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      Journal of Pain Research (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on reporting of high-quality laboratory and clinical findings in all fields of pain research and the prevention and management of pain. Sign up for email alerts here.

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      Epidural dexmedetomidine infusion for perioperative analgesia in patients undergoing abdominal cancer surgery: randomized trial

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          Abstract

          Objective

          To assess the postoperative analgesic efficacy of epidural dexmedetomidine added to bupivacaine infusion for patients undergoing major abdominal cancer surgery.

          Methods

          Patients scheduled for major upper abdominal cancer surgery were allocated to group bupivacaine (n =32), in which patients received epidural bupivacaine infusion (6 mL/h bupivacaine 0.1%) for 48 hours postoperatively, or group bupivacaine + dexmedetomidine (n=32), in which patients received epidural dexmedetomidine added to bupivacaine infusion (6 mL/h of bupivacaine 0.1% + dexmedetomidine, 0.5 µg/mL) for 48 hours postoperatively. The cumulative morphine consumption, the time to first analgesic request, and the VAS pain score were evaluated.

          Results

          The cumulative morphine consumption was significantly reduced in group bupivacaine + dexmedetomidine compared with group bupivacaine: mean ± SD of 10.40±5.16 mg vs 23.23±8.37 mg with an estimated difference (95% CI) of −12.83 (−16.43, −9.24), ( P<0.001). The time to the first analgesic demand was significantly delayed in group bupivacaine + dexmedetomidine compared with group bupivacaine: median (IQR) of 6 (1.75, 8.25) h vs 1 (0, 4)h, ( P<0.001). The mean collapsed over time of overall VAS pain scores at rest and movement was significantly reduced in group bupivacaine + dexmedetomidine compared with group bupivacaine : mean ± SE of 1.6±0.08 vs 2.38±0.08 with an estimated difference (95% CI) of −0.8 (−1, −0.86), ( P<0.001), and mean ± SE of 2.17±0.07 vs 3.25±0.07 with an estimated difference (95% CI) of −1.1 (−1.27, – 0.89), ( P<0.001), respectively.

          Conclusion

          Epidural infusion of dexmedetomidine added to bupivacaine for patients undergoing major abdominal cancer surgery significantly reduced morphine consumption, delayed time to first analgesic supplementation, and decreased pain intensity during the first 48 hours postoperatively without harmful derangement on hemodynamics.

          Most cited references41

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          The effects of increasing plasma concentrations of dexmedetomidine in humans.

          This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.
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            Validity and reliability of the Observer's Assessment of Alertness/Sedation Scale: study with intravenous midazolam.

            The Observer's Assessment of Alertness/Sedation (OAA/S) Scale was developed to measure the level of alertness in subjects who are sedated. This scale was tested in 18 subjects in a three-period crossover study to assess its reliability and its criterion, behavioral, and construct validity. After receiving either placebo or a titrated dose of midazolam to produce light or heavy sedation, each subject was administered two sedation scales (OAA/S Scale and a Visual Analogue Scale) and two performances tests (Digit Symbol Substitution Test and Serial Sevens Subtraction). Two raters individually evaluated the subject's level of alertness on each of the two sedation scales. The results obtained on the OAA/S Scale were reliable and valid as measured by high correlations between the two raters and high correlations between the OAA/S Scale and two of the three standard tests used in this study. The OAA/S Scale was sensitive to the level of midazolam administered; all pairwise comparisons were significant (p less than 0.05) for all three treatment levels at both test periods.
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              Effect of low-dose dexmedetomidine or clonidine on the characteristics of bupivacaine spinal block.

              The purpose of this study was to compare the onset and duration of sensory and motor block, as well as the hemodynamic changes and level of sedation, following intrathecal bupivacaine supplemented with either dexmedetomidine or clonidine. In a prospective, double-blind study, 60 patients undergoing transurethral resection of prostate or bladder tumor under spinal anesthesia were randomly allocated to one of three groups. Group B received 12 mg of hyperbaric bupivacaine, group D received 12 mg of bupivacaine supplemented with 3 microg of dexmedetomidine and group C received 12 mg of bupivacaine supplemented with 30 microg of clonidine. The onset times to reach peak sensory and motor levels, and the sensory and motor regression times, were recorded. Hemodynamic changes and the level of sedation were also recorded. Patients in groups D and C had a significantly shorter onset time of motor block and significantly longer sensory and motor regression times than patients in group B. The mean time of sensory regression to the S1 segment was 303 +/- 75 min in group D, 272 +/- 38 min in group C and 190 +/- 48 min in group B (B vs. D and B vs. C, P < 0.001). The regression of motor block to Bromage 0 was 250 +/- 76 min in group D, 216 +/- 35 min in group C and 163 +/- 47 min in group B (B vs. D and B vs. C, P < 0.001). The onset and regression times were not significantly different between groups D and C. The mean arterial pressure, heart rate and level of sedation were similar in the three groups intra-operatively and post-operatively. Dexmedetomidine (3 microg) or clonidine (30 microg), when added to intrathecal bupivacaine, produces a similar prolongation in the duration of the motor and sensory block with preserved hemodynamic stability and lack of sedation.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2018
                30 October 2018
                : 11
                : 2675-2685
                Affiliations
                [1 ]Anesthesia and Pain Management, South Egypt Cancer Institute, diabhetta25@ 123456gmail.com
                [2 ]Anesthesia and Intensive Care, Faculty of Medicine, Assuit University, Assuit, Egypt
                Author notes
                Correspondence: Diab Fuad Hetta, Anesthesia and Pain Management, South Egypt Cancer Institute, Assuit University, 71515 Assuit, Egypt, Tel +20 109 109 0009, Fax +20 88 234 8609, Email diabhetta25@ 123456gmail.com
                Article
                jpr-11-2675
                10.2147/JPR.S163975
                6214321
                4b77e0ee-65c4-4622-a2c3-be9bcd5582bf
                © 2018 Hetta et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Anesthesiology & Pain management
                dexmedetomidine,epidural,postoperative pain
                Anesthesiology & Pain management
                dexmedetomidine, epidural, postoperative pain

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