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Collecting And Measuring Wound Exudate Biochemical Mediators In Surgical Wounds
Published on: October 20, 2012
Postoperative pain and systemic inflammatory stress response after preoperative analgesia with clonidine or
Jasminka Persec1, Zoran Persec, Ino Husedzinovic
1Anesthesiology, Resuscitation and Intensive Care Medicine Clinic, University Hospital Dubrava, Zagreb, Croatia, jpersec@net.amis.hr.
Aim:
With adequate control of perioperative pain it is possible to control central and peripheral inflammatory responses to surgery and influence patient outcomes. Use of analgesics before the pain stimulus (preventive analgesia) obstructs development of neuroplastic changes in the central nervous system and reduces pain. Our investigation hypothesis is that preoperative central (epidural or intrathecal) clonidine will reduce postoperative pain and the systemic inflammatory stress response more effectively than levobupivacaine.
Design:
Randomized controlled study.
Methods:
Forty-two patients undergoing colorectal resection surgery were allocated into three groups receiving a preoperative epidural dose of (i) clonidine 5 microg/kg (n = 17), (ii) levobupivacaine 2.5 mg/ml (n = 12) or (iii) saline as a control group (n = 13). Procalcitonin, interleukin-6 and pain levels were assessed before operation, 1 h after starting, and then at 1, 6, 12 and 24 h after operation.
Results:
There were no significant differences between the groups of patients in age, sex, body-mass index, body surface area and operation time. We demonstrated significant reduction (P < 0.05) in levels of procalcitonin and interleukin-6 in the preoperative clonidine group compared with the preoperative levobupivacaine and control groups. Postoperative pain levels at rest and on movement were significantly lower (P < 0.05) in the clonidine group, especially 1 h after surgery (VAS 0.82 and 1.18), than in the levobupivacaine group (VAS 5.25 and 6.67) and the control group (VAS 7.08 and 8.31).
Conclusion:
These results support the importance of the central effect of clonidine on pain pathways and blockade of the systemic inflammatory stress response.
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