Dexmedetomidine versus remifentanil in postoperative pain control after spinal surgery: a randomized controlled study

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Abstract

Background

Total intravenous anesthesia (TIVA) is used widely in spinal surgery because inhalational anesthetics are known to decrease the amplitude of motor evoked potentials. Presently, dexmedetomidine is used as an adjuvant for propofol-based TIVA. We compared the effects of remifentanil and dexmedetomidine on pain intensity as well as the analgesic requirements after post-anesthesia care unit (PACU) discharge in patients undergoing spinal surgery.

Methods

Forty patients scheduled for posterior lumbar interbody fusion (PLIF) surgery under general anesthesia were enrolled. Anesthesia was maintained using propofol at 3–12 mg/kg/h and remifentanil at 0.01–0.2 μg/kg/min in Remifentanil group or dexmedetomidine at 0.01–0.02 μg/kg/min in Dexmedetomidine group, keeping the bispectral index between 40 and 60. Patient-controlled analgesia (PCA) made of hydromophone was applied once the patients opened their eyes in the PACU. The visual analog scale (VAS) score, PCA dosage administered, and postoperative nausea and vomiting (PONV) were recorded at the time of discharge from the PACU (T1) and at 2 (T2), 8 (T3), 24 (T4), and 48 hours (T5) after surgery.

Results

The VAS score in Remifentanil group was significantly higher than that in Dexmedetomidine group at immediate and late postoperative period (4.1 ± 2.0 vs. 2.3 ± 2.2 at T1, and 4.0 ± 2.2 vs. 2.6 ± 1.7 at T5; P < 0.05). Dexmedtomidine group had a statistically significantly lower PCA requirement at every time point after surgery except directly before discharge from the PACU (3.0 ± 1.2 ml vs. 2.3 ± 1.4 ml at T1; P > 0.05, but 69.7 ± 21.4 ml vs. 52.8 ± 10.8 ml at T5; P < 0.05). Patients in Remifentanil group displayed more PONV until 24 hours post-surgery.

Conclusions

Dexmedetomidine displayed superior efficacy in alleviating pain and in postoperative pain management for 48 hours after PLIF. Therefore, dexmedetomidine may be used instead of remifentanil as an adjuvant in propofol-based TIVA.

Trial registration

Clinical Research Information Service (CRiS) Identifier: KCT0001041.

Related collections

Most cited references 25

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The effects of increasing plasma concentrations of dexmedetomidine in humans.

Thomas Ebert, Judith Hall, Jill A. Barney … (2000)

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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A comprehensive review of opioid-induced hyperalgesia.

Marion Lee, Sanford M Silverman, Hans Hansen … (2011)

Opioid-induced hyperalgesia (OIH) is defined as a state of nociceptive sensitization caused by exposure to opioids. The condition is characterized by a paradoxical response whereby a patient receiving opioids for the treatment of pain could actually become more sensitive to certain painful stimuli. The type of pain experienced might be the same as the underlying pain or might be different from the original underlying pain. OIH appears to be a distinct, definable, and characteristic phenomenon that could explain loss of opioid efficacy in some patients. Findings of the clinical prevalence of OIH are not available. However, several observational, cross-sectional, and prospective controlled trials have examined the expression and potential clinical significance of OIH in humans. Most studies have been conducted using several distinct cohorts and methodologies utilizing former opioid addicts on methadone maintenance therapy, perioperative exposure to opioids in patients undergoing surgery, and healthy human volunteers after acute opioid exposure using human experimental pain testing. The precise molecular mechanism of OIH, while not yet understood, varies substantially in the basic science literature, as well as clinical medicine. It is generally thought to result from neuroplastic changes in the peripheral and central nervous system (CNS) that lead to sensitization of pronociceptive pathways. While there are many proposed mechanisms for OIH, 5 mechanisms involving the central glutaminergic system, spinal dynorphins, descending facilitation, genetic mechanisms, and decreased reuptake and enhanced nociceptive response have been described as the important mechanisms. Of these, the central glutaminergic system is considered the most common possibility. Another is the hypothesis that N-methyl-D-aspartate (NMDA) receptors in OIH include activation, inhibition of the glutamate transporter system, facilitation of calcium regulated intracellular protein kinase C, and cross talk of neural mechanisms of pain and tolerance. Clinicians should suspect OIH when opioid treatment's effect seems to wane in the absence of disease progression, particularly if found in the context of unexplained pain reports or diffuse allodynia unassociated with the original pain, and increased levels of pain with increasing dosages. The treatment involves reducing the opioid dosage, tapering them off, or supplementation with NMDA receptor modulators. This comprehensive review addresses terminology and definition, prevalence, the evidence for mechanism and physiology with analysis of various factors leading to OIH, and effective strategies for preventing, reversing, or managing OIH.

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Postoperative nausea and vomiting. Its etiology, treatment, and prevention.

M Watcha, Aaron P White (1992)

In a recent editorial, Kapur described perioperative nausea and vomiting as "the big 'little problem' following ambulatory surgery."257 Although the actual morbidity associated with nausea is relatively low in health outpatients, it should not be considered an unavoidable part of the perioperative experience. The availability of an emesis basin for every patient in the postanesthesia recovery unit is a reflection of the limited success with the available therapeutic techniques.257 There had been little change in the incidence of postoperative emesis since the introduction of halothane into clinical practice in 1956. However, newer anesthetic drugs (e.g. propofol) appear to have contributed to a recent decline in the incidence of emesis. Factors associated with an increased risk of postoperative emesis include age, gender (menses), obesity, previous history of motion sickness or postoperative vomiting, anxiety, gastroparesis, and type and duration of the surgical procedure (e.g., laparoscopy, strabismus, middle ear procedures). Anesthesiologists have little, if any, control over these surgical factors. However, they do have control over many other factors that influence postoperative emesis (e.g., preanesthetic medication, anesthetic drugs and techniques, and postoperative pain management). Although routine antiemetic prophylaxis is clearly unjustified, patients at high risk for postoperative emesis should receive special considerations with respect to the prophylactic use of antiemetic drugs. Minimally effective doses of antiemetic drugs can be administered to reduce the incidence of sedation and other deleterious side effects. Potent nonopioid analgesics (e.g., ketorolac) can be used to control pain while avoiding some of the opioid-related side effects. Gentle handling in the immediate postoperative period is also essential. If emesis does occur, aggressive intravenous hydration and pain management are important components of the therapeutic regimen, along with antiemetic drugs. If one antiemetic does not appear to be effective, another drug with a different site of action should be considered. With the availability of new antiserotonin drugs, the incidence of recurrent (intractable) emesis could be further decreased. Research into the mechanisms of this common postoperative complication may help in improving the management of emetic sequelae in the future. As suggested in a recent editorial, improvement in antiemetic therapy could have a major impact for surgical patients, particularly after ambulatory surgery. Patients as well as those involved in their postoperative care look forward to a time when the routine offering of an emesis basin after surgery becomes a historical practice.

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Author and article information

Contributors

Wonjung Hwang: amoeba79@catholic.ac.kr

Jaemin Lee: jmlee@catholic.ac.kr

Jihyun Park: leopard85@naver.com

Jin Joo: jiyo1004@catholic.ac.kr

Journal

Journal ID (nlm-ta): BMC Anesthesiol

Journal ID (iso-abbrev): BMC Anesthesiol

Title: BMC Anesthesiology

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2253

Publication date (Electronic): 24 February 2015

Publication date PMC-release: 24 February 2015

Publication date Collection: 2015

Volume: 15

Electronic Location Identifier: 21

Affiliations

Department of Anesthesiology and Pain Medicine, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, 222 Banpodaero, Seocho-gu, Seoul 137-701 South Korea

Article

Publisher ID: 4

DOI: 10.1186/s12871-015-0004-1

PMC ID: 4352285

PubMed ID: 25750586

SO-VID: 06bdcab3-94b1-4df1-93ab-9f4e47b20be9

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 29 August 2014

Date accepted : 18 February 2015

Custom metadata

ScienceOpen disciplines: Anesthesiology & Pain management

Keywords: dexmedetomidine,remifentanil,total intravenous anesthesia,postoperative pain

Data availability:

ScienceOpen disciplines: Anesthesiology & Pain management

Keywords: dexmedetomidine, remifentanil, total intravenous anesthesia, postoperative pain

Dexmedetomidine versus remifentanil in postoperative pain control after spinal surgery: a randomized controlled study

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Abstract

Background

Methods

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Conclusions

Trial registration

Related collections

Irish Journal of Paramedicine

Most cited references 25

The effects of increasing plasma concentrations of dexmedetomidine in humans.

A comprehensive review of opioid-induced hyperalgesia.

Postoperative nausea and vomiting. Its etiology, treatment, and prevention.

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