Shigeo Ohmura

Systemic toxicity and resuscitation in bupivacaine-, levobupivacaine-, or ropivacaine-infused rats.

We compared the systemic toxicity of bupivacaine, levobupivacaine, and ropivacaine in anesthetized rats. We also compared the ability to resuscitate rats after lethal doses of these local anesthetics. Bupivacaine, levobupivacaine, or ropivacaine was infused at a rate of 2 mg · kg−1 · min−1 while electrocardiogram, electroencephalogram, and arterial pressure were continuously monitored. When asystole was recorded, drug infusion was stopped and a resuscitation sequence was begun. Epinephrine 0.01 mg/kg was administered at 1-min intervals while external cardiac compressions were applied. Resuscitation was considered successful when a systolic arterial pressure ≥100 mm Hg was achieved within 5 min. The cumulative doses of levobupivacaine and ropivacaine that produced seizures were similar and were larger than those of bupivacaine. The cumulative doses of levobupivacaine that produced dysrhythmias and asystole were smaller than the corresponding doses of ropivacaine, but they were larger than those of bupivacaine. The number of successful resuscitations did not differ among groups. However, a smaller dose of epinephrine was required in the Ropivacaine group than in the other groups. We conclude that the systemic toxicity of levobupivacaine is intermediate between that of ropivacaine and bupivacaine when administered at the same rate and that ropivacaine-induced cardiac arrest appears to be more susceptible to treatment than that induced by bupivacaine or levobupivacaine.

Predicting difficult intubation with indirect laryngoscopy

Background It is not always possible to predict when tracheal intubation will be difficult or impossible. The authors wanted to determine whether indirect laryngoscopy could identify patients in whom intubation was difficult. Methods Indirect laryngoscopy was done in 2,504 patients. The Wilson risk sum score and the modified Mallampati score were also studied in a different series of 3,680 patients for comparison. These predictive methods were compared according to three parameters: positive predictive value, sensitivity, and specificity. Results Of 6,184 patients studied, the trachea proved difficult to intubate in 82 (1.3%). Positive predictive value (31%) and specificity (98.4%) with indirect laryngoscopy were greater than the other two predictive methods (P < 0.01), whereas sensitivity with indirect laryngoscopy (69.2%) was greater than that of the Wilson risk sum score (55.4%) (P < 0.01). Conclusions Although in 15% of patients indirect laryngoscopy could not be performed because of excessive gag reflex, indirect laryngoscopy can serve as an effective method to predict difficult intubation.

A comparison of the effects of propofol and sevoflurane on the systemic toxicity of intravenous bupivacaine in rats

UNLABELLED We compared the effects of propofol and sevoflurane on bupivacaine-induced central nervous system and cardiovascular toxicity in rats. Thirty-four male Sprague-Dawley rats were anesthetized with 70% N2O/30% O2 plus the 50% effective dose (ED50) of propofol (propofol group, n = 12); 70% N2O/30% O2 plus ED50 of sevoflurane (sevoflurane group, n = 11); or 70% N2O/30% O2 (control group, n = 11). Bupivacaine was infused at a constant rate of 2 mg x kg(-1) x min(-1) while electrocardiogram, electroencephalogram, and invasive arterial pressure were continuously monitored. The cumulative doses of bupivacaine that induced dysrhythmias, seizures, and 50% reduction of heart rate were larger in the propofol and sevoflurane groups than in the control group. The cumulative dose of bupivacaine that induced a 50% reduction in the mean arterial blood pressure was larger in the propofol group than in the sevoflurane and control groups. The margin of safety, assessed by the time between the onset of dysrhythmias and 50% reduction of mean arterial blood pressure, was wider in the propofol group than in the sevoflurane group. We conclude that propofol and sevoflurane attenuate bupivacaine-induced dysrhythmias and seizures and that propofol has a wider margin of safety than sevoflurane. IMPLICATIONS In anesthetized patients, dysrhythmias may be the only warning sign of intravascular injection of bupivacaine. Because propofol has a wider margin of safety than sevoflurane, life-threatening cardiovascular depression may be prevented by stopping the injection of bupivacaine at the onset of dysrhythmias during propofol anesthesia.

Left-molar Approach Improves the Laryngeal View in Patients with Difficult Laryngoscopy

Background The molar approach of laryngoscopy is reported to improve glottic view in sporadic cases of difficult laryngoscopy. The authors studied the effect of molar approaches and optimal external laryngeal manipulation (OELM) using the Macintosh blade. Methods A series of 1,015 adult patients who underwent general anesthesia and tracheal intubation was studied. Laryngoscopy was carried out using a Macintosh no. 3 or 4 standard blade. Three consecutive trials of direct laryngoscopy using the midline and left- and right-molar approaches were carried out under full muscle relaxation with optimal head and neck positioning. The best glottic views were recorded for each approach with and without OELM. Results Difficult laryngoscopy with a midline approach accounted for 6.5% (66 cases) before OELM and 1.97% (20 cases) after OELM. A left-molar approach with OELM further reduced difficult laryngoscopy to seven cases (P < 0.001 vs. midline approach with OELM); a right-molar approach with OELM reduced difficult laryngoscopy to 18 cases (P = 0.48). Conclusions The left-molar approach with OELM improves the laryngeal view in patients with difficult laryngoscopy.

The effects of arm position on central spread of local anesthetics and on quality of the block with axillary brachial plexus block

BACKGROUND AND OBJECTIVES Spread of local anesthetic solution in axillary brachial plexus block is thought to be influenced by the position of the arm and the use of compression maneuvers. We investigated how these two factors affected central local anesthetic spread and block quality. METHODS Radiographic spread of local anesthetic was studied in 80 adult patients. They received mepivacaine mixed with contrast agent through an indwelling catheter with the arm abducted to either 0 or 90 degrees , and with or without local digital compression. Central and peripheral spread of the contrast agent was evaluated with anteroposterior radiographs of the axilla. Block quality was studied in a separate series of 70 adult patients. They received mepivacaine with the arm abducted 0 degrees or 90 degrees . The degree of sensory and motor block was assessed 20 minutes after the injection. RESULTS Arm position at 0 degrees abduction promoted central spread of the contrast agent. Although digital compression suppressed peripheral spread effectively, it did not improve the central spread of the solution. Sensory block was comparable in all terminal nerves of the arm in both arm positions, whereas motor block of the radial nerve was promoted with no abduction. CONCLUSIONS The central spread of local anesthetics is facilitated by injection without abduction of the arm but not by the use of compression at the injection site. This, however, did not alter the quality of the block.

Pulmonary uptake of ropivacaine and levobupivacaine in rabbits.

Local anesthetic toxicity produced by an inadvertent IV injection is attenuated by the pulmonary uptake of local anesthetics. We compared the pulmonary uptake of ropivacaine and levobupivacaine after a bolus injection in rabbits. Sixteen anesthetized rabbits were randomly assigned to either a ropivacaine group or a levobupivacaine group. A bolus containing ropivacaine or levobupivacaine 0.5 mg/kg and indocyanine green (an intravascular indicator) 0.25 mg/kg was injected rapidly into the vena cava. Arterial blood samples were collected serially at 1.2-s intervals for 30 s. Concentrations of local anesthetic and indocyanine green in each sample were determined for the calculation of first-pass uptake of a local anesthetic in the lung. The first-pass uptake of levobupivacaine (31.4% ± 8.3%; mean ± sd) was larger than that of ropivacaine (22.9% ± 5.6%), and the maximum arterial concentration of ropivacaine (21.2 ± 2.8 &mgr;g/mL) was larger than that of levobupivacaine (18.6 ± 1.9 &mgr;g/mL). We conclude that the pulmonary uptake of levobupivacaine is larger than that of ropivacaine after a bolus injection. Therefore, the advantages of ropivacaine over levobupivacaine in terms of less cardiovascular toxicity may be offset by the smaller pulmonary uptake after an inadvertent IV injection.

The influence of hypoxia and hyperoxia on the kinetics of propofol emulsion

PurposeTo study the effect of hypoxia and hyperoxia on the pharmacokinetics of propofol emulsion, hepatic blood flow and arterial ketone body ratio in the rabbit.MethodsTwenty four male rabbits were anesthetized with isoflurane (1.5–2%) in oxygen. After the surgical procedure, isoflurane administration was discontinued and intravenous propofol infusion (30 mg · kg−1hr−1) was started. The infusion rate of propofol was maintained throughout the study. After an initial 90 min period of propofol infusion, rabbits were randomly allocated to one of three groups: hypoxia (F1O2= 0.l), normoxia (F1O2= 0.21), and hyperoxia (F1O2= 1.0). Propofol infusion was continued under the allocated F1O2 for 60 min. Propofol concentrations in arterial blood, total body clearance of propofol, hepatic blood flow and arterial ketone body ratio were measured.ResultsThe mean arterial propofol concentration at the end of infusion was higher in the hypoxia group (15.2 ± 2.8 μg · mL−1, mean ± SD) than in the normoxia (7.4 ± 1.7) and hyperoxia (8.0 ± 1.9) groups (P < 0.05). Total body clearance of propofol, hepatic blood flow and arterial ketone body ratio were all reduced in the hypoxia group (P < 0.05). Total ketone body concentration in arterial blood increased in the hyperoxia group (P < 0.01).ConclusionHypoxia produced an accumulation of propofol in blood and reduced propofol clearance. These changes could result from decreased hepatic blood flow and low cellular energy charge in the liver. Hyperoxia, on the other hand, increased total ketone body in arterial blood.ObjectifÉtudier l’effet de l’hypoxie et de l’hyperoxie sur la pharmacocinétique de l’émulsion de propofol et le ratio débit sanguin hépatique-corps cétoniques artériels chez le lapin.MéthodeVingt-quatre lapins mâles ont été anesthésiés avec un mélange de sévoflurane (1,5-2 %) et d’oxygène. Après l’opération, on a stoppé l’administration d’isoflurane et commencé la perfusion intraveineuse de propofol (30 mg · kg−1hr−1). La vitesse de perfusion du propofol a été maintenue tout au long de l’étude. À la suite d’une perfusion initiale de propofol de 90 min, les lapins ont été répartis au hasard en trois groupes : hypoxie (F1O2= 0,1), normoxie (F1O2= 0,21) et hyperoxie (F1O2= 1,0). La perfusion de propofol s’est poursuivie pendant 60 min quelle que soit la F1O2 choisie. On a mesuré : les concentrations de propofol dans le sang artériel, la clairance corporelle totale du propofol, le ratio débit sanguin hépatique-corps cétoniques artériels.RésultatsLa concentration artérielle moyenne de propofol, à la fin de la perfusion, était plus élevée dans le groupe hypoxie (15,2 ± 2,8μg·mL−1, moyenne ± écart type) que dans le groupe normoxie (7,4 ± 1,7) et hyperoxie (8,0 ± 1,9) (P < 0,05). La clairance corporelle totale du propofol, le ratio débit sanguin hépatiquecorps cétoniques artériels ont tous été réduits dans le groupe hypoxie (P < 0,05). La concentration corporelle totale de cétone dans le sang artériel était plus élevée dans le groupe hyperoxie (P < 0,01).ConclusionL’hypoxie a provoqué une accumulation de propofol dans le sang et a réduit la clairance du propofol. Ces changements peuvent résulter d’une réduction du débit sanguin hépatique et d’une faible charge énergétique cellulaire hépatique. Par ailleurs, l’hyperoxie augmente la concentration totale des corps cétoniques artériels.

Displacement of lidocaine from the lung after bolus injection of bupivacaine

The purpose of this study was to determine whether lidocaine was displaced from the lung after bolus injection of bupivacaine. Fourteen anaesthetized rabbits were randomly assigned to either a bupivacaine or a control group. Lidocaine was infused at a rate of 10 mg · kg−1 hr−1. After one hour of infusion, a bolus of bupivacaine (1 mg · kg−1) in normal saline (0.2 ml · kg−1) was injected into the central venous circulation in the bupivacaine group. The control group was injected with normal saline. After bolus injection, arterial blood samples were collected serially from an internal carotid artery at 1.2-sec intervals for 24 sec. The baseline concentration of lidocaine was 3.0 ±0.1 μg · ml−1 in the bupivacaine group and 3.2 ±0.1 μg · ml-1 in the control group (NS). Arterial concentrations of lidocaine increased to a maximum of 4.7 ±0.2 μg · ml−1 in the bupivacaine group (P = 0.0001). No increases were seen in the control group. These findings indicate that lidocaine was displaced from the lung into the blood after bolus injection of bupivacaine. The amount of lidocaine displaced during the first passage of bupivacaine through the lung was calculated to be 92.3 ±9.7 μg. It is concluded that lidocaine is displaced from the lung after bolus injection of bupivacaine.RésuméCette étude vise à déterminer si la lidocaïne est déplacée du poumon après un bolus de bupivacaïne. Quatorze lapins anesthésiés sont répartis au hasard entre un groupe bupivacaïne et un groupe contrôle. La lidocaïne est perfusée à la vitesse de 10 mg · kg−1 hr−1. Dans le groupe bupivacaïne, après une heure de perfusion, un bolus de bupivacaïne (1 mg · kg−1) dans du soluté physiologique (0,2 ml · kg−1) est injecté dans la circulation veineuse centrale. Le groupe contrôle ne reçoit que du physiologique. Après l’injection du bolus, on recueille des échantillons de sang artériel en série par la carotide interne à des intervalles de 1,2 sec pendant 24 sec. La concentration initiale de lidocaïne est de 3,0 ±0,1 μg · ml−1 dans le groupe bupivacaïne et de 3,2 ±0,1 μg · ml−1 dans le groupe contrôle (NS). Les concentrations artérielles de lidocaïne augmentent jusqu’à un maximum de 4,7 ±0,2 μg · ml−1 dans le groupe bupivacaïne (P = 0,0001). On ne trouve pas d’augmentation dans le groupe contrôle. Ces résultats indiquent que la lidocaïne est déplacée du poumon vers le sang après un bolus de bupivacaine. La quantité déplacée calculée lors du premier passage est de 92,3 ±9,7 μg. On conclut que la lidocaïne est déplacée du poumon après une injection en bolus de bupivacaïne.

Respiratory failure caused by massive pleural effusion in a patient with deep neck abscess.

for 2 days, but redness and swelling of the neck had developed gradually, followed by dyspnea. On admission, physical examination showed he was confused. Redness and swelling were seen on the left side of the neck, and the area around the left tonsil was extremely swollen. Blood pressure was 136/68mmHg and heart rate 125 bpm. The patient had a slight fever, temperature 37.6°C, his respiratory rate was 24 breaths per min, and stridor could be heard. SpO2 was 99% under oxygen administration (5 l·min 1) with a face mask. Blood examination showed that C-reactive protein (CRP) had increased to 47 mg·dl 1, and the white blood cell (WBC) count had increased to 12 400 ·mm 3. The examination also showed Na, 130mEq·l 1; K, 3.0 mEq·l 1; Cl, 93 mEq·l 1; blood glucose level, 422 mg·dl 1; hemoglobin A1c, 7.6%; and renal dysfunction (blood urea nitrogen [BUN], 45 mg·dl 1; creatinine [Cr], 1.5mg·dl 1). Computed tomography (CT) scan of the neck revealed an abscess extending from the peritonsillar space to the parapharyngeal and retropharyngeal space, and swelling of the area surrounding the glottis (Fig. 1), but the abscess did not extend directly into the mediastinum, and pleural effusion was not detected. Emergency surgical drainage was scheduled. In the operating room, tracheostomy was performed first, under local anesthesia because the pharynx was extremely edematous. Anesthesia was induced with thiopental (200 mg), and was maintained with sevoflurane (1.0%–1.5%) in 40% oxygen and 60% nitrous oxide under mechanical ventilation. Blood loss during the operation was 50g, and 2200 ml of acetated Ringer’s solution was administered during surgery. Bacterial examination revealed infection with a combination of aerobic ( -streptococcus) and anaerobic gram-negative rod bacteria. After surgery, PaO2 was 447 mmHg under 100% oxygen, and X-ray of the chest revealed no abnormalities. The patient was returned to a general ward. He received

Propofol pharmacokinetics in a patient with bilateral leg amputation

input 55 kg as his weight (termed the “hypothetical weight”) to the infusion pump for propofol. Without premedication, anesthesia was induced with 50 μg of fentanyl and 80mg of propofol intravenously. Before induction of anesthesia, an indwelling catheter was inserted into the left radial artery for blood sampling. A laryngeal mask airway was inserted without the use of muscle relaxants. Propofol was first infused at a rate of 10 mg·kg 1·h 1 based on the hypothetical weight, and the infusion rate was controlled between 5 and 10 mg·kg 1·h 1 according to clinical signs. During the operation, the patient’s blood pressure and heart rate were stable, his pupils were contracted, and no spontaneous movement was observed. The operation lasted 60 min, and propofol infusion was stopped (propofol was infused for 70min). About 10 min after the termination of propofol, he regained consciousness. In order to investigate the pharmacokinetics of propofol, 18 arterial blood samples (1.0 ml each) were appropriately obtained for 240 min after the start of propofol infusion. The propofol concentration was determined by using high-performance liquid chromatography, as described by Plummer [3]. The data were pharmacokinetically analyzed with NONMEM (GloboMax, Hanover, MD, USA) and are shown in Table 1 together with normal human adult values calculated by the parameter set by Marsh et al. [4]. Figure 1 shows the measured propofol concentrations, the curve fitted by NONMEM, and the simulation result of propofol concentrations based on the measured weight [“The patient (40kg)” in Table 1]. In the figure, propofol concentration can be kept high enough ( 3μg·ml 1) [5] when propofol is infused based on the hypothetical weight, whereas it fails in the case when the measured weight is chosen as the input of the propofol infusion pump. In this case, we infused propofol based on the hypothetical weight, assuming that the patient had both legs intact. As a result, the propofol concentration was kept