Abstract
The effect of different doses of fentanyl and nalbuphine on the spread of spinal analgesia produced by lidocaine was studied in 68 patients undergoing transurethral resection of the prostate (TURP) under spinal anesthesia. Patients were randomly assigned to six groupsfentanyl A, B, or C (FA, FB, FC) or nalbuphine A, B, or C (NA, NB, NC), which received intravenous (IV) 50, 100, or 150 μg of fentanyl or 10, 15, or 20 mg of nalbuphine, respectively, 20 min after spinal anesthesia with lidocaine. We tested the level of spinal analgesia with pinprick sensation 20 min after spinal anesthesia and 10 min after the opioid administration, when 0.4 mg of naloxone was administered IV. The levels of sensory analgesia were reassessed 10 min after naloxone. Ten minutes after fentanyl or nalbuphine, the level of analgesia increased (1.8 ± 1.7, 3.1 ± 1.2, and 4.1 ± 1.5 cm, in the FA, FB, and FC groups and 1.9 ± 0.9, 2.6 ± 1.4, and 3.7 ± 2.2 cm in the NA, NB, and NC groups, respectively). The increases in the level of analgesia differed significantly between the fentanyl groups (F = 8.0939; df = 2,35; P < 0.001), the increase produced by 150 μg being significantly higher than produced by 50 μg of fentanyl (limits of confidence −4.236809 and −0.4431909; P < 0.01). Naloxone reversed the effect of fentanyl and 10 min after its administration the fentanyl groups did not differ with regard to the level of spinal analgesia. Nalbuphine also enhanced the spread of sensory analgesia produced by lidocaine, but the nalbuphine groups did not differ significantly between them with regard to the level of analgesia 10 min after its administration as well 10 min after naloxone treatment. Naloxone completely antagonized the effect of fentanyl on spinal analgesia but only partially the effect of nalbuphine. Fentanyl 100 and 150 μg significantly increased the level of analgesia when compared with equipotent doses of nalbuphine 10 and 15 mg (P < 0.02 and P < 0.05, respectively). We conclude that systemic fentanyl and nalbuphine enhance the spread of spinal analgesia in a dose-dependent manner. This effect is antagonized by naloxone, and may be clinically important when a spinal block dissipates before completion of surgery.
