Seiitsu Murakami

Continuous axillary brachial plexus block

Continuous axillary brachial plexus block was performed in 597 patients undergoing prolonged operations on the hand. The technique required placement of a 5 cm 23 gauge teflon intravenous catheter in the axillary perivascular sheath. Lidocaine 1.5 per cent or mepivicaine 1.5 per cent (20-40 ml) were used for the initial block dose. Surgery was completed in 77.2 per cent of patients (460) with the axillary block alone while in 19.1 per cent of patients (114) supplementary narcotic administration or additional regional blocks were required. In 3.7 per cent of patients (22) the technique was considered a complete failure. Complications included local anaesthetic toxic reactions (2.85 per cent, 17 cases), nerve injury (0.50 per cent, three cases) and one case of major haematomaformation. The advantages of this technique and the possible complications are discussed.RésuméLe Mac continuel du plexus axillaire a été pratiqué chez 597 patients subissant une opération prolongée de la main. Pour cette technique, nous avons placé un cathéter intraveineux en teflon de calibre 23 et long de 5 cm dans l’axillaire de l’espace périvasculaire. Une dose de 1.5 pour cent de lidocaine ou de mépivicaine 1.5 pour cent (20–40 ml) a été injectée pour la dose initiale du bloc. L’opération chirurgicale fut compiétée chez 77.2 pour cent des patients (460) avec le bloc axillaire seulement alors que chez 191 pour cent des patients (114), une administration supplémentaire de narcotique fut injectée ou des blocs régionaux additionnels furent nécessaires. Dans le cas de 3.7 pour cent des patients (22), la technique Jut considérée un éckec total. Les complications ont entraîné des réactions toxiques avec l’agent d’anesthésie locale (2.85 pour cent, 17 cas), des lésions aux nerfs (0.50 pour cent, 3 cas) et un cas extrême deformation d’hématome. Les avantages de cette technique et les complications possibles sont discutées.

Effects of Epidural Anesthesia on Cardiovascular Response and Survival in Experimental Hemorrhagic Shock in Dogs

The purpose of the present study was to assess the effects of epidural anesthesia on cardiovascular responses and survival in experimental hemorrhagic shock in dogs. Thirty mongrel dogs were randomly assigned to one of three groups on the basis of anesthetic technique: the upper-level group (n = 10), receiving general anesthesia plus upper-level (mainly thoracic region) epidural anesthesia; the lower-level group (n = 10), receiving general anesthesia plus lower-level (mainly lumbar region) epidural anesthesia; and the control group (n = 10), receiving general anesthesia alone. After withdrawal of blood, the changes in mean arterial pressure (40 mmHg) and cardiac index were similar in all groups. In the upper-level group, a lower heart rate and systemic vascular resistance than the control group were maintained throughout in the presence of severe hypotension. A significant difference in survival was seen between the upper-level and control groups over the 100-min observation period as a whole (P less than 0.05 by the Generalized Wilcoxon test), since, at the end of the period, only two of the ten animals in the control group survived, whereas nine of ten in the upper-level group survived (P less than 0.001 by the Kaplan-Meier test). This result demonstrates that, in dogs lightly anesthetized with halothane and nitrous oxide, upper thoracic level epidural anesthesia significantly improves survival in experimental hemorrhagic shock (compared with survival in dogs with lumbar epidural or no epidural anesthesia) when the epidural is performed before hemorrhage and when the mean arterial pressure is constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased circulation time in the upper limb reduces the lag time of the finger pulse oximeter response

To observe the influence of circulatory changes on the lag time of the pulse oximeter response, eight healthy patients scheduled for hand surgery were studied. After breath holding, the patients took a breath of oxygen and the time to an increase in SpO2 was measured before and after axillary brachial plexus block. It was found that the lag time with finger probe decreased from 28.6 ±7.1 sec to 15.8 ± 1.1 sec (mean ± SD) following brachial block (P < 0.01), There was no change in arterial blood pressure. The results suggest that the lag time of the finger pulse oximeter response is primarily determined by blood flow.RésuméAfin d’observer l’influence des changements circulatoires sur le temps de réponse du saturomètre, huit patients en santé devant subir une chirurgie de la main ont été étudiés. Après avoir retenu leur respiration, les patients ont pris une respiration sous oxygène et le temps d’attente jusqu’à l’observation d’une augmentation de la SpO2 a été mesuré avant et après le bloc du plexus axillaire. Il a été noté que le temps de réponse avec la pièce digitale diminuait (P < 0,01) de 28,6 ± 7,1 sec à 15,8 ±1,1 sec (moyenne ± ET) après le bloc axillaire. Il n’y avait aucun changement de la tension artérielle. Ces résultats suggèrent que le temps de réponse de la pièce digitale du saturomètre est principalement déterminé par le débit sanguin.

BENEFICIAL EFFECT OF UPPER THORACIC EPIDURAL ANESTHESIA IN EXPERIMENTAL HEMORRHAGIC SHOCK IN DOGS : INFLUENCE OF CIRCULATING CATECHOLAMINES

The question as to whether reduction of plasma catecholamine concentration contributes to the beneficial effects of upper thoracic epidural anesthesia on survival during hemorrhagic shock was examined. Twenty-six dogs were anesthetized with halothane and nitrous oxide, and blood was withdrawn to reduce the mean arterial blood pressure (MAP) to 40 mmHg. The 12 dogs in group A received both upper thoracic epidural anesthesia before the hemorrhage and intravenous infusion of epinephrine (450 ng.kg-1.min-1) and norepinephrine (150 ng.kg-1.min-1) during hemorrhage. The 14 dogs in group B received none of these. At 20 min after the start of the bleeding, plasma catecholamine concentrations were increased in both groups more than ten-fold. There were no significant intergroup differences with respect to these concentrations at any point during the experimental period. During the 100-min period of hemorrhage, 1 of the 12 animals in group A and 10 of the 14 in group B died. A significant difference in survival was seen between the two groups over the 100-min hypotensive period (P less than 0.01 by the generalized Wilcoxon test). These results suggest that the survival benefit of upper thoracic epidural anesthesia cannot be explained simply by differences in the level of catecholamines in the plasma, and that perhaps differences in the level of catecholamines at the nerve endings or other factors may be more important.

Brainstem auditory evoked potentials during procaine toxicity in dogs

Although the toxic effect of local anaesthetics on the activity of cerebral cortex has been extensively studied, little is known about their toxic effect on brainstem. Accordingly, the influence of procaine on brainstem auditory evoked potentials (BAEPs) and on the electroencephalogram (EEG) was observed in 15 dogs. After the administration of procaine (15 mg · kg−1, iv), the amplitudes of wave I (1.88 ± 0.56 vs 2.06 ± 0.61 μV, mean ± SD) and wave II (1.91 ± 0.41 vs 2.06 ± 0.46 μV) in BAEPs increased (P < 0.05), while the amplitudes of wave III (0.97 ± 0.27 vs 0.81 ± 0.24 μV), wave IV (1.15 ± 0.43 vs 0.85 ± 0.29 μV) and wave V (1.04 ± 0.46 vs 0.92 ± 0.41 μV) were decreased (P < 0.05), and both the I–III inter-peak latency (1.57 ± 0.04 vs 1.70 ± 0.07 msec) and III–V inter-peak latency (2.15 ± 0.09 vs 2.35 ± 0.12 msec) were prolonged (P < 0.01). The EEG changed from an awake pattern to seizure activity. These results suggest that the electrical activity of the brainstem auditory pathway is suppressed even when the cerebral cortex is in an excitatory slate at the convulsive stage of procaine toxicity.RésuméLes anesthésiques locaux ont des effets toxiques bien définis sur l’activité cérébrale corticale, mais leurs effets sur le tronc cérébral sont moins bien connus. La présente étude faite chez 15 chiens évalue les effets de la procaine sur l’électroencé-phalogramme (EEG) et sur les potentiels évoqués auditifs (PEA) au niveau du tronc cérébral. L’administration intraveineuse de procaine (15 mg · kg−1) cause une augmentation des ondes I et II des PEA, de 1,88 ± 0,56 à 2,06 ± 0,61 μV et de 1,91 ± 0,41 à 2,06 ± 0,46 μV respectivement (moyenne ± écart-type P < 0,05), et une diminution des ondes III, IV et V de 0,97 ± 0,27 à 0,81 ± 0,24 μV, de 1,15 ± 0,43 à 0,86 ± 0,29 μV et de 1,04 ± 0,46 à 0,92 ± 0,41 μV respectivement (P < 0,05). La procaine prolonge la latence entre les pics I et III de 1,57 t 0,04 à 1,70 ± 0,07 msec (P < 0,01) et entre les pics III et V de 2,15 ± 0,09 à 2,35 ± 0,12 msec (P < 0,01). Après injection de la procaine, le tracé d’EEG présente une activité de type épileptique comparativement à un tracé d’éveil avant l’injection du médicament. Ces résultats suggèrent qu ’au moment où les effets toxiques de la procaïne causent une excitation de type convulsif au niveau du cortex cérébral, l’activité au niveau du tronc cérébral est supprimée.

False hyperchloremia in bromism

Plasma chloride concentration measured by an ion-specific electrode can be interfered by other ions. The authors experienced a case of phantom limb pain with a marked hyperchloremia (251 mEq ·l−1) which was measured by the ion-specific electrode method. The patient was diagnosed as bromide intoxication due to chronic ingestion of analgesic tablets which contain bromvalerylurea. A toxic level of plasma bromide concentration supported the diagnosis. Elevated plasma chloride and bromide concentrations were normalized in three weeks after discontinuation of the analgesic intake.Laboratory study revealed that fluoride ion did not affect chloride concentration measured by an ion-specific electrode. Bromide and iodide ions, however, interfered with the electrode and produced a large overestimation of chloride concentration.Hyperchloremia should be interpreted carefully when chloride was measured by an ion-specific electrode method.

Effects of Ketamine on Recovery of Auditory Brainstem Response after Total Brain Ischemia

L-glutamate was first proposed as a neuroexitatory agent1, 2. Progress has been particulary rapid in understanding the N-metyl-D-aspartate (NMDA) class of glutamate receptor3 and ketamine has been known as an antagonist of NMDA receptor4. Prolonged stimulation of exitatory amino acid receptors of either the NMDA or non-NMDA types evertually results in the central neuronal injury. The exact mechanism of neuronal injury is complicated, since depolarization can lead to neural swelling, calcium influx, and other consequences5.