Local anesthetic, the hydrochloride is Nesacaine Chloroprocaine Hydrochloride is a synthetic, aminoester, local, anesthetic agent. Chloroprocaine hydrochloride acts by inhibiting sodium influx through binding to specific membrane sodium ion channels in the neuronal cell membranes, restricting sodium permeability, and blocking nerve impulse conduction. This leads to a loss of sensation. Chloroprocaine hydrochloride is short-acting due to rapid hydrolysis by pseudocholinesterase into para-aminobenzoic acid in plasma. Chloroprocaine has a significantly shorter duration of action than lidocaine and is significantly less toxic.
BACKGROUND: Neuraxial anaesthesia is the desired method for Caesarean section. Bupivacaine is a well-known local anaesthetic. It has a long duration of action and can cause unpredictable levels of anaesthesia with subsequent prolonged discharge time. 2-Chloroprocaine has a rapid onset of action, producing an excellent sensory and motor block and has a rapid hydrolysis in the bloodstream by pseudocholinesterase. We compared bupivacaine and 2-chloroprocaine for spinal anaesthesia during Caesarean section. The primary endpoint was the earliest reversal sign of the motor block. METHODS: Sixty ASAI/II patients, planned for elective singleton Caesarean section, were equally randomised to three groups. All patients received a combined spinal-epidural anaesthesia. The first group received 2-chloroprocaine (40 mg) without sufentanil, the second group received 2-chloroprocaine (40 mg) with sufentanil (1 mug) and the third group received hyperbaric bupivacaine (7.5 mg) with sufentanil (1 mug) as a spinal anaesthetic. Motor and sensory blockade were assessed at specific time points. RESULTS: There was no difference between the three groups regarding the time to regression of the motor block. However, at 5 min post spinal injection, the level of sensory block was higher for both groups with 2-chloroprocaine, in comparison with the bupivacaine group. CONCLUSION: 2-Chloroprocaine can be used for low risk Caesarean section in healthy parturients. There is no difference in time to motor block resolution compared to bupivacaine. Motor recovery seems more predictable for 2-chloroprocaine and may be beneficial for the breastfeeding initiation.
Title: Continuous caudal anesthesia for inguinal hernia repair in former preterm infants Henderson K, Sethna NF, Berde CB Ref: Journal of Clinical Anesthesia, 5:129, 1993 : PubMed
STUDY OBJECTIVE: To determine the feasibility of continuous caudal anesthesia with 2-chloroprocaine in conscious former preterm infants undergoing inguinal hernia repair. DESIGN: Prospective study. SETTING: University-affiliated children's hospital. PATIENTS: Ten former preterm infants, ASA physical status II and III, who were 35 to 49.5 weeks postconceptional age at the time of surgery. INTERVENTIONS: Caudal anesthesia was administered via an indwelling catheter using a loading dose of 1 ml/kg (30 mg/kg) of 3% 2-chloroprocaine, followed by incremental doses of 0.3 ml/kg (9 mg/kg) to achieve a level of T4 to T2. The block was maintained by a minimum infusion rate of 30 mg/kg/hr (1 ml/kg/hr) of the same local anesthetic solution. MEASUREMENTS AND MAIN RESULTS: The mean cumulative dose of 2-chloroprocaine was 2.8 +/- 1.0 ml/kg/hr (84 +/- 30 mg/kg/hr) infused over a mean duration of 95 +/- 35 minutes. Serum cholinesterase concentration and plasma 2-chloroprocaine concentration were measured in five infants. CONCLUSIONS: Three percent 2-chloroprocaine can be used effectively for continuous caudal anesthesia in conscious, former preterm infants for inguinal hernia and penoscrotal surgical procedures lasting 85 to 170 minutes.
Title: Genetic variants of human serum cholinesterase influence metabolism of the muscle relaxant succinylcholine. Lockridge O Ref: Pharmacol Ther, 47:35, 1990 : PubMed
People with genetic variants of cholinesterase respond abnormally to succinylcholine, experiencing substantial prolongation of muscle paralysis with apnea rather than the usual 2-6 min. The structure of usual cholinesterase has been determined including the complete amino acid and nucleotide sequence. This has allowed identification of altered amino acids and nucleotides. The variant most frequently found in patients who respond abnormally to succinylcholine is atypical cholinesterase, which occurs in homozygous form in 1 out of 3500 Caucasians. Atypical cholinesterase has a single substitution at nucleotide 209 which changes aspartic acid 70 to glycine. This suggests that Asp 70 is part of the anionic site, and that the absence of this negatively charged amino acid explains the reduced affinity of atypical cholinesterase for positively charged substrates and inhibitors. The clinical consequence of reduced affinity for succinylcholine is that none of the succinylcholine is hydrolyzed in blood and a large overdose reaches the nerve-muscle junction where it causes prolonged muscle paralysis. Silent cholinesterase has a frame shift mutation at glycine 117 which prematurely terminates protein synthesis and yields no active enzyme. The K variant, named in honor of W. Kalow, has threonine in place of alanine 539. The K variant is associated with 33% lower activity. All variants arise from a single locus as there is only one gene for human cholinesterase (EC 3.1.1.8). Comparison of amino acid sequences of esterases and proteases shows that cholinesterase belongs to a new family of serine esterases which is different from the serine proteases.
