BackgroundThe purpose of this systematic review and meta-analysis of randomized controlled trials (RCTs) was to evaluate the effect of combined femoral and sciatic nerve block (SNB) versus femoral and local infiltration anesthesia (LIA) after total knee arthroplasty (TKA).MethodsThe electronic databases PubMed, Embase, Cochrane Library, and Web of Science were searched from their inception to 15 June 2016. Articles comparing combined femoral and SNB versus femoral and LIA for pain control were eligible for this meta-analysis. This systematic review and meta-analysis was performed according to the PRISMA statement criteria. The primary endpoint was the visual analogue scale (VAS) score with rest at 12, 24, and 48 h, which represents the pain control after TKA. Data regarding active knee flexion, length of hospital stay, anesthesia time, and morphine use at 24 and 48 h were also compiled. The complications of postoperative nausea and vomiting (PONV) and fall were also noted to assess the safety of morphine-sparing effects. After testing for publication bias and heterogeneity across studies, the data were aggregated for random-effects modeling when necessary.ResultsSeven clinical trials with 615 patients were included in the meta-analysis. The pooled results indicated that SNB was associated with a lower VAS score at 12 h (MD = −6.96; 95% CI −8.36 to −5.56; P < 0.001) and 48 h (MD = −2.41; 95% CI −3.90 to −0.91; P < 0.001) after TKA. There was no significant difference between the SNB group and the LIA group in terms of the VAS score at 24 h (MD = 0.67; 95% CI −0.31 to 1.66; P = 0.182). The anesthesia time in the LIA group was shorter than in the SNB group, and the difference was statistically significant (MD = 4.31, 95% CI 1.34 to 7.28, P = 0.004). There were no significant differences between the groups in terms of active knee flexion, length of hospital stay, morphine use, PONV, and the occurrence of falls.ConclusionsSNB may provide earlier anesthesia effects than LIA when combined femoral nerve block (FNB); however, there were no differences in morphine use, active knee flexion, and PONV between the groups. The LIA group spent less time under anesthesia, suggesting that LIA may offer a practical and potentially safer alternative to SNB.Electronic supplementary materialThe online version of this article (doi:10.1186/s13018-016-0495-6) contains supplementary material, which is available to authorized users.
Abstract. The pain induced by local acute inflammation results in mild to severe discomfort, in addition to the possibility of physiological dysfunction and psychiatric disorders, such as sleep disorders and depression. However, the pathogenesis of pain is yet to be fully elucidated. In the present study, the effects of bupivacaine were explored in rat models inflammatory pain in order to investigate the anti-pain mechanism of bupivacaine. Complete Freund's adjuvant (CFA) was injected into the right rear foot of the rats to establish a model of transient inflammation-induced pain. Rats were randomly divided into four groups (n=8): CFA, CFA plus bupivacaine, CFA plus saline and untreated. The mechanical withdrawal threshold (MWT) of the rats was detected prior to and following CFA injection, and the results demonstrated that the MWT in the right rear foot significantly decreased from the 1st day of CFA injection (P<0.01; n=8), as compared with the untreated controls. Bupivacaine treatment was demonstrated to significantly increase the MWT of rats treated with CFA stimulation, as compared with the CFA group (P<0.01). Rotarod testing was performed to assess the motor activity of the rats, and the results demonstrated no significant differences among the four groups (P>0.05). Furthermore, the respective body weights of the rats were determined every two days before and after CFA injection, and no significant differences were detected among the four groups (P>0.05). Western blot analysis was performed to analyze expression levels of IκB and nuclear factor (NF)-κB, and the results demonstrated that bupivacaine increased the expression of IκB and decreased the expression levels of NF-κB, as compared with the rats with CFA-induced inflammatory responses, suggesting that bupivacaine inhibited NF-κB activation in the dorsal horn of the lumbar spinal cord of the model rats. Furthermore, reverse transcription-quantitative polymerase chain reaction analysis was performed to analyze the expression levels of inflammatory cytokines, which demonstrated that bupivacaine significantly inhibited the expression of TNF-α, IL-1β and IL-6, as compared with the untreated group (P<0.01). Moreover, bupivacaine treatment significantly decreased the expression of spinal microglial marker OX42 and astrocyte marker-glial fibrillary acidic protein, as compared with the rats in the CFA group (P<0.01). The present findings demonstrated that treatment with bupivacaine significantly decreased the activation of microglia and astrocytes in rat models of inflammatory pain. Therefore, the present results may provide clarification of the pathogenesis and mechanism of inflammation-induced pain and may provide novel therapeutic strategies for the clinical treatment of pain.
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