Okuda Y

Use of the Pentax-AWS in 293 patients with difficult airways.

Background:Several case reports have shown that the Pentax-AWS® (Hoya Corporation, Tokyo, Japan), a new video laryngoscope, is useful in patients with difficult airways. Methods:We assessed the effectiveness of the Pentax-AWS® in two groups. Group 1 included 270 patients in whom direct laryngoscopy using a Macintosh laryngoscope had been difficult. Group 2 included 23 patients with predicted difficult intubation and difficult mask ventilation without previous use of the Macintosh laryngoscope. Results:In group 1, the view of the glottis with the Macintosh laryngoscope was Cormack and Lehane grade 2 in 14 patients, grade 3 in 208 patients, and grade 4 in 48 patients. In 256 patients in whom the grade was 3 or 4 with the Macintosh laryngoscope, the view with the Pentax-AWS® was either grade 1 or 2 in 255 patients (99.6%; 95% confidence intervals 97.8–100%). Tracheal intubation was successful with the Pentax-AWS® in 268 of 270 patients (99.3%; 95% confidence interval 97.4–100%), and it failed (after two attempts) in two patients. In group 2, tracheal intubation was successful in 22 of 23 patients, and it failed in one patient. The reasons for failed intubation using the Pentax-AWS® were failure to position the blade toward the glottic side of the epiglottis, inability to maneuver the endotracheal tube away from the arytenoids and into the trachea, and bleeding and swelling of the oropharynx. Conclusion:The success rate of tracheal intubation using the Pentax-AWS® was high in patients with difficult laryngoscopy with a Macintosh laryngoscope and in patients with predicted difficult intubation.

The Pentax-AWS video-laryngoscope: the first experience in one hundred patients.

We studied the efficacy of the Pentax-AWS (Tokyo, Japan), a new portable, battery-operated video-laryngoscope, in 100 patients. It was possible to insert the blade of the Pentax-AWS and to see a full view of the glottis on the first attempt in 99 of 100 patients. In the remaining patient, insertion of the Pentax-AWS was abandoned because of a risk of damaging teeth that were already loose. Tracheal intubation was successful in 98 patients. The median time taken for tracheal intubation was 35 s (range, 5–120 s).

Propofol prevents lipid peroxidation following transient forebrain ischemia in gerbils

Purpose: To ascertain whether propofol prevents lipid peroxidation on delayed neuronal death induced by transient forebrain ischemia in the hippocampal CAI subfield in gerbils.Methods: Forty gerbils were randomly assigned to five groups: Group I, control, sham operation treated with physiological saline solution (PSS); Group II, ischemia/reperfusion treated with PSS; Group III, ischemia/reperfusion treated with 50 mg·kg−1 propofol; Group IV, ischemia/reperfusion treated with 100 mg·kg−1 propofol; Group V, ischemia/reperfusion treated with 150 mg·kg−1 propofol. Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes under N2O/O2/halothane anesthesia after propofol or PSS. Five days later, the cerebrum was removed and each forebrain was cut into two including the hippocampus. Lipid peroxidation was determined using the production of malondialdehyde (MDA), and histopathological changes in the hippocampal CAI subfield were examined.Results: In group II, the pyramidal cells were atrophic and pycnotic, vacuolation and structural disruption of the radial striated zone was observed. In the other four groups, these changes were not observed. Degenerative ratios of pyramidal cells were: Group I: 4.9±2.3, Group II: 94.1±4.5 (P<0.01), Group III: 12.5±5.7, Group IV: 11.0±4.6, Group V: 9.6±4.9%. Production of MDA was: Group I: 83±22, Group II: 198±25 (P<0.01), Group III: 153±39, Group IV: 113±34, Group V: 106±27 nmol·g−1 wet tissue.Conclusion: Propofol attenuated delayed neuronal death by preventing lipid peroxidation induced by transient forebrain ischemia in the hippocampal CAI subfield in gerbils.RésuméObjectif: Vérfier si le propofol empêche la peroxydation lipidique qui survient à la mort neuronale différée induite par une ischémie transitoire du prosencéphale, dans le sous-champ CAI de l’hippocampe chez des gerbilles.Méthode: On a réparti au hasard 40 gerbilles en cinq groupes: dans le groupe I, témoin, elles ont subi une opération fictive traitée avec une solution physiologique salée (SPS); dans le groupe II, une ischémie/reperfusion traitée avec une SPS; dans le groupe III, une ischémie/reperfusion traitée avec 50 mg·kg−1 de propofol; dans le groupe IV, une ischémie/reperfusion traitée avec 100 mg·kg−1 de propofol et dans le groupe V, une ischémie/reperfusion traitée avec 150 mg·kg−1 de propofol. L’ischémie transitoire du cerveau antérieur a été induite par l’occlusion bilatérale des artères carotides communes pendant quatre minutes sous anesthésie au N2O/O2/halothane après l’administration de propofol ou de SPS. Cinq minutes plus tard, le cerveau a été retiré et chaque prosencéphale a été coupé en deux, induant l’hippocampe. La peroxydation lipidique a été déterminée en utilisant la production de malondialdéhyde (MDA), et les changements histopathologiques du sous-champ CAI de l’hippocampe ont été examinés.Résultats: Dans le groupe II, les cellules pyramidales étaient atrophiques et pycnotiques; une rupture vacuolaire et structurale de la zone radiale striée a été observée. Dans les autres groupes, ces changements n’ont pas été notés. Les taux de cellules pyramidales dégénératives ont été: groupe I: 5,8±2,5 %, groupe II: 94,1±4,5 (P<0,01), groupe III: 12,5±5,7 %, group IV: 11,0±4,6 %, groupe V: 9,4±6,6 %. La production de MDA a été dans le groupe I: 83±22, II: 198±25 (P<0,01), III: 153±39, IV: 113±34 et V: 106±27 nmol·g−1 de tissu.Conclusion: Le propofol a réduit la mort neuronale différée en empêchant la peroxydation lipidique induite par l’ischémie transitoire du prosencéphale dans le sous-champ CAI de l’hippocampe de gerbilles.

Propofol prevents delayed neuronal death following transient forebrain ischemia in gerbils.

PurposeThis study was conducted to ascertain whether propofol may protect against delayed neuronal death in the hippocampal CA1 subfield in gerbils.MethodsThirty-five gerbils were randomly assigned to five groups: Group I, the control group, a sham operation treated with physiological saline solution (PSS); Group II, ischemia/reperfusion treated with PSS; Group III, ischemia/reperfusion treated with 50 mg · kg−1 propofol; Group IV ischemia/reperfusion treated with 100 mg · kg−1 propofol; Group V ischemia/reperfusion treated with 150 mg · kg−1 propofol. Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes under N2O/O2/halothane anesthesia after administration of propofol or PSS. Five days later, histopathological changes in the hippocampal CA1 subfield were examined using a light microscope and degenerative ratio of the pyramidal cells were measured according to the following formula: (number of degenerative pyramidal cellsAotal number of pyramidal cells per I mm of hippocampal CA1 subfield) × 100.ResultsIn group II, the pyramidal cells were atrophic and pycnotic; vacuolation and structural disruption of the radial striated zone was observed. In the other four groups, these changes were not observed. The degenerative ratios of pyramidal cells were as follows; group 1: 5.9 ± 1.9%, group II: 94.6 ± 2.5% (P < 0.01), group III: 10.7 ± 1.7%, group IV: 9.7 ± 1.8%, group V: 9.2 ± 1.9%.ConclusionThis study suggests that propofol may prevent delayed neuronal death in the hippocampal CA1 subfield after cerebral ischemia/reperfusion in gerbils.RésuméObjectifLa présente étude a été menée pour vérifier si le propofol peut protéger contre la mort neuronale retardée du sous-champ CA1 hippocampique chez des gerbilles.MéthodeTrente-cinq gerbilles ont été répartis au hasard en cinq groupes: le groupe I, témoin, subit une opération fictive traitée avec une solution physiologique salée (SPS); les autres gerbilles subissent une ischémie/reperfusion traitée dans le groupe II avec une SPS; dans le groupe III, avec 50 mg · kg−1 de propofol; dans le groupe IV avec 100 mg · kg−1 de propofol et dans le groupe V avec 150 mg · kg−1 de propofol. L’ischémie transitoire du cerveau antérieur a été induite par l’occlusion bilatérale des artères carotides communes pendant quatre minutes sous anesthésie au N2O/O2/halothane après l’administration de propofol ou de SPS. Cinq jours plus tard, on a vérifié les changements histopathologiques survenus dans le sous-champ CA1 hippocampique à l’aide d’un microscope optique et le taux de dégénérescence des cellules pyramidales a été mesuré comme suit: (nombre de cellules pyramidales dégénératives/nombre total de cellules pyramidales par mm de sous-champ CA1 hippocampique) x 100.RésultatsDans le groupe II, on a noté des cellules pyramidales atrophiques et pycnotiques; on a aussi observé la vacuolisation et la rupture structurale de la zone radiale striée. Dans les quatre autres groupes, ces changements n’ont pas été notés. Les taux de cellules pyramidales dégénératives étaient pour le groupe 1: 5.9 ± 1.9.%, le groupe II: 94.6 ± 2.5 % (P < 0.01), le groupe III: 10.7 ± 1.7 %, le groupe IV: 9.7 ± 1.8 %, le groupe V: 9.2 ± 1.9%.ConclusionCette étude suggère que le propofol peut prévenir la mort neuronale tardive dans le sous-champ CA1 hippocampique à la suite d’une ischémie/reperfusion chez les gerbilles.

Delayed severe airway obstruction due to hematoma following stellate ganglion block

Background and Objectives. Delayed onset of airway obstruction following stellate ganglion block (SGB) may be life threatening. We treated a patient who developed a severe airway obstruction caused by a large hematoma several hours after an SGB. Methods. A 62‐year‐old woman suffering from sudden deafness developed dyspnea 2 hours after undergoing her fourth SGB, and evidenced swelling and tenderness in her anterior neck and chest. Her pharyngolaryngeal tissues were edematous, and the glottis was markedly narrowed. Computed tomograms and magnetic resonance images revealed a large soft tissue mass extending from the first cervical vertebra to the diaphragm. Results. Surgical tracheotomy was performed to maintain her airway. Swelling of the vocal cord disappeared on the eleventh day after the operation. Conclusions. We believe that the SGB needle injured the vertebral artery and caused massive hemorrhage anterior to the cervical vertebra, subsequently inducing pharyngolaryngeal edema by obstructing the venous and lymphatic drainage of the cervical region.

Use of a nerve stimulator for phrenic nerve block in treatment of hiccups

HICCUPS may be managed with several methods, such as stimulation of the pharynx, compression of the eyeballs, gastric lavage, sedation, and inhalation of carbon dioxide. If these treatments fail, block of the phrenic nerve has been suggested as the last resort. Moore has suggested that if hiccups did not stop after the first attempt at blocking, the procedure should be repeated. Fluoroscopy or chest radiographs taken during inspiration and expiration (double-exposure method)4 can confirm the paralysis of the diaphragm after phrenic nerve block. However, even when the phrenic nerve is blocked, the diaphragm may not be paralyzed. Therefore, objective tests that would detect the successful phrenic nerve block are useful. We report the use of a nerve stimulator for confirmation of phrenic nerve block.

A sevoflurane induction of anesthesia with gradual reduction of concentration is well tolerated in elderly patients

PurposeTo establish the appropriate inhalation induction technique using a high concentration of sevoflurane in the elderly.MethodsForty-five patients, aged 70–79-yr-old, were randomly divided into three groups: 1) Group I: anesthesia was induced with propofol 2 mg·kg−1 and sevoflurane 2% (n = 15); 2) Group II: anesthesia was induced with a threeminute inhalation of sevoflurane 8%; 3) Group III: anesthesia was induced with inhalation of sevoflurane using a gradual reduction technique (8, 6, 4% for each minute). In Groups II and III, a modified vital capacity inhalation induction was performed. Mean arterial pressure (MAP), heart rate (HR) and oxygen saturation (SpO2) were measured continuously during induction. In addition, induction time and adverse events related to anesthetic induction were recorded.ResultsThe induction time in Group I was significantly shorter than that in Groups II and III (P < 0.05). However, there was no difference in the induction time between Groups II and III. In Groups II and III, the majority of patients required additional breaths. In comparison with the other groups, stability of MAP was maintained in Group III. The variations of HR in all groups were small. During induction, no patient experienced a decrease in SpO2 below 96%, except for two patients in Group I. Severe respiratory adverse events were not observed. Other adverse events were similar in all groups.ConclusionsOur results suggest that a high concentration sevoflurane induction using a gradual reduction technique may be an acceptable alternative to standard iv induction in elderly patients.RésuméObjectifRéaliser la technique appropriée d’induction par inhalation en utilisant une forte concentration de sévoflurane chez des patients âgés.MéthodeQuarante-cinq patients de 70–79 ans, ont été répartis de façon aléatoire en trois groupes : 1) groupe I : anesthésie induite avec 2 mg·kg−1 de propofol et du sévoflurane à2%(n = 15) ; 2) groupe II : anesthésie induite avec l’inhalation de sévoflurane à 8 % pendant 3 min ; 3) groupe III : anesthésie induite avec l’inhalation de sévoflurane selon la technique de réduction graduelle de la concentration (8, 6, 4 % pour chaque minute). Dans les groupes II et III, une induction par inhalation, avec modification de la capacité vitale, a été réalisée. La tension artérielle moyenne (TAM), la fréquence cardiaque (FR) et la saturation du sang en oxygène (SpO2) ont été mesurées en continu pendant l’induction. De plus, le temps nécessaire à l’induction et les événements indésirables reliés à l’induction anesthésique ont été notés.RésultatsLe temps d’induction a été significativement plus court dans le groupe I que dans les groupes II et III (P < 0,05). Aucune différence de temps d’induction n’a été relevée entre les groupes II et III. Dans ces groupes II et III, la majorité des patients ont eu besoin de ventilation supplémentaire. Comparativement aux autres groupes, la stabilité de la TAM a été maintenue dans le groupe III. Les variations de FC ont été faibles dans tous les groupes. Pendant l’induction, aucun patient n’a subi de baisse de la SpO2 en dessous de 96 %, sauf deux patients du groupe I. Aucune complication respiratoire sévère n’a été observée. Les autres événements indésirables ont été comparables d’un groupe à l’autre.ConclusionNos résultats montrent qu’une induction avec une forte concentration de sévoflurane, selon une technique de réduction graduelle, peut remplacer l’induction iv habituelle de façon acceptable chez les patients âgés.

Recovery of psychomotor function after propofol sedation is prolonged in the elderly

PurposeTo assess the effects of age on recovery of psychomotor function for propofol sedation during spinal anesthesia.MethodsPropofol was continuously infused during surgery and spinal anesthesia in 15 elderly patients (65–85 yr-old) and 15 younger patients (20–50 yr-old). Infusion rates were adjusted to maintain an appropriate level of sedation using the bispectral index (range 60–70). The sedative infusion was discontinued at the end of surgery. The early recovery times from the end of propofol infusion to opening of eyes on command, sustaining a hand grip, and recall of name were noted. Psychomotor function, as measured by the Trieger’s dot test, was evaluated before anesthesia and 30, 60, 90, 120 min after the end of propofol infusion.ResultsThe duration of anesthesia was 142 ± 55 min and 134 ±61 min in the elderly and younger patients, respectively. No differences were observed in early recovery times between elderly and younger patients (opened their eyes on command, 6.3 ± 4.0 min and 5.2 ± 2.6 min; sustained a hand grip, 7.2 ± 3.9 min and 6.1 ± 3.5 min and recalled their name, 8.0 ± 4.5 min and 6.5 ± 3.8 min,P > 0.05). The recovery of psychomotor function in the elderly took longer compared with the younger patients, and psychomotor function in the elderly recovered at 120 min after the end of propofol infusion.ConclusionEarly recovery times following propofol sedation is similar between elderly and younger patients, but recovery of psychomotor function in the elderly is delayed compared with younger patients.RésuméObjectifÉvaluer les effets de l’âge sur la récupération de la fonction psychomotrice à la suite d’une sédation au propofol pendant la rachianesthésie.MéthodeUne perfusion continue de propofol a été utilisée pendant une intervention chirurgicale sous rachianesthésie chez 15 patients âgés (65–85 ans) et 15 patients plus jeunes (20–50 ans). Les vitesses de perfusion ont été réglées de façon à maintenir un niveau approprié de sédation à l’aide de l’index bispectral (intervalle de 60–70). La perfusion a été interrompue à la fin de l’opération. On a noté le temps écoulé entre la fin de la perfusion jusqu’à l’ouverture des yeux sur commande, le moment où le patient peut maintenir la préhension de la main et se nommer. La fonction psychomotrice, mesurée par le test de Trieger, a été évaluée à 30, 60, 90 et 120 min après la fin de la perfusion de propofol.RésultatsLa durée de l’anesthésie a été de 142 ± 55 min et de 134 ± 61 min chez les patients âgés et les plus jeunes, respectivement. Aucune différence des temps de récupération précoce n’a été observée entre les patients âgés et les autres (l’ouverture des yeux sur commande: 6,3 ± 4,0 min et 5,2 ± 2,6 min; la préhension de la main: 7,2 ± 3,9 min et 6,1 ± 3,5 min et la capacité de se nommer: 8.0 ± 4,5 min et 6,5 ± 3,8 min, P > 0,05). Le rétablissement de la fonction psychomotrice a été plus long chez les gens âgés comparés aux plus jeunes et s’est produit à 120 min après la fin de la perfusion de propofol chez les patients âgés.ConclusionLes temps de récupération précoce qui suit la sédation au propofol sont similaires chez les patients âgés ou plus jeunes, mais le rétablissement de la fonction psychomotrice est retardé chez les patients âgés comparés à des patients plus jeunes.

A combination of heparin and an intermittent pneumatic compression device may be more effective to prevent deep-vein thrombosis in the lower extremities after laparoscopic cholecystectomy

BackgroundThe purpose of this study was to clarify the effect of a combination of heparin and an intermittent pneumatic compression device on thrombogenesis and platelet activation in the upper and lower extremities after laparoscopy.MethodsA blinded study was performed on 30 patients. Patients were randomly injected with either heparin or physiological saline solution (PSS) subcutaneously. The intermittent compression boot was used during surgery. Plasma D-dimer (D-D), a, marker of thrombogenesis, and β-thromboglobulin (β-TG), a marker of platelet activation, were measured in the upper and lower extremities.ResultsIn the heparin group, D-Ds in the upper and lower extremities increased significantly 24 h after surgery, but they were significantly lower than those of the PSS group. β-TG in the low-r extremities of patients in the PSS group increased significantly 24 h after surgery.ConclusionA combination of low-molecular-weight heparin and intermittent pneumatic compression may be more effective to prevent deep-vein thrombosis in the legs.

Assessment of QT interval and QT dispersion following stellate ganglion block using computerized measurements.

Background and Objectives Prolongation of QT interval and QT dispersion (QTD) may be associated with an increased risk of arrhythmias. This study was designed to investigate the effects of right or left stellate ganglion block (SGB) on RR interval, QT interval, the rate-corrected QT (QTc) interval, QTD and the rate-corrected QTD (QTcD) using computerized measurements. Methods Ten healthy volunteers underwent both right and left SGBs using 7 mL 1% mepivacaine with a 7-day interval between the 2 blocks. The measurement from the 12-lead electrocardiogram was performed for 60 minutes after SGB. Results Right SGB induced a significant decrease of RR interval immediately after the block, and significant increases of QT interval, QTc interval, QTD, and QTcD from immediately through 50 minutes after the block (P < .01). Left SGB induced a significant decrease of RR interval, and significant increases of QTc interval and QTD immediately after the block (P < .01). Left SGB also produced a significant decrease of QT interval from 20 through 50 minutes after the block, and a significant decrease of QTc interval from 30 through 50 minutes after the block (P < .05). Conclusions Right SGB induces increases of the QT interval, QTc interval, QTD, and QTcD, and left SGB induces decreases of the QT interval and QTc interval.