AMPRES

Indications

• Local anesthesia for surgical procedures
• Regional anesthesia for obstetric analgesia
• Dental procedures requiring local anesthesia
• Pain management in certain acute conditions

Dosage

Children: Refer to the BNF for Children for specific pediatric dosing information.

Adults: Refer to the BNF for specific dosing information. Generally, the dosage varies based on the procedure and the patient's condition.

Mechanism of action

Chloroprocaine binds to the alpha subunit of voltage-gated sodium channels, inhibiting sodium influx into neuronal cells. This action decreases the permeability of nerve membranes to sodium, thereby reducing the rate of rise of the action potential. Consequently, it blocks nerve signal conduction, resulting in a loss of sensation in the targeted area. The order of loss of nerve function typically follows pain, temperature, touch, proprioception, and skeletal muscle tone.

Pharmacodynamics

Chloroprocaine produces local or regional anesthesia with minimal effects on cardiovascular and central nervous systems at therapeutic doses. Unlike other local anesthetics, it has shorter ambulation and discharge times. However, high plasma concentrations can lead to serious adverse effects, including cardiovascular issues such as atrioventricular block, cardiac arrest, and decreased cardiac output. Central nervous system effects may range from stimulation to depression, including symptoms like restlessness, tremors, convulsions, and potentially respiratory arrest.

Pharmacokinetics

Chloroprocaine is rapidly metabolized by plasma esterases, resulting in a short duration of action. The onset of anesthesia is quick, typically occurring within minutes. Its elimination half-life is brief, contributing to its rapid recovery profile. The pharmacokinetics may vary depending on the route of administration and patient-specific factors, such as age and hepatic function. The drug's effects can be influenced by the site of injection and the vascularity of the area.

Adverse effects

• Cardiovascular adverse effects
• Atrioventricular block
• Cardiac arrest
• Decreased cardiac output
• Decreased arterial blood pressure
• Central nervous system stimulation or depression
• Restlessness
• Tremors
• Shivering
• Convulsions
• Depression
• Coma
• Respiratory arrest

Interactions

• chloroprocaine+sulfonamides: Severe (decreases effects)
• chloroprocaine+antiarrhythmics: Unknown (increases risk of cardiovascular adverse effects)
• chloroprocaine+amiodarone: Unknown (increases risk of cardiovascular adverse effects)
• chloroprocaine+dronedarone: Unknown (increases risk of cardiovascular adverse effects)
• chloroprocaine+vernakalant: Unknown (increases risk of cardiovascular adverse effects)
• chloroprocaine+sotalol: Unknown (increases risk of cardiovascular adverse effects)
• chloroprocaine+beta blockers, non-selective: Unknown (increases risk of cardiovascular adverse effects)

Pregnancy

Safety in pregnancy has not been established, use with caution.

Breast-feeding

Chloroprocaine may be excreted in breast milk, use with caution.

Storage

Store at room temperature, protect from light. Do not freeze.

Formulations

• Chloroprocaine hydrochloride injection

Indications

• Local anaesthesia for minor surgical procedures
• Regional anaesthesia as part of a balanced anaesthetic technique
• Epidural anaesthesia for childbirth or lower extremity surgeries

Dosage

Children: Refer to the BNF for Children for appropriate dosing information as it is dependent on the specific procedure and patient's age and weight.

Adults: Refer to the product literature as licensed doses may vary based on the specific clinical scenario and patient characteristics.

Mechanism of action

Chloroprocaine hydrochloride works by inhibiting sodium ion influx through voltage-gated sodium channels in neuronal cell membranes. This blockade prevents the depolarization and subsequent propagation of action potentials along nerve fibers, thereby resulting in a loss of sensation in the targeted area.

Pharmacodynamics

Chloroprocaine has a rapid onset of action, typically within 5 to 15 minutes, and provides effective analgesia for a duration of approximately 30 to 60 minutes, depending on the concentration used and the method of administration. It is particularly effective for short surgical procedures, allowing for quick recovery of sensory and motor functions after the anaesthetic wears off.

Pharmacokinetics

Chloroprocaine is rapidly metabolized by plasma cholinesterases into inactive metabolites, which contributes to its short duration of action. It is primarily eliminated via hydrolysis in the plasma, with minimal renal excretion of unchanged drug. The onset and duration of action can be influenced by factors such as the site of injection and the presence of additives like vasoconstrictors.

Contra-indications

• Avoid injection into infected tissues
• Avoid injection into inflamed tissues
• Hypovolaemia
• Impaired cardiac conduction
• Severe anaemia

Adverse effects

• Anxiety
• Dizziness
• Hypotension
• Nausea
• Vomiting

Interactions

• Adrenaline may be hazardous in patients with severe hypertension or unstable cardiac rhythm
• Consider dose reduction in patients with low plasma-cholinesterase activity

Precautions

• Increased absorption into the blood may increase systemic side effects
• Local anaesthetic effect may be reduced by altered local pH
• Should be administered by or under the direct supervision of personnel experienced in anaesthesia

Pregnancy

Chloroprocaine is classified as a Category B drug. Use during pregnancy should only be considered if the potential benefits justify the potential risks to the fetus.

Breast-feeding

Caution is advised; it is not known whether chloroprocaine is excreted in human milk.

Storage

Store in a cool, dry place, away from direct sunlight. Protect from light and keep out of reach of children.

Formulations

• Chloroprocaine hydrochloride solution for injection

Mechanism of action

Chloroprocaine acts mainly by binding to the alpha subunit on the cytoplasmic region of voltage-gated sodium channels and inhibiting sodium influx in neuronal cell membranes. This lowers the nerve membrane permeability to sodium and decreases the rate of rise of the action potential. Therefore, chloroprocaine inhibits signal conduction and leads to a reversible nerve conduction blockade. The progression of anesthesia depends on the diameter, myelination and conduction velocity of nerve fibers, and the order of loss of nerve function is the following: 1) pain, 2) temperature, 3) touch, 4) proprioception, and 5) skeletal muscle tone. Local anesthetics prevent the generation and the conduction of the nerve impulse. Their primary site of action is the cell membrane. ... Local anesthetics 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. ... As the anesthetic action progressively develops in a nerve, the threshold for electrical excitability gradually increases, the rate of rise of the action potential declines, impulse conduction slows, and the safety factor for conduction decreases; these factors decrease the probability of propagation of the action potential, and nerve conduction fails. ... /Local anesthetics/ can block K+ channels. ... blockade of conduction is not accompanied by any large or consistent change in resting membrane potential due to block of K+ channels. /Local anesthetics/ ... SITE AT WHICH LOCAL ANESTHETICS ACT, AT LEAST IN ... CHARGED FORM, IS ACCESSIBLE ONLY FROM THE INNER SURFACE OF THE MEMBRANE. ... LOCAL ANESTHETICS APPLIED EXTERNALLY FIRST MUST CROSS THE MEMBRANE BEFORE THEY CAN EXERT A BLOCKING ACTION. /LOCAL ANESTHETICS/ ... /TWO 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/ ... ACID SALT MUST BE NEUTRALIZED IN TISSUE & FREE AMINE LIBERATED BEFORE DRUG CAN PENETRATE TISSUES & PRODUCE ANESTHETIC ACTION. ... FORM OF MOLECULE ACTIVE IN NERVE FIBERS IS CATION. ... CATION ... COMBINES WITH SOME RECEPTOR IN MEMBRANE TO PREVENT GENERATION OF ACTION POTENTIAL. /LOCAL ANESTHETICS/ ... /SUGGESTED/ THAT PROCAINE ... DIMINISHES RELEASE OF ACETYLCHOLINE BY MOTOR-NERVE ENDINGS. /PROCAINE/

Pharmacodynamics

Chloroprocaine is an ester local anesthetic agent indicated for the production of local or regional anesthesia with effects on the cardiovascular and central nervous systems. Compared with lidocaine and bupivacaine, chloroprocaine has shorter ambulation and discharge times. Chloroprocaine has minimal effects on cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance at therapeutic doses. However, at toxic blood concentrations, chloroprocaine may cause atrioventricular block and cardiac arrest, as well as decreased cardiac output and arterial blood pressure. A high concentration of chloroprocaine in plasma can also lead to central nervous system stimulation, depression, or both. Some signs of central stimulation include restlessness, tremors and shivering, which may progress to convulsions. Depression, coma and respiratory arrest may also occur. As with other local anesthetics, patients may experience depression of the central nervous system without a prior stage of stimulation.