P. Lavandhomme

Pain after knee arthroplasty: an unresolved issue

AbstractPurpose Despite the recent advances in the understanding of pain mechanisms and the introduction of new drugs and new techniques in the postoperative management, pain after total knee arthroplasty (TKA) is still an unresolved issue. It affects the quality of life and rehabilitation of an important percentage of patients undergoing TKA. The aim of this narrative review was to give an overview on pain mechanisms and multimodal pain management.MethodsA review of all peer-reviewed articles on pain after knee arthroplasty was performed by two reviewers. Recent articles on incisional pain mechanisms were included because of their importance in the understanding of postsurgical pain. Search was performed in Pubmed, Cochrane and Google Scholar data bases.ResultsPostsurgical pain mechanisms are based on both local and systemic inflammatory reactions. Peri-operative pain management starts with the anaesthetic technique and resides on a multimodal analgesia regimen. New concepts, drugs and techniques have shown their efficacy in reducing the severity of acute postoperative pain and the risk of developing chronic pain after TKA.ConclusionThis narrative review offers a clear overview of pain mechanism after knee arthroplasty and an understanding on how multimodal pain management can reduce the intensity and duration of pain after knee arthroplasty.Level of evidenceIV.

Use of dexmedetomidine for pain control.

For many years, clonidine, an α2-adrenergic receptor (α2-AR) agonist, has been widely used as an analgesic adjuvant in perioperative conditions and pain therapy. Dexmedetomidine (DMET) is currently the most potent α2-AR agonist available and was first approved as a sedative agent for use in the intensive care unit. However, DMET has recently been investigated for its analgesic effects and has the potential to become an alternative to clonidine.

Does the perioperative analgesic/anesthetic regimen influence the prevalence of long-term chronic pain after mastectomy?

STUDY OBJECTIVE To investigate if the anesthetic/analgesic regimen is associated with the risk of reporting long-term chronic postmastectomy pain (CPMP). DESIGN Cross-sectional survey SETTING Academic hospital PATIENTS A total of 267 women having undergone mastectomy with axillary lymph node dissection between 2003 and 2008 INTERVENTIONS: All patients were contacted between October and December 2012, with a questionnaire asking for persistent pain after surgery and its characteristics. MEASUREMENTS Besides demographical data, tumor characteristics, and adjuvant treatment, we recorded type and doses of intraoperative anesthetics/analgesics (sufentanil, ketamine, clonidine, nonsteroidal anti-inflammatory drugs, MgSO4, propofol, or halogenated agents). RESULTS Of the 128 patients returning analyzable questionnaires, 43.8% reported chronic pain (48.2% with neuropathic characteristics). Multivariate logistic/linear regression model showed 4 factors independently associated with persistent pain: recall of preoperative pain (odds ratio [OR], 1.27; 95% confidence interval [CI], 1.09-1.48), chemotherapy (OR, 1.32; 95% CI, 1.13-1.55), need for strong opioids in postanesthesia care unit (OR, 1.30; 95% CI, 1.11-1.53), and halogenated agent anesthesia (OR, 0.81; 95% CI, 0.70-0.95). CONCLUSION In conclusion, our study confirms the high prevalence of CPMP, 4 to 9 years after surgery. Recall of preoperative pain, chemotherapy, and need for strong opioids in the postanesthesia care unit were all associated with the presence of chronic pain. Of the intraoperative analgesics/anesthetics studied, only use of halogenated agents was associated with a lower prevalence of CPMP.

2p24.1p23.2 deletion and delayed recovery after a general anesthesia for gastrointestinal endoscopic procedure

Interstitial 2p deletions are very rare and may include proopiomelanocortin (POMC) gene (2p23.3). Our 10‐year‐old patient, known to carry this genetic anomaly, underwent an endoscopic interventional procedure under general anesthesia. After a sevoflurane induction, alfentanil (8.5 μg·kg−1) was given. The procedure lasted 22 min. There was an unexpected delayed recovery likely reflecting an unexpected delayed recovery likely due to opioid hypersensitivity. The deletion of POMC may cause a deficit in endorphin and may lead to an up‐regulation of opioid receptors. Exogenous opioids should be used with particular caution in patients suffering a deficit of POMC.

Analgesic and hyperalgesic effect of single intrathecal dose of morphine under normal and neuropathic conditions: 14AP2-10

plasma O2 . production was the highest at the just reperfusion and lasted at least 1 week. Mechanical and cold allodynia were present in both hindpaws as early as 4 hr after reperfusion, and lasted at least 4 weeks. Pain behavior was significantly attenuated in G1, G2 and G3 compared with control. In G3, pain behavior was less attenuated than G1 and G2. Microscopic findings showed less inflammatory reaction in the G1 and G2. Conclusion(s): This study suggests that the O2 . is partly responsible for development of the CRPS-I. Even though O2 . inhibition is less effective after CRPS-I has been already developed, O2 . inhibition is still effective for reduce CRPS-I pain. References: 1 White FA, Bhangoo SK, Miller RJ. Nat Rev Drug Discov 2005; 4: 834–44. 2 Kim HK, Park SK, Zhou JL, et al. Pain 2004; 111: 116–24. 3 Coderre TJ, Xanthos DN, Francis L, et al. Pain 2004; 112: 94–105.

Local effect of bupivacaine and amitriptyline infiltration on wound NGF expression after plantar incision in rats: A-739

life in the spinal fluid phase2. We have collected respiratory depression data from 661 patients receiving intrathecal diamorphine up to 1mg for nonobstetric surgery. Materials and Methods: Over a one-year period, details of naloxone administration were collected from 1732 patients undergoing major non-obstetric surgery, of which 77% was major orthopaedic surgery. Patients received either intraoperative intrathecal diamorphine plus postoperative intravenous patient-controlled morphine analgesia (ITD PCA) or PCA alone (PCA group). Intrathecal diamorphine dosage varied from 0.1 mg to 1 mg, although the majority of patients received either 0.5 mg (ITD 0.5 PCA) or 1 mg (ITD1.0 PCA). The relative risk (RR) for receiving naloxone was calculated for each group, using the PCA group as a control. Where available, relative risk stratified by age above and below 80 years was calculated. Results and Discussions: Data are shown in the table.

Effect of abdominal surgery with or without vagotomy on tumor cells proliferation in rat: A-480

dependently from all 2-AR subtypes. At a concentration of 13 mM this displacement was almost complete. In 2A-AR-KO-mice a reduced signal intensity of specifically bound [125J]-PIC – according to the dominant role of this 2-AR subtype – was seen but the displacement by remifentanil was comparable to 2Band 2C-KO mice. Conclusion: Our findings suggest that remifentanil but not sufentanil interact with all subtypes of 2-AR in the central nervous system. This may indicate that clinical effects of remifentanil could be partially mediated by 2-AR. References: 1 Krause T, Tonner PH, Scholz J, et al. Anesthesiology 1999; V91, A388. 2 Takada K, et al. Anesthesiology 2002; 96: 1420–1426.