Takahiko Okuda

Anesthetic management for the minimally invasive Nuss procedure in 21 patients with pectus excavatum

The aim of this study was to assess the anesthetic management and postoperative analgesic effect of continuous epidural infusion for the minimally invasive Nuss procedure. A total of 21 operated cases were analyzed retrospectively. Thoracoscopy was used in all cases. General anesthesia with endotracheal intubation was induced and maintained with oxygen, air, sevoflurane, and fentanyl in all cases. Thoracic epidural anesthesia was performed after induction at the level between Th4 and 12. When the bar was placed via insertion under the sternum, six patients exhibited sinus tachycardia and one showed premature atrial contraction for 2–4 beats before recovering spontaneously within 1 min. Operations were uneventful. The mean operating time was 115 min and anesthetic time was 193 min. In X-ray findings, residual pneumothorax and pleural effusion were found in seven (33.3%) and eight (38.0%) patients, respectively. In all cases, these symptoms were resolved spontaneously within 5 days. Epidural fentanyl (0.3 µg·kg−1·h−1) in 0.125% bupivacaine (0.15 ml·kg−1·h−1) or 0.2% ropivacaine (0.15 ml·kg−1·h−1) were used for 3 days to relieve postoperative pain. Postoperatively, 12 (57.1%) patients required no additional analgesics, and 4 (19.0%) patients required a single dose of dicrofenac sodium or pentazocine. Although the Nuss procedure is minimally invasive, we should pay attention to the possibility of many intra- and postoperative complications. Continuous epidural infusion of fentanyl with local anesthetics provides effective postoperative pain relief and prevents complications such as bar displacement after the Nuss procedure.

Suppressant effects of midazolam on responses of spinal dorsal horn neurones in rabbits.

Recordings of noxious intra-arterial bradykinin (BK)-induced chemonociceptive and spontaneous activity from 30 single spinal lamina V neurones of the dorsal horns in non-anaesthetized and decerebrated rabbits, were performed with tungsten microelectrodes. Intravenous injection of midazolam (0.2 mg/kg; 7 neurones) depressed BK-induced neural discharges by 55.0 +/- 6.2% (P less than 0.05) and 57.9 +/- 8.4% (P less than 0.05) 5 and 25 min after administration, respectively. Treatment with flumazenil (0.2 mg/kg, i.v.; 7 neurones), administered 20 min after midazolam, completely reversed the inhibition by midazolam of the BK-induced spinal lamina V neural responses and spontaneous neuronal activity. In contrast, a large dose of naloxone (1.0 mg/kg, i.v.; 6 neurones), administered 20 min after midazolam, failed to alter the midazolam-induced depressant effects on the nociceptive responses, at the spinal dorsal horn. Treatments with flumazenil (5 neurones) and naloxone (5 neurones) did not influence either the spontaneous or the BK-induced neuronal discharges, recorded in spinal lamina V cells. Midazolam depressed the nociceptive responses probably through its agonistic activity on the binding to the GABA-benzodiazepine-barbiturate system in the spinal dorsal horn.

Roles of endotracheal tubes and slip joints in respiratory pressure loss: a laboratory study

PurposeThe endotracheal tube (ETT) constitutes a significant component of total airway resistance. However, a discrepancy between measured and theoretical values has been reported in airway resistance through ETTs. The causes of the discrepancy were estimated by physical and rheological simulations.MethodsThe pressure losses through total lengths of ETTs and slip joints under a volumetric flow rate of 30 L/min were measured, and the pressure losses through the tubular parts of ETTs with internal diameters (IDs) of 6.0-, 6.5-, 7.0-, 7.5-, and 8.0 mm were measured. The Reynolds number of each setting was calculated, and the pressure losses through the total length of the ETT, the tubular part, and the slip joint of each size of tube were estimated.ResultsThe Reynolds numbers were >5000 in all sizes of ETTs. Measured pressure losses were larger in small sized ETTs than in large sized ETTs—520.9 Pascals (Pa) in 6.0-mm ID and 136.4 Pa in 8.0-mm ID tubes. The measured pressure losses through the tubular part were comparable to the predicted values. The measured pressure losses through the slip joints were larger than the predicted values, and they accounted for approximately 25–40% of total pressure losses of the ETTs.ConclusionEspecially in small sized tubes, the pressure loss through the slip joint accounts for a large percentage of the total pressure loss through the ETT. The pressure loss through the slip joint may play a role in the discrepancy between measured and theoretical pressure losses through ETTs.

Naloxone and flumazenil fail to antagonize the isoflurane-induced suppression of dorsal horn neurons in cats.

Effects of naloxone and flumazenil on isoflurane activities were examined on dorsal horn neurons in cats. Isoflurane suppressed bradykinin-induced nociceptive responses in transected feline spinal cords. The bradykinin-induced neuronal firing rates were significantly suppressed by 60.0%, 35.3% and 32.2% at 10, 20 and 30 min after isoflurane administration, respectively. The 32.2% suppression on bradykinin-induced neuronal responses at 30 min after isoflurane administration was not reversed 5 min after administration of naloxone (36.4% suppression). The suppressive effects of isoflurane were not reversed by naloxone (0.2 mg·kg−1, i.v. Similarly, the benzodiazepine antagonist, flumazenil (0.2 mg·kg−1 i.v., did not affect the suppressive effects of isoflurane. Failure of naloxone and flumazenil to reverse the suppressive effects of isoflurane suggests that isoflurane interacts with neither opioid nor benzodiazepine receptors in producing its suppressive action on nociceptive responses in dorsal horn neurons of the feline spinal cord.

Yohimbine and flumazenil: effect on nitrous oxide-induced suppression of dorsal horn neurons in cats

PurposeThe purpose of this study was to determine the mechanisms of nitrous oxide (N2O) antinociception at the spinal level with yohimbine (an α2-adrenergic antagonist) and flumazenil (a specific benzodiazepine antagonist) using chemonociceptive stimuli in spinal dorsal horn neurons in the cat.MethodsA lumbar laminectomy extending from L4 to L6 was performed to allow insertion of a extracellular recording device via a microelectrode. Additional laminectomy was performed at the T12 level to transect the spinal cord. As a noxious stimulus, bradykinin (BK) was injected via the cannula inserted into the femoral artery. Animals were divided into four treatment groups for subsequent experiments: N2O+flumazenil, N2O+yohimbine, flumazenil (alone), and yohimbine (alone).ResultsN2O suppressed BK-induced nociceptive responses in transected feline spinal cords. The BK-induced neuronal firing rates were significantly suppressed: to 69.2%, 61.8%, and 52.2% of the baseline firing rate at 10, 20, and 30 min, respectively, after N2O administration. The 47.8% suppression on BK-induced neuronal responses at 30 min after N2O administration was reversed 5 min after administration of yohimbine (25.2% suppression). Similarly, N2O suppression (42.5%) on chemically induced neuronal responses was reversed by flumazenil (24.9% suppression) at identical postadministration intervals.ConclusionThese data imply that N2O suppresses the nociceptive responses in part probably through its agonistic binding activity to the α2-adrenergic, γ-aminobutyric acid (GABA)-benzodiazepine, or both receptor systems in dorsal born neurons of the feline spinal cord.

The Influence of Volatile Anesthetics on Portwine Stain

To examine the relationship between volatile inhalation anesthetics and the fading of portwine stain (PWS), the study retrospectively investigated the incidence of termination of pulsed dye laser treatment vis-à-vis PWS fade during use of a general inhalation anesthetic in 107 infants and children with facial PWS. The fading of PWS is disadvantageous to the pulsed dye laser treatment. All patients received pulsed dye laser treatment under general anesthesia using one of four kinds of volatile inhalation anesthetics (halothane, enflurane, isoflurane, and sevoflurane). Two hours before the induction of anesthesia, all patients were rectally irrigated. Treatment was discontinued in none of the 44 patients in the halothane group or the 7 patients in the enflurane group; in one of the 29 in the isoflurane group; and in 10 of the 27 patients in the sevoflurane group. The sevoflurane group showed a significantly (P < 0.01) higher incidence of PWS fading. Thus, when using a volatile inhalation anesthetic in combination with pulsed dye laser treatment for PWS, caution should be exercised if sevoflurane is selected, as PWS fading is harmful to the pulsed dye laser.

Suppressive action of enflurane on dorsal horn neurons in rabbits

The neurophysiologic mechanism of the suppressive action of enflurane on spinal nociceptive transmission was examined in rabbits with intact and with transected spinal cords. Enflurane suppressed nociceptive responses in both intact and transected spinal cord groups. The suppressive effects of enflurane were significantly greater in the intact group than in the transected group. The suppressive effects of enflurane were not reversed by the addition of 0.2 mg·kg−1 of naloxone. These results suggest that enflurane suppresses nociceptive responses by activating descending inhibitory systems and directly suppressing activity at the spinal level. This suppressive action of enflurane does not interact with the opioid receptor.

Anesthesia in Shy-Drager syndrome

The Shy-Drager syndrome (SDS) is characterizes by autonomic dysfunction, accompanied by additional central neurologic symptoms. The main clinical manifestations of the autonomic dysfunction include orthostatic hypotension, vesicorectal dysfunction, hydrohidrosis and extrapyramidal syndrome. During anesthesia, the cardiovascular instability due to autonomic dysfunction represent a potential danger. The present paper reports the anesthetic course of a patient with SDS undergoing abdonimal surgery.

Recurrent coronary artery spasm during a non-cardiac surgical procedure

Coronary artery spasm is often reported in the perioperative period1 ll • Myocardial ischemia caused by coronary artery spasm as characterized by ST-segment elevation occurs suddenly and is not preceded by an increase in blood pressure or heart rate. This may frequently result in premature contractions, atrioventricular block, severe hypotension and even cardiac arrest. We report a case of coronary artery spasm occurred 4 times during a noncardiac surgical procedure.

Effect of preanesthetic famotidine on gastric volume and pH.

The effect of preanesthetic 20 mg of famotidine on gastric fluid volume and pH were studied in patients scheduled for elective surgery. One hundred and twenty-eight patients were divided into four groups-control, intravenous, intramuscular and oral with 32 patients in each group. Patients in placebo group received no famotidine and served as control. Patients in the intravenous and intramuscular groups were administered famotidine one hour before surgery. Patients in the oral group were administered famotidine the night before and on the morning of surgery. Gasric volume in the control group was 19.1±10.8 ml; in the intravenous group, 7.4±6.4 ml; in the intramuscular group, 7.3±6.9 ml: and in the oral group, 7.1±6.9 ml. Gastric pH was 3.4±2.3, 6.8±1.1, 6.9±1.6, and 6.7±1.2 in groups one through four, respectively. When compared to the control group, famotidine significantly decreased gastric. volume and increased gastric pH. There were no statistical differences among the different modes of administration. No adverse effects were observed in this study. It is concluded that preanesthetic management of 20 mg of famotidine reduced the risk of acid aspiration pneumonitis.