Hiroyoshi Kawaai

Intravenous Sedation with Low-Dose Dexmedetomidine: Its Potential for Use in Dentistry

This study investigated the physiologic and sedative parameters associated with a low-dose infusion of dexmedetomidine (Dex). Thirteen healthy volunteers were sedated with Dex at a loading dose of 6 mcg/kg/h for 5 minutes and a continuous infusion dose of 0.2 mcg/kg/h for 25 minutes. The recovery process was observed for 60 minutes post infusion. The tidal volume decreased significantly despite nonsignificant changes in respiratory rate, minute ventilation, oxygen saturation, and end-tidal carbon dioxide. The mean arterial pressure and heart rate also decreased significantly but within clinically acceptable levels. Amnesia to pin prick was present in 69% of subjects. A Trieger dot test plot error ratio did not show a significant change at 30 minutes post infusion despite a continued significant decrease in bispectral index. We conclude that sedation with a low dose of Dex appears to be safe and potentially efficacious for young healthy patients undergoing dental procedures.

Dexmedetomidine decreases the oral mucosal blood flow

There is an abundance of blood vessels in the oral cavity, and intraoperative bleeding can disrupt operations. There have been some interesting reports about constriction of vessels in the oral cavity, one of which reported that gingival blood flow in cats is controlled by sympathetic α-adrenergic fibres that are involved with vasoconstriction. Dexmedetomidine is a sedative and analgesic agent that acts through the α-2 adrenoceptor, and is expected to have a vasoconstrictive action in the oral cavity. We have focused on the relation between the effects of α-adrenoceptors by dexmedetomidine and vasoconstriction in oral tissues, and assessed the oral mucosal blood flow during sedation with dexmedetomidine. The subjects comprised 13 healthy male volunteers, sedated with dexmedetomidine in a loading dose of 6 μg/kg/h for 10 min and a continuous infusion of 0.7 μg/kg/h for 32 min. The mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), systemic vascular resistance (SVR), and palatal mucosal blood flow (PMBF) were measured at 0, 5, 10, 12, 22, and 32 min after the start of the infusion. The HR, CO, and PBMF decreased significantly during the infusion even though there were no differences in the SV. The SVR increased significantly but the PMBF decreased significantly. In conclusion, PMBF was reduced by the mediating effect of dexmedetomidine on α-2 adrenoceptors.

A Comparison of Intravenous Sedation With Two Doses of Dexmedetomidine: 0.2 µg/kg/hr Versus 0.4 µg/kg/hr

The present study investigated the physiologic and sedative effects between two different continuous infusion doses of dexmedetomidine (DEX). Thirteen subjects were separately sedated with DEX at a continuous infusion dose of 0.2 µg/kg/hr for 25 minutes after a loading dose of 6 µg/kg/hr for 5 minutes (0.2 group) and a continuous infusion dose of 0.4 µg/kg/hr for 25 minutes after a loading dose of 6 µg/kg/hr for 5 minutes (0.4 group). The recovery process was then observed for 60 minutes post infusion. The tidal volume, mean arterial pressure, and heart rate in both groups decreased significantly during infusion, but they were within a clinically acceptable level. A Trieger dot test plot error ratio in the 0.4 group was significantly higher than that in the 0.2 group until 15 minutes post infusion. Sedation appears to be safe at the infusion doses of DEX studied. However, increasing maintenance infusion doses of DEX from 0.2 µg/kg/hr to 0.4 µg/kg/hr delays some recovery parameters.

Changes in leukocyte migration during carbonic anhydrase activity inhibition.

Experiment 1 evaluated changes in leukocyte migration during acetazolamide (AZ) inhibition of carbonic anhydrase activity in leukocytes. AZ induced changes in the intracellular calcium concentration, and extracellular calcium is thought to be a factor inducing an increase in leukocyte migration. Next, Experiment 2 determined whether extracellular calcium concentration was a primary factor influencing leukocyte migration in the absence of AZ. The distance of leukocyte migration increased in a dose-dependent manner with AZ despite the presence of IL-8 or LPS in Experiment 1. The extracellular calcium concentration used in the present study had no influence on the distance in leukocyte migration in Experiment 2. The distance of leukocyte migration showed a tendency to increase in a dose-dependent manner with LPS concentration. In conclusion, AZ may stimulate leukocyte migration due to its participation in the regulation of intracellular pH controlled by CA activity without an effect of low extracellular calcium concentration. In addition, AZ was thus suggested to possibly have an anti-inflammatory effect in supporting leukocyte migration during inflammatory reactions.

Intravenous Sedation for Implant Surgery: Midazolam, Butorphanol, and Dexmedetomidine Versus Midazolam, Butorphanol, and Propofol

We compared the amnesic action, recovery process, and satisfaction of patients and surgeons after the use of 2 different sedation regimens for 40 patients undergoing scheduled implant surgery. Butorphanol, midazolam, dexmedetomidine (BMD) was administered to 20 patients who were maintained with continuous infusion of dexmedetomidine after the induction with butorphanol and midazolam, and butorphanol, midazolam, propofol (BMP) was administered to 20 patients who were maintained with continuous infusion of propofol after the induction with butorphanol and midazolam. To assess the amnesic action, the memory of local anesthesia, auditory memory, and visual memory were evaluated. The Trieger Dot Test (TDT) was applied during the recovery process. A questionnaire regarding the patients feelings of the management of sedation was taken from each patient and was also filled out by the surgeon. The comparison between groups was analyzed by the Mann-Whitney U test. No significant differences in the amnesic action and the TDT were noted. Both methods also satisfied the patients and surgeons, as determined by the questionnaire results. In conclusion, both sedation regimens are appropriate for implant surgery.

Continuous infusion propofol general anesthesia for dental treatment in patients with progressive muscular dystrophy.

Progressive muscular dystrophy may produce abnormal reactions to several drugs. There is no consensus of opinion regarding the continuous infusion of propofol in patients with progressive muscular dystrophy. We successfully treated 2 patients with progressive muscular dystrophy who were anesthetized with a continuous infusion of propofol. In case 1, a 19-year-old, 59-kg man with Becker muscular dystrophy and mental retardation was scheduled for dental treatment under general anesthesia. General anesthesia was maintained by a continuous infusion of 6-10 mg/kg propofol per hour and an inhalational mixture of 67% nitrous oxide and 33% oxygen. No complications were observed during or after the operation. In case 2, a 5-year-old, 11-kg boy with Fukuyama type congenital muscular dystrophy and slight mental retardation was scheduled for dental treatment under general anesthesia. General anesthesia was maintained with a continuous infusion of 6-12 mg/kg propofol per hour and an inhalational mixture of 0.5-1.5% sevoflurane in 67% nitrous oxide and 33% oxygen. No complications were observed during or after the operation. It is speculated that a continuous infusion of propofol in progressive muscular dystrophy does not cause malignant hyperthermia because serum levels of creatine phosphokinase and myoglobin decreased after our anesthetic management. Furthermore, our observations suggest that sevoflurane may have some advantages in patients with progressive type muscular dystrophies other than Duchenne muscular dystrophy and Becker muscular dystrophy. In conclusion, our cases suggest that a continuous infusion of propofol for the patients with progressive muscular dystrophy is a safe component of our anesthetic strategy.

Lidocaine Concentration in Oral Tissue by the Addition of Epinephrine

The vasoconstrictive effect due to the addition of epinephrine to local anesthetic has been clearly shown by measuring blood-flow volume or blood anesthetic concentration in oral mucosal tissue. However, there are no reports on the measurement of anesthetic concentration using samples directly taken from the jawbone and oral mucosal tissue. Consequently, in this study, the effect of lidocaine concentration in the jawbone and oral mucosal tissue by the addition of epinephrine to the local anesthetic lidocaine was considered by quantitatively measuring lidocaine concentration within the tissue. Japanese white male rabbits (n = 96) were used as test animals. General anesthesia was induced by sevoflurane and oxygen, and then cannulation to the femoral artery was performed while arterial pressure was constantly recorded. Infiltration anesthesia was achieved by 0.5 mL of 2% lidocaine containing 1 : 80,000 epinephrine in the upper jawbone (E(+)) and 0.5 mL of 2% of epinephrine additive-free lidocaine (E(0)) under the periosteum. At specified time increments (10, 20, 30, 40, 50, and 60 minutes), samples from the jawbone, oral mucosa, and blood were collected, and lidocaine concentration was directly measured by high-performance liquid chromatography. No significant differences in the change in blood pressure were observed either in E(+) or E(0). In both E(+) and E(0) groups, the serum lidocaine concentration peaked 10 minutes after local anesthesia and decreased thereafter. At all time increments, serum lidocaine concentration in E(+) was significantly lower than that in E(0). There were no significant differences in measured lidocaine concentration between jawbone and mucosa within either the E(+) or the E(0) groups at all time points, although the E(0) group had significantly lower jawbone and mucosa concentrations than the E(+) group at all time points when comparing the 2 groups to each other. Addition of epinephrine to the local anesthetic inhibited systemic absorption of local anesthetic into the blood such that a high concentration could be maintained in the tissue. Epinephrine-induced vasoconstrictive effect was observed not only in the oral mucosa but also in the jawbone.

Maximum opening of the mouth by mouth prop during dental procedures increases the risk of upper airway constriction

From a retrospective evaluation of data on accidents and deaths during dental procedures, it has been shown that several patients who refused dental treatment died of asphyxia during dental procedures. We speculated that forcible maximum opening of the mouth by using a mouth prop triggers this asphyxia by affecting the upper airway. Therefore, we assessed the morphological changes of the upper airway following maximal opening of the mouth. In 13 healthy adult volunteers, the sagittal diameter of the upper airway on lateral cephalogram was measured between the two conditions; closed mouth and maximally open mouth. The dyspnea in each state was evaluated by a visual analog scale. In one subject, a computed tomograph (CT) was taken to assess the three-dimensional changes in the upper airway. A significant difference was detected in the mean sagittal diameter of the upper airway following use of the prop (closed mouth: 18.5 ± 3.8 mm, maximally open mouth: 10.4 ± 3.0 mm). All subjects indicated upper airway constriction and significant dyspnea when their mouth was maximally open. Although a CT scan indicated upper airway constriction when the mouth was maximally open, muscular compensation was admitted. Our results further indicate that the maximal opening of the mouth narrows the upper airway diameter and leads to dyspnea. The use of a prop for the patient who has communication problems or poor neuromuscular function can lead to asphyxia. When the prop is used for patient refusal in dentistry, the respiratory condition should be monitored strictly, and it should be kept in mind that the “sniffing position” is effective for avoiding upper airway constriction. Practitioners should therefore consider applying not only systematic desensitization, but also general anesthesia to the patient who refuses treatment, because the safety of general anesthesia has advanced, and general anesthesia may be safer than the use of a prop and restraints.

Elevation of a Periosteal Flap With Irrigation of the Bone for Minor Oral Surgery Reduces the Duration of Action of Infiltration Anesthesia

The aim of this study is to assess the difference in duration of action after infiltration anesthesia when elevation of a periosteal flap (EPF) was accomplished with water or saline irrigation versus nonelevation of a periosteal flap (NEPF). The 57 patients in this study were under conscious sedation. A long treatment time of more than 1 hour was used. Instances where peripheral nerve block or opioids were administered and infiltration anesthesia over 2 fields were excluded before the study. Patients were included in either an EPF group (n = 29) or an NEPF group (n = 28). Statistically significant differences were detected in the initial dose of anesthetic (EPF: 4.3 +/- 1.4 mL, NEPF: 1.8 +/- 0.9 mL), the time until initial supplemental anesthesia (EPF: 38 +/- 26 minutes, NEPF: 65 +/- 27 minutes), and the frequency of anesthesia administration (EPF: 2.5 +/- 1.2 times, NEPF: 1.3 +/- 0.7 times). These results suggest that the duration of anesthesia action in EPF decreases to half compared with NEPF, even if the anesthetic was infiltrated in double the amount. Although supplemental anesthesia is required frequently in EPF, it is not efficacious. We speculated that the residual anesthetics in tissue were washed out by irrigation and hemorrhage and that supplemental anesthesia became ineffective because of leakage from the opened flap. Elevation of a periosteal flap reduces the effect of infiltration anesthetics.

Lidocaine Concentration in Mandibular Bone After Subperiosteal Infiltration Anesthesia Decreases With Elevation of Periosteal Flap and Irrigation With Saline

It has been reported that the action of infiltration anesthesia on the jawbone is attenuated significantly by elevation of the periosteal flap with saline irrigation in clinical studies; however, the reason is unclear. Therefore, the lidocaine concentration in mandibular bone after subperiosteal infiltration anesthesia was measured under several surgical conditions. The subjects were 48 rabbits. Infiltration anesthesia by 0.5 mL of 2% lidocaine with 1 : 80,000 epinephrine (adrenaline) was injected into the right mandibular angle and left mandibular body, respectively. Under several surgical conditions (presence or absence of periosteal flap, and presence or absence of saline irrigation), both mandibular bone samples were removed at a fixed time after subperiosteal infiltration anesthesia. The lidocaine concentration in each mandibular bone sample was measured by high-performance liquid chromatography. As a result, elevation of the periosteal flap with saline irrigation significantly decreased the lidocaine concentration in the mandibular bone. It is suggested that the anesthetic in the bone was washed out by saline irrigation. Therefore, supplemental conduction and/or general anesthesia should be utilized for long operations that include elevation of the periosteal flap with saline irrigation.