ABSTRACT
Intrathecal clonidine mimics the activation of the descending noradrenergic pathways and produces analgesia by a specific action on post-synaptic alpha 2 adrenoceptors thus inhibiting dorsal horn neurone firing [1]. It produces dose dependent postoperative analgesia and enhances labor analgesia with intrathecal narcotics. The authors evaluated the dose-response potency of intrathecal clonidine alone during first stage of labor with the respect to analgesia and maternal and fetal side effects. Forty-five parturients were included in this prospective, randomized, double-blind study. Parturients with less than 6-cm cervical dilatation received 30, 60, or 180 micro g intrathecal clonidine. The authors recorded visual analog pain score [VAS], maternal blood pressure and heart rate, ephedrine requirements, and sedation at regular intervals and fetal heart rate tracings continuously. Duration of analgesia was defined as time from intrathecal clonidine administration until request for additional analgesia. clonidine produces a reducion in VAS with all three doses. The duration of analgesia was significantly longer in patients receiving 180 micro g [median, 135; range, 60-200 min] and 60 micro g [median, 120.6; range, 60-l80 min] than 30 micro g [median, 58.4; range, 22-150 min], and VAS was lower in the 180-micro g group than in the 30-micro g group. In the 180-micro g group, hypotension required significantly more often treatment with ephedrifle than in the other groups. No adverse events or fetal heart rate abnormalities occurred. Thirty to 180 micro g intrathecal clonidine produces dose-dependent analgesia during first stage of labor. Although duration and quality of analgesia were more pronounced with 60 and 180 micro g than with 30 micro g, high incidence of hypotension requires caution with the use of 180 micro g for labor analgesia