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Wei-Hung Chan,1,2 Yu-Juei Hsu,3 Chiao-Pei Cheng,1 Kuan-Nien Chou,2,4 Chin-Li Chen,5 Shih-Ming Huang,6 Wei-Chih Kan,7,8,* Yi-Lin Chiu6,* 1Department of Anesthesiology, Tri-Service General Hospital, National Defense Medical Center, Taipei City, Taiwan, Republic of China; 2Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei City, Taiwan, Republic of China; 3Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei City, Taiwan, Republic of China; 4Department of Neurosurgery, Tri-Service General Hospital, National Defense Medical Center, Taipei City, Taiwan, Republic of China; 5Division of Urology, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei City, Taiwan, Republic of China; 6Department of Biochemistry, National Defense Medical Center, Taipei City, Taiwan, Republic of China; 7Department of Nephrology, Department of Internal Medicine, Chi-Mei Medical Center, Tainan City, Taiwan, Republic of China; 8Department of Biological Science and Technology, Chung Hwa University of Medical Technology, Tainan City, Taiwan, Republic of China*These authors contributed equally to this workCorrespondence: Yi-Lin Chiu, Department of Biochemistry, National Defense Medical Center, Rm. 7323, 7F, No. 161, Sec. 6, Minquan E. Road, Neihu Dist, Taipei City, 114201, Taiwan, Republic of China, Tel +886 02 87923100#18828, Fax +886 02 87910776, Email yilin1107@mail.ndmctsgh.edu.twPurpose: In this study, we use animal models combined with bioinformatics strategies to investigate the potential changes in overall renal transcriptional expression after traumatic brain injury.Methods: Microarray analysis was performed after kidney acquisition using unilateral controlled cortical impact as the primary mouse TBI model. Multi-oriented gene set enrichment analysis was performed for differentially expressed genes.Results: The results showed that TBI affected the gene set associated with mitochondria function in kidney cells, and a negative enrichment of gene sets associated with immune cell migration and epidermal development was also observed. Analysis of the disease phenotype gene set revealed that differential expression of mitochondria-related genes was associated with lactate metabolism. Alternatively, activation and adhesion of immune cells associated with the complement system may promote autoinflammation in kidney tissue. The simulated immune cell infiltration analysis showed an increase in the proportion of activated memory CD4 T cells and a decrease in the proportion of resting memory CD4 T cells, suggesting that activated memory CD4 T cell infiltration may be involved in the inflammation of renal tissue and cause damage to renal cells, such as principal cells, mesangial cells and loops of Henle cells.Conclusion: This study is the first to reveal the effects of brain trauma on the kidney. TBI may affect the expression of mitochondria function-related gene sets in renal cells by increasing lactate. It may also affect renal mesangial cells by inducing increased infiltration of immune cells through mechanisms related to complement system activation or autoimmune antibodies.Keywords: traumatic brain injury, nephropathy, complement system, lactate metabolism, immune cell infiltration

BACKGROUND The Trachway Videolight Intubating Stylet is a video-assisted system with a rigid but malleable intubating stylet that facilitates endotracheal intubation. Minimizing cervical spine movement with manual in-line stabilization is essential for patients with cervical spine injuries such as multiple trauma. However, the intubation time of the Trachway Videolight Intubating Stylet and complications associated with intubation in patients with manual in-line stabilization in the neutral-head and head-lift positions remain unclear. METHODS Patients (20-80 years old) who were scheduled to undergo surgery that required general anesthesia with tracheal intubation were randomly allocated to either a neutral-head (n = 62) or a head-lift position (n = 62) group. Manual in-line stabilization was performed to limit cervical spine mobility. We aimed to evaluate orotracheal intubation time and success rate in these 2 positions with the Trachway Videolight Intubating Stylet. RESULTS Intubation was faster in the head-lift than in the neutral-head position (20 ± 10 and 25 ± 13 seconds, respectively, P = .000); intubation was equally successful in the 2 positions (96.8% vs 96.8%). Responses to intubation did not differ between positions (heart rate, P = .142; visual analog scale scores for throat soreness, P = .54). The only significant predictor of intubation time was the body mass index in the head-lift position group (P = .005). CONCLUSIONS Intubation using the Trachway Videolight Intubating Stylet with manual in-line stabilization is faster in the head-lift position, and therefore preferable. However, if the head-lift position is not suitable, the neutral-head position is a sensible alternative, with comparable intubation success rate, heart rate change, and postoperative throat soreness.

Background Acute water intoxication after hysteroscopy is a rare, life-threatening condition, often accompanied with delayed diagnosis owing to masked symptoms because of general anesthesia. Case presentation Herein we presented a 39-year-old female who presented with cardiac arrest after hysteroscopic myomectomy because of acute water intoxication and survived after extracorporeal membrane oxygenation, continuous venous–venous hemofiltration, and aggressive high sodium fluid resuscitation. Conclusion Failure to recognize and treat this condition appropriately may lead to potentially lethal cardiopulmonary complications.

The effects of intravenous (IV) catheter gauge and pressurization of IV fluid (IVF) bags on fluid flow rate have been studied. However, the pressure needed to achieve a flow rate equivalent to that of a 16 gauge (G) catheter through smaller G catheters and the potential for endothelial damage from the increased kinetic energy produced by higher pressurization are unclear. Constant pressure on an IVF bag was maintained by an automatic adjustable pneumatic pressure regulator of our own design. Fluids running through 16 G, 18 G, 20 G, and 22 G catheters were assessed while using IV bag pressurization to achieve the flow rate equivalent to that of a 16 G catheter. We assessed flow rates, kinetic energy, and flow injury to rabbit inferior vena cava endothelium. By applying sufficient external constant pressure to an IVF bag, all fluids could be run through smaller (G) catheters at the flow rate in a 16 G catheter. However, the kinetic energy increased significantly as the catheter G increased. Damage to the venous endothelium was negligible or minimal/patchy cell loss. We designed a new rapid infusion system, which provides a constant pressure that compresses the fluid volume until it is free from visible residual fluid. When large-bore venous access cannot be obtained, multiple smaller catheters, external pressure, or both should be considered. However, caution should be exercised when fluid pressurized to reach a flow rate equivalent to that in a 16 G catheter is run through a smaller G catheter because of the profound increase in kinetic energy that can lead to venous endothelium injury.

BACKGROUND The pneumatic tourniquet is frequently used in total knee arthroplasty. Tourniquet deflation may result in hypotension and tachycardia caused by the rapid shift of blood volume back to the ischaemic limb and a decrease in cardiac preload. Passive leg raising (PLR) represents a 'self-volume challenge' that can result in an increase in preload. Such a PLR-induced increase in preload was hypothesised to attenuate the decrease in preload resulting from tourniquet deflation. OBJECTIVE To evaluate the effect of PLR on hypotension and tachycardia following tourniquet deflation. DESIGN A randomised controlled trial. SETTING Single medical centre. PATIENTS Seventy patients who underwent unilateral total knee arthroplasty were randomised into two groups: tourniquet deflation with PLR (n = 35) or without PLR (control group, n = 35). INTERVENTION(S) Patients in both groups were administered a single dose of plain bupivacaine for spinal anaesthesia. The pneumatic tourniquet was inflated on the thigh and the surgery was performed. The study composed of four steps: for the PLR group, step 1 - inflation of the tourniquet while the patient was supine; step 2 - the patient's legs were raised to a 45° angle; step 3 - the tourniquet was deflated while the patient's legs were still raised; and step 4 - the legs were returned to the supine position. In the control group, the same perioperative procedure was used, but PLR was not conducted. MAIN OUTCOME MEASURES The patients' blood pressure and heart rate were measured before, during and after tourniquet deflation. RESULTS After tourniquet deflation, the magnitude of the changes in blood pressure and heart rate was less in the PLR group than that in the control group. In addition, the blood pressure nadir also occurred later in the PLR group than in the controls. CONCLUSION Bilateral PLR is a simple, reversible manoeuvre that mimics rapid fluid loading. Bilateral PLR attenuates the severity of, and delays the time to, hypotension and tachycardia following deflation of a lower limb tourniquet. TRIAL REGISTRATION ClinicalTrials.gov number NCT01592669.

Objective To investigate whether target-controlled infusion (TCI) with propofol, a method that has theoretically better control of drug concentration, produces less cardiovascular and respiratory suppression than an intermittent bolus of a sedative cocktail regimen in deep sedation for gastrointestinal endoscopy. Methods In total 100 participants who had undergone esophagoduodenoscopy (EGD) and 120 who had undergone colonoscopy were prospectively and randomly enrolled to receive TCI with propofol or intermittent bolus of cocktail regimen containing midazolam, alfentanil and propofol until they were unresponsive to verbal commands. The target concentration was adjusted and the bolus of the cocktail regimen was added based on their responses. The nadir values of heart rate, blood pressure and oxygen saturation during and after the procedure were recorded. Results The nadir systolic blood pressure during the endoscopy in the cocktail regimen group was significantly lower than that in the TCI with propofol group. In the cocktail regimen group, the incidence of hypotension during colonoscopy and that of bradycardia during EGD were higher than those in the TCI with propofol group. No participants in the TCI with propofol group experienced hypoxia during endoscopy. In the cocktail regimen group, six participants who had undergone EGD and six who had undergone colonoscopy showed transient hypoxic episodes during or after endoscopy. Conclusion TCI with propofol produced less cardiovascular and respiratory suppression than intermittent bolus of a sedative cocktail regimen in deep sedation for gastrointestinal endoscopy.

We conducted a retrospective study to investigate the anesthesia-controlled time and factors that contribute to prolonged extubation in open colorectal surgery. Using our hospital database, demographic data, various time intervals (waiting for anesthesia time, anesthesia time, surgical time, emergence time, exit from operating room after extubation, total operating room time, and post-anesthesia care unit stay time), and incidence of prolonged extubation (≥ 15 mins), were compared between patients who received desflurane/fentanyl-based anesthesia and total intravenous anesthesia via target-controlled infusion with fentanyl/propofol. Logistic regression analyses were performed to assess the association between variables that contributed to prolonged extubation. In conclusion, the anesthesia-controlled time was similar in desflurane anesthesia and propofol-based total intravenous anesthesia for open colorectal surgery in our hospital. Surgical time greater than 210 minutes, as well as age, contributed to prolonged extubation.

Motorcycle exhaust (ME) from two-stroke engines contains many toxicants and poses a potential health hazard. The major objectives of the present study were to investigate the male reproductive toxicity of ME and the underlying mechanisms of toxicity. Male Wistar rats were exposed to ME by inhalation 1 h each in the morning and afternoon, Monday through Friday. Exposures to 1:50 diluted ME for 4 weeks or to 1:10 diluted ME for 2 and 4 weeks showed concentration- and time-dependent decreases of testicular weight, spermatid number, and cauda epididymal sperm number. Subsequent studies were done using 4-week exposure to 1:10 diluted ME. ME caused histopathological changes including testicular spermatocytic necrosis and seminiferous tubule atrophy and cauda epididymal formation of clusters of pyknotic and necrotic sperm cells. ME-exposed male rats mated with untreated females showed decreases of male mating index and female fertility index and an increase of implantation site loss. ME decreased 7-ethoxycoumarin O-deethylase and superoxide dismutase activities but induced proinflammatory cytokine interleukin-6 (IL-6) messenger RNA (mRNA) in the testis. Male rats were exposed to ME with or without cotreatment with 50 mg/kg vitamin E orally for 4 weeks. ME decreased serum testosterone concentration. This effect was reversed by cotreatment with vitamin E. ME decreased testicular spermatid number and induced IL-6 mRNA and protein. These effects were also reversed by the vitamin E cotreatment. The present findings show that ME causes male reproductive effects and induces testicular IL-6 in rats by mechanisms involving induction of oxidative stress and inhibition of steroidogenesis.

Nasogastric tube insertion is a routine procedure in medical care. However, misplacement of the tube can cause a variety of complications, which can be life threatening in some instances. We report a case of fatal hemorrhagic shock immediately after nasogastric tube insertion in a patient undergoing debridement by video-assisted thoracoscopic surgery for mediastinitis. Emergency endoscopy showed that the bleeding came from the nasogastric tube which had perforated the esophagus and possibly tore an intrathoracic large vessel. The nasogastric tube insertion was considered to have directly produced the perforation because no esophageal perforation had been found on preoperative endoscopy. Factors contributing to the risk of esophageal perforation in this case included coexisting mediastinitis, surgical manipulation, endotracheal intubation, inability to cooperate during general anesthesia, and repetitive advancement of the nasogastric tube. Prompt clamping of the nasogastric tube or delayed insertion after failed attempts might have improved the outcome. This report illustrates the complication of massive bleeding that can occur immediately after misplaced insertion of a nasogastric tube. Extraordinary care should be taken to avoid misplacement of the nasogastric tube during insertion.

Ketamine is a common intravenous anesthetic and a frequent drug of abuse, alone or in combination with cocaine. However, the pharmacokinetic effects of ketamine have not been fully investigated. This study determined the effects of ketamine on cytochrome P-450 (P-450)-dependent catalytic activities, protein levels, and hepatotoxicity using male Wistar rats treated with 10, 20, 40, or 80 mg/kg ketamine intraperitoneally twice daily for 4 d. Treatment with ketamine produced a dose-dependent increase of pentoxyresorufin O-dealkylation activity of liver microsomes. Treatment with 80 mg/kg ketamine resulted in 14-, 3-, and 2-fold rise in O-dealkylation of pentoxyresorufin, ethoxyresorufin, and methoxyresorufin of rat liver microsomes, respectively. The treatment produced 31% and 86% increases in 7-ethoxycoumarin O-deethylation and erythromycin N-demethylation, respectively. In addition, aniline hydroxylation activity was elevated by 62%. Protein blot analysis of liver microsomal proteins revealed that 80 mg/kg ketamine induced P-450 1A, 2B, 2E1, and 3A proteins by 2-, 13-, 2-, and 2-fold, respectively. In reversibility study, ketamine-induced pentoxyresorufin O-dealkylation, 7-ethoxycoumarin O-deethylation, erythromycin N-demethylation, and methoxyresorufin O-demethylation activities of liver microsomes prepared from rats 4 d after ketamine treatment were 75%, 48%, 29%, and 38% lower than the respective activities of liver microsomes prepared from rats 1 d after treatment. Protein blot analysis showed that ketamine-induced P-450 2B1/2 proteins also decreased in a time-dependent manner in 4 d. In hepatotoxicity study, treatment of rats with 1 ml/kg CCl4 produced a 7-fold increase in serum alanine aminotransferase activity level and a 17-fold rise in rats pretreated with 80 mg/kg ketamine for 4 d. Treatment of ICR mice with 120 mg/kg cocaine produced a 17% mortality, whereas the same dose of cocaine produced a 50% mortality in mice pretreated with ketamine. Treatment of mice with 100 mg/kg cocaine produced a 76-fold increase in serum alanine aminotransferase activity level and a 260-fold rise in mice pretreated with 80 mg/kg ketamine for 4 d. The present study shows that ketamine induces the expression of multiple forms of P-450 in rat liver microsomes and increases CCl4-induced liver toxicity and cocaine-mediated acute toxicity. Other potential pharmacological or toxicological events related to ketamine use need to be further explored.

Previous study showed that patients under general anesthesia (GA) had nasopharyngeal secretions on the face at the end of ocular surgery, especially in propofol-based total intravenous anesthesia (TIVA), it might induce postoperative endophthalmitis. Therefore, we conducted a retrospective study to compare the incidence of endophthalmitis after ocular surgery under topical, inhalation anesthesia, and propofol-based TIVA in our medical center from 2011 to 2015. A total of 21,032 patients were included, and we evaluated epidemiologic factors, systemic diseases, other ocular pathologic characteristics, complications during the surgery, technique of ocular surgery, method of antibiotic prophylaxis, vitreous culture, and vision outcome in these patients. Fifteen endophthalmitis cases among 21,032 operations reported, equaling an incidence of 0.071%. The incidence rates under topical, inhalation anesthesia, and propofol-based TIVA were 0.083%, 0.039%, and 0%, respectively (P = 0.39). Moreover, the risk of endophthalmitis under GA (0.024%) was significantly lower than topical anesthesia (0.083%) (P

We studied the hypothermic effect of adding 150 microg morphine during spinal anaesthesia in 60 parturients scheduled for elective caesarean section. All the parturients received intrathecal injection of a solution containing 150 mug morphine or normal saline in addition to 10-12 mg hyperbaric bupivacaine 0.5%. In both groups, a significant decrease in body temperature was noted. There was no difference in the area under the curve for temperature against time for the two groups; however, the maximum decrease in temperature from baseline was significantly larger after morphine than after saline injection (mean (SD) 1.11 (0.61) degrees C vs 0.76 (0.39) degrees C, respectively; p = 0.01) and the time to nadir temperature was significantly longer (59.5 (17.6) min vs 50.4 (15.9) min, respectively; p = 0.047). The lowest temperature observed in the morphine group was 34.3 degrees C. We conclude that intrathecal injection of 150 microg morphine intensified the intra-operative hypothermic effect of bupivacaine spinal anaesthesia for caesarean section.

To investigate whether target-controlled infusion (TCI) with propofol, a method that has theoretically better control of drug concentration, produces less cardiovascular and respiratory suppression than an intermittent bolus of a sedative cocktail regimen in deep sedation for gastrointestinal endoscopy.In total 100 participants who had undergone esophagoduodenoscopy (EGD) and 120 who had undergone colonoscopy were prospectively and randomly enrolled to receive TCI with propofol or intermittent bolus of cocktail regimen containing midazolam, alfentanil and propofol until they were unresponsive to verbal commands. The target concentration was adjusted and the bolus of the cocktail regimen was added based on their responses. The nadir values of heart rate, blood pressure and oxygen saturation during and after the procedure were recorded.The nadir systolic blood pressure during the endoscopy in the cocktail regimen group was significantly lower than that in the TCI with propofol group. In the cocktail regimen group, the incidence of hypotension during colonoscopy and that of bradycardia during EGD were higher than those in the TCI with propofol group. No participants in the TCI with propofol group experienced hypoxia during endoscopy. In the cocktail regimen group, six participants who had undergone EGD and six who had undergone colonoscopy showed transient hypoxic episodes during or after endoscopy.TCI with propofol produced less cardiovascular and respiratory suppression than intermittent bolus of a sedative cocktail regimen in deep sedation for gastrointestinal endoscopy.

Motorcycle exhaust (ME) is a major source of air pollution and a potential health hazard in urban areas where motorcycles are a popular means of transportation. The main objectives of this study were to determine the ability of ME to cause cardiotoxicity in rats and investigate the possible mechanisms of toxicity. Male rats were exposed to 1:10 diluted ME by inhalation 2 h daily and Monday through Friday for 8 weeks. Exposure to ME increased heart weight and decreased cardiac antioxidant enzymes glutathione S-transferase (GST), superoxide dismutase and glutathione peroxidase activities in a concentration- and time-dependent manner. Analysis of echocardiographic parameters indicated that ME increased left ventricle posterior wall thickness, interventricular septum thickness and left ventricle mass. Histopathological examinations of the hearts revealed that ME exposure caused focal cardial degeneration and necrosis, mononuclear cell infiltration, and fibrosis. The results of reverse transcriptase-polymerase chain reaction studies showed that ME decreased GST-M1 and GST-P1 mRNA expression and increased the expression of proinflammatory cytokine interleukin-1β, hypertrophy marker atrial natriuretic peptide, fibrosis markers type I and III collagen, profibrotic cytokine connective tissue growth factor, and hypertrophy and fibrosis mediator transforming growth factor (TGF)-β1 in the heart. The data of Western blot analysis showed that cardiac TGF-β1 protein was induced by ME. These findings demonstrate that subchronic ME exposure caused hypertrophy and fibrosis, and modulated GST and TGF-β1 expression in rat heart possibly by mechanisms involving oxidative stress and inflammation.

An 84-year-old male was scheduled for coronary artery bypass graft surgery under general anesthesia. During cardiopulmonary bypass, the leakage of blood into the syringe being used for balloon inflation and the thermistor connector of the pulmonary artery catheter (PAC) was detected. Resistance was encountered when trying to withdraw the PAC. A surgical suture of the right atrium cannulation was stitched to PAC and was immediately released. Early detection of surgical damage to PAC and recognition of the entrapped PAC by gently withdrawing it avoided possible life-threatening complications, including pulmonary air embolism, and the inevitable of resternotomy. Transesophageal echocardiography, chest radiography, and fluoroscopy can help confirm any postoperative surgical damage following closure of the sternum or while in the intensive care unit.

Background: Ketamine has been shown to induce rat cytochrome P-450 in a way similar to phenobarbital. However, whether ketamine is able to induce glutathione S-transferase (GST) and UDP-glucuronosyltransferase (UGT), two major phase II drugmetabolizing enzymes, remains unclear. The present study aimed to investigate the effect of ketamine on GST and UGT activities in rats. Methods: In a dose-response study, male adult Wistar rats were treated with 10, 20, 40 or 80 mg/kg ketamine intraperitoneally twice daily for 4 days. Livers were removed 1 day after ketamine treatment and hepatic GST and UGT activities were determined. In a reversibility study, rats were treated with 80 mg/kg ketamine intraperitoneally twice daily for 4 days and killed 1, 2, 3 or 4 days after the last dose of ketamine. Livers were removed and hepatic GST and UGT activities were determined. Results: The results of the dose-response study showed that treatment of rats with 10, 20, 40, or 80 mg/kg ketamine produced 19%, 20%, 18%, and 25% increases respectively in the catalytic activity of hepatic cytosolic GST, and 41%, 41%, 35%, and 38% increases respectively in the catalytic activity of microsomal UGT. The results of the reversibility study showed that the GST activities of the rats killed 1, 2, 3, or 4 days after ketamine treatment were 62%, 88%, 46% and 65% higher than the activity of the control group. The UGT activities of the rats killed 1, 2, 3, or 4 days after ketamine treatment were 56%, 53%, 54% and 72% higher than the activity of the control group. Conclusion: Ketamine is able to induce the activities of hepatic GST and UGT in rats. The induced GST and UGT activities persist for at least 4 days after cessation of ketamine. The results suggest the possibility of interactions of drugs related to phase II enzyme induction in chronic ketamine users.

Background In a series of ex vivo and in vivo studies we investigated the ability of repetitive ketamine administration to alter the metabolism and anaesthetic effect of propofol and the role of ketamine-mediated P-450 2B induction in rats. Methods Male Wistar rats were pretreated with 80 mg kg −1 ketamine i.p. twice daily for 4 days. Pentoxyresorufin O -dealkylation (PROD), P-450 2B protein and mRNA were determined. Residual propofol concentration was measured after incubating hepatic microsomes with 100 μM propofol. Sleeping times induced by i.p. 80 mg kg −1 propofol were determined. Orphenadrine, a P-450 2B inhibitor, was added in both ex vivo and in vivo studies. Finally, serial whole blood propofol concentrations were determined after i.v. infusion of 15 mg kg −1 propofol. Results Ketamine pretreatment produced 5.4-, 3.4- and 1.7-fold increases in hepatic PROD activity, P-450 2B protein and mRNA, respectively. Residual propofol concentration was 46% lower after incubation with microsomes from ketamine-pretreated rats than in the control group. The addition of orphenadrine to ketamine-pretreated microsomes produced an increase in residual propofol concentration in a concentration-dependent manner. Ketamine pretreatment reduced propofol sleeping time to 12% of the control, which was reversed by orphenadrine. The whole blood propofol concentration in ketamine-pretreated rats was significantly lower than that of control rats at 1, 2, 4 and 8 min after cessation of propofol infusion. Conclusions Repetitive ketamine administration enhances propofol metabolism and reduces propofol sleeping time in rats. We suggest that P-450 2B induction may produce ketamine–propofol interaction in anaesthetic practice.

The aim of this study is to investigate the optimal injection time of alfentanil during induction of anesthesia to blunt the circulatory responses induced by laryngoscopy and tracheal intubation.Seventy-five patients of ASA class I or II were randomly assigned to five groups. Group I was the placebo group in which the patients received normal saline 2 ml just before induction. Patients in groups II, III, IV and V received alfentanil 10 microg/kg at 5, 3, 1 and 0.5 min before intubation respectively. Anesthesia was maintained with 1.5% isoflurane and nitrous oxide in 50% oxygen (2:2 L/min). The patients' heart rate and blood pressure before and after intubation were documented and compared. The occurrence of adverse effects was also recorded.Patients' demographic data, baseline hemodynamic profile and the laryngoscopic time did not differ among the five groups. The patients in groups II, III and IV showed decreased heart rate compared with group I within 3 min after intubation. The patients in group V like those in group I did not show a reduction in heart rate 1 min after intubation. The patients in groups II, III, IV and V all showed reduced systolic blood pressure and rate-pressure product (RPP) 2 min after intubation. The occurrence of hypotension and bradycardia was not different among the five groups; hypertension and high RPP were less in groups II, III and IV as compared with group I. Ninety-three percent patients in group II and group III suffered from dizziness after alfentanil administration. One patient in group II had nausea and another one patient displayed hypoxemia after alfentanil administration.Considering equal effectiveness and fewer side effects, one minute before intubation is the optimal injection time of alfentanil to blunt the circulatory responses induced by laryngoscopy and tracheal intubation.

The aim of this study was to evaluate the effectiveness of lidocaine, propofol and ephedrine in suppressing fentanyl-induced cough.One hundred and eighteen patients were randomly assigned into four groups and the following medications were given intravenously: patients in Group I (n = 31) received normal saline 2 mL, Group II (n = 29) received lidocaine 2 mg.kg(-1), Group III (n = 30) received propofol 0.6 mg.kg(-1) and Group IV (n = 28) received ephedrine 5 mg. At one minute after the study medication, fentanyl 2.5 microg.kg(-1) was given intravenously within two seconds. The occurrence of cough and vital sign profiles were recorded within two minutes after fentanyl bolus by an anesthesiologist blinded to study design.Sixty-five percent of patients in the placebo group had cough, whereas the frequency was significantly decreased in Groups II (14%) and IV (21%). Although a numerically lower frequency of cough was noted in Group III (37%), it was not statistically different from that of the placebo group. SpO(2) decreased significantly in patients of Group III compared to placebo; one patient experienced hypoxemia necessitating mask ventilation. Patients in Group III showed a decrease in heart rate and systolic blood pressure (2 beats.min(-1) and 8 mmHg vs baseline). Patients in Group IV showed an increase in both measurements (5 beats.min(-1) and 8 mmHg vs baseline). No truncal rigidity was observed throughout the study.Intravenous lidocaine 2 mg.kg(-1) or ephedrine 5 mg, but not propofol 0.6 mg.kg(-1), was effective in preventing fentanyl-induced cough. The results provide a convenient method to decrease fentanyl-induced cough.

Pruritus is a common side effect of intrathecal morphine injection for postoperative pain control. Its incidence is especially high in patients undergoing cesarean delivery. We investigated the effectiveness of ondansetron in preventing intrathecal morphine-induced pruritus in such patients. We included 60 consecutive nonbreastfeeding women who were scheduled for elective cesarean delivery. After the administration of spinal anesthesia with bupivacaine and intrathecal morphine 0.15 mg injection, the patients were randomly divided into three groups. Group 1 received placebo (normal saline) IV injection, Group 2 diphenhydramine 30 mg IV injection, and Group 3 ondansetron 0.1 mg/kg IV injection. The incidence of pruritus was significantly lower in the ondansetron group (25%) when compared with that in the placebo group (85%) and in the diphenhydramine group (80%) (both P0.05). The postoperative pain score and time to flatus passage were not significantly different among the three groups. There were no headache or extrapyramidal signs associated with ondansetron use. In conclusion, ondansetron prophylaxis significantly reduced the incidence of intrathecal morphine-induced pruritus in patients undergoing cesarean delivery.Ondansetron prophylaxis significantly decreases the incidence of pruritus, a common side effect of intrathecal morphine used to treat postcesarean delivery pain.

For decades, water-mill murmur, decrease in end-tidal CO(2) (Petco(2)), hypotension, and hypoxemia have been accepted as diagnostic criteria for gas embolism. In this case report, a 19-yr-old male patient developed a sudden reduction in Petco(2) and profound circulatory collapse 15 min after intramedullary irrigation with H(2)O(2). However, arterial oxygen desaturation never developed throughout the entire course of resuscitation from presumed massive oxygen embolism.