Persistent pain following knee arthroplasty.

BACKGROUND AND OBJECTIVE: The prevalence of persistent pain after orthopaedic surgery has been the subject of only few studies and the risk factors for persistent pain have been evaluated even more rarely. The purpose of the present study was to evaluate the degree and the risk factors of persistent pain after knee arthroplasty. METHODS: The prevalence of persistent postoperative pain after knee replacement was evaluated with a questionnaire in a large, register-based cross-sectional prevalence study. The main hypothesis was that the type of operation (primary, bilateral, revision) would influence the prevalence of persistent postoperative pain. Logistic regression analysis was performed to test the hypothesis and to find other possible risk factors for the development of persistent pain. RESULTS: The total number of patients was 855. The operation was a primary arthroplasty in 648 patients (75.7%), a bilateral arthroplasty in 137 patients (21.1%) and a revision arthroplasty in 70 patients (8.2%). The response rate was 65.7%. The type of operation was not associated with the prevalence of persistent pain, but the degree of early postoperative pain was the strongest risk factor. If the degree of pain during the first postoperative week was from moderate to intolerable, the risk for the development of persistent pain was three to 10 times higher compared with patients complaining of mild pain during the same period. Other risk factors were the long duration of preoperative pain and female sex. CONCLUSION: Intensity of early postoperative pain and delayed surgery increase the risk of the persistent pain after knee arthroplasty.

Bile high-mobility group box 1 contributes to gut barrier dysfunction in experimental endotoxemia.

Lipopolysaccharide (LPS) is an important factor in sepsis. LPS given by intraperitoneal injection induces intestinal hyperpermeability and bacterial translocation in animals and stimulates hepatic Kupffer cells to release TNF-alpha into the bile. This study aims to test the hypothesis that in response to LPS stimulation, hepatic Kupffer cells and extrahepatic macrophages release a large amount of the inflammatory cytokine high-mobility group box 1 (HMGB1) into the bile and that bile containing HMGB1 contributes to gut barrier dysfunction in experimental endotoxemia. To test this, rat common bile ducts were catheterized and bile flow rate was monitored before and during the LPS administration. Eight hours after LPS challenge, anti-HMGB1 neutralizing antibody or nonimmune (sham) IgG was injected into the duodenal lumen of endotoxemic rats; normal mice were also gavaged with normal or endotoxemic rat bile (bile collected from LPS-treated rats). We found that after LPS challenge, the bile flow rate in rats was significantly decreased at the 4- to 12-h time points, TNF-alpha concentration in the bile was markedly elevated at the 3- to 4-h time points, and bile HMGB1 levels were significantly increased at the 8- to 12-h time points. Duodenal injection with anti-HMGB1 antibody reversed LPS-induced gut barrier dysfunction in rats. In addition, feeding endotoxemic rat bile to normal mice significantly increased both mucosal permeability and bacterial translocation. The increase in permeability and bacterial translocation was reversible following removal of HMGB1 from the endotoxemic rat bile. These findings document that bile HMGB1 mediates gut barrier dysfunction in experimental endotoxemia.

Potentially detrimental effects of N-acetylcysteine on renal function in knee arthroplasty.

Ischaemia/reperfusion induces systemic inflammation and oxidative stress and thereby remote organ injury in the kidney. In a double-blind, placebo-controlled clinical trial of 30 patients undergoing knee arthroplasty with tourniquet, this study evaluated the effect of N-acetylcysteine (NAC) infusion on renal function by measuring urine alpha-1-microglobulin, N-acetyl-beta-D-glucosaminidase (NAG), glutathione-S-transferase-alpha and -phi and serum creatinine and cystatin C concentrations up to 24 h post-operatively. Compared to the baseline, urine alpha-1-microglobulin/creatinine increased in both groups and was higher in the NAC group than in the placebo group at tourniquet deflation and at 3 h thereafter. Urine NAG/creatinine increased at deflation and at 3 h thereafter in the NAC group and the ratio was higher than in the placebo group. The two sensitive indicators of proximal tubular damage and function used in the present study suggest that use of NAC in clinical setting of ischaemia/reperfusion injury may increase the risk of remote kidney injury.

The effect of parecoxib on kidney function at laparoscopic hysterectomy.

Conventional nonsteroidal anti-inflammatory drugs (NSAIDs) have a well-documented nephrotoxic action. Still, there are only few studies that have investigated the nephrotoxicity of cyclo-oxycenase-2-inhibitors during the perioperative period. Thirty patients scheduled for elective laparoscopic hysterectomy were enrolled in this prospective, randomized double-blind study. Patients were randomized into two groups: a saline-treated control group (placebo) and 80 mg parecoxib-treated group (parecoxib). The samples for the analyses of serum and urine were collected at the induction of anesthesia, two hours thereafter, two hours from the end of anesthesia, and on the first postoperative day (POD). S-crea, S-urea, S-cystatin C, S-Na, S-K, U-1mikroglobulin/U-crea, U-GST/U-crea, and U-GST/U-crea were analyzed from the samples. Urine output was measured every hour for the first five hours, and total amount of urine was measured until the first postoperative day. There were no clinical and few statistical significant differences between the two groups in the renal measurements during the study period. The urinary output was also similar in the two groups. A single dose of 80 mg of parecoxib was well tolerated by the kidneys in the short-term perioperative use in patients undergoing laparoscopic hysterectomy with ASA physiological status I-II and age under 60 years.

Deep sedation with dexmedetomidine in a porcine model does not compromise the viability of free microvascular flap as depicted by microdialysis and tissue oxygen tension.

BACKGROUND: Deep sedation is often necessary after major reconstructive plastic surgery in the face and neck regions to prevent sudden spontaneous movements capable of inflicting mechanical injury to the transplanted musculocutaneous flap(s). An adequate positioning may help to optimize oxygenation and perfusion of the transplanted tissues. We hypothesized that dexmedetomidine, a central alpha2-agonist and otherwise potentially ideal postoperative sedative drug, may induce vasoconstriction in denervated flaps, and thus increase the risk of tissue deterioration. METHODS: Two symmetrical myocutaneous flaps were raised on each side of the upper abdomen in 12 anesthetized pigs. The sympathetic nerve fibers were stripped from the arteries in one of the flaps (denervated flap), while nerve fibers were kept untouched in the other (innervated flap). After simulation of ischemia and reperfusion periods, the animals were randomized to deep postoperative sedation with either propofol (n = 6) or dexmedetomidine (n = 6). Flap tissue metabolism was monitored by microdialysis and tissue-oxygen partial pressure. Glucose, lactate, and pyruvate concentrations were analyzed from the dialysate every 30 min for 4 h. RESULTS: Mean arterial blood pressure was higher in the dexmedetomidine group (P = 0.036). Flap tissue metabolism remained stable throughout the experiment as measured by lactate-pyruvate and lactate-glucose ratios (median ranges 14.3-24.5 for lactate-pyruvate and 0.3-0.6 for lactate-glucose) and by tissue-oxygen partial pressure, and no differences were found between groups. CONCLUSIONS: Our data suggest that dexmedetomidine, even if used for deep sedation, does not have deleterious effects on local perfusion or tissue metabolism in denervated musculocutaneous flaps.