Spinal 2-Chloroprocaine: The Effect of Added Dextrose

Abstract

Spinal 2-chloroprocaine is being investigated as an alternative short-acting spinal anesthetic to replace lidocaine for outpatient surgery. Adding dextrose increases the baricity of solutions and alters the characteristics of spinal anesthesia. In this study, we compared 2-chloroprocaine spinal anesthesia performed with or without the addition of dextrose (1.1%). Eight volunteers underwent 2 spinal anesthetics, receiving 40 mg 2-chloroprocaine (2 mL, 2%) with 0.25 mL saline with one and 0.25 mL 10% dextrose with the other in a double-blinded, randomized, balanced crossover manner. Pinprick anesthesia, tolerance to transcutaneous electrical stimulation, and tourniquet, motor strength measurements, and time to ambulation and void were assessed. Postvoid residual bladder volume was measured via ultrasound. Spinal anesthesia was successful in all subjects and regressed within 110 (80-110) min. There was no significant difference in peak height T4 (T7-C6), time to achieve peak block height (14 +/- 6 min), time for 2-segment regression (44 +/- 9 min), regression to L1 (66 +/- 12 min), tolerance of tourniquet (43 +/- 9 min), or return of motor function (81 +/- 14 min). Mean postvoid residual volume was larger with dextrose (74 +/- 67 mL versus 16 +/- 35 mL; P = 0.02). No subject reported signs of transient neurologic symptoms (TNS). In conclusion, spinal 2-chloroprocaine provides adequate potency with reliable regression, seemingly without TNS. Adding dextrose does not significantly alter spinal block characteristics but increases residual bladder dysfunction. Therefore, the addition of glucose to 2-chloroprocaine for spinal anesthesia is not necessary. Spinal chloroprocaine provides adequate potency with reliable regression, seemingly without concerns of transient neurologic symptoms, and hence an appealing profile for outpatient surgery. The addition of dextrose does not alter peak block height or tolerance of thigh tourniquet, and increases the degree of residual bladder dysfunction.