METHODS: Perioperative data from consecutive cardiac surgery patients were prospectively collected between September 2005 and June 2006 in a university-affiliated clinic (n = 1188). During the first 5 mo, 596 patients received aprotinin (Group A); in the next 5 mo, 592 patients were treated with tranexamic acid (Group T). Except for antifibrinolytic therapy, the anesthetic and surgical protocols remained unchanged.

RESULTS: The pre- and intraoperative variables were comparable between the treatment groups. Postoperatively, a significantly higher incidence of seizures was found in Group T (4.6% vs 1.2%, P < 0.001). This difference was also significant in the primary valve surgery and the high risk surgery subgroups (7.9% vs 1.2%, P = 0.003; 7.3% vs 2.4%, P = 0.035, respectively). Persistent atrial fibrillation (7.9% vs 2.3%, P = 0.020) and renal failure (9.7% vs 1.7%, P = 0.002) were also more common in Group T, in the primary valve surgery subgroup. On the contrary, among primary coronary artery bypass surgery patients, there were more acute myocardial infarctions and renal dysfunction in Group A (5.8% vs 2.0%, P = 0.027; 22.5% vs 15.2%, P = 0.036, respectively). The 1-yr mortality was significantly higher after aprotinin treatment in the high risk surgery group (17.7% vs 9.8%, P = 0.034).

CONCLUSION: Both antifibrinolytic drugs bear the risk of adverse outcome depending on the type of cardiac surgery. Administration of aprotinin should be avoided in coronary artery bypass graft and high risk patients, whereas administration of tranexamic acid is not recommended in valve surgery.

METHODS: In a prospective trial, a standardized questionnaire was used in 100 patients for aspirin intake within the 5 days immediately before coronary artery bypass grafting. Whole blood platelet aggregation triggered by arachidonic acid was investigated using the Multiplate® platelet function analyzer.

RESULTS: Eleven of 23 patients with aspirin intake within the 5 days before the intervention showed an abnormal aggregation response. Nine of 77 patients who reported no aspirin intake before surgery had an abnormal aggregation response. There were no significant differences in chest tube drainage and red blood cell transfusion over the first 24 h postoperatively between patients with and without reported aspirin intake. There was no significant difference in chest tube drainage over the first 24 h postoperatively between patients showing normal or abnormal aggregation response. Patients with abnormal aggregation before intervention (<51 U) received significantly more platelet transfusion than patients with normal aggregation (1.1 U compared to 0.3 U, P = 0.001).

CONCLUSIONS: Our results suggest that arachidonic acid-induced aggregation in whole blood may be a better predictor of platelet-related coagulopathy and platelet transfusion than the assessment of aspirin intake by patient self-reporting.

METHODS: Multiplate (M) assays, measuring changes in electrical resistance as aggregation units over time (AU*min), and LTA assays induced by collagen (COL), adenosine diphosphate (ADP) or arachidonic acid (AA) and PFA-100 testing, using epinephrine (PFA100-EPI) or ADP (PFA100-ADP) cartridges, were performed simultaneously using arterial blood samples obtained before induction of anesthesia in 70 consecutive patients scheduled for elective coronary artery bypass grafting. Patients in group A (n = 48) served as controls, patients in group B (n = 11) received aspirin 100 mg/d and those in group C (n = 11) aspirin 100 mg/d and clopidogrel 75 mg/d until the day before surgery.

RESULTS: In controls the median (1st, 3rd quartiles) change in impedance AU*min for M-COL (374 [231–469]) was significantly greater than in patients receiving aspirin (164 [86–211], P = 0.0009) or receiving aspirin and clopidogrel (118 [101–244], P = 0.004). M-ADP values in controls were 258 (158–389), in patients receiving aspirin 261 (159–393), and in patients receiving aspirin and clopidogrel 88 (48–231, P = 0.054). M-AA values were significantly lower in patients receiving aspirin alone (45 [28–60], P = 0.0004) or aspirin and clopidogrel (44 [26–221], P = 0.008) than in controls (200 [86–345]).

The areas under the receiver operating characteristic curves indicating the ability to discriminate patients taking aspirin from those not taking aspirin were comparable for COL and AA assays using whole blood impedance aggregometry or classical LTA (M-COL 0.84 [P = 0.001], LTA-COL 0.85 [P = < .001], M-AA 0.84 [P = < .001] and LTA-AA 0.87 [P = < .001]), but only 0.74 for PFA-100-EPI (P = 0.03). Similarly, for discrimination of patients not taking antiplatelet drugs from patients taking clopidogrel and aspirin the areas under the receiver operating characteristic curve were also comparable for both aggregometry methods M-COL 0.77 (P = 0.006), LTA-COL 0.78 (P = 0.004), M-ADP 0.74 (P = 0.015), LTA-ADP 0.73 (P = 0.018).

CONCLUSION: Results achieved with the bedside Multiplate assays were not different than those obtained with classical aggregometry for detecting the effects of aspirin and clopidogrel in preoperative patients scheduled for elective cardiac surgery.

METHODS: Anesthetized male Wistar rats were instrumented with a coronary artery occluder. After 7 d of recovery, animals were randomized to 1 of 5 groups each containing 8 animals. The i-LPC group underwent 5 min of coronary occlusion to induce i-LPC. Xe-LPC was achieved by administration of xenon (70 volume%) for 15 min. Additional rats were pretreated with the COX-2 inhibitor NS-398 (5 mg kg^–1 body weight i.p.) with and without Xe-LPC. A group of sham operated animals not undergoing i-LPC or Xe-LPC served as controls (Con). After 24 h, all animals were anesthetized and underwent 25 min of myocardial ischemia induced by tightening of the coronary artery occluder followed by 2 h of reperfusion. Myocardial infarct size was assessed by triphenyltetrazolium chloride staining. In additional experiments, hearts were excised at different time points after preconditioning to investigate COX-2 mRNA and protein expression by polymerase chain reaction and infrared Western blot, respectively.

RESULTS: Both i-LPC and Xe-LPC reduced myocardial infarct size (% of the area at risk) compared with Con (i-LPC: 29 ± 7%; Xe-LPC 31 ± 8%, both P < 0.05 vs Con 64 ± 6%). NS-398 abolished the cardioprotective effect of Xe-LPC (61 ± 6%, P < 0.05 vs Xe-LPC). COX-2 mRNA and protein expression was only increased in the i-LPC group, but not in the Xe-LPC group.

CONCLUSION: Xenon induces late myocardial preconditioning that is abolished by functional blockade of COX-2 activity. In contrast to i-LPC, Xe-LPC did not lead to an increased expression of COX-2 mRNA and protein. These data suggest differences in COX-2 regulation in i-LPC and Xe-LPC.

METHODS: One hundred sixty-six patients (aged 18–75 yr) scheduled for thoracic surgery with a DLT were enrolled. Before induction of general anesthesia, 0.1 mg/kg dexamethasone (Group D1), 0.2 mg/kg dexamethasone (Group D2), or a placebo (Group P) were infused IV in a double-blind and prospectively randomized manner. Glottic exposure as defined by Cormack and Lehane score, resistance to DLT insertion, number of intubation attempts, time to achieve intubation, and the duration of tracheal intubation were recorded. At 1 h and 24 h after tracheal extubation, the patients were evaluated for sore throat and hoarseness using a visual analog scale (VAS; where 0 = no pain and 100 = worst pain imaginable).

RESULTS: One hour after tracheal extubation, the incidence of postoperative sore throat and hoarseness, along with the severity of sore throat were lower in Group D1 (31%, P = 0.021; 11%, P = 0.003; and VAS 12.4, P < 0.001, respectively) and D2 (11%, P = 0.001; 4%, P = 0.001; and VAS 6.6, P < 0.001, respectively) compared with Group P (53%, 36% and VAS 30.9, respectively). Twenty-four hours after tracheal extubation, the incidence of postoperative sore throat, hoarseness, and the severity of sore throat were significantly lower in Group D2 (27%, P = 0.002; 15%, P = 0.001; and VAS 29.9, P < 0.002, respectively) compared with Group D1 (47%, 31%, and VAS = 43.9, respectively) and Group P (57%, 45%, and VAS = 51.3, respectively). There was no complication associated with the dexamethasone administration.

CONCLUSION: The prophylactic use of 0.2 mg/kg of dexamethasone significantly decreases the incidence and severity of sore throat and hoarseness 1 h and 24 h after tracheal extubation of a DLT.

METHODS: Forty ASA 1 or 2 children, 1–10 yr of age, were randomized to receive either dexmedetomidine-midazolam or propofol for maintenance of anesthesia for MRI after a sevoflurane induction. Dexmedetomidine was administered as an initial loading dose (1 µg/kg) followed by a continuous infusion (0.5 µg · kg^–1 · h^–1). Midazolam (0.1 mg/kg) was administered IV when the infusion commenced. Propofol was administered as a continuous infusion (250–300 µg · kg^–1 · min^–1). Recovery times and hemodynamic responses were recorded by one nurse who was blinded to the treatments.

RESULTS: We found that the times to fully recover and to discharge from the ambulatory unit after dexmedetomidine administration were significantly greater (by 15 min) than those after propofol. Analysis of variance demonstrated that heart rate was slower and systolic blood pressure was greater with dexmedetomidine than propofol. Respiratory indices for the two treatments were similar. During recovery, hemodynamic responses were similar. Cardiorespiratory indices during anesthesia and recovery remained within normal limits for the children’s ages. No adverse events were recorded.

CONCLUSION: Dexmedetomidine-midazolam provides adequate anesthesia for MRI although recovery is prolonged when compared with propofol. Heart rate was slower and systolic blood pressure was greater with dexmedetomidine when compared with propofol. Respiratory indices were similar for the two treatments.

METHODS: A retrospective chart review of all children presenting as outpatients to a tertiary care, freestanding children’s hospital for elective cardiac surgery between January 1, 2000 and January 31, 2003 was performed. All patient charts in which the admission date matched the cardiac surgical date were examined. Patients were excluded if the preoperative laboratory evaluation was performed outside of our facility, preoperative laboratory investigation was not performed, or the patient was transported by medical transport to our hospital. Patients were grouped according to three methods: the number of cardiac medications (none to four), and cardiac medications, noncardiac medications, and no medications. The presence of electrolyte abnormalities was also examined in the context of cardiac medications with various pharmacologic effects. The primary outcome measure was the incidence of abnormal laboratory values for children taking various cardiac medications.

RESULTS: Of the 933 initial entries found, 774 met the investigational criteria and were included in the analysis. Although statistically significant differences in preoperative electrolytes were associated with the use of cardiac and noncardiac medication, there was no clinical value to this correlation. The data demonstrate a very low incidence of hypokalemia and hypomagnesemia in the entire study population.

CONCLUSION: Preoperative electrolyte disturbances in children and young adults presenting for cardiac surgery are uncommon. The concern of hypokalemia or hypomagnesemia important in the adult population taking cardiac medications was not identified in the pediatric population. These data do not support the need for routine preoperative electrolyte evaluation in children taking cardiac medications.

METHODS: Information was collected on a standardized data collection form. Clinical information obtained included user characteristics, patient characteristics, type and duration of operation, details of airway management and anesthetic technique, details of adverse events, and postoperative status of the patient.

RESULTS: Use of the PLMA was documented in 2114 patients by 81 anesthesiologists (57% trainee, 43% staff grade). The insertion success rate was 99% within a maximum of 3 attempts. Mean airway leak pressure was 28 (11–40) cm H₂O. In 3.2% of cases, the PLMA was abandoned in favor of the endotracheal tube. Ventilation was controlled in 98%. Clinically "relevant" adverse events were recorded in 3.3% of all cases, of which 0.6% were classified as "serious." No long-term adverse sequelae resulted. No signs of aspiration were found in 12 patients with apparent regurgitation of gastric fluid through the drain tube of the PLMA. Five cases of difficult ventilation and 16 cases of difficult endotracheal intubation were successfully managed by the use of the PLMA.

CONCLUSION: This study demonstrates that airway management using the PLMA is safe and effective in a general practice setting. The results support the assumption that a correctly positioned PLMA can protect from pulmonary aspiration of regurgitate gastric fluid. The data also support use of the PLMA for the management of the difficult airway.

METHODS: In 107 ASA physical status I–III patients, anesthesia was induced with propofol, tracheal intubation facilitated with neuromuscular blockade, and ventilation controlled with 50% nitrous oxide in oxygen to maintain end-tidal carbon dioxide concentrations between 35 and 45 mm Hg. Isoflurane or desflurane was administered in a 1 L/min inflow rate at FD concentrations sufficient to maintain FA at 0.6 minimum alveolar anesthetic concentration (0.7% or 3.7%, respectively). FD, FI, and FA were measured 5, 10, 20, 40, 60, 90, 120,150, and 180 min after starting potent inhaled anesthetic delivery.

RESULTS: Fifty-nine patients received isoflurane and 48 received desflurane. BMI ranged between 18 and 63 kg/m² and demographic variables did not differ between anesthetic groups. For isoflurane, FD/FA or FI/FA weakly (but significantly) correlated with BMI at 9/18 time points whereas for desflurane FD/FA or FI/FA correlated significantly with BMI at only one time point (P < 0.01). After dividing each group into nonobese (BMI < 30) and obese (BMI ≥ 30) patients, with isoflurane, FD/FA or FI/FA was higher in obese patients at four time points whereas there was no difference between nonobese and obese patients for desflurane. Patients receiving isoflurane took longer to respond to command after discontinuing anesthesia but obesity did not increase or decrease awakening time for either isoflurane or desflurane. When BMI was used to normalize FI/FA and FD/FA the median values for isoflurane consistently exceeded the median value for desflurane by factors ranging from 3 to 5, values comparable to the ratios of their blood/gas (3.1), muscle/gas (4.6), and fat/gas (5.4) partition coefficients.

CONCLUSION: BMI modestly affects FD/FA and FI/FA, and this effect is most apparent for an anesthetic having a greater solubility in all tissues. An increased BMI increases anesthetic uptake and, thus, the need for delivered anesthetic to sustain a constant alveolar anesthetic concentration, particularly with a more soluble anesthetic. However, the increase with an increased body mass is small.

METHODS: Sixty patients undergoing lower abdominal surgery were randomly divided into four groups according to the anesthetic to be administered; namely, sevoflurane (group S), propofol (group P), both sevoflurane and dexmedetomidine (group SD), or propofol and dexmedetomidine (group PD) as maintenance general anesthetics. After induction, anesthesia was maintained with sevoflurane (0.6%–1.5%) in group S, propofol (2–5 mg/kg/h) in group P, sevoflurane and dexmedetomidine (1 µg/kg over 10 min followed by 0.4 µg/kg/h until the end of surgery) in group SD, and propofol and dexmedetomidine in group PD with continuous epidural infusion. Bispectral Index values were maintained within 45 ± 5 by changing the concentration of sevoflurane or the infusion rate of propofol in all groups. The time between the interruption of maintenance general anesthetics and eye opening was measured. Postoperative cognitive function was evaluated using the Short Orientation Memory Concentration Test.

RESULTS: The time to eye opening of groups S (8.5 ± 2.5 min, mean ± sd; n = 15) and SD (12.0 ± 3.3 min) were comparable, whereas that of group PD (21.7 ± 7.1 min) was longer than that of group P (11.0 ± 4.4 min). The time to eye opening of group PD was significantly (P < 0.001) longer than those of the other three groups. The scores of Short Orientation Memory Concentration Test between groups S and P were similar and were not changed by co-administration of dexmedetomidine.

CONCLUSION: When co-administered with dexmedetomidine, sevoflurane produced a shorter time to eye opening than propofol. Postoperative cognitive function was not affected by dexmedetomidine administration. These results suggest dexmedetomidine may delay recovery when given as an adjuvant to propofol during total IV anesthesia.

METHODS: The influence of propofol on wild type and mutant (₁S267M, ₁S267I, ₁S267Mβ, ₁S267Iβ) glycine receptors expressed in human embryonic kidney 293 cells was investigated by using the whole-cell clamp technique.

RESULTS: Mutation of the ₁ subunit TM2 serine residue to either isoleucine or methionine decreased the sensitivity of the receptor to glycine, and abolished the direct activation of the glycine receptor by propofol. Additionally, the methionine and particularly the isoleucine mutation decreased the glycine-enhancing actions of propofol.

CONCLUSIONS: The nature of the TM2 residue (267) of the glycine ₁ subunit influences the glycine modulatory effect of propofol and direct activation of the receptor by this anesthetic. A comparison of the impact of such complementary mutations on the interaction of propofol with glycine and GABA_A receptors should permit a better understanding of the molecular determinants of action of propofol on these structurally related receptors and may aid in the development of selective glycine receptor modulators.

METHODS: Rat II/R injury was produced by clamping the superior mesenteric artery for 1 h followed by 3 h of reperfusion. Thirty rats were randomly allocated into control, injury (II/R) and propofol (pretreatment) groups (n = 10 per group). In the propofol group, propofol 50 mg/kg, a dose that has been shown to cause the loss of reflex responses to a painful stimulus while remaining sensitive to skin incision in rats, was administered intraperitoneally 30 min before inducing intestinal ischemia, while animals in control and untreated injury groups received an equal volume of intralipid. Intestinal mucosal epithelial apoptosis was detected via electron microscopy and TUNEL analysis. Lipid oxidation product malondialdehyde and the activities of superoxide dismutase were assessed by colorimetric analyses. Ceramide generation and sphingomyelinase mRNA expression in intestinal mucosa were determined by high performance thin layer chromatography and reverse transcriptase polymerase chain reaction, respectively.

RESULTS: II/R caused intestinal mucosal epithelial apoptosis and over-production of ceramide accompanied by up-regulation of sphingomyelinase mRNA expression and increases in lipid oxidation (all P < 0.01 versus control). Propofol pretreatment significantly attenuated these changes (all P < 0.01, propofol versus injury).

CONCLUSION: The findings indicate that propofol pretreatment attenuates II/R-induced intestinal epithelial apoptosis, which might be attributable to its antioxidant property modulating the ceramide pathway.

METHODS: PC12 cells were stimulated with ACh in the presence or absence of nicorandil, and phosphorylation of ERK was examined by a Western blot analysis. We also examined the effects of nicorandil on the ERK activation induced by 4β-phorbol 12-myristate 13-acetate, an activator of protein kinase C, or ionomycin, a calcium ionophore. Intracellular Ca²⁺ increase was visualized in fluo-3-loaded PC12 cells using fluorescence microscopy.

RESULTS: Nicorandil inhibited ACh-induced ERK activation in a concentration-dependent manner. The inhibition was abolished by glibenclamide, an adenosine triphosphate-sensitive potassium channel blocker. Nicorandil suppressed the ERK activation induced by ionomycin but not 4β-phorbol 12-myristate 13-acetate. Pretreatment of PC12 cells with nicorandil reduced the intracellular Ca²⁺ concentration stimulated by ACh.

CONCLUSIONS: Nicorandil inhibits muscarinic activation of the ERK signaling pathway by reducing the intracellular Ca²⁺ concentration.

METHODS: Ovalbumin-sensitized rabbits were randomly assigned to several protocol groups: Group C comprised untreated animals; in the other three groups, either H1 and H2 histaminic receptor blockade was performed, leaving the M1, M2, and M3 muscarinic receptors functional (Group M123), or combining this treatment with M3 muscarinic receptor blockade (Group M12), or with vagotomy (Group M3). Respiratory system impedance was measured over a 90-s period, during which succinylcholine, mivacurium or atracurium was administered. To monitor the changes in lung mechanics, respiratory system impedance was averaged in a 2-s time window and fitted by a model featuring airway resistance and inertance and tissue damping and elastance.

RESULTS: The peak increases in airway resistance in Group C were greatest with succinylcholine (79 ± 17[SE]%) and mivacurium administration (75% ± 12%), whereas they were lower after attracurium (40% ± 11%). These changes were markedly attenuated by both histamine and muscarinic receptor blockade with the largest reduction in Group M3 for succinylcholine (14% ± 5.2%), and in Group M123 for mivacurium (5.1% ± 9.1%) and attracurium (7.8% ± 4.0%).

DISCUSSION: Although the bronchospasm developing in the allergic airways after muscle relaxants is mediated primarily by the histaminic pathway, the interactions of succinylcholine on the M1, M2, and M3 receptors, those of atracurium on the M1 and M2 receptors, and those of mivacurium on the M3 receptors may also play a role.

METHODS: The amount of total O₂ consumed by the Magellan-2200 (Oceanic Medical Products, Atchison, KS) FAM with pneumatically controlled ventilator was calculated using the ideal gas law and the measured mass of O₂ consumed from E cylinders. DG to the bellows canister assembly was measured with the Wright Respirometer Mk 8 (Ferraris Respiratory Europe, Hertford, UK). PC gas consumption was calculated by subtracting DG and fresh gas flow (FGF) from the total O₂ consumed from the E cylinder. The delivered tidal volume (V_T) was measured with a pneumotach (Hans Rudolph, KS City, MO). Three different V_T were tested (500, 750, and 1000 mL) with two lung models (HC and LC) using the Vent Aid Training Test Lung (MI Instruments, Grand Rapids, MI). Respiratory variables included an I:E of 1:2, FGF of 1 L/min, and respiratory rate of 10 breaths/min.

RESULTS: Total O₂ consumption was directly proportional to V_T and inversely proportional to compliance. The smallest total O₂ consumption rate (including FGF) was 9.3 ± 0.4 L/min in the HC-500 model and the largest was 15.9 ± 0.5 L/min in the LC-1000 model (P < 0.001). The mean PC circuitry consumption was 3.9 ± 0.24 L/min or 390 mL ± 24 mL/breath.

CONCLUSIONS: To prepare for loss of central DG supply, patient safety will be improved by estimating cylinder duration for low total thoracic compliance. Using data from the smaller compliance and greatest V_T model (LC-1000), a full O₂ E cylinder would be depleted in <42 min, whereas a full H cylinder would last approximately 433 min.

METHODS: Eighty-five adults with a Body Mass Index >30 kg/m², scheduled for elective surgery, consented to participate in this prospective randomized equivalence study conducted in a teaching hospital. The randomization scheme used permuted blocks with subjects equally allocated to be positioned using either the blanket method or the table-ramp method. The end-point in either case was to achieve a head-elevated position, where the patient's external auditory meatus and sternal notch were in the same horizontal plane. Although all patients were positioned by the same anesthesiologist, laryngoscopy and tracheal intubation were performed by trainees with various levels of expertise. Standard IV induction and tracheal intubation techniques were used. The time from loss of consciousness to the time after tracheal intubation when end-tidal CO₂ was detected was recorded. The effectiveness of mask ventilation and quality of laryngeal exposure were also noted.

RESULTS: The mean time (sd) to tracheal intubation was 175 (66) s in the blanket group, as compared to 163 (71) s in the table-ramp group. Assuming the bounds for equivalence are –55,55 s, our study found a 95% confidence interval of –36.22, 13.52 s using two one-sided tests for equivalence corresponding to a significance level of 0.05. There was no difference in the number of attempts at laryngoscopy (P = 0.21) and tracheal intubation (P = 0.76) required to secure the airway between the two groups.

CONCLUSIONS: Before induction of anesthesia, obese patients can be positioned with their head elevated above their shoulders on the operating table, on a ramp created by placing blankets under their upper body or by reconfiguring the OR table. For the purpose of direct laryngoscopy and tracheal intubation, these two methods are equivalent.

METHODS: We performed a prospective study of adult patients with a Body Mass Index (BMI) ≥40 over a 12-mo period comparing the MMP and EMS. The performance of the MMP, EMS, and other commonly used tests was compared for the ability to predict difficult laryngoscopy, defined as a Cormack-Lehane grade of 3 or 4. Positioning and direct laryngoscopic techniques were not standardized. The incidence of difficult laryngoscopy and difficult intubation was compared in patients with BMI ≥ or <40.

RESULTS: Three-hundred-forty-six patients with a BMI ≥40 were evaluated with both the MMP and EMS and received direct laryngoscopy. On average, craniocervical extension decreased the MMP class (P < 0.0001). Compared to the MMP, the EMS improved specificity and predictive value while maintaining sensitivity. Compared to the MMP and other tests, an EMS class of 3 or 4 and a diagnosis of diabetes mellitus were the only statistically significant predictors of difficult laryngoscopy in the morbidly obese. There was no difference in the incidence of difficult laryngoscopy or intubation in the morbidly obese compared to patients with a BMI <40.

CONCLUSIONS: The EMS was superior to the MMP in the prediction of difficult laryngoscopy in the morbidly obese population. A diagnosis of diabetes mellitus also warrants further investigation as a predictor of difficult laryngoscopy in this population. Finally, this study supports previous findings that morbid obesity is not itself a predictor of difficult laryngoscopy or intubation.

METHODS: We analyzed 815,077 ASA physical status 1, 2, and 3 elective surgery patients in the Department of Veterans Affairs National Surgical Quality Improvement Program database to identify patients who died on the day of surgery. We then attempted to identify factors predictive of unexpected death and to identify potential areas for improvement in care. A subset of the cases underwent individual chart review as well to identify areas for improvement in anesthesia care.

RESULTS: Of the total patients, 0.08% died on the day of surgery. The strongest predictive factor by multiple variable regression was the type of surgery, with aortic surgery resulting in an odds ratio of 13.67, (95% CI 9.76–19.17). Other factors predictive of death were identified by multiple variable regressions and included low albumin, existence of dyspnea, and elevated bilirubin or creatinine. Chart reviews of 88 of the deaths found that opportunities for improved anesthesia care were present in 13 of the 88. We estimated that a death that might have been prevented by improved anesthesia care occurred in approximately 1/13,900 cases. Myocardial infarction and hemorrhage were frequently identified factors. An unexpected factor was that the period between the conclusion of surgery and the final transfer of care in recovery was a time when many of the deaths occurred.

CONCLUSIONS: We conclude that, although patient and surgical factors lead to the vast majority of deaths on the day of surgery, there are identifiable areas for reducing the incidence of such deaths by improvements in anesthesia care.

METHODS: Before each trial, the anesthesia machine was contaminated for 2 h with 3% sevoflurane and then prepared by changing the CO₂ absorbent, removing the vaporizer(s), and mounting a clean circuit and artificial lung. The basic flush procedure consisted of oxygen 10 L/min with the ventilator set to a tidal volume of 600 mL at a rate of 10/min. Residual sevoflurane in the inspiratory limb of the circuit was measured using an ambient air analyzer capable of measuring sevoflurane to <1 ppm. Results were analyzed using log-linear regression of residual concentration as a function of time. This model was used to estimate the time required to achieve a desired residual anesthetic concentration.

RESULTS: Times to achieve 10 and 5 ppm in the Dräger Narkomed GS were 11 and 18 min, respectively. For the Dräger Fabius anesthesia machine, times to 10 and 5 ppm were 75 and 104 min, respectively. Several maneuvers to accelerate clearance of residual sevoflurane from the Dräger Fabius resulted in only modest reductions in these times (10 and 5 ppm times 40–50 min and 60–80 min, respectively). Insertion of an activated charcoal filter (QED®, Anecare Laboratories, Salt Lake City, UT) into the inspiratory limb of the Dräger Fabius circuit reduced the residual anesthetic concentration to <5 ppm within 10 min; this concentration was maintained for >6 h despite a fresh gas flow of only 2 L/min after the first 15 min.

DISCUSSION: Preparation of the Dräger Fabius anesthesia machine using conventional flushing techniques required almost 10 times as long as an older, conventional anesthesia machine. If a prolonged flush is impractical or impossible, we describe a procedure using an activated charcoal filter inserted on the inspiratory limb of the breathing circuit which can effectively scrub residual sevoflurane to a concentration <5 ppm within 10 min. This procedure includes an initial 5 min flush without the activated charcoal filter followed by a 5 min flush with the charcoal filter, after which the machine is ready for use in the malignant hyperthermia-susceptible patient. The charcoal filter must remain on the machine for the remainder of the anesthetic, and the fresh gas flow should be maintained ≥10 L/min for the first 5 min, and ≥2 L/min thereafter.

METHODS: We measured levels of blood hydroperoxides as an index of oxidative injury of cellular components, as well as plasma ferric-reducing ability as an index of total antioxidant potential, during sigmoidectomy under four conditions: open sigmoidectomy with sevoflurane anesthesia, laparoscopic sigmoidectomy with sevoflurane anesthesia, open sigmoidectomy with propofol anesthesia, and laparoscopic sigmoidectomy with propofol anesthesia.

RESULTS: Ferric-reducing ability decreased significantly during surgery for the open sigmoidectomy with sevoflurane anesthesia, by 387 ± 153 mmol/L, though the hydroperoxides level did not change, showing that oxidative stress increases in surgical patients. However, its toxicity may not be high enough to injure cellular components, since hydroperoxides, which are typical oxidized products of cellular components, did not increase. There were no changes in the hydroperoxides level or the ferric-reducing ability for the laparoscopic sigmoidectomy with sevoflurane anesthesia, indicating that this procedure does not increase surgical oxidative stress. Only hydroperoxides decreased significantly at the end of surgery for the open sigmoidectomy with propofol anesthesia and laparoscopic sigmoidectomy with propofol anesthesia, by 120 ± 73 and 144 ± 107 UCarr (1 UCarr corresponds to 0.8 mg/L H₂O₂), respectively.

CONCLUSIONS: It seems certain that open abdominal surgery of the intestinal tract increases intraoperative oxidative stress. A laparoscopic procedure was not associated with oxidative stress, and propofol anesthesia reduced it by apparently functioning as an antioxidant.

METHODS: We performed a long-term prospective study in a medical-surgical ICU. Patients with severe sepsis (n = 170) admitted for >48 h were included in the study. We used the Short-form 36 to evaluate the HRQOL of severe sepsis patients before ICU and hospital stay and at 3 and 6 mo after ICU discharge. Furthermore, we compared the results for ICU admission and 6 mo after ICU discharge with those of an age-matched general Dutch population.

RESULTS: At 6 mo after ICU discharge, 95 patients could be evaluated (eight patients were lost to follow-up, 67 died). HRQOL showed a multidimensional decline during the ICU stay and gradual improvement over the 6 mo after ICU discharge for the social functioning, vitality, role-emotional, and mental health dimensions. However, 6 mo after ICU discharge, scores for the physical functioning, role-physical, and general health dimensions were still significantly lower than preadmission values. Physical and Mental Component Scores changed significantly over time. In particular, the Mental Component Score showed a small decline at ICU discharge but recovered rapidly, and at 6 mo after ICU discharge had improved to near normal values. In addition, Short-form 36 scores were lower than those in a matched general population in six of the eight dimensions, with the exception of social functioning and bodily pain. Interestingly, the preadmission HRQOL in surviving patients was already lower in three of the eight dimensions (role-physical, mental health, and vitality) when compared with the general population.

CONCLUSIONS: Severe sepsis patients demonstrate a sharp decline of HRQOL during ICU stay and a gradual improvement during the 6 mo after ICU discharge. Recovery begins after ICU discharge to the general ward. Nevertheless, recovery is incomplete in the physical functioning, role-physical, and general health dimensions at 6 mo after ICU discharge compared with preadmission status.

METHODS: In this prospective, randomized, double-blind study, we examined the analgesic efficacy of demand-only PCEA and PCEA with background infusion. We recruited 300 nulliparous parturients. Analgesia was initiated with intrathecal ropivacaine 2 mg and fentanyl 15 µg and maintained with epidural ropivacaine 0.1% with fentanyl 2 µg/mL. Parturients were randomized to one of three groups. Group 0: demand-only PCEA, bolus of 5 mL, lockout interval of 15 min. Group 5: background infusion of 5 mL/h, bolus of 5 mL, lockout interval of 12 min. Group 10: background infusion of 10 mL/h, bolus of 5 mL, lockout interval of 10 min. The maximum dose of all groups was 20 mL/h. The primary outcome was incidence of breakthrough pain. Secondary outcomes included intrapartum pain scores, neuraxial blockade characteristics, side effects, the total and hourly volume of ropivacaine, neonatal outcomes, and obstetric outcomes.

RESULTS: The incidence of breakthrough pain and the maximum visual analog scale (0–100 mm scale) pain scores were higher in Group 0 versus Groups 5 and 10 (43% vs 17% and 11%, P < 0.001 and 37 ± 28 vs 22 ± 26 and 16 ± 25 [mean ± sd], P < 0.001), respectively. Group 10 had a longer duration of effective analgesia compared with Group 0 (mean 895 min, 95% CI 823–966 vs 565 min, 95% CI 454–677, P < 0.001) and increased ropivacaine consumption, and was associated with a longer duration of the second stage of labor.

CONCLUSION: Demand-only PCEA (5-mL bolus, 15-min lockout interval) resulted in less local anesthetic consumption but an increased incidence of breakthrough pain, higher pain scores, shorter duration of effective analgesia, and lower maternal satisfaction, when compared with PCEA with background infusion (5-mL bolus, 10–12-min lockout interval, and 5–10 mL/h infusion).

METHODS: The base salary system was stratified according to rank and clinical experience. The supplemental pay structure was linked to electronic patient records and a scheduling database to award points for clinical activity; educational, research, and administrative points systems were constructed in parallel. We analyzed monthly American Society of Anesthesiologist (ASA) unit data for operating room activity and physician compensation from 2000 through mid-2007, excluding the 1-yr implementation period (July 2004–June 2005) for the new model.

RESULTS: Comparing 2005–2006 with 2000–2004, quarterly ASA units increased by 14% (P = 0.0001) and quarterly ASA units per full-time equivalent increased by 31% (P < 0.0001), while quarterly ASA units per anesthetizing location decreased by 10% (P = 0.046). Compared with a baseline year (2001), Instructor and Assistant Professor faculty compensation increased more than Associate Professor and Professor faculty (P < 0.001) in both pre- and postimplementation periods. There were larger compensation increases for the postimplementation period compared with preimplementation across faculty rank groupings (P < 0.0001). Academic and educational output was stable.

DISCUSSION: Implementing a productivity-based faculty compensation model in an academic department was associated with increased mean supplemental pay with relatively fewer faculty. ASA units per month and ASA units per operating room full-time equivalent increased, and these metrics are the most likely drivers of the increased compensation. This occurred despite a slight decrease in clinical productivity as measured by ASA units per anesthetizing location. Academic and educational output was stable.

METHODS: (A) There were 164 nomination letters submitted from 2004 through 2007 for 45 nominees. The letters contained n = 2659 full sentences and n = 50,821 words. We systematically created a list of 36 terms related to finance, profit, and productivity. We also analyzed the frequency of use of these terms relative to the use of the 15 most common relationship-oriented terms (e.g., compassion, encourage, mentor, and respect). (B) The salary/career survey’s questions relevant to anesthesia group productivity had responses from 303 US OR directors, 97% of whom were nurses. We tested the strength of the relationship between the budget responsibility of the OR nursing director and his or her annual salary.

RESULTS: (A) 2.6% of sentences in the nomination letters included at least one term related to profit and productivity (95% confidence interval 2.0%–3.2%). Relationship-oriented terms were 9.0 times more prevalent (95% confidence interval 7.1–11.4). (B) There was statistically significant positive proportionality between the OR nursing director’s operational budget (including personnel) and his or her salary (Pearson r = 0.64, P < 0.001). The 10th percentile of the operational budget was $1 million and the 90th percentile was $36 million. The budget of $1 million was associated with a salary 22% less than the median and the budget of $36 million was associated with a salary 22% larger than the median.

CONCLUSION: Through (A) organizational constituencies, and (B) compensation, many US OR nursing directors likely are encouraged to enhance relations with nursing staff, not to champion organizational initiatives that would reduce under-utilized OR time and OR nursing labor costs. Resulting decisions can differ from those that would increase the productivity (profit) of the anesthesia group. Anesthesia groups need to champion initiatives to increase anesthesia productivity, while being sensitive to institutional expectations of nursing directors.

METHODS: Individual published equations (derived from prior animal and human studies) were implemented into a comprehensive simulation program. Included in the normal physiological modeling was cerebral blood flow, arterial blood pressure, and carbon dioxide (CO₂) partial pressure. We also added external and pathological perturbations, such as head-up position and intracranial hemorrhage.

RESULTS: The model performed clinically realistically given inputs of published traumatized patients and cases encountered by clinicians. The pulsatile nature of the output graphics was easy for clinicians to interpret. The maneuvers simulated include changes of basic physiological inputs (e.g., arterial blood pressure, central venous pressure, CO₂ tension, head-up position, and respiratory effects on vascular pressures) as well as pathological inputs (e.g., acute intracranial bleeding, and obstruction of cerebrospinal outflow).

CONCLUSIONS: Based on the results, we believe the model would be useful to teach complex relationships of brain hemodynamics and study clinical research questions such as the optimal head-up position, the effects of intracranial hemorrhage on cerebral hemodynamics, as well as the best CO₂ concentration, to reach the optimal compromise between intracranial pressure and perfusion. With the ability to vary the model’s complexity, we believe it would be useful for both beginners and advanced learners. The model could also be used by practicing clinicians to model individual patients (entering the effects of needed clinical manipulations and then running the model to test for optimal combinations of therapeutic maneuvers).

METHODS: To induce brain ischemia reperfusion, we introduced a silicone-coated monofilament nylon suture into the origin of the middle cerebral artery, withdrawing it after 90 min. Treatment groups (n = 32), received propofol (0.1 mL · kg^–1 · min^–1) infusion for 30 min before occlusion; the vehicle group (n = 32) and the sham-operated group (n = 28), which received the intralipid vehicle at the same time and rate. To assess cerebral infarct volume, we used 2, 3, 5-triphenyl-tetrazolium chloride staining; wet–dry weight ratio was the basis for cerebral edema estimation, and we used immunohistochemistry and Western blot to detect AQP4 expression.

RESULTS: The wet–dry weight ratio decreased from 86.89% ± 0.71% in the vehicle group (n = 6) to 72.42% ± 0.74% in the propofol group (n = 6), corresponding to an average decrease of 16%. In parallel and based on immunohistochemical semi-quantification, the propofol group exhibited remarkable attenuation of AQP4 over-expression in the ischemic border zone compared with the vehicle group: 1.28 ± 0.03 vs 1.40 ± 0.05, n = 7, respectively; P < 0.05. Values derived from Western blot quantification were similarly decreased in the propofol group compared to the vehicle group: 20.85% ± 4.18% vs 31.67% ± 3.23%, n = 4, respectively; P < 0.05. However, infarct volume and neurologic deficit in postischemic rats in the propofol group were not statistically different from values in the vehicle group.

CONCLUSIONS: We conclude that prestroke treatment with propofol reduces postischemic cerebral edema in rats, possibly through inhibiting AQP4 over-expression in the boundary zone of ischemia.

METHODS: Two-hundred-twenty-five patients with moderate-to-severe pain after third molar extraction were randomized to receive a single dose of IN morphine 7.5 mg or 15 mg, IV morphine 7.5 mg, oral morphine 60 mg or placebo. Pain intensity was assessed using visual analog and categorical scales, and pain relief using a categorical scale. Outcomes included total pain relief, pain intensity difference, summed pain intensity difference, time to analgesic onset, time to requesting rescue medication, and patients’ global evaluation of their treatment. Safety assessments included adverse event recording and nasal examinations.

RESULTS: Across the various efficacy outcomes, both IN morphine doses were statistically similar to the positive comparators (IV and oral morphine), and all four morphine treatments were statistically superior to placebo. Overall, IN morphine 15 mg presented an efficacy profile similar to IV morphine 7.5 mg; both treatments demonstrated rapid onset of efficacy, generally persistent throughout the 6-h assessment period. The lower dose of IN morphine, 7.5 mg, was statistically similar to the other active treatments at 2 h and 6 h and similar to placebo at 4 h. Study medications were generally well tolerated, with no withdrawals due to adverse events or other safety concerns, and no serious adverse events reported. The most frequently reported adverse events were typical systemic opioid effects.

CONCLUSIONS: IN morphine offers a noninvasive alternative to IV morphine for postoperative analgesia.

METHODS: This was a double-blind, placebo-controlled study in patients undergoing major surgery who were randomized to receive intranasal ketorolac, 10 mg or 30 mg, or placebo every 8 h for 40 h. After surgery, patients with pain intensity of at least 40 on a 100-mm visual analog scale were assessed at 30 min and at 1, 2, 3, 4, 5, 6, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, and 48 h after receiving the study drug. Patient-controlled IV morphine provided supplemental analgesia.

RESULTS: Among 127 patients enrolled, morphine use during the first 24 h was significantly less in patients receiving 30 mg of ketorolac (37.8 mg) than in the placebo group (56.5 mg) and in the 10-mg ketorolac group (54.3 mg). Over 48 h, the 30-mg ketorolac group used significantly less morphine than the placebo group. Summed pain intensity differences at 4 and 6 h significantly favored the 30-mg ketorolac group over the other groups. The rates of pyrexia and tachycardia were significantly lower in the ketorolac 30-mg group than in the placebo group. Other adverse events were reported with similar frequency in all treatment groups and most were considered unrelated to treatment.

CONCLUSION: Thirty milligrams of intranasal ketorolac demonstrated significant analgesic efficacy compared to 10 mg of intranasal ketorolac and placebo.

METHODS: Ninety females undergoing total abdominal hysterectomy with spinal anesthesia were randomly assigned to six groups consisting of placebo (normal saline, C), fentanyl (three bolus of 1 µg · kg^–1, F), ketamine (infusion of 15 µg · kg^–1 · min^–1, K), ketamine and fentanyl (infusion of 15 µg · kg^–1 · min^–1 ketamine plus three bolus of 1 µg · kg^–1 fentanyl, FK), lornoxicam (one bolus of 8 mg, L), and lornoxicam and fentanyl (one bolus of 8 mg lornoxicam plus three bolus of 1 µg · kg^–1 fentanyl, FL). Cumulative morphine consumption, pain score, and adverse effects were recorded at 1, 3, 6, 12, 24, and 48 h postoperatively.

RESULTS: Cumulative morphine consumption in Group F was significantly more than that in Group C at 3, 6, and 12 h postoperatively (P < 0.05). Postoperative cumulative morphine consumption was similar in Groups C, K, FK, L, and FL. No differences in postoperative pain scores were observed among groups. More patients in Groups K and FK had hallucinations during and/or after surgery than those in Group C (P < 0.05).

CONCLUSIONS: Our data suggest that the increase of postoperative morphine requirements induced by intraoperative administration of fentanyl could be prevented by ketamine or lornoxicam.

METHODS: We searched the databases of Medline (1966–2007), CINAHL, The Cochrane Central Register of Controlled Trials (2006), and Scopus for randomized controlled trials investigating the use of acupuncture for chronic headache. Studies were included in which adults with chronic headache, including migraine, tension-type headache or both, were randomized to receive needling acupuncture treatment or control consisting of sham acupuncture, medication therapy, and other nonpharmacological treatments. We extracted the data on headache intensity, headache frequency, and response rate assessed at early and late follow-up periods.

RESULTS: Thirty-one studies were included in this review. The majority of included trials comparing true acupuncture and sham acupuncture showed a trend in favor of acupuncture. The combined response rate in the acupuncture group was significantly higher compared with sham acupuncture either at the early follow-up period (risk ratio [RR]: 1.19, 95% confidence interval [CI]: 1.08, 1.30) or late follow-up period (RR: 1.22, 95% CI: 1.04, 1.43). Combined data also showed acupuncture was superior to medication therapy for headache intensity (weighted mean difference: –8.54 mm, 95% CI: –15.52, –1.57), headache frequency (standard mean difference: –0.70, 95% CI: –1.38, –0.02), physical function (weighted mean difference: 4.16, 95% CI: 1.33, 6.98), and response rate (RR: 1.49, 95% CI: 1.02, 2.17).

CONCLUSION: Needling acupuncture is superior to sham acupuncture and medication therapy in improving headache intensity, frequency, and response rate.

METHODS: Patients undergoing mandibular third molar extraction and experiencing moderate-to-severe pain postsurgery were randomized to receive single, oral doses of tapentadol HCl (25, 50, 75, 100, or 200 mg), morphine sulfate (60 mg), ibuprofen (400 mg; used to establish model sensitivity), or placebo. Mean total pain relief over 8 h (TOTPAR-8) was the primary end point. Secondary end points included mean total pain relief over 4 h (TOTPAR-4) and onset of analgesia. Pairwise comparisons of study drug to placebo were assessed using the Fisher least significant difference test. Adverse events were recorded.

RESULTS: Four hundred patients were randomized to treatment and completed the study. Compared with placebo, mean TOTPAR-8 was significantly greater for tapentadol HCl 50 mg (P = 0.041), 75 mg (P = 0.001), 100 mg (P < 0.001), and 200 mg (P < 0.001); morphine sulfate 60 mg (P < 0.001); and ibuprofen 400 mg (P < 0.001) in a nonparametric analysis of the primary end point. The significantly higher TOTPAR-8 score for ibuprofen compared with placebo established the sensitivity of the model. Mean TOTPAR-4 was higher and onset of action appeared more rapid for tapentadol HCl 200 mg than morphine sulfate 60 mg. Pain relief scores with morphine sulfate 60 mg were between those of tapentadol HCl 100 and 200 mg. The incidence of nausea and vomiting appeared to be lower with all doses of tapentadol HCl compared with morphine sulfate 60 mg, but was not statistically significant.

CONCLUSION: Single oral doses of tapentadol 75 mg or higher effectively reduced moderate-to-severe postoperative dental pain in a dose-related fashion and were well-tolerated relative to morphine. These data suggest that tapentadol is a highly effective, centrally acting analgesic with a favorable side effect profile and rapid onset of action.

METHODS: Fifty females undergoing elective total abdominal hysterectomy were randomized to undergo TAP block with ropivacaine (n = 24) versus placebo (n = 26) in addition to standard postoperative analgesia comprising patient-controlled IV morphine analgesia and regular diclofenac and acetaminophen. All patients received a general anesthetic and, before surgical incision, a bilateral TAP block was performed using 1.5 mg/kg ropivacaine (to a maximal dose of 150 mg) or saline on each side. Each patient was assessed postoperatively by a blinded investigator in the postanesthesia care unit and at 2, 4, 6, 12, 24, 36, 48 h postoperatively.

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