RÉSUMÉ
PURPOSE: This randomized noninferiority trial aimed to evaluate whether combined suprascapular, axillary nerve, and the articular branch of lateral pectoral nerve block (3NB) is noninferior to interscalene nerve block (ISB) for pain control after arthroscopic rotator cuff repair (ASRCR). MATERIALS AND METHODS: Eighty-five patients undergoing ASRCR were randomized to either 3NB (n = 43) or ISB (n = 42) group. We used 5 and 15 ml of 0.2% ropivacaine for each nerve in the 3NB and ISB groups, respectively. The primary outcome was the visual analog scale (VAS) pain score at 4 h postoperatively measured assessed on an 11-point scale (ranging from 0 = no pain to 10 = worst pain) that was analyzed using noninferiority testing. The secondary outcome was VAS pain scores in the recovery room and at 8, 12, 24, 36, 48, and 72 h postoperatively. Rebound pain, IV-PCA usage during 48 h, dyspnea, muscle weakness, and satisfaction were evaluated. RESULTS: Regarding the primary outcome, the mean difference in VAS pain scores between the 3NB (2.5 ± 1.6) and ISB (2.2 ± 2.3) groups at 4 h postoperatively was 0.3, with a 95% confidence interval (CI) of -0.56 to 1.11. The upper limit of 95% CI is lower than the noninferiority margin of 1.3 (p < 0.001). At all other time points, except in the recovery room, 3NB showed noninferior to ISB. Rebound pain, IV-PCA usage during the second 24 h, and muscle weakness were lower in the 3NB group (all p < 0.005). The satisfaction was similar in both groups (p = 0.815). CONCLUSION: Combined 3NB is noninferior to ISB in terms of pain control after ASRCR; and is associated with low levels of rebound pain, IV-PCA usage, and muscle weakness. LEVEL OF EVIDENCE: Randomized controlled trial, Level I.
Sujet(s)
Bloc du plexus brachial , Coiffe des rotateurs , Analgésiques , Anesthésiques locaux , Arthroscopie , Humains , Douleur postopératoire/étiologie , Douleur postopératoire/prévention et contrôleRÉSUMÉ
BACKGROUND: Various methods have been used to reduce postoperative pain after thoracic surgery. However, these methods may affect the patient's respiratory response and delay recovery from anesthesia. We aimed to evaluate the effects of fentanyl and remifentanil during extubation after video-assisted thoracic surgery (VATS). METHODS: This study included 45 randomly-selected male patients who underwent VATS for pneumothorax between July 2011 and August 2012. We divided the participants into 3 groups: the F group, which received a bolus injection of 1.0 µg/kg of fentanyl; the R1 group, which received a 0.04 µg/kg/min remifentanil infusion; and the R2 group, which received a 0.08 µg/kg/min remifentanil infusion. Hemodynamics, pain, cough, consciousness level, and nausea were assessed for each group. RESULTS: The number and severity of coughs were lower in the R1 and R2 groups than in the F group, and there were no differences between the R1 and R2 groups. Respiratory depression and loss of consciousness were not observed in any of the patients, and there were no differences in hemodynamics. CONCLUSION: In comparison with fentanyl, remifentanil did not result in a wide fluctuation of blood pressure and heart rate upon emergence from general anesthesia. Moreover, remifentanil contributed to cough suppression and postoperative pain control. Remifentanil seems to be a safe and effective analgesic after VATS.
RÉSUMÉ
Whole lung lavage (WLL) is a therapeutic procedure to remove accumulated material by infusing and draining the lungs with lavage fluid. This procedure has been regarded as the current standard of care to treat pulmonary alveolar proteinosis. However, the WLL protocol has not yet been standardized and the technique has been refined and modified a number of times. A rapid infusion system is a device used to infuse blood or other fluids at precise rates and normothermic conditions. This device is not typically used in WLL, which relies on the passive infusion of fluids using the gravitational force. However, in this study we performed WLL using a rapid infusion system, since we aimed to take advantage of its shorter operation time and greater degree of control over fluid volume and temperature. The patient's symptoms improved without the occurrence of any complications.
RÉSUMÉ
Submucosal infiltration and the topical application of epinephrine as a vasoconstrictor produce excellent hemostasis during surgery. The hemodynamic effects of epinephrine have been documented in numerous studies. However, its metabolic effects (especially during surgery) have been seldom recognized clinically. We report two cases of significant metabolic effects (including lactic acidosis and hyperglycemia) as well as hemodynamic effects in healthy patients undergoing orthognathic surgery with general anesthesia. Epinephrine can induce glycolysis and pyruvate generation, which result in lactic acidosis, via ß2-adrenergic receptors. Therefore, careful perioperative observation for changes in plasma lactate and glucose levels along with intensive monitoring of vital signs should be carried out when epinephrine is excessively used as a vasoconstrictor during surgery.
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Castleman's disease (CD) is a rare lymphoproliferative disorder of undetermined etiology. Unicentric Castleman's disease is confined to a single lymph node; it is usually asymptomatic though sometimes has local manifestations related to mass effects. In contrast, multicentric Castleman's disease (MCD) typically presents with lymphoid hyperplasia at multiple sites; it is associated with systemic symptoms and abnormal laboratory findings, with a less favorable prognosis. In case of anesthesia in CD, an exhaustive preanesthetic evaluation is essential to identify associated clinical manifestations which may influence the management of the anesthesia. Perioperative careful monitoring and proper anesthetic management are both important. We report a case of general anesthesia with anesthetic management in a patient with MCD that has not been documented in the literature.
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BACKGROUND: Cerebral hypotension and desaturation can occur during shoulder surgery in the seated position. We evaluated the correlation of cerebral oxygen saturation (rSO(2)) using near infra-red spectroscopy (NIRS) and mean arterial pressures (MAP) (at the levels of the brain and heart). METHODS: Fifty patients, scheduled for the arthroscopic shoulder surgery in the seated position, were enrolled to monitor the rSO(2), bispectral Index (BIS), and MAPs at the levels of the brain and heart. The values of each parameter were collected at 5 min after intubation, immediately after placing the patient in the sitting position, 5 min after the patient was seated, immediately after the surgical incision, and every 30 min after incision. RESULTS: A correlation between the cerebral rSO(2) and the MAP at the level of brain were statistically significant. Cerebral rSO(2) and MAP after a change of posture from supine to sitting position were significantly decreased, compared to the baseline value. CONCLUSIONS: Monitoring cerebral rSO(2) and MAP at the level of brain can be helpful to detect the possibility of cerebral deoxygenation earlier.
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Liver ischemia/reperfusion has been shown to result in injury of remote organs such as the heart and lungs. Whether or not acute liver injury also results in kidney injury has so far not been adequately addressed. In anesthetized Wistar rats, partial (70%) normothermic hepatic ischemia was applied for 75 min. After 24 h of reperfusion, renal injury was assessed by histology, creatinine and blood urea nitrogen (BUN) serum concentrations, renal expression of proinflammatory genes [quantitative real-time polymerase chain reaction (qRT-PCR)], caspase-3 activation (Western blot), and neutrophil accumulation (myeloperoxidase assay). Twenty-four hours after hepatic ischemia, creatinine (0.57+/-0.06 vs. 0.32+/-0.04 mg/dL) and BUN (40.7+/-15.3 vs. 14.3+/-2.0 mg/dL) were increased when compared to sham. qRT-PCR revealed higher renal intercellular adhesion molecule-1 gene expression following hepatic ischemia (166+/-45% when compared to sham) but no differences in renal monocyte chemoattractant protein-1, macrophage inflammatory protein-2, and inducible NO synthase expression. In both groups, kidneys showed no morphological damage and no increase in caspase-3 and myeloperoxidase activity. Severe hepatic ischemia results in a moderate impairment of renal function in rats but does not trigger an inflammatory response in the kidney and does not result in morphological damage of the kidney.
Sujet(s)
Foie/vascularisation , Insuffisance rénale/étiologie , Lésion d'ischémie-reperfusion/complications , Animaux , Apoptose/physiologie , Caspase-3/métabolisme , Créatinine/sang , Immunotransfert , Rein/anatomopathologie , Mâle , Myeloperoxidase/métabolisme , Rats , Rat Wistar , Insuffisance rénale/anatomopathologie , Insuffisance rénale/physiopathologie , Lésion d'ischémie-reperfusion/physiopathologieRÉSUMÉ
We report a case of Baker's cyst that induced compression of both the tibial and common peroneal nerves. The patient presented with calf atrophy and foot drop over a 6-month period. These signs and symptoms could have been mistaken for those of spinal origin. Based on an electrodiagnostic study and magnetic resonance imaging, compression of nerves by an asymptomatic Baker's cyst measuring 6x4 cm was confirmed. This cyst communicated with the articular joint which was also associated with a medial meniscal lesion. We treated the patient arthroscopically by performing partial medial meniscectomy, and through the posterolateral and the posteromedial portal, decompression of the Baker's cyst was performed. Approximately 6 weeks after the arthroscopic decompression, the cyst recurred. Therefore open resection was performed. At 1-year follow-up, the patient had considerable improvement in motor as well as sensory function and showed no evidence of recurrence. Although the electrodiagnostic studies showed an improvement in symptoms, the patient continued to complain of lower leg weakness owing to delayed diagnosis and cyst decompression. We believe that Baker's cysts should also be considered in the differential diagnoses of patients who present with neuromuscular dysfunction in the calf and leg.
Sujet(s)
Syndromes de compression nerveuse/étiologie , Nerf fibulaire commun , Kyste poplité/complications , Nerf tibial , Arthroscopie , Électrodiagnostic , Femelle , Troubles neurologiques de la marche/étiologie , Troubles neurologiques de la marche/chirurgie , Humains , Imagerie par résonance magnétique , Ménisques de l'articulation du genou/chirurgie , Adulte d'âge moyen , Syndromes de compression nerveuse/chirurgie , Kyste poplité/diagnostic , Kyste poplité/chirurgieRÉSUMÉ
OBJECTIVES: To determine the effect of a single dose of methylphenidate on the cognitive performance of patients with traumatic brain injury (TBI), and particularly on working memory and visuospatial attention. DESIGN: A double-blind placebo-controlled study. The subjects were randomly divided into an experimental group taking methylphenidate and a control group taking a placebo. SETTING: The Department of Rehabilitation Medicine of a university hospital. SUBJECTS: Eighteen subjects with TBI (16 male and two female) were enrolled. INTERVENTIONS: The patients were given 20 mg methylphenidate or a placebo. Cognitive assessments were performed at three times: before the medication as a baseline, 2 h after medication and at follow-up (48 h later). MAIN MEASURES: Cognitive assessments consisted of working memory tasks and endogenous visuospatial attention tasks designed using SuperLabPro 2.0 software. Response accuracy and reaction time were measured. RESULTS: There were significant improvements in response accuracy in the methylphenidate group compared with the placebo group for both the working memory and visuospatial attention tasks. A significant decrease in the reaction time was also observed in the methylphenidate group only for the working memory task. CONCLUSIONS: The administration of single-dose methylphenidate has an effect in improving cognitive functioning following a TBI. The effects were most prominent regarding the reaction time of the working memory.
Sujet(s)
Lésions encéphaliques/traitement médicamenteux , Stimulants du système nerveux central/pharmacologie , Cognition/effets des médicaments et des substances chimiques , Méthylphénidate/pharmacologie , Adulte , Attention/effets des médicaments et des substances chimiques , Lésions encéphaliques/rééducation et réadaptation , Stimulants du système nerveux central/administration et posologie , Méthode en double aveugle , Femelle , Humains , Mâle , Mémoire/effets des médicaments et des substances chimiques , Méthylphénidate/administration et posologie , Temps de réaction , Statistique non paramétriqueRÉSUMÉ
PURPOSE: We undertook a study to determine whether propofol may attenuate Kupffer cell (KC) activation, thus protecting the cells against hypoxia-reoxygenation injury through the modulation of intracellular calcium ([Ca2+]i). METHODS: [Ca2+]i, the expression of tumour necrosis factor (TNF)-alpha mRNA, and KC viability were measured in response to hypoxia-reoxygenation following pretreatment with propofol 0.5 and 5 microg.mL(-1) (Groups P1 and P2, respectively) or without propofol (Group HRC). KCs were isolated and cultured from male Sprague-Dawley rats. KCs were incubated under an atmosphere of hypoxia (95% N2 + 5% CO2) for 60 min with subsequent 120 min reoxygenation (95% air + 5% CO2). [Ca2+]i for the first 12 min after reoxygenation, TNF-alpha mRNA, and KC viability at the end of reoxygenation in groups P1 and P2 were compared with those of HRC. RESULTS: The increase of [Ca2+]i from the baseline was attenuated in P1 (96.6 +/- 6.9%) and P2 (96.1 +/- 5.4%) compared with HRC (143.8 +/- 11.5%), (P < 0.001), with no difference between P1 and P2. The expression of TNF-alpha mRNA increased only in HRC during hypoxia-reoxygenation. KC viability increased in P1 (97.5 +/- 2.6%) and P2 (94.6 +/- 2.9%), compared with HRC (89.9 +/- 1.4%), (P < 0.005), with no difference between P1 and P2. CONCLUSION: The results indicate that propofol attenuates KC activation and protects KC from hypoxia-reoxygenation injury at clinically relevant concentrations. This attenuation seems to result from inhibition of [Ca2+]i increase in KC.