METHODS: Patients were randomly assigned to receive saline (n = 38) or a modified full-dose regimen of aprotinin (n = 37) IV during OPCAB surgery. Blood sampled perioperatively from the coronary sinus, skin wounds, and systemic circulation was analyzed to test coagulation and platelet function. Major adverse cardiovascular events were monitored by obtaining troponin I at 24 h (myocardial infarction), predischarge computed tomography angiography (vein graft thrombosis), and by clinical examination for stroke.

RESULTS: Coronary sinus blood obtained immediately after OPCAB surgery showed significantly less activation in the aprotinin group, as judged by reduced formation of platelet-leukocyte conjugates (P < 0.02) and platelet-derived microparticles (P < 0.05). The aprotinin group showed inhibition of platelet aggregation induced by thrombin (P = 0.007) but not adenosine diphosphate. Thrombin generation, defined by F1.2 levels, was significantly reduced by aprotinin in the coronary sinus but not in skin wound incisions. Major adverse cardiovascular events were significantly reduced in aprotinin-treated patients (5.4% vs 29.7%, P < 0.05). Aprotinin also demonstrated antifibrinolytic properties through diminished red blood cell transfusion (P < 0.04) and reduced blood loss postoperatively (603 ± 330 vs 810 ± 415 mL, P < 0.004).

CONCLUSION: This study demonstrates that aprotinin protects patients undergoing OPCAB surgery from a hypercoagulable state by diminishing thrombin-induced platelet activation and thrombin generation within saphenous vein grafts, while maintaining systemic hemostatic and antifibrinolytic benefits. These results support further investigation of aprotinin and other PAR-1 antagonists in OPCAB surgery.

METHODS: After surgical instrumentation, we divided male Sprague-Dawley rats into 3 sets. The first set was divided into groups, which received methadone (0.03–3 mg/kg), morphine (0.03–3 mg/kg), or water (placebo) 30 min before ischemia. Some animals of the first set also received the -opioid antagonist naltrindole (5 mg/kg) before methadone (0.3 mg/kg), morphine (0.3 mg/kg), or placebo administration. The second set of animals was divided into groups that received methadone (0.3 mg/kg) 5 min before reperfusion or 10 s after reperfusion. These 2 sets of animals were subjected to 30 min of myocardial ischemia by left anterior descending coronary artery occlusion and then 2 h of reperfusion. The third set of animals received placebo, methadone (0.3 mg/kg), or morphine (0.3 mg/kg) 5 min before reperfusion and were subjected to 45 min of ischemia by left anterior descending coronary artery occlusion with 2 h of reperfusion. Myocardial IS was assessed by staining myocardial tissue with triphenyltetrazolium chloride and expressed as a percentage of the area at risk (mean ± sem).

RESULTS: Methadone or morphine administered before ischemia reduced myocardial IS. The greatest effect was achieved at a dose of 0.3 mg/kg (methadone, 46% ± 1%, P < 0.001 and morphine, 47% ± 1%, P < 0.001 versus placebo, 61% ± 1%, respectively). Naltrindole (5 mg/kg) blocked methadone-induced (0.3 mg/kg) and morphine-induced (0.3 mg/kg) cardioprotection (naltrindole + methadone, 58% ± 1%, P < 0.001 versus methadone; and naltrindole + morphine, 58 ± 1%, P < 0.001 versus morphine). Methadone (0.3 mg/kg) reduced myocardial IS when given 5 min before reperfusion (46% ± 1%, P < 0.001 versus placebo) but not 10 s after reperfusion (60% ± 1%, P = 0.675 versus placebo). No significant myocardial IS differences were seen for placebo when comparing the 45-min ischemia group (64% ± 1%) with the 30-min ischemia group (60% ± 1%, P = 0.069). The longer ischemia time of 45 min abrogated methadone-induced IS reduction (64% ± 2%, P = 0.867 versus 45-min ischemia placebo group) and morphine-induced IS reduction (65% ± 1%, P = 0.836 versus 45-min ischemia placebo group).

CONCLUSIONS: These findings demonstrate that methadone and morphine produce similar myocardial IS-sparing effects that are -opioid receptor mediated and that are dependent on the duration of myocardial ischemia.

METHODS: A detailed cardiac history, resting echocardiography, and hemoglobin and NT-proBNP levels were obtained in 666 patients before vascular surgery. Anemia was defined as serum hemoglobin <13 g/dL for men and <12 g/dL for women. Troponin T measurements and 12-lead electrocardiograms were performed on postoperative days 1, 3, 7, and 30 and whenever clinically indicated. The primary end point of the study was the composite of 30-day postoperative cardiovascular death, nonfatal myocardial infarction, and troponin T release. Receiver operating characteristic curve analysis was used to assess the optimal cutoff value of NT-proBNP for the prediction of the composite end point. Multivariable regression analysis was used to assess the additional value of NT-proBNP for the prediction of postoperative cardiac events in nonanemic and anemic patients.

RESULTS: Anemia was present in 206 patients (31%) before surgery. Hemoglobin level was inversely related with the NT-proBNP levels (β coefficient = –2.242; P = 0.025). The optimal predictive cutoff value of NT-proBNP for predicting the composite cardiovascular outcome was 350 pg/mL. After adjustment for clinical cardiac risk factors, both anemia (odds ratio [OR] 1.53; 95% confidence interval [CI]: 1.07–2.99) and increased levels of NT-proBNP (OR 4.09; 95% CI: 2.19–7.64) remained independent predictors for postoperative cardiac events. However, increased levels of NT-proBNP were not predictive for the risk of adverse cardiac events in the subgroup of anemic patients (OR 2.16; 95% CI: 0.90–5.21).

CONCLUSIONS: Both anemia and NT-proBNP are independently associated with an increased risk for postoperative cardiac events in patients undergoing vascular surgery. NT-proBNP has less predictive value in anemic patients.

METHODS: Children (aged 5–15 yr) who underwent general anesthesia were included, and all perioperative data including anesthetic drugs were collected prospectively. Children were interviewed three times postoperatively using a semistructured questionnaire. All cases of possible or probable awareness were discussed with the child's care providers to confirm or refute the memories. Internal consensus among investigators across sites was reached, and these cases and a random selection of others were reviewed by three external reviewers. For the purpose of this study, possible/probable awareness was defined as cases with agreement between the internal consensus and at least two of the three external reviewers.

RESULTS: One thousand seven hundred eighty-four children completed at least one interview. Thirty-two cases were coded as possible or probable awareness by at least one entity (i.e., either the internal consensus or one of the external reviewers). Fourteen of these cases met the definition for possible/probable awareness, making the incidence of awareness 0.8%. Six of the 14 children with awareness (43%) remembered feeling scared during their surgery and three (21%) reported hurting. Two children in this group (14%) said they would feel worse if they had to have surgery again, which was not significantly different from reports of children with no recall (15%). None of the children with awareness required psychological follow-up. Endoscopic procedures were associated with a higher risk for awareness (relative risk = 4.5 [confidence interval 1.5–13.6]).

CONCLUSIONS: Although 0.8% of children experienced possible/probable awareness in this study, none experienced short-term psychological distress.

Our aim in this exploratory study was to first compare BIS values at 4 different stages of anesthesia between intellectually disabled children and controls. Our second aim was to investigate the discriminative properties of BIS between consciousness and unconsciousness for intellectually disabled children and for controls.

METHODS: Eighteen intellectually disabled children and 35 control children, aged 2–13 yr, were included. BIS values, landmark events, and standard monitoring values of vital functions were recorded throughout the whole procedure. The performance of BIS in distinguishing between a conscious and unconscious state was assessed from receiver operating characteristic curves.

RESULTS: Median (interquartile range) BIS values for the intellectually disabled group were significantly lower than those for controls in the awake state (72 [48–77] vs 97 [84–98], P < 0.001), during stable intraoperative anesthesia (34 [21–45] vs 43 [33–52], P = 0.02), and during return of consciousness (59 [36–68] vs 73 [64–78], P = 0.009). The discriminative properties of the BIS monitor for the state of consciousness were comparable between the 2 groups according to the receiver operating characteristic curves. Nevertheless, the optimal cutoff BIS value for discrimination between conscious and unconscious state was 28 points lower for the intellectually disabled group.

CONCLUSIONS: We advise anesthesiologists to be alert to possible lower BIS values in intellectually disabled children. There is a risk that they will inadvertently misinterpret the state of consciousness in intellectually disabled children. New multicenter studies must find the optimal manner of evaluating (un)consciousness in intellectually disabled patients with documented and confirmed specific etiologies of their intellectual disability.

METHOD: Digital audiovisual recordings of 293 children undergoing outpatient elective surgery were coded using Observer XT software and the validated Revised Perioperative Child-Adult Medical Procedure Interaction Scale. Multiple pass second-by-second data recording was used to capture children’s behaviors across phases of anesthesia induction.

RESULTS: More than 40% of children aged 2–10 yr displayed some distress behavior during induction with 17% of these children displaying significant distress and more than 30% of children resisting anesthesiologists during induction. Children’s distress and nondistress behaviors displayed four profiles over the course of anesthesia induction: Acute Distress, Anticipatory Distress, Early Regulating Behaviors, and Engagement with Procedure. Older children had higher scores on early regulating and engagement profiles whereas younger children had higher scores on Acute Distress. There were no differences across age in children’s Anticipatory Distress. Construct validity of behavior profiles was supported via correlations of profile score (overall and on the walk to the operating room) with a validated assessment of children’s anxiety at induction.

CONCLUSIONS: Children undergoing anesthesia display a range of distress and nondistress behaviors. A group of behaviors was identified that, when displayed on the walk to the operating room, is associated with less distress at anesthesia induction. These data provide the first examination of potentially regulating behaviors of children, but more detailed sequential analysis is required to validate specific functions of these behaviors.

METHODS: We included 95 patients who had suffered from postoperative vomiting (POV) after general anesthesia and 94 control patients. After DNA isolation, the entire HTR3A and HTR3B coding regions, the 5' flanking regions, and exon/intron boundaries were screened for genetic variants. Correlation of identified genetic variants with POV was determined by logistic regression.

RESULTS: We identified 16 different variants in the HTR3A gene and 19 in the HTR3B gene. By using a multivariate logistic regression model that also included classical risk factors, the HTR3A variant c1377A>G was associated with a significantly higher risk (odds ratio [OR] 2.972; 95% confidence interval [CI] 1.466–6.021; P = 0.003) and the HTR3B variants c5+201_+202delCA (OR 0.421; 95% CI 0.257–0.69; P = 0.001) and c6-137C>T (OR 0.034; 95% CI 0.003–0.332; P = 0.004) were associated with a lower risk for POV. However, all significant genetic variants were located in noncoding regions of their gene.

CONCLUSIONS: Genetic variations in the HTR3A and HTR3B gene seem to be associated with the individual risk of developing POV. How strong their influence is within the multifactorial genesis of POV needs to be investigated in additional studies with an appropriate sample size.

METHODS: Two hundred adult patients presenting for elective outpatient colonoscopy were randomized to receive propofol alone or propofol plus midazolam, and/or fentanyl for IV sedation. Baseline cognitive function was measured using the computerized CogState test battery (Cogstate^TM, Melbourne, Australia) before sedation. During the procedure, sedative drug doses, depth of sedation (via the bispectral index and observer’s assessment of alertness/sedation score), complications, and treatability were recorded. Patients were interviewed about recall immediately after emerging from sedation, and cognitive testing was repeated at hospital discharge. Recovery times, quality of recovery, and satisfaction with care were also recorded.

RESULTS: In the propofol plus adjuvants group, 84 patients received fentanyl 50 µg (25–100) (median [range]) and 57 patients received midazolam 2 mg (0.5–10). Patients’ cognitive function at discharge was worse than their performance at baseline. However, the changes in cognitive function between discharge and baseline were not significantly different between the two groups. At discharge, 18.5% of patients were cognitively impaired to an extent equivalent to a blood-alcohol concentration of 0.05%. Sedation with propofol plus midazolam and/or fentanyl produced better operating conditions than sedation with propofol alone and was associated with shorter procedure times. Recovery times, recall, dreaming, quality of recovery, and patient satisfaction with care were similar between the groups. Administration of >2 mg of midazolam was a predictor of impaired cognitive function at discharge.

CONCLUSIONS: Significant cognitive impairment was common at discharge from elective outpatient colonoscopy. However, the addition of midazolam and/or fentanyl to propofol sedation did not result in more cognitive impairment than the use of propofol alone. Furthermore, the use of adjuvants improved the ease of colonoscopy without increasing the rate of complications or prolonging early recovery times..

METHODS: In this double-blind study, 52 healthy women scheduled to undergo tubal sterilization were randomly assigned to receive either intrathecal 10 mg lidocaine 2% plus 10 µg fentanyl (Group I) or intrathecal 3 mg levobupivacaine 0.5% plus 10 µg fentanyl (Group II), each solution made to a total volume of 3 mL with sterile water. The following variables were monitored intraoperatively: anesthesia onset time, need for anesthesia-analgesia supplementation, depth of sedation, surgical conditions, and occurrence of hemodynamic events. After surgery, motor block, proprioception, vibration sense, light touch, and Romberg’s test were performed to evaluate whether the patients could bypass the postanesthesia care unit and be allowed to walk by themselves. Sensory block level was determined at 5, 10, and 15 min after anesthetic injection, and then every 15 min until resolution was complete. A difference of 25 min in sensory block resolution time was considered clinically relevant.

RESULTS: Onset time and intraoperative conditions were comparable in both groups. No patient required general anesthesia to complete surgery. All patients from both groups bypassed the postanesthesia care unit. Ambulation took place after 27 (18–45) min in Group I and 30 (18–56) min in Group II (P = 0.24). Complete regression of spinal anesthesia occurred after 93 (65–120) min in Group I and 105 (78–150) min in Group II (P = 0.019); however, no differences were observed in time for home discharge 185 (150–300) min in Group I and 188 (125–300) min in Group II (P = 0.62). Global patient satisfaction was comparable between both groups.

CONCLUSIONS: Levobupivacaine 3 mg plus 10 µg fentanyl may be used as a suitable alternative to 10 mg lidocaine plus 10 µg fentanyl for spinal anesthesia of short duration. It achieved a clinically equivalent time for resolution of sensory block, similar intraoperative conditions, and comparable patient satisfaction..

METHODS: Sixty-five female patients (ASA physical status I–II) scheduled for transabdominal hysterectomy were recruited to this randomized, placebo-controlled study. Thirty-two patients in the treatment group received IV lidocaine starting 20 min before surgery, whereas the control group (33 patients) received a matched saline infusion. Both groups received patient-controlled epidural analgesia during the postoperative period. Blood samples were collected before, 24, 48, and 72 h after surgery to measure ex vivo cytokine production of interleukin (IL)-1 receptor antagonist (IL-1ra) and IL-6, as well lymphocyte mitogenic response to phytohemagglutinin-M. A 10-cm visual analog scale was used to assess pain intensity at rest and after coughing.

RESULTS: Patients in the lidocaine + patient-controlled epidural analgesia group experienced less severe postoperative pain in the first 4 and 8 h after surgery (visual analog scale 4/3.7 at rest and 5.3/5 during coughing versus 4.5/4.2 and 6.1/5.3, respectively, in the placebo group). There was significantly less ex vivo production of IL-1ra and IL-6, whereas the lymphocyte proliferation response to phytohemagglutinin-M was better maintained than in the control group.

CONCLUSION: The present findings indicate that preoperative and intraoperative IV lidocaine improves immediate postoperative pain management and reduces surgery-induced immune alterations.

METHODS: Data from 45 patients scheduled for a radical prostatectomy were analyzed. After lumbar epidural catheterization, patients received remifentanil and propofol solely for induction of anesthesia. Thereafter, epidural analgesia was initiated, and isoflurane, sevoflurane, or desflurane (15 patients each) was added to maintain unconsciousness. At least 45 min later, end-tidal concentrations were varied between 0.5 and 2 minimum alveolar anesthetic concentration. We estimated an individual k_e0 value for each patient by optimizing the prediction probability P_K (P_K-based k_e0) or by minimizing the area within the hysteresis loop (area-based k_e0). Data are mean ± sd.

RESULTS: Both semiparametric approaches led to comparable k_e0 values with 0.18 ± 0.06 min^–1 (P_K based) and 0.15 ± 0.04 min^–1 (area based) for isoflurane and 0.17 ± 0.08 min^–1 (P_K based) and 0.16 ± 0.11 min^–1 (area based) for sevoflurane. k_e0 values for desflurane (P_K based: 0.30 ± 0.17min^–1; area based: 0.32 ± 0.25 min^–1) were significantly higher than for isoflurane and sevoflurane.

CONCLUSION: Maximizing the prediction probability P_K for estimating k_e0 seems to be a promising method that researchers could use on an exploratory basis.

METHODS: We first examined changes in blood glucose levels in rats undergoing sigmoid colostomy under sevoflurane, sevoflurane/buprenorphine, propofol, and propofol/buprenorphine anesthesia. We then examined changes in blood glucose levels after glucose administration using awake rats, rats under sevoflurane anesthesia, and rats under propofol anesthesia.

RESULTS: Blood glucose levels increased markedly after sigmoid colostomy under sevoflurane anesthesia; the marked increases could not be prevented by the coadministration of buprenorphine. Under propofol anesthesia, blood glucose levels did not change after sigmoid colostomy at the highest dose, but increased slightly at the lowest and intermediate doses; the slight increases were completely prevented by the coadministration of buprenorphine. Whereas changes in blood glucose levels after glucose administration in rats under sevoflurane anesthesia were significantly greater than those in awake rats, the changes in rats under propofol anesthesia were similar to those in awake rats.

CONCLUSIONS: During surgery, hyperglycemia was observed under sevoflurane and sevoflurane/buprenorphine anesthesia, but blood glucose levels were relatively stable under propofol and propofol/buprenorphine anesthesia. Whereas sevoflurane exaggerates glucose intolerance, propofol has no significant effects on glucose tolerance. We speculate that this feature of propofol contributes, at least in part, to the stable glucose metabolism during surgery observed in this study. The results of this study confirm the marked difference in the effects of sevoflurane and propofol on glucose metabolism.

METHODS: A reversible ATP depletion (antimycin A) followed by restoration of substrate supply in LLC-PK1 cells was used as an in vitro model of renal I-R. Cell viability was assessed by dimethylthiazol-diphenyltetrazol bromide and trypan blue dye exclusion test assays. Apoptosis was evaluated by annexin V–fluorescein isothiocyanate staining by flow cytometry and immunofluorescence. Propofol treatments were initiated at various time intervals: 1 or 24 h before ischemia, only during ischemia, or only during reperfusion. To evaluate the mechanisms of propofol protection, specific K_ATP channel inhibitors or activators were used in some experiments during propofol pretreatment.

RESULTS: Propofol attenuated I-R injury on LLC-PK1 cells when present either 1 or 24 h before initiated I-R, and also during the recovery period, but not when added only during ischemia. Propofol pretreatment significantly protected LLC-PK1 from I-R-induced apoptosis. The protective effect of propofol was prevented by glibenclamide (a sarcolemmal ATP-dependent K⁺ channel blocker) and decreased by 5-hydroxidecanoic acid (a mitochondrial ATP-dependent K⁺ channel blocker), but it was not modified by diazoxide (a selective opener of ATP-sensitive K⁺ channel).

CONCLUSION: Propofol protected cells against apoptosis induced by I-R. This protection was probably due to a preconditioning effect of propofol and was, at least in part, mediated by K_ATP channels.

METHODS: Neocortical astrocytes were exposed to OGD in an anaerobic chamber. After 6 h of OGD exposure, astrocytes were subsequently subjected to 24 h of reoxygenation. Propofol was added during the OGD phase of the model. Cell morphology was assessed by light microscopy. Astrocyte viability was assessed by measuring 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide absorbency (optical density value) and the percentage of lactate dehydrogenase released by injured astrocytes. AQP4 expression was evaluated with Western blot analysis. To investigate the possible mechanism of propofol’s effects on AQP4 expression, cultured astrocytes were pretreated for 24 h with the PKC activator, 12-O-tetradecanoylphorbol 13-acetate, before the propofol treatment/OGD 6 h/reoxygenation 24 h.

RESULTS: We found by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide testing that astrocyte viability began to decrease after about 4 h of OGD exposure and decreased to 60% after 6 h of OGD. When 6 h of OGD was followed by 24 h of reoxygenation, cell viability was further decreased. AQP4 expression was attenuated after 6 h of OGD exposure but was reversed and exceeded baseline levels after 24 h of reoxygenation. Propofol dose-dependently reduced cell death assessed by lactate dehydrogenase test (P < 0.05), and 10 µM propofol significantly down-regulated AQP4 expression in astrocytes after 6 h of OGD followed by 24 h of reoxygenation (P < 0.01). Prolonged (24 h) pretreatment with the phorbol ester, 12-O-tetradecanoylphorbol 13-acetate before OGD significantly reversed the effect of propofol on AQP4 expression (P < 0.01).

CONCLUSION: Propofol, administered during OGD, provided neuroprotective effects and down-regulated AQP4 expression in the OGD/reoxygenation model of cultured rat astrocytes. Activation of the PKC pathway may block the effects of propofol.

METHODS: We anesthetized homozygous G_i2 GS/GS and wild-type (WT) mice with isoflurane and quantified time (in seconds) to loss and resumption of righting response. During recovery from isoflurane anesthesia, breathing was quantified in a plethysmography chamber for both lines of mice.

RESULTS: G_i2 GS/GS mice required significantly less time for loss of righting and significantly more time for resumption of righting than WT mice. During recovery from isoflurane anesthesia, G_i2 GS/GS mice exhibited significantly greater respiratory depression. Poincaré analyses show that GS/GS mice have diminished respiratory variability compared with WT mice.

CONCLUSION: Modulation of G_i2 signaling by RGS proteins alters loss and resumption of wakefulness and state-dependent changes in breathing.

METHODS: Rat EAAT3 was expressed in Xenopus oocytes. l-glutamate- and l-cysteine-induced membrane currents were recorded using the 2-electrode voltage clamp technique. The peak current was quantified to reflect the amount of transported substrates because transport of substrates via EAATs is electrogenic.

RESULTS: Exposure of oocytes to 5 mM tert-butyl hydroperoxide, an organic oxidant, for 10 min reduced the V_max, but did not affect the K_m, of EAAT3 for l-cysteine. The volatile anesthetics isoflurane, sevoflurane, and desflurane at concentrations from 1% to 3% attenuated the tert-butyl hydroperoxide-reduced EAAT3 activity for l-glutamate and l-cysteine.

CONCLUSIONS: Our results suggest that volatile anesthetics preserve EAAT3 function to transport l-glutamate and l-cysteine under oxidative stress, which may be a mechanism for the neuroprotective effects of volatile anesthetics.

METHODS: We randomly allocated 66 adult obese patients with a body mass index between 30 and 50 kg/m² scheduled to undergo laparoscopic bariatric surgery into 3 groups. According to the recruitment maneuver used, the zero end-expiratory pressure (ZEEP) group (n = 22) received the vital capacity maneuver (VCM) maintained for 7–8 s applied immediately after intubation plus ZEEP; the positive end-expiratory pressure (PEEP) 5 group (n = 22) received the VCM maintained for 7–8 s applied immediately after intubation plus 5 cm H₂O of PEEP; and the PEEP 10 group (n = 22) received the VCM maintained for 7–8 s applied immediately after intubation plus 10 cm H₂O of PEEP. All other variables (e.g., anesthetic and surgical techniques) were the same for all patients. Heart rate, noninvasive mean arterial blood pressure, arterial oxygen saturation, and alveolar-arterial Pao₂ gradient (A-a Pao₂) were measured intraoperatively and postoperatively in the postanesthesia care unit (PACU). Length of stay in the PACU and the use of a nonrebreathing O₂ mask (100% Fio₂) or reintubation were also recorded. A computed tomographic scan of the chest was performed preoperatively and postoperatively after discharge from the PACU to evaluate lung atelectasis.

RESULTS: Patients in the PEEP 10 group had better oxygenation both intraoperatively and postoperatively in the PACU, lower atelectasis score on chest computed tomographic scan, and less postoperative pulmonary complications than the ZEEP and PEEP 5 groups. There was no evidence of barotrauma in any patient in the 3 study groups.

CONCLUSIONS: Intraoperative alveolar recruitment with a VCM followed by PEEP 10 cm H₂O is effective at preventing lung atelectasis and is associated with better oxygenation, shorter PACU stay, and fewer pulmonary complications in the postoperative period in obese patients undergoing laparoscopic bariatric surgery.

METHODS: In this prospective observational study conducted in a biochemistry laboratory, we analyzed 179 routine blood samples from consecutive patients over a 3-mo period using two automated blood chemistry analyzers, the LX20 (Beckman) and the Modular (Roche). Measured and calculated parameters from the two analyzers were compared.

RESULTS: Although the correlation between measured values was satisfactory, there were large differences in the limits of agreement for calculated values (SID_app: 9.6 mEq/L, SID_eff: 6.4 mEq/L, and SIG: 11.7 mEq/L) and a weak correlation (SID_app: r² = 0.54 and SIG: r² = 0.12) between the analyzers.

CONCLUSIONS: The results of the Stewart-Fencl approach for interpretation of acid-base status can vary according to the analyzer used. These differences may have important clinical and research implications..

METHODS: A syringe pump infused a saline carrier solution at a low flow rate frequently used in an intensive care unit (10 mL/h) through a multiport manifold connected to the 16-gauge lumen of a standard 16-cm triple-lumen catheter. The model drug methylene blue (3 mL/h) joined the carrier flow at the first, second, or fourth stopcock of a traditional manifold or 1 of 2 positions in a microinfusion manifold, a new device designed to minimize dead volume. Effluent samples were collected every minute for quantitative spectrophotometric analysis of delivery onset and offset.

RESULTS: Onset and offset times differed significantly among individual ports of the traditional 4-stopcock manifold. There was also a significant difference between the 2 ports of the microinfusion manifold, but this was less pronounced. Both ports of the microinfusion manifold yielded delivery dynamics that were similar to the most downstream port of the 4-stopcock manifold. There was good correlation between dynamic data and dead volume for each of the manifolds.

CONCLUSIONS: Using a traditional stopcock manifold, port selection significantly affects drug delivery dynamics for continuous infusions. The findings provide quantitative support for the concept that the most critical infusion should join the system at the manifold port closest to the patient. Port selection was less important for the microinfusion manifold and dynamics were faster compared with the second and fourth ports of the stopcock manifold. The smaller dead volumes of the microinfusion manifold minimize unwanted delays in drug delivery onset and offset allowing more precise control over drug delivery by continuous infusion.

METHODS: More than 5.6 million patients in the Nationwide Inpatient Sample who underwent principal procedures of knee arthroplasty, cholecystectomy, hip/femur surgical treatment, spinal fusion, appendectomy, colorectal resection, laminectomy without fusion, coronary artery bypass grafting, and cardiac valve procedures from 1996 to 2005 were included. Rates of POVL, defined as any discharge with an International Classification of Diseases, Ninth Revision, Clinical Modification code of ischemic optic neuropathy (ION), cortical blindness (CB), or retinal vascular occlusion (RVO), were estimated. Potential risk factors were assessed by univariate and multivariable analyses.

RESULTS: Cardiac and spinal fusion surgery had the highest rates of POVL. The national estimate in cardiac surgery was 8.64/10,000 and 3.09/10,000 in spinal fusion. By contrast, POVL after appendectomy was 0.12/10,000. Those undergoing cardiac surgery, spinal fusion, and orthopedic surgery had a significantly increased risk of developing ION, RVO, or CB. Patients younger than 18 yr had the highest risk for POVL, because of higher risk for CB, whereas those older than 50 yr were at greater risk of developing ION and RVO. Other significant positive predictors for some diagnoses of POVL were male gender, Charlson comorbidity index, anemia, and blood transfusion. There was no increased risk associated with hospital surgical volume. During the 10 yr from 1996 to 2005, there was an overall decrease in POVL in the procedures we studied.

CONCLUSIONS: The results confirm the clinical suspicion that the risk of POVL is higher in cardiac and spine fusion surgery and show for the first time a higher risk of this complication in patients undergoing lower extremity joint replacement surgery. The prevalence of POVL in the eight most commonly performed surgical operations in the United States has decreased between 1996 and 2005. Increased odds of POVL with male gender and comorbidity index indicate that some risk factors for POVL may not presently be modifiable. The conclusions of this study are limited by factors affecting data accuracy, such as lack of data on the intraoperative course and inability to confirm the diagnostic coding of any of the discharges in the database.

METHODS: Twenty-four nonsedated adult volunteers underwent neck magnetic resonance imaging with and without CP. Measurements were made of the postcricoid hypopharynx, airway compression, and lateral displacement of the cricoid ring during the application of CP. The relevant anatomy was reviewed.

RESULTS: The hypopharynx, not the esophagus, is what lies behind the cricoid ring and is compressed by CP. The distal hypopharynx, the portion of the alimentary canal at the cricoid level, was fixed with respect to the cricoid ring and not mobile. With CP, the mean anterioposterior diameter of the hypopharynx was reduced by 35% and the lumen likely obliterated, and this compression was maintained even when the cricoid ring was lateral to the vertebral body.

CONCLUSIONS: The location and movement of the esophagus is irrelevant to the efficiency of the Sellick’s maneuver (CP) in regard to prevention of gastric regurgitation into the pharynx. The hypopharynx and cricoid ring move together as an anatomic unit. This relationship is essential to the efficacy and reliability of Sellick’s maneuver. The magnetic resonance images show that compression of the alimentary tract occurs with midline and lateral displacement of the cricoid cartilage relative to the underlying vertebral body.

METHODS: In this prospective, observational study, we interviewed 600 patients during the preoperative visit in a tertiary referral educational hospital in northwest Iran. The definition of substance abuse and dependence was according to DSM-IV criteria. Postoperative complications and in-hospital mortality of patients with substance (cigarette, opium, and alcohol) dependence and abuse were compared with those in control patients who did not use these substances.

RESULTS: In 600 studied patients, the prevalence of cigarette smoking was 42.1% (ex-smokers 26.0% and current smokers 16.1%), prevalence of opium use was 12.0% (opium abuse 7.0% and opium dependence 5.0%), and alcohol consumption was 8.1% (alcohol abuse 7.4% and alcohol dependence 0.7%). The prevalence of cigarette smoking was 58.9% in men and 7.6% in women (P = 0.001). Postoperative cardiac complications in current smokers (21.5%) and ex-smokers (20.5%) were not significantly different from the control group (28.2%). Also, pulmonary complications were not different in current smokers (24.7%) and ex-smokers (17.9%) from the control group (26.8%; P = 0.196). However, in men, pulmonary complications in current smokers were more prevalent than in the control group (P = 0.044). In opium and alcohol dependents and abusers, postoperative complications were not statistically different from the control group (all P values >0.05). No increase was observed regarding in-hospital mortality in patients with substance use.

CONCLUSIONS: In cardiac surgery patients in northwest Iran, the prevalence of cigarette smoking is relatively low (very low in women), as is alcohol use, compared with Western countries; however, opium use is twice as prevalent. We found higher pulmonary complication rates in men who smoked, but no increase in postoperative cardiopulmonary complications and in-hospital mortality rates in patients who abused opium and consumed alcohol.

METHODS: One hundred fifty consecutive adult morbidly obese patients (body mass index >35 kg/m²) were randomly selected to receive one of 3 VLSs: GlideScope®, Storz® V-Mac^TM, and McGrath®. Direct laryngoscopy scored the best possible view of the glottis; subsequently, the respective VLS was used, and the patient's trachea was intubated. Common preprocedural (e.g., Mallampati grade) and intraprocedural (Cormack-Lehane grade) metrics of intubation difficulty were measured, as well as the dependent variables of intubation time, number of attempts, and subjective difficulty.

RESULTS: All 3 VLSs tested offered an equal or better view of the glottis compared with traditional direct laryngoscopy. The number of attempts necessary to intubate the trachea differed significantly among VLSs (average 2.6 ± 1.0 attempts for the GlideScope, 1.4 ± 0.7 for the Storz, and 2.9 ± 0.9 for the McGrath VLS). The average intubation times were 33 ± 18 s for the GlideScope, 17 ± 9 s for the Storz, and 41 ± 25 s for the McGrath VLS.

CONCLUSIONS: In this study, the VLS with the Macintosh blade (Storz VLS) had a better overall satisfaction score, intubation time, number of intubation attempts, and necessity of extra adjuncts, compared with the 2 other tested devices.

METHODS: In 16 anesthetized pigs (31.4 ± 3.4 kg), a jugular vein, a carotid artery, the pulmonary artery (thermodilution), the portal vein, and a hepatic vein were cannulated for hemodynamic monitoring and blood sampling. Ultrasonic flowprobes were placed around the portal vein, the hepatic artery, and the superior mesenteric artery (SMA). In addition to 30 mL/kg of dextran 70 given before baseline, all animals received 10 mL · kg^–1 · h^–1 of IV fluids throughout the experiment. An endotoxin infusion (2 µg · kg^–1 · h^–1) was given for 300 min; 100 min after the start of endotoxin, the pigs were randomized to receive levosimendan (50 µg · kg^–1 · h^–1, n = 8) or placebo (n = 8). To evaluate the isolated effects of endotoxemia, all data before randomization were pooled into one group. Data were analyzed by analysis of variance and presented as mean ± sem.

RESULTS: Endotoxemia (t = 90 min, pooled data) decreased systemic vascular resistance (SVR, 2526 ± 203 to 1946 ± 122 dyn · s · cm^–5, P = 0.003) and mean arterial blood pressure (MAP, 109 ± 6 to 84 ± 3 mm Hg, P < 0.05), whereas heart rate (66 ± 4 to 98 ± 8 bpm), and mean pulmonary arterial pressure (MPAP, 20 ± 1 to 38 ± 2 mm Hg) increased (P < 0.001). Cardiac output (CO, 3.4 ± 0.2 L/min) and systemic oxygen delivery (414 ± 33 mL/min) were unchanged, but blood flows in the SMA (575 ± 34 to 392 ± 38 mL/min) and the portal vein (881 ± 62 to 568 ± 39 mL/min) decreased (P < 0.001). Although hepatic arterial blood flows increased (36 ± 8 to 219 ± 38 mL/min), gut (114 ± 11 to 84 ± 7 mL/min) and hepatic (94 ± 11 to 67 ± 8 mL/min) oxygen deliveries decreased (P < 0.05). At t = 300 min, the levosimendan group showed lower MPAP (39 ± 3 vs 49 ± 2 mm Hg, P = 0.025), lower SVR (2158 ± 186 vs 3069 ± 370 dyn · s · cm^–5, P = 0.052), and lower MAP (55 ± 9 vs 87 ± 9 mm Hg, P < 0.001) than the control group. In both groups, CO, portal vein, and hepatic arterial blood flows decreased (P < 0.001); the mean values for the levosimendan group at t = 300 min were 2.0 ± 0.4 L/min, 390 ± 83 mL/min, and 36 ± 12 mL/min, respectively. SMA blood flow decreased only in the levosimendan group (432 ± 40 to 320 ± 78 mL/min, P < 0.001), whereas gut oxygen delivery decreased in the levosimendan (85 ± 12 to 63 ± 12 mL/min, P < 0.001) and in the control (83 ± 6 to 59 ± 3 mL/min, P = 0.03) groups.

CONCLUSION: Levosimendan administered after the establishment of endotoxemic shock to pigs receiving moderate fluid resuscitation prevented further increases in MPAP and maintained a low SVR. There were, however, no improvements in CO, MAP decreased, and levosimendan neither prevented the development of circulatory shock nor improved hepatosplanchnic perfusion.

METHODS: Twenty anesthetized pigs (26.8 ± 0.5 kg) were instrumented with flow probes and catheters to monitor systemic and regional perfusion as described in our companion article in this issue of the journal. Two animals were excluded because of surgical complications. Oxygen consumption (VO₂) was measured by indirect calorimetry. Starting 1 h after instrumentation, an endotoxin infusion (Escherichia coli lipopolysaccharide, 2 µg · kg^–1 · h^–1) was administered for 300 min. Sixty minutes after the start of endotoxin, the animals were fluid resuscitated (20 mL/kg dextran 70); at 120 min, they were randomized into three groups of six animals each: levosimendan (25–50 µg · kg^–1 · h^–1), dobutamine (10–20 µg · kg^–1 · min^–1), and control. In the first two groups, norepinephrine (0.5–2 µg · kg^–1 · min^–1) was added when mean arterial blood pressure (MAP) ≤ 65 mm Hg. Crystalloids were given to maintain filling pressures ≥ baseline. The data were divided into two subsets: before (0–120 min, all animals) and after (120–300 min, three groups) randomization, and analyzed by analysis of variance. P < 0.05 was considered significant.

RESULTS: At 120 min, cardiac output was 15% higher (P < 0.001), systemic vascular resistance was 30% lower (P < 0.001), and MAP decreased 12.5% (P = 0.004); blood flow in the hepatic artery, superior mesenteric artery, and portal vein had increased by 100% (P = 0.004), 60% (P < 0.001), and 20% (P < 0.001), respectively. Between 120 and 300 min, cardiac output and systemic oxygen delivery decreased 50% in control animals (P < 0.05), remained unchanged in the levosimendan group, and increased 60% with dobutamine (P = 0.05). MAP (P = 0.043) and VO₂ (P = 0.001) decreased 20% in the control group. Portal vein flow decreased in the control (50%) and levosimendan (30%) groups (P < 0.001) and was therefore higher in the dobutamine group (P = 0.003) at 300 min. Hepatic and gut oxygen deliveries decreased in the levosimendan (50%, and 30%, respectively, P < 0.001) and control groups (70% and 45%, respectively, P < 0.05); thus, regional oxygen deliveries were greater in the dobutamine group (P < 0.05). In this group, mixed venous and hepatic vein oxygen saturation were maintained; the latter variable was higher than in the other groups (P < 0.05). Although unchanged with dobutamine, arterial (P = 0.020), portal (P = 0.020), and hepatic vein (P = 0.034) lactate concentrations increased twofold with levosimendan.

CONCLUSION: In volume-resuscitated endotoxemic pigs, the association of either levosimendan or dobutamine with norepinephrine preserved systemic blood flow, oxygen delivery, and VO₂. However, only dobutamine-norepinephrine maintained portal blood flow, which was associated with preservation of splanchnic and hepatic oxygen homeostasis and stable lactate concentrations.

METHODS: We performed a prospective observational cohort study in a 21-bed polyvalent intensive care unit in a university hospital.

RESULTS: Three hundred sixty-one intubated adult patients with a duration of mechanical ventilation (MV) of 6 days or more were admitted over a 28-mo period. Late-onset VAP was confirmed in 76 patients (21%) by the presence of at least one microorganism at a concentration ≥10⁴ colony-forming units/mL on the bronchoalveolar lavage. Gram-negative bacilli represented 75% and Staphylococcus aureus 21% of recovered organisms. Factors independently associated with late-onset VAP by multivariate analysis included a high simplified acute physiology score II score (odds ratio: 1.021; 95% confidence interval [CI]: 1.005–1.038; P = 0.01), development of acute respiratory distress syndrome during the first 5 days of MV (odds ratio: 1.98; 95% CI: 1.05–3.67; P = 0.04), and size of the endotracheal tube ≥7.5 (odds ratio: 2.06; 95% CI: 1.88–3.90; P = 0.03). EN started within 48 h of MV onset was not associated with a higher risk for late-onset VAP.

CONCLUSION: In our nontrauma patient population, early EN was not associated with development of late-onset VAP. In this population, severity of the disease during the first 5 days of MV seemed to be associated with late-onset VAP. In addition, our results suggest that the risk of late-onset VAP is higher in patients with a tube size ≥7.5 than in patients with a tube size <7.5.

METHODS: Male Sprague-Dawley rats weighing 250-300 g were randomly assigned to 1 of 4 groups: sham rats (injected intraperitoneally [IP] with saline) pretreated with vehicle (100% O₂) (sham-vehicle); sham rats pretreated with isoflurane (sham-ISO); LPS rats (injected IP with LPS) pretreated with vehicle (vehicle-LPS); and LPS rats pretreated with isoflurane (ISO-LPS). Endotoxemia was induced by IP injection of LPS. Isoflurane 1.4% was administered 30 min before LPS injection. The animals were then observed for 6 h. We monitored arterial blood pressure, heart rate, and blood gas. The extent of ALI was evaluated by lung wet/dry ratio, Evans blue dye extravasation, and histologic examination. We also measured pulmonary nitric oxide (NO), tumor necrosis factor (TNF)-, interleukin (IL)-1β, and IL-6 levels. In addition, survival statistics and pulmonary inducible NO synthase (iNOS) gene expression were also determined.

RESULTS: LPS caused systemic hypotension and severe ALI, as evidenced by the increases in the extent of ALI, impairment of pulmonary functions, and increases in pulmonary NO, TNF-, IL-1β, and IL-6. Isoflurane preconditioning mitigated systemic hypotension and the development of ALI. Isoflurane preconditioning also attenuated the LPS-induced increases in pulmonary nitrate/nitrite and proinflammatory cytokine release and improved survival of rats with severe sepsis. The expression of iNOS was upregulated by LPS and reduced by isoflurane pretreatment.

CONCLUSIONS: Isoflurane preconditioning can attenuate pulmonary proinflammatory cytokine release and decrease the mortality induced by severe sepsis. Early protection seems to be mediated partly through inhibition of iNOS-NO pathway activation.

METHODS: Sixty women presenting for elective cesarean delivery were randomly assigned to one of the 3 groups. Group 7 received intrathecal hyperbaric bupivacaine 7 mg, Group 8 received 8 mg, and Group 9 received 9 mg. Women in all 3 groups received intrathecal morphine 100 µg and IV hydroxyethyl starch 15 mL/kg at the time of initiation of combined spinal-epidural anesthesia. Surgery began when a sensory level of T4 was achieved. Patients were monitored for block characteristics and side effects by a blinded observer. Our primary outcome was the maximum cephalad sensory block height.

RESULTS: There was a difference in the maximum extent of cephalad sensory block among groups (Group 7: median T2 [interquartile range T2–T3]; Group 8: median T2 [T1–T2]; Group 9: median T1 [C8–T2]; P = 0.02). However, the time taken to reach T4 was similar in all 3 groups. The incidence of hypotension requiring vasopressors was different among groups (30% in Group 7, 55% in Group 8, and 70% in Group 9; P = 0.04). No patient had inadequate anesthesia. Neonatal outcomes were similar in all 3 groups.

CONCLUSION: The lowest dose of hyperbaric bupivacaine (7 mg) provided equally rapid onset and effective anesthesia for cesarean delivery while reducing the incidence of hypotension compared with 8 and 9 mg. However, because of its shorter duration of anesthesia, it may be feasible only when the block can be reinforced using a functional epidural catheter.

METHODS: Two hundred eight parturients who developed moderate to severe pruritus after the administration of intrathecal morphine were randomly allocated to 2 groups: IV pentazocine 15 mg (n = 104) and IV ondansetron 4 mg (n = 104). The successful treatment of pruritus (no or mild pruritus) and other adverse effects were determined 15 min after study drug administration, and patients were observed for recurrence of pruritus for 4 h.

RESULTS: The treatment success rate at 15 min was higher in the pentazocine group (96.1%) than in the ondansetron group (80.8%) (95% confidence interval of difference: 7.0%, 23.8%; P = 0.001). The recurrence rate of moderate to severe pruritus within 4 h after treatment in the pentazocine group (12.0%) was lower than in the ondansetron group (32.1%) (P = 0.001). There were no significant differences between groups in nausea/vomiting, sedation, shivering, pain scores, and pain at injection site. No respiratory depression was observed.

CONCLUSIONS: Pentazocine 15 mg is superior to ondansetron 4 mg for the treatment of intrathecal morphine-induced pruritus and has a lower recurrence rate. The side effects after treatment are mild.

METHODS: The setting is the preanesthesia evaluation clinic (PAC) of a university hospital, where patients consult several medical professionals, either by walk-in or appointment. Queuing theory was used to model the initial set-up of the clinic, and later to model possible alternative designs. With the queuing model, possible improvements in efficiency could be investigated. Inputs to the model were patient arrival rates and expected service times with clinic employees, collected from the clinic's logging system and by observation. The performance measures calculated with the model were patient length of stay and employee utilization rate. Supported by the model outcomes, a working group consisting of representatives of all clinic employees decided whether the initial design should be maintained or an intervention was needed.

RESULTS: The queuing model predicted that 3 of the proposed alternatives would result in better performance. Key points in the intervention were the rescheduling of appointments and the reallocation of tasks. The intervention resulted in a shortening of the time the anesthesiologist needed to decide upon approving the patient for surgery. Patient arrivals increased sharply over 1 yr by more than 16%; however, patient length of stay at the clinic remained essentially unchanged. If the initial set-up of the clinic would have been maintained, the patient length of stay would have increased dramatically.

CONCLUSIONS: Queuing theory provides robust methods to evaluate alternative designs for the organization of PACs. In this article, we show that queuing modeling is an adequate approach for redesigning processes in PACs.

METHODS: Three hundred forty-seven fasting patients had a preoperative glucose measurement determined from blood residue left on the IV needle, measured with an Accu-Chek glucometer (Roche Diagnostics, Indianapolis, IN).

RESULTS: After excluding patients with a diabetes history, 4.0% had a glucose measurement between 100 and 125 mg/dL, at a cost of $14.22 per identification, and 1.2% had a glucose measurement more than 125 mg/dL, at a cost of $32.00 per identification.

CONCLUSIONS: This preoperative blood glucose screening test was implemented at a cost of approximately one-tenth of current methods.

METHODS: Eighty patients undergoing craniotomy for supratentorial tumor resection were randomly assigned into two groups. Patients in Group G (n = 40) received oral gabapentin (3 x 400 mg), and patients in Group P (n = 40) received oral phenytoin (3 x 100 mg) for 7 days before the operation and postoperatively. An identical anesthesia protocol was performed for both the groups. Anesthesia was maintained with propofol and remifentanil infusion. Patient-controlled analgesia with morphine was used, and pain levels were measured. The antiepileptic-related side effects, anesthetic consumption, duration of anesthesia and surgery, tracheal extubation time, postoperative pain scores, morphine consumption, and sedation scores were recorded.

RESULTS: Thirty-seven patients in Group G and 38 patients in Group P completed the study. During the preoperative period in Group G, one patient had severe fatigue, one had severe dizziness, and one patient’s surgical procedure was changed. The median plasma levels of gabapentin were 34 µmol/mL (range, 23-51 µmol/mL) in 34 patients. In Group P, one patient withdrew from the study preoperatively and one developed transient neurological symptoms postoperatively.

The demographic data and mean duration of anesthesia and surgery were similar in both the groups. The total propofol and remifentanil consumption in Group G (1847 ± 548 mg/3034 ± 1334 µg) was significantly less than that of Group P (2293 ± 580 mg/4287 ± 1282 µg) (P = 0.01). However, tracheal extubation could be done earlier in Group P (4.5 ± 2 min) than in Group G (16.6 ± 22 min) (P < 0.001). Pain scores were significantly higher in Group P at 15 min, 30 min, and 1 h (P < 0.001). The total morphine consumption was also significantly higher in Group P (33 ± 17 mg vs 24 ± 19 mg) (P = 0.01). The postoperative sedation scores were significantly higher in Group G at 15 min, 30 min, 1 h, and 2 h (P < 0.001).

CONCLUSIONS: The administration of gabapentin to patients undergoing craniotomy for supratentorial tumor resection was effective for acute postoperative pain. It also decreased analgesic consumption after surgery. However, it may lead to side effects such as delayed tracheal extubation and increased sedation postoperatively.

METHODS: Seventy male sevoflurane-anesthetized Sprague Dawley rats were randomly assigned to the following treatment groups: normothermic ischemia, intraischemic hypothermia, and postischemic hypothermia with corresponding sham-operated controls. Fifteen naïve rats were investigated as reference for natural neurogenesis. Forebrain ischemia was induced by bilateral common carotid artery occlusion and hemorrhagic hypotension. In normothermic groups, the pericranial temperature was maintained at 37.5°C. Animals in the hypothermic groups were cooled to a pericranial temperature of 33°C for 45 min. All animals received 5-bromo-2-deoxyuridine for 7 days. Histopathological damage and 5-bromo-2-deoxyuridine-positive neurons of the hippocampus were analyzed after 28 days.

RESULTS: Hypothermia had no impact on natural neurogenesis. Cerebral ischemia increased the number of new neurons regardless of pericranial temperature. Forty-five minutes of hypothermia beginning before ischemia diminished hippocampal injury to <10% in the CA1 and CA3 regions, whereas 45 min of postischemic hypothermia beginning after reperfusion did not reduce neuronal injury compared with normothermia.

CONCLUSIONS: Neither intraischemic nor postischemic hypothermia affected the ischemia-induced increase in endogenous neurogenesis. Intraischemic hypothermia reduced hippocampal damage, whereas postischemic hypothermia as applied here did not prevent formation of histopathological injury. This indicates that, 28 days after cerebral ischemia, postischemic neurogenesis is not significantly increased by mild peri-ischemic hypothermia and not affected by the severity of histopathological damage.

METHODS: Sixty patients undergoing abdominal hysterectomy were randomly assigned to 1 of the following 3 groups: control group received oral placebo capsules and bolus plus infusion of saline; ketamine group received oral placebo capsules and, before incision, 0.3 mg/kg IV bolus and 0.05 mg·kg^–1·h^–1 infusion of ketamine until the end of surgery; and gabapentin group received oral gabapentin 1.2 g and bolus plus infusion of saline. The anesthetic technique was standardized, and the postoperative assessments included verbal rating scales for pain and sedation, IV morphine usage, quality of recovery assessment, recovery of bowel function, resumption of normal activities, and patient satisfaction with their pain management. Patients were questioned at 1, 3, and 6 mo after surgery for chronic postoperative pain.

RESULTS: Postoperative pain scores were significantly lower in the gabapentin group compared with the ketamine and control groups, and patient-controlled analgesia morphine use was significantly reduced in both treatment groups (versus control group) (P < 0.001). Total patient-controlled analgesia morphine use was decreased by 35% and 42% in the ketamine and gabapentin groups, respectively, compared with the control group (P < 0.001). Patient satisfaction with pain treatment was significantly improved in the ketamine and gabapentin groups compared with the control group (P < 0.001).

The incidence of incisional pain and related pain scores at the 1-, 3-, and 6-mo follow-up were significantly lower in the gabapentin group compared with the ketamine and control groups (P < 0.001).

CONCLUSION: Gabapentin and ketamine are similar in improving early pain control and in decreasing opioid consumption; however, gabapentin also prevented chronic pain in the first 6 postoperative months.

METHODS: One hundred thirty-two patients with acute herpes zoster diagnosed 1–7 days after the onset of the rash were randomly assigned to receive either standard therapy (oral antivirals and analgesics) or standard therapy with additional repetitive paravertebral injections of a mixture of 10 mL 0.25% bupivacaine and 40 mg methylprednisolone acetate every 48 h for a week. Efficacy was evaluated at 1, 3, 6, and 12 mo after the end of the treatments. The primary end point was the proportion of patients with zoster-associated pain and/or allodynia 1 mo after inclusion. Statistical analysis was performed based on the intent-to-treat population.

RESULTS: One hundred thirteen patients completed the 1-yr follow-up. At 1 mo posttherapy, 13% of patients in the paravertebral group reported zoster-related pain, compared with 45% in the standard group (P < 0.001). At 3, 6, and 12 mo posttherapy, the incidence of PHN was still significantly lower in the paravertebral group than in the standard group. The quality of life improved in both groups at each follow-up time point with no significant difference between groups.

CONCLUSION: Repetitive paravertebral anesthetic block in combination with steroids plus standard treatment with acyclovir and analgesics significantly reduced the incidence of PHN than the standard treatment alone.

METHODS: Therefore, a spinal block was administered in male Wistar rats by administering a local anesthetic (bupivacaine) through an intrathecal catheter at the mid-thoracic level. This thoracic spinal block completely suppressed the noxious stimulation-induced withdrawal reflex that is normally elicited by electrical stimulus. Fos immunoreactivity (Fos-IR) was quantified in all laminae of the L4 segment of the spinal cord.

RESULTS: Noxious stimulation resulted in a general and strong increase in Fos-IR in the ipsilateral dorsal horn, mainly in Laminae I, II, and V. Thoracic spinal block caused a remarkable increase in the amount of Fos-IR in Lamina V, but had no significant effect on the Fos-IR in Laminae I and II.

CONCLUSIONS: The increase in Fos-IR in Lamina V may have resulted from the interruption of a pain-modulating descending mechanism from the brain. A known modulating descending mechanism is the serotonergic system, controlled by the periaqueductal gray. This system inhibits the neurons in the superficial laminae. Another nonserotonergic system originates in the anterior pretectal nucleus. The latter facilitates neurons in the superficial laminae, while neurons in Lamina V are inhibited. We conclude that both systems are probably involved in the observed effects of the peripheral noxious stimulation given in the present model.

METHODS: Rats were divided into four groups (n = 24 each): control, trauma, trauma (T) + sham EA, and T + EA. EA was applied to Zusanli (ST36) and Lanwei (Extra37) acupoints at 20 min after surgery for 30 min, and then performed once a day on postoperative days 1–5. Splenic T cells were isolated and the production and mRNA expression of interleukin (IL)-2, interferon-, IL-4, and IL-10 were assayed. The activation of mitogen-activated protein kinase and the DNA binding activity of nuclear factor (NF)-B and activator protein (AP)-1 were examined.

RESULTS: Paw withdrawal threshold and paw withdrawal latency were significantly increased in the T + EA group compared with the trauma group from postoperative day 1 (paw withdrawal threshold: 5.8 ± 0.7 vs 3.0 ± 0.7 g; paw withdrawal latency: 7.0 ± 0.8 vs 4.5 ± 0.5 s; P < 0.001) to day 5 (9.0 ± 0.6 vs 5.5 ± 0.6 g; 12.0 ± 1.3 vs 7.0 ± 0.8 s; P < 0.001). Th1 cytokine (IL-2 and interferon-) production and mRNA expression in splenic T cells of traumatized rats were significantly decreased on postoperative day 3 (P < 0.001, trauma group versus control group), whereas Th2 cytokine (IL-4 and IL-10) production and mRNA expression were increased (P < 0.001). This was accompanied with a significant depression in the activity of extracellular-regulated protein kinase (ERK)1/2, p38, NF-B, and AP-1 (P < 0.001, trauma group versus control group). EA administration increased Th1 cytokine protein and mRNA expression, suppressed Th2 cytokine protein and mRNA expression (P < 0.05, T + EA group versus trauma group), and increased the activity of ERK1/2, p38, NF-B, and AP-1 (P < 0.001, T + EA group versus trauma group).

CONCLUSIONS: EA regulates a balance between Th1 and Th2 cytokines at protein and mRNA levels in splenic T cells, and, at least in part, involves the signaling pathways of ERK1/2, p38, NF-B, and AP-1. The findings suggest that EA may improve immune suppression after surgical trauma.

METHODS: After premedication and single-injection femoral nerve block, 60 patients undergoing knee arthroscopy were randomly allocated to receive a sciatic nerve block with either NS (n = 30) or US (n = 30). In the US group, the sciatic nerve was localized between the ischial tuberosity and the greater trochanter. In the NS group, the appropriate muscular response (foot plantar flexion or inversion) was elicited (1.5 mA, 2 Hz, 0.1 ms) and maintained to ≤0.5 mA. The volume of the injected local anesthetic was varied for consecutive patients based on an up-and-down method, according to the response of the previous patient. The initial volume was 12 mL. An independent observer evaluated the occurrence of complete loss of pinprick sensation and motor block: positive or negative responses within 20 min after the injection determined a 2-mL decrease or increase for the next patient, respectively.

RESULTS: The mean MEAV₅₀ for sciatic nerve block was 12 mL (95% confidence interval [CI], 10–23 mL) in Group US and 19 mL (95% CI, 15–23 mL) in Group NS (P < 0.001). The effective dose in 95% of cases was 14 mL (95% CI, 12–17 mL) in Group US and 29 mL (95% CI, 25–40 mL) in Group NS (P = 0.008).

CONCLUSIONS: US provided a 37% reduction in the MEAV₅₀ of 1.5% mepivacaine required to block the sciatic nerve compared with NS.

METHODS: One hundred twelve patients scheduled for elective forearm surgery under axillary brachial plexus block were randomly allocated to receive 34 mL lidocaine 1.5% with 3 mL of isotonic saline chloride (control group, n = 28), 34 mL lidocaine 1.5% with 2 mL (100 µg) of fentanyl and 1 mL of isotonic saline chloride (fentanyl group, n = 28), 34 mL lidocaine 1.5% with 2 mL saline chloride and 100 ng (1 mL) naloxone (naloxone group, n = 28), or 34 mL lidocaine 1.5% with 2 mL (100 µg) of fentanyl and 100 ng (1 mL) naloxone (naloxone + fentanyl group, n = 28). A multiple stimulation technique was used in all patients. After performing the block, sensory and motor blockades of radial, median, musculocutaneous, and ulnar nerves were recorded at 5, 15, and 30 min. The onset time of the sensory and motor blockades was defined as the time between the last injection and the total abolition of the pinprick response and complete paralysis, respectively. The duration of sensory and motor blocks was considered as the time interval between the complete block and the first postoperative pain and complete recovery of motor functions.

RESULTS: Sensory and motor onset times were longer in the naloxone (sensory onset time: 15 ± 3, and motor onset time: 21 ± 4) and naloxone + fentanyl group than control or fentanyl groups (sensory onset time: 10 ± 3 min in control group, 10 ± 4 min in fentanyl group, and 17 ± 3 min in naloxone + fentanyl group, motor onset time: 15 ± 5 min in control group, 14 ± 7 min in fentanyl group, and 17.3 ± 3.4 min in naloxone + fentanyl group) (P < 0.001). The duration of time to first postoperative pain and motor blockade was significantly longer in the naloxone (92 ± 10 and 115 ± 10 min) and naloxone + fentanyl groups (98 ± 12 and 122 ± 16 min) than control (68 ± 7 and 89 ± 11 min) and fentanyl groups (68 ± 11 and 90 ± 12 min) (P < 0.001). The time to first postoperative pain was significantly longer in the naloxone and naloxone + fentanyl groups than in the control or fentanyl groups (P < 0.001).

CONCLUSIONS: The addition of an ultra-low dose of naloxone to lidocaine 1.5% solution with or without fentanyl solution in axillary brachial plexus block prolongs the time to first postoperative pain and motor blockade but also lengthens the onset time.

METHODS: Fifty male patients undergoing transurethral surgery received either 8 mg oral ondansetron the evening before surgery plus IV 8 mg ondansetron 15 min before subarachnoid anesthesia or placebo. All patients received 2.2 mL of 0.75% plain ropivacaine intrathecally. Sensory and motor block were assessed 30 min after the intrathecal injection and every 30 min thereafter until recovery from the motor block.

RESULTS: Thirty minutes after spinal injection of ropivacaine, we first measured, in both groups, the time to maximum block for both sensory and motor modalities. The maximum level of the sensory block, defined as decreased sensation, was T8 in the control and T6 in the ondansetron group, and absence of sensation was defined as T11 and T9 for the control and the ondansetron groups, respectively. Regarding block duration, 180 min after spinal injection, sensory block was detected in 11 of 22 and 16 of 24 patients and motor block in 1 of 22 and 0 of 24 in the control and ondansetron groups, respectively. Sensory and motor block did not differ between groups at any measured time point.

CONCLUSIONS: Ondansetron had no effect on the subarachnoid sensory or motor block produced by ropivacaine.