Dominique Fletcher

Are psychological predictors of chronic postsurgical pain dependent on the surgical model? A comparison of total knee arthroplasty and breast surgery for cancer.

UNLABELLED Anxiety, depression, and catastrophizing are generally considered to be predictive of chronic postoperative pain, but this may not be the case after all types of surgery, raising the possibility that the results depend on the surgical model. We assessed the predictive value of these factors for chronic postsurgical pain in 2 different surgical models: total knee arthroplasty for osteoarthritis (89 patients, 65% women, age = 69 ± 9 years, baseline pain intensity = 4.7 ± 2.1) and breast surgery for cancer (100 patients, 100% women, age = 55 ± 12 years, no preoperative pain). Data were collected before surgery, then 2 days and 3 months after surgery. Anxiety, depression, and catastrophizing were measured with the Spielberger State-Trait Anxiety Inventory, Beck Depression Inventory, and Pain Catastrophizing Scale, respectively. Pain was assessed with the Brief Pain Inventory. Neuropathic pain was detected with the DN4 questionnaire. Multivariate logistic regression analyses for the total knee arthroplasty and breast surgery models considered together indicated that the presence of clinically meaningful chronic pain at 3 months (pain intensity ≥3/10) was predicted independently by age (P = .04), pain intensity on day 2 (P = .009), and state anxiety (P = .001). Linear regression models also showed that pain magnification, one of the dimensions of catastrophizing, independently predicted chronic pain intensity (P = .04). These results were not affected by the surgical model or by the neuropathic characteristics of the pain. Thus, state anxiety and pain magnification seem to constitute psychological risk factors for chronic postsurgical pain relevant in all surgical models. PERSPECTIVE This prospective study performed in patients with total knee arthroplasty or breast surgery for cancer shows that state anxiety, amplification of pain, and acute postoperative pain independently predict postsurgical pain at 3 months and that this does not depend on the surgical model.

Lack of Impact of Intravenous Lidocaine on Analgesia, Functional Recovery, and Nociceptive Pain Threshold after Total Hip Arthroplasty

Background:The analgesic effect of perioperative low doses of intravenous lidocaine has been demonstrated after abdominal surgery. This study aimed to evaluate whether a continuous intravenous low-dose lidocaine infusion reduced postoperative pain and modified nociceptive pain threshold after total hip arthroplasty. Methods:Sixty patients participated in this randomized double-blinded study. Patients received lidocaine 1% (lidocaine group) with a 1.5 mg/kg−1 intravenous bolus in 10 min followed by a 1.5 mg · kg−1 · h−1 intravenous infusion or saline (control group). These regimens were started 30 min before surgical incision and stopped 1h after skin closure. Lidocaine blood concentrations were measured at the end of administration. In both groups, postoperative analgesia was provided exclusively by patient-controlled intravenous morphine. Pain scores, morphine consumption, and operative hip flexion were recorded over 48 h. In addition, pressure pain thresholds and the extent of hyperalgesia around surgical incision were systematically measured at 24 and 48 h. Results:In comparison with the placebo, lidocaine did not induce any opioid-sparing effect during the first 24 h (median [25–75% interquartile range]; 17 mg [9–28] vs. 15 mg [8–23]; P = 0.54). There was no significant difference regarding the effects of lidocaine and placebo on pain score, pressure pain thresholds, extent in the area of hyperalgesia, and maximal degree of active hip flexion tolerated. Mean plasma lidocaine concentration was 2.1 ± 0.4 &mgr;g/ml. Conclusion:Low dose perioperative intravenous lidocaine after total hip arthroplasty offers no beneficial effect on postoperative analgesia and does not modify pressure and tactile pain thresholds.

Influence of timing on the analgesic effect of intravenous ketorolac after orthopedic surgery

&NA; This study evaluated the pre‐emptive analgesic effect of intravenous (i.v.) ketorolac (KET) for total hip replacement (THR). Sixty patients who underwent surgery for THR under general anesthesia were randomly allocated to 3 groups. Two i.v. injections were administered: one before induction and one after surgery. The patients were studied prospectively in a double‐blind manner. The control group (CONT; n = 20) received 2 ml of normal saline (NS) for both injections. The pre‐operative KET group (PRE; n = 20) received 60 mg of KET and then 2 ml of NS. The postoperative KET group (POST; n = 20) received 2 ml of NS and then 60 mg Of KET. General anesthesia was standardized with a intra‐operative cumulated dose of fentanyl limited to 4&mgr;g/kg. In the recovery room (RR), pain was controlled with an i.v. titration of morphine; thereafter, on the surgical ward, patients used a patient‐controlled analgesia (PCA) pump (Abbott). Pain was evaluated with a visual analogue scale (VAS) at rest and movement in the RR, then every hour for 6 h and every 6 h for 2 days. The side effects monitored were: sedation, respiratory depression, nausea, perioperative bleeding. The patients and surgery were similar for the 3 groups. Upon arrival in the RR, VAS scores taken at rest and at movement were lower for the PRE group than for the CONT and POST groups. Otherwise, VAS scores were similar in all 3 groups. The cumulative dose of morphine in the PRE group was lower than that for the CONT and POST groups from 0 to 6 h. However, the hourly consumption of morphine after titration was similar in all 3 groups for the entire study. Four patients, 2 in the PRE and 2 in the POST group had abnormal bleeding. In this study 60 mg of pre‐operative KET had greater analgesic effect than the same dose administered at skin closure. This beneficial effect was important in the immediate postoperative period but was not sustained with time.

Antiinflammatory effect of peripheral nerve blocks after knee surgery: clinical and biologic evaluation.

Background:Nerve blocks provide analgesia after surgery. The authors tested whether nerve blocks have antiinflammatory effects. Methods:Patients had combined sciatic (single-shot) and continuous femoral block (48 h) (block group) or morphine patient-controlled analgesia after total knee arthroplasty. Pain at rest and upon movement was monitored at 1 (D1), 4 (D4), and 7 days (D7) and 1 (M1) and 3 months (M3) after surgery. Knee inflammation was evaluated (skin temperature, knee circumference) before surgery and at D1, D4, D7, M1, and M3. Plasma cytokine concentrations (interleukin [IL]-6, IL-1&bgr;, tumor necrosis factor [TNF], IL-10, soluble receptor 1 of TNF [sTNF-R1]) were measured before surgery and at 4 h, D1, D4, and D7 after surgery. Capsule and synovial membrane cytokines were measured (IL-6, TNF, IL-1, IL-10). Knee flexion was evaluated before surgery and at D1, D4, D7, M1, and M3. Morphine use and recovery time to autonomy were monitored. Results:Pain at rest and upon movement was lower in the block group than in patient-controlled analgesia patients between D1 and D7 (analysis of variance, P < 0.005). Knee flexion was improved in the block group for D1 to M1 (analysis of variance, P < 0.0001). Block group patients recovered nonassisted mobilization (t test, P = 0.04) and toilet use (t test, P = 0.03) more rapidly. Knee circumference and skin temperature were lower in the block group between D1 and D7 (analysis of variance, P < 0.05). Synovial membrane IL-1 (P < 0.05) and IL-10 (P < 0.01) increased, and plasma IL-6 and sTNF-R1 peaked at 24 h, with no difference between groups. Conclusion:Nerve blocks inhibited clinical inflammation after total knee arthroplasty, with no change in tissue and plasma cytokine concentrations.

Perioperative pregabalin administration does not prevent chronic postoperative pain: systematic review with a meta-analysis of randomized trials

Abstract The efficacy of perioperative pregabalin treatment for preventing chronic pain remains a matter of debate. We searched the MEDLINE, EMBASE, LILACS, Cochrane, and Clinical Trial Register databases, and other sources, for randomized controlled trials comparing the effects of pregabalin and placebo. The primary outcome was the incidence of chronic postsurgical pain (CPSP) at 3 months. The secondary endpoints were CPSP at 3, 6, and 12 months and the incidence of chronic postsurgical neuropathic pain at the same time points. A random-effect meta-analysis was performed on the combined data. Evidence quality was rated by the GRADE method. We included 18 studies (2485 patients) in the meta-analysis. Overall, 60% of the trials reporting the primary outcome at 3 months were unpublished; the unpublished trials corresponded to 1492/1884 (79%) of the patients included in these studies. No difference in CPSP incidence between pregabalin and placebo was found at any time point; the risk ratio was 0.87 (0.66, 1.14), I2 = 57% at 3 months. The evidence was considered to be of moderate quality. Subgroup analysis by publication status, daily dose, type of administration, and type of surgery did not highlight any differences between subgroups. Insufficient data concerning the incidence of chronic postsurgical neuropathic pain were available for any firm recommendation to be made. Pooled data from published and unpublished studies provide no support for the efficacy of pregabalin for preventing CPSP.

A targeted remifentanil administration protocol based on the analgesia nociception index during vascular surgery

BACKGROUND The intraoperative modulation of opioids continues to be based on clinical signs. This may result in adverse events such as sympathetic reactivity or opioid-induced hyperalgesia. Recently, the Analgesia/Nociception Index (ANI), a non-invasive 0-100 index derived from heart rate variability analysis, has been proposed for nociception assessment. However, the ability of the ANI to adequately guide intraoperative opioid administration has never been demonstrated. We designed a prospective study to evaluate the ability of the ANI to guide remifentanil administration in vascular surgery. METHODS One hundred and eighty adults presenting for elective surgery were included. All received total intravenous anaesthesia with propofol adjusted to entropy and remifentanil adjusted to the ANI. The primary endpoint was the number of patients without any episode of reactivity defined as a 20% increase in heart rate or arterial pressure or the occurrence of movement. Secondary endpoints included opioid use and maximal pain rate in the first postoperative day. RESULTS Anaesthesia was achieved without any episode of reactivity in 160 (89%) patients. Twenty-five episodes of reactivity occurred in 20 (11%) patients. The median remifentanil dose was 0.042 [0.040-0.044]μg.kg-1.min-1. At 24hours, the maximal NRS pain score was 2 [2,3]. One hundred and fifty-five patients (86%) did not receive any postoperative opioids, whereas 25 (14%) received a median dose of 5[5-10] mg of oxycodone. CONCLUSION This prospective study demonstrated that the ANI can be used to adequately guide intraoperative remifentanil administration during vascular surgery. Such guidance resulted in low remifentanil consumption, low postoperative pain rates and low opioid rescue analgesia.

Additivity of bupivacaine and morphine for peripheral analgesia in rats.

Abstract— Infiltration of the surgical wound is a classical technique for post‐operative analgesia. Recent studies have suggested that local anaesthetic may be combined with other drugs such as opioids. This study has evaluated, in rat, the infiltration with morphine, bupivacaine and their combination. In all groups, the two hind paws were injected with carrageenin. The left hind paw was used as control. The vocalisation threshold to paw pressure (VTPP) of both hind paws was evaluated 2 h after induction of carrageenin inflammation (baseline value), then every lOmin until the return to baseline value after injection of analgesic drugs. The development of oedema was evaluated in both hind paws by measurement of paw circumference (PC) before, then after, carrageenin injection. All analgesic drugs were injected in the right inflamed paw diluted in 0.2 mL of normal saline. The analgesic effect of bupivacaine (0.1, 0.25 and 0.5%), morphine (25, 50 and 100 μg) and their combination (bupivacaine 0.1%/morphine 20 μg, bupivacaine 0.2%/morphine 40 μg and bupivacaine 0.4 %/morphine 80 μg) was tested. The effect of naloxone on morphine induced analgesia was tested. The interaction between bupivacaine and morphine was evaluated with an isobolographic analysis. Bupivacaine produced a dose‐dependent antinociceptive effect. Morphine infiltration produced a peripheral, dose‐dependent analgesic effect antagonised by naloxone. This analgesic effect of morphine was associated with an anti‐inflammatory effect. The isobolographic analysis revealed only additivity between bupivacaine and morphine. The infiltration with morphine offers a peripheral analgesic effect which is additive with the effect of bupivacaine. An anti‐inflammatory effect of morphine participates in this peripheral analgesic effect.

Eye protection in anaesthesia and intensive care

French Society for Anaesthesia and Intensive Care (SFAR), French Ophthalmology Society (SFO), French-speaking Intensive Care Society (SRLF), Hawa Keita *, Jean-Michel Devys , Jacques Ripart , Marie Frost , Isabelle Cochereau , Frédérique Boutin , Claude Guérin , Dominique Fletcher , Vincent Compère i a Department of anaesthesia, AP–HP, CHU Louis-Mourier, 178, rue des Renouillers, 92700 Colombes, France b Department of anaesthesia and intensive care, fondation Adolphe-Rotschild, 29, rue Manin, 75019 Paris, France c Department of anaesthesia, pain and intensive care, GHU Caremeau, place du Pr-Debré, 30029 Nimes cedex 09, France d Department of anaesthesia, hôpital Michallon, BP 217, 38043 Grenoble cedex 9, France e Fondation Adolphe-Rotschild, 29, rue Manin, 75019 Paris, France f Department of anaesthesia and critical care III, CHU de Bordeaux, groupe hospitalier Pellegrin, place Amélie-Raba-Leon, 33000 Bordeaux, France g Department of intensive care, hôpital de la Croix-Rousse, 103, grande rue de la Croix-Rousse, 69317 Lyon cedex 04, France h Department of anaesthesia and intensive care, hôpital Ambroise-Paré, 9, avenue Charles-de-Gaulle, 92104 Boulogne-Billancourt, France i Department of anaesthesia and intensive Care, CHU de Rouen, 1, rue de Germont, 76031 Rouen, France