increases risk of methaemoglobinaemia)
• dapsone: Moderate (increases risk of methaemoglobinaemia)
• nitrofurantoin: Moderate (increases risk of methaemoglobinaemia)
• paracetamol: Moderate (increases risk of methaemoglobinaemia)
• nitroprusside: Unknown (increases risk of methaemoglobinaemia)

Precautions

• Use with caution in patients with compromised cardiovascular function
• Careful monitoring in patients with respiratory conditions
• Consider alternative anesthetics in patients with history of methaemoglobinaemia
• Administer in a controlled setting where resuscitation equipment is available

Pregnancy

Prilocaine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult relevant guidelines for specific use.

Breast-feeding

Prilocaine is excreted in human milk. Caution should be exercised when administering to nursing mothers.

Storage

Store at room temperature (15-25 degrees Celsius). Protect from light and moisture.

Formulations

• Prilocaine hydrochloride injection
• Topical prilocaine cream

Indications

• Infiltration anesthesia
• Nerve block anesthesia
• Dental procedures
• Regional anesthesia

Dosage

Children: Consult the BNF for Children for specific dosing guidelines, as pediatric doses vary based on age, weight, and the procedure being performed.

Adults: For infiltration anesthesia, the typical adult dose is 100–200 mg/minute, adjusted according to the site of administration and patient response, with a maximum of 400 mg per course. For spinal anesthesia, a usual dose is 40–60 mg (maximum 80 mg).

Mechanism of action

Prilocaine exerts its local anesthetic effects by reversibly binding to and inhibiting voltage-gated sodium channels in the neuronal cell membrane. This action prevents sodium influx during depolarization, thereby interrupting the propagation of action potentials along sensory nerves and leading to a loss of sensation in the targeted area.

Pharmacodynamics

Prilocaine demonstrates a dose-dependent effect on nerve conduction. It has a rapid onset of action, typically occurring within minutes, with a duration of anesthesia that can last from 1 to 2 hours depending on the dose and route of administration. The drug is less likely to induce systemic toxicity compared to other local anesthetics, but high doses can lead to complications such as methaemoglobinaemia.

Pharmacokinetics

Prilocaine is metabolized primarily in the liver by cytochrome P450 enzymes. Its systemic absorption and elimination are influenced by the route of administration, with infiltration anesthesia resulting in slower absorption compared to nerve blocks. The half-life of prilocaine is approximately 1.5 to 2 hours, and the drug is excreted in urine primarily as metabolites.

Contra-indications

• Hypersensitivity to prilocaine or any component of the formulation
• Acquired methaemoglobinaemia
• Congenital methaemoglobinaemia
• Severe cardiac conduction disorders
• Infection at the injection site
• Inflamed tissues

Adverse effects

• Dizziness
• Nausea
• Vomiting
• Paraesthesia
• Hypotension
• Hypertension
• Respiratory depression
• Methaemoglobinaemia
• Cardiac arrest

Interactions

• Other local anaesthetics
• Sympathomimetics
• Vasoconstrictors

Precautions

• Use with caution in elderly or debilitated patients
• Caution in hepatic impairment due to increased risk of toxic plasma concentrations
• Caution in renal impairment due to increased risk of side effects
• Use with caution during early pregnancy
• Only to be administered by trained personnel with resuscitation equipment available

Pregnancy

Use with caution in early pregnancy, large doses during delivery may cause neonatal respiratory depression, hypotonia and bradycardia.

Breast-feeding

Present in milk but not known to be harmful; use with caution.

Storage

Store in a cool, dry place, protected from light. Follow specific storage instructions as per product literature.

Formulations

• Citanest 1% solution for injection (prilocaine hydrochloride 10 mg per 1 ml) available in 50 ml vials

Mechanism of action

Prilocaine acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. ... BLOCK CONDUCTION IN NERVE PERHAPS BY COMPETING WITH CA @ SOME SITE THAT CONTROLS PERMEABILITY OF MEMBRANE ... CA IS ALSO INVOLVED IN ACTION OF LOCAL ANESTHETICS ON SMOOTH MUSCLE ... & ON ADRENAL MEDULLA ... /LOCAL ANESTHETICS/ ... PREVENT THE GENERATION & THE CONDUCTION OF THE NERVE IMPULSE. THEIR PRIMARY SITE OF ACTION IS THE CELL MEMBRANE. ... BLOCK CONDUCTION BY DECREASING OR PREVENTING THE LARGE TRANSIENT INCREASE IN THE PERMEABILITY OF EXCITABLE MEMBRANES TO NA+ THAT NORMALLY IS PRODUCED BY A SLIGHT DEPOLARIZATION OF THE MEMBRANE. /LOCAL ANESTHETICS/ AS ANESTHETIC ACTION PROGRESSIVELY DEVELOPS IN A NERVE, THRESHOLD FOR ELECTRICAL EXCITABILITY INCR & SAFETY FACTOR FOR CONDUCTION DECR; WHEN THIS ACTION IS SUFFICIENTLY WELL-DEVELOPED, BLOCK OF CONDUCTION IS PRODUCED. /LOCAL ANESTHETICS/ .../2 POSSIBILITIES:/ ACHIEVE BLOCK BY INCR SURFACE PRESSURE OF LIPID LAYER THAT CONSTITUTES NERVE MEMBRANE...CLOSING PORES THROUGH WHICH IONS MOVE. ... /OR:/ AFFECT PERMEABILITY BY INCR DEGREE OF DISORDER OF MEMBRANE. /LOCAL ANESTHETICS/

Pharmacodynamics

Prilocaine binds to the intracellular surface of sodium channels which blocks the subsequent influx of sodium into the cell. Action potential propagation and nerve function is, therefore, prevented. This block is reversible and when the drug diffuses away from the cell, sodium channel function is restored and nerve propagation returns.