The effects of clonidine added to mepivacaine for paronychia surgery under axillary brachial plexus block

We hypothesized that onset of sensory block is delayed in infected versus healthy tissues within the same nerve distribution after axillary brachial plexus block (ABPB) and that clonidine added to mepivacaine would enhance anesthesia and postoperative analgesia. Forty-one outpatients undergoing thumb/index paronychia surgery under ABPB were randomly assigned to receive in a double-blind fashion 400 mg mepivacaine plus either 100 μg clonidine (clonidine group, n = 21) or 2 mL saline (placebo group, n = 20). Onset of sensory block in the infected area was delayed compared with healthy areas of the same nerve distribution (24.7 ± 5.5 min versus 21.3 ± 7.2; P = 0.02 for median and 21.6 ± 7.8 min; P = 0.04 for radial) within the placebo group. In the clonidine group, when compared to placebo i) onset of sensory block in both the median and radial nerve territories was accelerated (11.1 ± 5.6 and 10.5 ± 5.2 versus 21.3 ± 7.2 and 21.6 ± 7.8 min, respectively; P < 0.001), ii) onset of sensory block in the region of infection was accelerated (9.1 ± 1.9 versus 24.7 ± 5.5 min; P < 0.001), iii) duration of anesthesia (275 ± 75 versus 163 ± 57; P = 0.04) and time to first analgesic requirement (279 ± 87 versus 197 ± 84 min; P = 0.002) were prolonged with decreased visual analog scale scores at this time (30 ± 18 versus 70 ± 24; P < 0.001), and iv) verbal numeric rating scores were decreased at 24 h (1.7 ± 2.2 versus 4.1 ± 3.0; P = 0.002) and 48 h (0.1 ± 0.5 versus 1.5 ± 2.4; P = 0.01) postoperatively. Our findings suggest that in the setting of distal infected tissue surgery under ABPB infected tissues are resistant to anesthesia compared with healthy areas within the same nerve distribution and clonidine added to mepivacaine enhances both anesthesia and postoperative analgesia.