Evaluation of the inhibition of hyperalgesia of intravenous Tenoxicam after abdominal total hysterectomy

Autor: YaaHui Dong, 東雅惠
Rok vydání: 2001
Druh dokumentu: 學位論文 ; thesis
Popis: 89
Tenoxicam, an injectable nonsteroidal anti-inflammatory drug (NSAID) with a prolonged elimination half-life, has been applied in the management of acute postoperative pain. Certain studies demonstrate its analgesic efficacy when be used as adjuncts to opioid analgesics. However, few data mention its mechanisms in the central nervous system. In this study, we apply three different doses of tenoxicam to patients undergoing abdominal total hysterectomy postoperatively. Patients are randomly assigned to receive IV either normal saline 6 ml (placebo), tenoxicam 0.4 mg/kg or tenoxicam 0.8 mg/kg after completion of surgery in a double-blinded fashion. Secondary hyperalgesia is measured by applying North Coast™ Semmes-Weinstein Monofilaments to the skin 5 cm proximal and perpendicular to the left, middle and right of the surgical incision. The three locations are labeled with “a”, “b” and “c” point, respectively. Patient-controlled analgesia setting with morphine is used to assist postoperative pain control. Pain intensity at rest or in motion is assessed with visual analogue scale score. The pain threshold, the morphine consumption, the pain intensity, the possible adverse drug events and the first flatus time are evaluated and recorded at 2, 4, 6, 24, and 48 hour postoperatively. All data collected are analyzed statistically with the SPSS software program. Three groups of patients are similar with respect to age, height, weight, total amount of fentanyl used intraoperatively, operative and anaesthetic time, and the amount of blood loss. No statistically significant differences are identified in morphine consumption among three groups. There are no differences in pain intensity at rest and in motion, either. The incidence of adverse drug events (nausea / vomiting, dizziness, pruritis, sedation status, liver and renal toxicity and bleeding tendency) are also similar. However, there is statistically significant difference in secondary hyperalgesia. At “a” point, there is significantly less (p=0.044) in the group of patients receiving 0.4 mg/kg tenoxicam compared to the placebo group. At “b” point, there is significantly less (p=0.011) in the group of patients receiving 0.4 mg/kg tenoxicam compared to the placebo group. Also, there is significantly less (p=0.026) in the group of patients receiving 0.8 mg/kg tenoxicam compared to the placebo group. However we can’t differentiate the effect in the group of patients receiving 0.4 mg/kg tenoxicam to patients receiving 0.8 mg/kg tenoxicam. We conclude that tenoxicam may contribute in the central mechanism, such as modulating the process of neuronal plasticity and thereafter prevent secondary hyperalgesia.
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