Anesth Analg 2002 Jun;94(6):1614-6
Departments of Anesthesiology and Orthopedics, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
[Medline record in process]
We conducted a randomized, double-blinded study to examine the onset time of tourniquet pain during epidural lidocaine anesthesia either with or without morphine in the epidural solution. Forty-five patients undergoing knee surgery with a thigh tourniquet were randomly allocated into 3 groups of 15 patients each: epidural morphine (EM; epidural administration of 17 mL of 2% lidocaine plus 2 mg of morphine, followed by IV injection of 0.2 mL of normal saline), IV morphine (IVM; 17 mL of 2% lidocaine plus 0.2 mL of normal saline, followed by IVM 2 mg IV), and control (17 mL of 2% lidocaine plus 0.2 mL of normal saline, followed by 0.2 mL of normal saline IV). The onset time of tourniquet pain was recorded. The level of sensory block was determined by the pinprick method at the occurrence of tourniquet pain. Hemodynamic changes and side effects of EM were also recorded. The onset time of tourniquet pain from both the epidural injection and the tourniquet inflation were significantly longer in the EM group (103 +/- 15 min and 80 +/- 15 min, respectively) compared with the IVM group (74 +/- 12 min and 50 +/- 12 min, respectively; P < 0.05) and the Control group (67 +/- 9 min and 45 +/- 9 min, respectively; P < 0.05). The level of sensory block at the onset of tourniquet pain and hemodynamic changes were not different among the three groups. Only two and three patients in the EM group complained of nausea/vomiting and pruritus, respectively. Respiratory depression was not observed in any patient. We conclude that epidural injection of the mixture of 2 mg of morphine and 2% lidocaine solution delayed the onset of tourniquet pain during epidural lidocaine anesthesia without significant morphine-related side effects. IMPLICATIONS: We examined the effect of epidural morphine on the onset of tourniquet pain during epidural lidocaine anesthesia. We found that the addition of 2 mg of morphine to epidural 2% lidocaine significantly delayed the onset of tourniquet pain without increasing morphine-related side effects.
PMID: 12032038, UI: 22027022
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Anesth Analg 2002 Jun;94(6):1553-7
Departments of Anesthesiology, Institute of Anesthesiology and Intensive Care, Rome University "La Sapienza," Rome.
To investigate a possible antinociceptive role of serotonin receptor subtype 3 (5-HT(3)), we evaluated the effects of a coadministration of ondansetron, a 5-HT(3) selective antagonist, and tramadol, a central analgesic dependent on enhanced serotonergic transmission. Fifty-nine patients undergoing ear, throat, and nose surgery, using tramadol for 24-h postoperative patient-controlled analgesia (bolus = 30 mg; lockout interval = 10 min) were randomly allocated either to a group receiving ondansetron continuous infusion (1 mg. mL(-1). h(-1)) for postoperative nausea and vomiting (Group O) or to a control group receiving saline (Group T). Pain and vomiting scores and tramadol consumption were evaluated at 4, 8, 12, and 24 h. Pain scores were never >4, according to a 0-10 numerical rating scale, in both groups. Group O required significantly larger doses of tramadol at 4 h (213 versus 71 mg, P < 0.001), 8 h (285 versus 128 mg, P < 0.002), and 12 h (406 versus 190 mg, P < 0.002). Vomiting scores were higher in Group O at 4 h (P < 0.05) and 8 h (P = 0.05). We conclude that ondansetron reduced the overall analgesic effect of tramadol, probably blocking spinal 5-HT(3) receptors. IMPLICATIONS: Serotonin is an important neurotransmitter of the descending pathways that down-modulate spinal nociception. In postoperative pain, ondansetron, a selective 5-HT(3) receptor antagonist, increased the analgesic dose of tramadol. We suggest that, when antagonized for antiemetic purpose, 5-HT(3) receptors foster nociception, because of their site-dependent action.
PMID: 12032025, UI: 22027009
Anesth Analg 2002 Jun;94(6):1517-1520
Departments of Anaesthesiology and Biostatistics, Trakya University, Edirne, Turkey.
[Record supplied by publisher]
We compared the efficacy of ondansetron, lidocaine, tramadol, and fentanyl in minimizing pain caused by the injection of rocuronium in 250 patients. After tourniquet application on the forearm, the patients were given saline (3 mL) (Group 1, n = 50), ondansetron (4 mg) (Group 2, n = 50), lidocaine (30 mg) (Group 3, n = 50), tramadol (50 mg) (Group 4, n = 50), or fentanyl (100 &mgr;g) (Group 5, n = 50) diluted into a 3-mL solution. The occlusion was released after 20 s and rocuronium was injected over 10-15 s. The patients were observed and asked immediately if they had pain in the arm, and the response was assessed. Reactions such as discomfort and pain, withdrawal of the hand, and so on after the administration of rocuronium were recorded as side effects for 24 h. Ten patients in Group 1, 28 patients in Group 2, 37 patients in Group 3, 30 patients in Group 4, and 15 patients in Group 5 reported no pain. Light pain was seen in 11 patients in Group 1, 14 patients in Group 2, 11 patients in Group 3, 12 patients in Group 4, and 20 patients in Group 5. Moderate pain was seen in 15 patients in Group 1, 6 patients in Group 2, 2 patients in Group 3, 8 patients in Group 4, and 10 patients in Group 5. Severe pain was seen in 14 patients in Group 1, 2 patients in Group 2, 0 patients in Group 3, 0 patients in Group 4, and 5 patients in Group 5. Correlation determined with log-linear analysis found in Group 1 pain score 0 (P < 0.001), Group 1 pain score 1 (P < 0.001), and Group 3 pain score 0 (P < 0.001). We conclude that ondansetron, lidocaine, tramadol, and fentanyl decrease the level of rocuronium injection pain. Among these drugs, lidocaine is the most effective, whereas fentanyl is the least effective. IMPLICATIONS: We compared the efficacy of ondansetron, lidocaine, tramadol, and fentanyl in minimizing the pain on injection of rocuronium in 250 patients. Ondansetron, lidocaine, tramadol, and fentanyl were effective in preventing and decreasing the level of rocuronium injection pain. Among these drugs, lidocaine was the most effective, and fentanyl was the least effective.
PMID: 12032018
Anesth Analg 2002 Jun;94(6):1469-73
Departments of Anesthesiology and Pediatrics, Children's National Medical Center, George Washington University, Washington, DC.
In this double-blinded, randomized, multicenter study, we examined analgesic efficacy and tolerability of tramadol in postoperative pediatric patients. Eighty-one postsurgical ASA physical status I and II patients ages 7-16 yr received oral tramadol (approximately 1 or 2 mg/kg) for postoperative analgesia when they were ready to transition from morphine patient-controlled analgesia to oral analgesics. Rescue analgesia consisted of morphine patient-controlled analgesia or an oral equivalent dose of oxycodone. Patients rated their pain just before the administration of tramadol and at regular intervals for 8 h afterwards using the Wong-Baker Faces Pain Rating Scale. The 2-mg/kg group required approximately half as much rescue analgesia as the 1-mg/kg group (P = 0.006). Parents rated the larger dose more favorably. Adverse events were generally mild to moderate in severity (vomiting [10%], nausea [9%], pruritus [7%], rash [4%]) and similar between the two treatment groups. There were no significant changes in hemodynamic variables, respiratory rate, or SpO(2) percentages between the two treatment groups or in all patients compared with pretreatment values. IMPLICATIONS: Oral tramadol 1-2 mg/kg is well tolerated and effective in postoperative children ready to transition from morphine patient-controlled analgesia. The group receiving 2 mg/kg required less rescue analgesic compared with those receiving 1 mg/kg.
PMID: 12032009, UI: 22026993
Anesth Analg 2002 Jun;94(6):1460-1
Departments of Anesthesiology and Nephrology Indira Gandhi Institute of Medical Sciences, Patna, India.
IMPLICATIONS: This case describes pain in the ear resulting from inadvertent placement of a subclavian dialysis catheter into the ipsilateral internal jugular vein. The pain subsided when the catheter was withdrawn.
PMID: 12032006, UI: 22026990
Anesthesiology 2002 May;96(5):1109-14
Department of Anesthesia and Intensive Care, Karolinska Institutet Danderyd Hospital, Stockholm, Sweden. eva.oddby@ane.ds.sll.se
BACKGROUND: Postoperative nausea and vomiting (PONV) is still common, especially among female patients. Our hypothesis is that coinduction with clonidine reduces the incidence of PONV in adult patients undergoing breast cancer surgery. METHODS: Sixty-eight women premedicated with midazolam were randomly allocated to coinduction with intravenous clonidine (group C) or placebo (group P) in this prospective, double-blind study. Anesthesia was standardized (laryngeal mask airway, fentanyl, propofol, sevoflurane, nitrous oxide, and oxygen). Hemodynamic parameters and the requirements for propofol, sevoflurane, and the postoperative need for ketobemidone were noted. The primary endpoints studied were the number of PONV-free patients and patient satisfaction with respect to PONV. RESULTS: Patients in group C had a significantly reduced need for propofol (P < 0.04) and sevoflurane (P < 0.01) and a reduced early need for ketobemidone (P < 0.04). There were significantly more PONV-free patients in group C compared with group P (20 and 11 of 30, respectively; P < 0.04). The number needed to treat was 3.3 (95% confidence interval, 1.8, 16.9). Intraoperative blood pressure, postoperative heart rate, and postoperative blood pressure were all significantly lower in group C compared with group P, but were not considered to be of clinical importance. No negative side effects were recorded. CONCLUSION: Coinduction with clonidine significantly increased the number of PONV-free patients after breast cancer surgery with general anesthesia.
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PMID: 11981150, UI: 21976888
Anesthesiology 2002 May;96(5):1062-9
Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands. B.Th.Veering@lumc.nl
BACKGROUND: Changing plasma protein concentrations may affect the protein binding and pharmacokinetics of drugs in the postoperative period. This study examined the effect of postoperative increases (in response to surgery) in plasma alpha1-acid-glycoprotein (AAG) concentrations on the plasma concentrations of the enantiomers of bupivacaine during continuous epidural infusion of racemic bupivacaine for postoperative pain relief. METHODS: Six patients scheduled for total hip surgery with combined epidural and general anesthesia received a bolus dose of bupivacaine (65 mg) followed by constant-rate (8 ml/h) epidural infusion of 2.5 mg/ml bupivacaine for 48 h. Total and unbound plasma concentrations of the enantiomers of bupivacaine and plasma AAG concentrations during the 48-h epidural infusion were determined. RESULTS: Total plasma concentrations of the enantiomers of bupivacaine increased steadily during the infusion (P < 0.0001), whereas unbound concentrations did not change after 12 h (P > 0.1). Total plasma concentrations of S(-)-bupivacaine were higher than those of R(+)-bupivacaine (P < 0.02), whereas unbound concentrations of S(-)-bupivacaine were lower than those of R(+)-bupivacaine (P < 0.002). AAG concentrations initially decreased, but thereafter increased steadily (P < 0.0001). Consequently, free fractions of the enantiomers initially increased and then decreased with time (P = 0.0002). Free fractions of S(-)-bupivacaine were smaller than those of R(+)-bupivacaine (P = 0.0003). CONCLUSIONS: The study confirmed that the pharmacokinetics of bupivacaine are enantioselective. During postoperative epidural infusion, changing plasma AAG concentrations affect the protein binding of both enantiomers of bupivacaine. Consequently, total plasma concentrations of the enantiomers increase with time, whereas unbound concentrations reach a plateau.
PMID: 11981143, UI: 21976881
BMJ 2002 Jun 1;324(7349):1308
Objective: To explore and explain socioeconomic variations in perceptions of and behavioural responses to chest pain. Design: Qualitative interviews. Setting: Community based study in Glasgow, Scotland. Participants: 30 respondents (15 men and 15 women) from a socioeconomically deprived area of Glasgow and 30 respondents (15 men and 15 women) from an affluent area of Glasgow. Outcome measures: Participants' reports of their perceptions of and actions in response to chest pain. Results: Residents of the deprived area reported greater perceived vulnerability to heart disease, stemming from greater exposure to heart disease in family members and greater identification with high risk groups and stereotypes of cardiac patients. This greater perceived vulnerability was not associated with more frequent reporting of presenting to a general practitioner. People from the deprived area reported greater exposure to ill health, which allowed them to normalise their chest pain, led to confusion with other conditions, and gave rise to a belief that they were overusing medical services. These factors were associated with a reported tendency not to present with chest pain. Anxiety about presenting among respondents in the deprived area was heightened by self blame and fear that they would be chastised by their general practitioner for their risk behaviours. Conclusions: Important socioeconomic variations in responses to chest pain may contribute to the known inequities in uptake of secondary cardiology services. Primary care professionals and health promoters should be aware of the ways in which perceptions of symptoms and illness behaviour are shaped by social and cultural factors.
PMID: 12039824, UI: 22035069
Clin J Pain 2002 Mar-Apr;18(2):136-7
PMID: 11882779, UI: 21876850
Eur J Pharmacol 2002 Mar 1;438(1-2):85-91
Seccion Externa de Farmacologia, Centro de Investigacion y de Estudios Avanzados del Instituto Politecnico Nacional, Mexico, D.F., Mexico.
The involvement of K(+) channels in the antinociceptive action of diclofenac was assessed in the formalin test. Local administration of diclofenac produced a dose-dependent antinociceptive effect due to a local action because drug administration in the contralateral paw was ineffective. Pretreatment of the injured paw with glibenclamide and tolbutamide (ATP-sensitive K(+) channel inhibitors), charybdotoxin and apamin (large- and small-conductance Ca(2+)-activated K(+) channel blockers, respectively), 4-aminopyridine or tetraethylammonium (voltage-dependent K(+) channel inhibitors) prevented diclofenac-induced antinociception. Given alone, K(+) channel inhibitors did not modify formalin-induced nociceptive behavior. Pinacidil (an ATP-sensitive K(+) channel opener) also produced antinociception which was blocked by glibenclamide. The peripheral antinociceptive effect of morphine (positive control) was blocked by glibenclamide and 4-aminopyridine but not by charybdotoxin or apamin. The results suggest that the peripheral antinociceptive effect of diclofenac may result from the activation of several types of K(+) channels, which may cause hyperpolarization of peripheral terminals of primary afferents.
PMID: 11906715, UI: 21904153
J Clin Oncol 2002 May 1;20(9):2409; discussion 2409-10
PMID: 11981019, UI: 21977750
J Clin Oncol 2002 May 1;20(9):2409-10
PMID: 11981018, UI: 21977749
J Clin Oncol 2002 May 1;20(9):2353-9
Department of Hematology and Oncology, Benjamin Franklin Klinik der Freien Universitat, and St Hedwigs-Krankenhaus, Berlin, Germany. hmenssen@zedat.fu-berlin.de
PURPOSE: Bisphosphonates have been found to reduce the incidence of skeletal-related events (SREs) in patients with multiple myeloma. This is the first double-blind, randomized, placebo-controlled study to assess the efficacy of ibandronate, a third-generation amino-bisphosphonate, in preventing SREs in advanced-stage multiple myeloma patients. PATIENTS AND METHODS: Patients with multiple myeloma stage II or III were randomly assigned to receive either ibandronate 2 mg or placebo as a monthly intravenous (IV) bolus injection for 12 to 24 months in addition to conventional chemotherapy. SREs such as peripheral pathologic or vertebral fractures, hypercalcemia, severe bone pain, and bone radiotherapy or surgery were analyzed. Bone-turnover markers were also studied. Finally, post hoc analyses of bone morbidity and survival were performed. RESULTS: Ninety-nine patients per treatment group were assessable for efficacy analysis. The occurrence of SRE per patient year and the time to first SRE were not significantly different between the two treatment groups. In overall evaluation, no differences were found between the treatment groups regarding bone pain, analgesic drug use, quality of life, and median survival (33.1 v 28.2 months, respectively). Explorative post hoc analyses revealed that ibandronate patients with strongly suppressed bone-turnover markers (> or = 30% and > or = 50% mean reduction of serum osteocalcin and urinary C-terminal telopeptides) developed significantly less bone morbidity. Ibandronate was tolerated well during as many as 25 therapy cycles. CONCLUSION: Monthly injections of ibandronate 2 mg IV neither reduced bone morbidity nor prolonged survival in the overall population of stage II/III multiple myeloma patients.
PMID: 11981007, UI: 21977738
J Pain Symptom Manage 2002 Apr;23(4):268-70
PMID: 11997193, UI: 21993043
N Engl J Med 2002 May 30;346(22):1732-8
PMID: 12037154, UI: 22033610
N Engl J Med 2002 May 23;346(21):1667-9
PMID: 12030261, UI: 22023547
Neurology 2002 May 28;58(10):1532
London, United Kingdom.
PMID: 12034792, UI: 22030770
Pain 2002 May;97(1-2):163-9
Department of Oral and Craniofacial Biological Sciences, Dental School, University of Maryland, Room # 5-A-14, 666 W Baltimore Street, 21201, Baltimore, MD, USA
PMID: 12031789, UI: 22028840
Pain 2002 May;97(1-2):151-61
Klinik und Poliklinik fuer Anesthesiologie und operative Intensivmedizin, Westfaelische Wilhelms-Universitaet, 48129, Muenster, Germany
PMID: 12031788, UI: 22028839
Pain 2002 May;97(1-2):139-50
Department of Cell and Animal Biology, Institute of Life Sciences, Hebrew University of Jerusalem, 01094, Jerusalem, Israel
PMID: 12031787, UI: 22028838
Pain 2002 May;97(1-2):117-25
Department of Anesthesiology and Center for the Study of Pharmacologic Plasticity in the Presence of Pain, Wake Forest University School of Medicine, Medical Center Boulevard, 27157-1009, Winston-Salem, NC, USA
PMID: 12031785, UI: 22028836
Pain 2002 May;97(1-2):93-103
Department of Anatomy and Neurobiology, Program in Neuroscience, University of Maryland School of Medicine, 21201, Baltimore, MD, USA
PMID: 12031783, UI: 22028834
Pain 2002 May;97(1-2):87-92
Arthritis Research Campaign (ARC) Epidemiology Unit, School of Epidemiology and Health Sciences, Stopford Building, University of Manchester, Oxford Road, M13 9PT, Manchester, UK
PMID: 12031782, UI: 22028833
Pain 2002 May;97(1-2):65-73
Department of Occupational Therapy, School of Health and Rehabilitation Sciences, The University of Queensland, Queensland 4072, Brisbane, Australia
PMID: 12031780, UI: 22028831
Pain 2002 May;97(1-2):53-63
Institute of Medical Science, University of Toronto, Ontario, M5T 2S8, Toronto, Canada
PMID: 12031779, UI: 22028830
Pain 2002 May;97(1-2):47-51
University Laboratory of Physiology, Oxford University, Parks Road, OX1 3PT, Oxford, UK
PMID: 12031778, UI: 22028829
Pain 2002 May;97(1-2):23-31
Back Pain Unit, King's Mill Centre for Healthcare Services, Mansfield Road, NG17 4JL, Sutton-in-Ashfield, UK
PMID: 12031776, UI: 22028827
Pain 2002 May;97(1-2):5-10
University Dental Hospital of Manchester, Higher Cambridge Street, M15 6FH, Manchester, UK
PMID: 12031774, UI: 22028825
Pain 2002 May;97(1-2):1-4
University of Pittsburgh School of Medicine, 3520 Fifth Avenue, Suite 300, 15213-3313, Pittsburgh, PA, USA
PMID: 12031773, UI: 22028824
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