Kazim Karaaslan

The effects of levobupivacaine versus levobupivacaine plus magnesium infiltration on postoperative analgesia and laryngospasm in pediatric tonsillectomy patients

BACKGROUND The aim of this study was to evaluate whether the addition of magnesium to levobupivacaine will decrease the postoperative analgesic requirement or not, and to investigate the possible preventive effects on laryngospasm. METHODS Seventy-five children undergoing elective tonsillectomy and/or adenoidectomy surgery. The drug was prepared as only NaCl 0.9% for the first group (Group S, n=25), levobupivacaine 0.25% for the second group (Group L, n=25), and levobupivacaine 0.25% plus magnesium sulphate 2mg/kg for the third group (Group M, n=25). Pain was recorded at 15th minute, 1st, 4th, 8th, 16th, and 24th hour postoperatively. Pain was evaluated using a modified Childrens Hospital of Eastern Ontario pain scale (mCHEOPS). Incidence of postoperative nausea and vomiting (PONV) was assessed at various time intervals (0-2, 2-6, 6-24h) by numeric rank score. Patients were followed for laryngospasm for 1h in recovery room after extubation. Other complications appeared within 24h postoperatively were recorded. RESULTS All postoperative CHEOPS values were lower than control in both groups. Analgesic requirement was decreased significantly in both groups in comparison with control patients, but this requirement was significantly lower in Group M (p<0.05). Although laryngospasm was not observed in Group M, the difference between groups was not statistically significant. PONV was similar in both groups. CONCLUSIONS Levobupivacaine and Levobupivacaine plus magnesium infiltration decrease the post-tonsillectomy analgesic requirement. Insignificant preventive effect of low doses of magnesium infiltration on laryngospasm observed in this study needs to be clarified by larger series.

Preconditionin effects of dexmedetomidine on myocardial ischemia/reperfusion injury in rats

BACKGROUND Preconditioning might protect the myocardium against ischemia/ reperfusion injury by reducing infarct size and preventing arrhythmias. Dexmedetomidine (DEX) is a highly selective α2-agonist used for sedoanalgesia in daily anesthetic practice. The cardioprotective effects of DEX on infarct size and on the incidence of arrhythmias observed after regional ischemia/reperfusion injury in vivo have not been reported. OBJECTIVE The aim of this study was to determine whether DEX exhibits a preconditioning effect and reduces infarct size and the incidence and duration of arrhythmias in a regional cardiac ischemia/reperfusion model in rats. METHODS Adult male Sprague-Dawley rats were anesthetized with sodium thiopental and mechanically ventilated (0.9 mL/100 g at 60 strokes/min) through a cannula inserted into the trachea after tracheotomy. Cardiac ischemia was then produced by ligating the left main coronary artery for 30 minutes, followed by a reperfusion period of 120 minutes. Blood pressure (BP) and heart rate (HR) were monitored and echocardiograms (ECGs) were performed. Arrhythmia was scored based on incidence and duration. The animals were randomly divided into 3 groups. The ischemic preconditioning (IPC) group underwent 5 minutes of ischemia followed by 5 minutes of reperfusion before the 30-minute ischemia/120-minute reperfusion period. In the DEX group, intraperitoneal (IP) DEX 1 mL (100 μg/kg) was administered 30 minutes before the ischemia/ reperfusion period. In the control group, IP saline 1 mL was administered 30 minutes before the ischemia/reperfusion period. After reperfusion, the heart was excised, demarcated with saline and ethanol to identify the occluded and nonoccluded myocardium, and cut into slices ~2 mm thick, that were then stained and placed between 2 glass plates. The risk zone and the infarct zone were compared between groups. The investigator assessing the infarcts was blinded to the study group. RESULTS Twenty-one adult (aged 4-6 months) male Sprague-Dawley rats weighing 280 to 360 g were included in the study; 7 rats were assigned to each group. BP, HR, and ECG readings were not significantly different between groups and did not change during the study. Arrythmias occurred during ischemia and reperfusion in all groups. The duration of the arrhythmias was significantly shorter and the arrhythmia score was significantly lower in the IPC group (all, P<0.05), compared with the control group; however, they were not significantly different in the DEX group. During the ischemic period, duration of ventricular tachycardia (VT) and ventricular premature contractions (VPC) in the DEX group was significantly longer than that observed in the IPC group (all, P<0.05). The duration of VPC was also significantly shorter than that observed in the control group (both, P<0.05). Duration of VT during the reperfusion period in the DEX group was significantly longer than that observed in both IPC and control groups (both, P<0.05). The mean (SD) percentage of damage was significantly lower in the IPC group (44.1% [2.0%]) and the DEX group (26.7% [2.0%]) compared with the control group (69.0% [3.0%]; both, P<0.05). The percentage of damage in the DEX group was also significantly lower compared with the IPC group (P<0.05). CONCLUSIONS This small, experimental in vivo study found that DEX was associated with reduced infarct size in ischemia/reperfusion injury in regional ischemia in this rat model but had no effect on the incidence of arrhythmias. Future studies are needed to clarify these findings.

Comparison of dexmedetomidine and midazolam for monitored anesthesia care combined with tramadol via patient-controlled analgesia in endoscopic nasal surgery: A prospective, randomized, double-blind, clinical study

UNLABELLED Abstract. BACKGROUND Monitored anesthesia care (MAC) may be applied for septoplasty or endoscopic sinus surgery in which an adequate sedation and analgesia without respiratory depression are desired for comfort of both the patient and the surgeon. Several combinations with different agents have been used for this purpose in these patients. However, analgesic properties for these agents have not been reported. OBJECTIVE The aim of this study was to investigate the analgesic and sedative effects of dexmedetomidine or midazolam infusion combined with tramadol that was used via patient-controlled analgesia (PCA), and to document the effects of these drugs on early cognitive functions. METHODS This prospective, randomized, double-blind, clinical study enrolled patients undergoing septoplasty or endoscopic sinus surgery at the Abant Izzet Baysal University Hospital, Bolu, Turkey, between February and September 2006. Patients were randomly allocated in a 1:1 ratio into 1 of 2 groups: the dexmedetomidine group (group D) patients received IV dexmedetomidine 1 μg/kg for 10 minutes followed by continuous infusion of 0.5 μg/kg · h(-1); and the midazolam group (group M) patients were administered a loading dose of IV midazolam 40 μg/kg for 10 minutes followed by infusion at the rate of 50 μg/kg · h(-1). A 1-minute bolus dose of IV tramadol (1.5 mg/kg) was administered in both groups 10 minutes after the administration of the primary drug, and continued via infusion using a PCA device. After baseline measurements, systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), heart rate (HR), oxygen saturation, and rate of respiration were recorded after the loading dose of study drug, after the bolus tramadol dose, at 10-minute intervals during the operation, and twice in the recovery rooms; 5 minutes after arrival and 5 minutes before discharge. Verbal rating score (VRS) and Ramsay sedation score were determined at baseline (after surgery was started), every 10 minutes thereafter until the end of the operation, and 2 times during recovery. All patients were assessed with the Wechsler Memory Scale-Revised at baseline (preoperatively) and 4 hours after the operation. RESULTS Seventy patients were enrolled in the study and randomly assigned to 1 of 2 groups: group D (sex, male/female, 23/12; mean [SEM] age, 32.53 [2.07] years; mean [SEM] weight, 73.03 [2.41] kg) or group M (sex, male/female, 21/14; mean [SEM] age, 34.43 [1.83] years; mean [SEM] weight, 67.90 [2.32] kg). All hemodynamic parameters (SAP, DAP, MAP, HR) were significantly higher in group M compared with group D from the onset of the surgery to discharge time (P < 0.05). Pain and sedation scores were similar in both groups, but the amount of PCA-administered rescue tramadol was significantly higher in group M (P = 0.001). A higher, though not statistically significant, prevalence of adverse events (ie, hypotension, bradycardia, and perioperative nausea and vomiting) were observed in group D. Postoperative logical verbal memory and digit span values were significantly higher in group D when compared with group M (P < 0.05). Postoperative digit span and visual reproduction scores were significantly higher than preoperative values in group D (P < 0.05). Postoperative personality functioning scores were significantly higher than preoperative values in group M (P < 0.05). CONCLUSIONS Based on VRS, Ramsay sedation scores, and surgeon and anesthesiologist satisfaction scores, dexmedetomidine or midazolam combined with tramadol PCA provided adequate analgesia and sedation in these adult patients undergoing septoplasty or endoscopic sinus surgery with MAC. A significantly larger amount of rescue tramadol was used by group M, suggesting that a better analgesic effect was achieved with dexmedetomidine.

Two different doses of caudal neostigmine co-administered with levobupivacaine produces analgesia in children

Background:  This study was aimed to evaluate the analgesic efficacy, duration of analgesia, and side effects of two different doses of caudal neostigmine used with levobupivacaine in children.

Detection of a retained epidural catheter fragment.

To the Editor: We thank the editor for a chance to respond to comments by Drs. Rocco and Philip1 concerning our paper.2 The idea that our study corroborates the findings of Rocco et al.3 is not correct. We measured epidural space pressure as saline was infused at several different flow rates in each animal and found a linear flow-pressure relation with a calculated Y-axis intercept that was within 1 to 2 mm Hg of the actual pressure obtained in the absence of flow. These data argue strongly against the presence of “Starling resistor (SR)” anatomy in the normal pig’s epidural space. If an SR were present, the calculated Y intercept would have been higher than observed, or the relation would have curved down, which indicates recruitment of additional exit pathways with critical opening pressures for fluid leaving the epidural space. In comparison, Rocco et al.3 measured epidural space pressure only at a single flow rate in each patient and, thus, cannot determine whether or not an SR is present. Their best evidence for an SR is the fact that “visible flow” of fluid passively leaving a syringe barrel and entering the epidural space “did not start” until the syringe had been raised some 10 to 15 cm above the spine—not a very scientific approach, because flow rates were not measured and low infusion pressures may have resulted in flow that escaped notice. Thus, the two studies differ in their methods, results, and interpretation. Rocco et al.3 determined their “initial pressure” after infusing small volumes of saline into the epidural space (legend to their Figure 1) and determined their “critical opening pressure” after infusing 3 to 9 mL; hence, to criticize us for doing the same is disingenuous. Their initial pressures were reported as 12 to 15 mm Hg, but these numbers come from only 13 of 25 patients studied. What were the pressures in the other 12 patients, and why were they excluded from analysis? Of additional note, the technique used by Rocco et al.3 for calculating “pressure at zero flow” was invalid because they extrapolated epidural space pressure versus time, rather than versus flow. On the other hand, we are pleased to note the similarity between our Figure 1 and their Figure 4, a tracing of pressure recorded during constant-flow volume infusion in an apparently healthy patient scheduled for surgery. The feature that is common to the two figures is a plateau in epidural space pressure as flow continues. We believe this plateau means that saline leaves the epidural space through pathways with constant resistance and enters a system with large capacitance. Otherwise, pressure would continue to increase rather than plateau. Our study was done in normal pigs, and finding similar results in a human is encouraging. Rocco et al.3 think certain technical aspects of our study precluded demonstration of SR-type hydrodynamic behavior. The linearity of our flow-pressure relations (R2 0.98 1.0) means that extrapolation to determine the Y-axis intercept is reasonable and accurate; hence, we would have found evidence of a critical opening pressure had it been present. The linearity of the relation adequately rules out recruitment of additional pathways with higher opening pressures as well. Rocco et al.3 are correct that infused fluid needs to reach the pressure-sensing needle before a reliable measurement can be made, but this distance was only 2 to 3 cm in our study because the needles were located at adjacent interspaces. They miss the bigger picture, however, which is that fluid spreads up and down the epidural space and through a variety of exit pathways, all of which might well demonstrate SR behavior. Rocco et al.3 confuse terms when they state that “once the critical opening pressure (initial pressure) is reached. . .” We strongly disagree with the concept that pressure measured in the absence of flow (initial pressure) corresponds to a critical opening pressure, and Rocco et al.3 make this distinction in Table 2 of their previous publication. Frankly, we were surprised to observe a pressure plateau during fluid infusion and that our flow-pressure relations were linear. We think the situation is more analogous to the flow of saline into a vein than into a “space” with limited capacitance and run off. Further studies are necessary to determine the location and nature of the exit pathways from the spinal epidural space that influence the hydrodynamics we have observed.

Effect of epidural levobupivacaine and levobupivacaine with fentanyl on stress response and postoperative analgesia after total knee replacement.

BACKGROUND Providing sufficient and convenient analgesia is crucial during the postoperative period after totalknee replacement (TKR) to enhance patient mobility and reduce stress response to surgery. The scope of this study is to compare the effects of levobupivacaine and levobupivacaine plus fentanyl on stress response and analgesic efficiency after TKR. METHOD In this study, 40 ASA I - II patients scheduled to undergo TKR were subjected to combined spinal epidural anesthesia (CSEA) injecting of 15 mg levobupivacaine and randomly assigned to receive either levobupivacaine 0.125% (Group L) or levobupivacaine 0.125% plus fentanyl 4 μg ml-1 (Group F) during postoperative period via the epidural route. Patient controlled epidural analgesia (PCEA) was offered for 24 hours. Venous blood samples were assayed for adrenocorticotropic hormone (ACTH), cortisol and prolactin levels before surgery and after analgesia administration. Analgesia was assessed using a visual analogue scale (VAS) at rest (VASR) and during movement (VASM). RESULTS There was no statistically significant difference between the groups in terms of total doses, bolus requests, bolus delivered and side effects (p > 0.05). The ACTH, cortisol and prolactin levels increased following the surgery and decreased during PCA infusion in both groups where the decline in Group F was significant (p < 0.05) at 24 hours after the analgesic treatment and 48 hours after the surgery. CONCLUSION We have demonstrated that infusion of levobupivacaine (0.125%) in combination with fentanyl (4 μg ml-1) using PCEA suppressed stress response to surgery significantly and provided better pain relief than levobupivacaine (0.125%) alone after TKR.

The treatment of postoperative inspiratory stridor with intraoral epinephrine

SIR—A 5-year-old, 20-kg boy presented for reoperation because of bleeding 5 h after tonsillectomy. Anesthesia was induced on both occasions with pentothal 5 mgÆkg, fentanyl 1 lgÆkg and vecuronium 0.1 mgÆkg, then maintained with nitrous oxide, oxygen and sevoflurane. Reversal of the relaxant was with atropine 0.01 mgÆkg and neostigmine 0.02 mgÆkg. The patient developed inspiratory stridor immediately after extubation. His peripheral oxygen saturation (SpO2) decreased to 85%. We ventilated him with 100% oxygen and gave him IV 20 mg lidocaine and 20 mg prednisolone. Success was partial and suprasternal and intercostal recessions continued with 100% oxygen and given intravenous 20 mg lidocaine and 20 mg prednisolone. But, the success of treatment was partial and added suprasternal and intercostal indrawings. Despite giving cold humidified oxygen via facemask the patient remained tachypneic with forced respiration. At that time, the peripheral venous catheter became displaced. While attempting venous access, 20 lg of epinephrine was instilled intraorally. In a few minutes, respiration improved significantly. The final values before discharge from the recovery room without oxygen support were: pulse rate; 140 bÆmin, blood pressure; 100/60 mmHg, respiratory rate; 17 min, SpO2; 97% and no recessions. Epinephrine posseses beneficial effects on respiration and has been used to treat croup (1) by the activation of beta-receptors. To our knowledge, this is the first report of using epinephrine intraorally as a bronchodilatator agent during postoperative stridor. We conclude that intraoral epinephrine may be a readily available and low-cost agent to treat postoperative inspiratory stridor. Further studies will be needed to detect the effects of intraorally used epinephrine for postoperative upper airway obstruction. Nebahat Gulcu* Kaz ım Karaaslan* Ahmet E. Suslu† Hasan Kocoglu* Departments of *Anesthesiology and †Ear Throat Nose Surgery, Abant Izzet Baysal University Medical Faculty, Bolu, Turkey (email: gulcune@yahoo.com.tr).

554 A NEW METHOD FOR EPIDURAL CATHETER FIXATION

M. Escher1 °, A. Cahana2, L. Robert2, S. Pautex3. 1Pain and Palliative Care Consultation, Division of Clinical Pharmacology and Toxicology, Geneva University Hospitals, Geneva, 2Interventional Pain Program, Division of Anesthesiology, Geneva University Hospitals, Geneva, 3Pain and Palliative Care Consultation, Department of Rehabilitation and Geriatrics, Geneva University Hospitals, Geneva, Switzerland