An evaluation of the postoperative antihyperalgesic and analgesic effects of intrathecal clonidine administered during elective cesarean delivery.

BACKGROUND: Intrathecal clonidine improves intraoperative anesthesia and postoperative analgesia after cesarean delivery. Clonidine also possesses antihyperalgesic properties. Hyperalgesia contributes to postoperative pain and may be associated with increased risk of chronic pain after surgery. In this study, we evaluated the postoperative antihyperalgesic effect of intrathecal clonidine after caesarean delivery. METHODS: Ninety-six parturients undergoing elective cesarean delivery were randomly assigned to receive intrathecal bupivacaine-sufentanil (BS group), bupivacaine-sufentanil-clonidine 75 microg (BSC group), or bupivacaine-clonidine 150 microg (BC group). The primary outcome was the extent and the incidence of periincisional punctate mechanical hyperalgesia as assessed by response to application of a von Frey filament at 24 and 48 h after cesarean delivery. Postoperative morphine requirements and pain scores, as well as residual pain at 1, 3, and 6 mo, were also assessed. RESULTS: The BC group had a significantly reduced area of periincisional hyperalgesia at 48 h (median, 25th-75th percentiles): 1.0 (1.0 - 3.3) cm(2) vs 9.5 (5.0-14.0) cm(2) in the BS group vs 5.0 (2.5-12.3) cm(2) in the BSC group (P = 0.02 with the BS group). The incidence of hyperalgesia at 48 h was also lower in the BC group: 16% vs 41% in the BS group vs 34% in the BSC group (P = 0.03 with BS group). Postoperative morphine consumption, pain scores, and incidence and intensity of residual pain did not differ among groups. CONCLUSIONS: Intrathecal clonidine 150 mug combined with bupivacaine had a postoperative antihyperalgesic effect expressed as a significant reduction in the extent and incidence of periincisional punctate mechanical hyperalgesia at 48 h after elective cesarean delivery compared with intrathecal bupivacaine-sufentanil and intrathecal clonidine 75 mug-bupivacaine-sufentanil.

Postoperative analgesic effects of continuous wound infiltration with diclofenac after elective cesarean delivery.

BACKGROUND: Postoperative pain mostly results from sensitization of afferent fibers at injury sites driving central sensitization. Recently, peripheral processes have gained attention as mechanisms of hyperalgesia, and prostaglandins are among highly sensitizing agents. To date, perioperative administration of a single local dose of nonsteroidal antiinflammatory drugs has shown inconclusive efficacy. Rather than a single bolus, the current study evaluates the postoperative analgesic effect of diclofenac continuous intrawound infusion after elective cesarean delivery. METHODS: Ninety-two parturients were randomly allocated to receive a 48-h continuous intrawound infusion with 240 ml containing 300 mg diclofenac, 0.2% ropivacaine, or saline. In the ropivacaine and saline groups, patients also received 75 mg intravenous diclofenac every 12 h for 48 h. Postoperative evaluation included intravenous morphine consumption by patient-controlled analgesia and visual analog pain scores. Punctate mechanical hyperalgesia surrounding the wound and presence of residual pain after 1 and 6 months were also assessed. RESULTS: Continuous diclofenac infusion significantly reduced postoperative morphine consumption (18 mg; 95% confidence interval, 12.7-22.2) in comparison with saline infusion and systemic diclofenac (38 mg; 95% confidence interval, 28.8-43.7) (P=0.0009) without unique adverse effects. Postoperative analgesia produced by local diclofenac infusion was as effective as local ropivacaine infusion with systemic diclofenac. CONCLUSIONS: After elective cesarean delivery, continuous intrawound infusion of diclofenac demonstrates a greater opioid-sparing effect and better postoperative analgesia than the same dose administered as an intermittent intravenous bolus.

The clinical role of NMDA receptor antagonists for the treatment of postoperative pain.

Recent advances in the understanding of postoperative pain have demonstrated its association with sensitization of the central nervous system (CNS) which clinically elicits pain hypersensitivity. N-methyl-D-aspartate (NMDA) receptors play a major role in synaptic plasticity and are specifically implicated in CNS facilitation of pain processing. Therefore, NMDA receptor antagonists, and specifically ketamine commonly used in clinical practice, have been implicated in perioperative pain management. At subanesthetic (i.e. low) doses, ketamine exerts a specific NMDA blockade and hence modulates central sensitization induced both by the incision and tissue damage and by perioperative analgesics such as opioids. However, the mechanisms underlying ketamine anti-hyperalgesic effect are not totally understood, and neither is the relationship between central sensitization and the risk of developing residual pain after surgery. This chapter examines the role of low doses of ketamine as an adjuvant drug in current perioperative pain management and questions the anti-hyperalgesic mechanisms involved.