2022
DOI: 10.1016/j.jclinane.2022.110652
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Perioperative ketamine for postoperative pain management in patients with preoperative opioid intake: A systematic review and meta-analysis

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Cited by 36 publications
(29 citation statements)
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“…The addition of Ketamine significantly decreased the pain intensity and consumption of opioids. This reduction in the patients' postoperative pain score in the ketamine group might be on account of the analgesic properties of this drug, as well as strengthening the opioid effect, which is applied via cholinergic, and monoaminergic mechanisms (12). On the other hand, ketamine prevents intense drug tolerance and hyperalgesia, which decreases morphine consumption.…”
Section: Discussionmentioning
confidence: 95%
“…The addition of Ketamine significantly decreased the pain intensity and consumption of opioids. This reduction in the patients' postoperative pain score in the ketamine group might be on account of the analgesic properties of this drug, as well as strengthening the opioid effect, which is applied via cholinergic, and monoaminergic mechanisms (12). On the other hand, ketamine prevents intense drug tolerance and hyperalgesia, which decreases morphine consumption.…”
Section: Discussionmentioning
confidence: 95%
“…ketamine, which disrupts the NMDA-MOR interaction associated with OIH, as discussed in the next section, has been suggested as potentially useful in the perioperative period in these patients [ 59 , 60 ]. A recent meta-analysis of nine RCTs in adult opioid users, with at least two weeks preoperative opioid intake, undergoing surgery showed that perioperative ketamine reduced cumulative mean opioid consumption by 97.3 mg (95%CI: −164.8 to −29.7) after 24 h and 186.4 mg (95%CI: −347.6 to −25.2) after 48 h [ 61 ] ( Table 3 ).…”
Section: Resultsmentioning
confidence: 99%
“…Indeed, the interaction between MOR and the NMDA receptor has been documented before, at the PAG level, but presented as a mechanism to explain opioid tolerance [ 112 ]; however, since the effect of the opioid is to promote pain signaling through increased neuronal activity, via NMDA activation through the calmodulin-dependent protein kinase (CAMKII) pathway [ 102 , 112 ], the resulting hyperalgesia in this case is opioid-induced, and not due to lack of opioid receptor stimulation, constituting a phenomenon of OIH, by definition. Additionally, individuals that show clinical OIH may have been prone to enhanced manifestation of this interaction because of previous opioid exposure modifying the MOR-isoform profile itself [ 11 , 61 ]. Additionally, Zhang and collaborators contributed to the consideration of genetic variability as a determinant of the individual-specific sum of impact from the mentioned molecular signaling pathways, and therefore a determinant for opioid-response and observable clinical variability, as the team demonstrated OPRM1 gene polymorphisms influenced individual women’s response to fentanyl analgesia after lower segment caesarean section surgeries [ 113 ].…”
Section: Resultsmentioning
confidence: 99%
“…They do note that it may increase the psychotomimetic adverse event rate. Another meta-analysis looked at the effect of ketamine in the treatment of postoperative pain in patients who use opioids [ 31 ]. This meta-analysis looked at nine studies that included a total of 802 patients with at least two weeks of opioid use.…”
Section: Introductionmentioning
confidence: 99%
“…This meta-analysis looked at nine studies that included a total of 802 patients with at least two weeks of opioid use. The authors found a clinically relevant opioid-sparing effect without an increased risk of postoperative sedation [ 31 ]. This shows that ketamine can be useful in the setting of pain control but with close monitoring.…”
Section: Introductionmentioning
confidence: 99%