Patients with intellectual disabilities frequently have concomitant epilepsy requiring medication with multiple antiepileptic drugs. Some previous studies have reported a drug interaction between propofol and antiepileptics. We report an outpatient with a delayed emergence from a general anesthesia with propofol that was attributed to multi-drug therapy for epilepsy.

  The patient was a 44-year-old man who was scheduled to undergo dental treatment requiring two sessions of ambulatory anesthesia using propofol. His preoperative tests were normal, including a routine blood examination, liver and kidney function, ECG and chest radiograph. He was receiving multiple antiepileptic drugs for the treatment of epilepsy.

  Anesthesia was induced using propofol, remifentanil, and rocuronium bromide. After the discontinuation of propofol administration, spontaneous eye opening and a response to verbal commands were both delayed, occurring about 1 hour after the first session of general anesthesia and about 1.5 hours after the second session.

  The patient was not obese, and his perioperative liver and renal functions were normal. Hypothermia and central nervous system (CNS) abnormalities caused by sequela were both ruled out. He had been receiving multiple antiepileptic drugs, so synergistic effects at propofol’s site of action in the CNS were suspected as the main cause of the delayed emergence. Furthermore, hypovolemia could have resulted in an elevated blood level of propofol and its delayed metabolism/excretion, delaying the emergence from sedation.

  We could not identify a clear cause because we did not measure the blood concentrations of the antiepileptics or propofol in the patient. In the presently reported patient, a drug interaction between propofol and antiepileptics was thought to be a possible cause of the delayed emergence from sedation.

  Neuropathic pain is caused by damage or diseases of the somatosensory nervous system. We report the effect of mirogabalin on chronic pain after maxillary molar extraction in a 74-year-old woman despite pregabalin, carbamazepine, and amitriptyline not having any effect.

  The patient began to feel contact pain in the right upper molar to anterior gingiva, the right palate, and the tongue after a maxillary molar extraction. At first, her doctor prescribed pregabalin. As this medication had no effect on her pain, so she was referred to our department for consultation. At the first consultation, no evidence suggesting the cause of the pain in the oral cavity was found. We suspected trigeminal neuralgia and prescribed carbamazepine, but her symptoms did not improve much. We then changed the medication to amitriptyline, but once again her symptoms did not improve. Next, we prescribed mirogabalin ; her symptoms finally began to improve gradually, and the extent of her pain was also reduced. She has continued to take mirogabalin, and her pain remains well controlled. Furthermore, she has not experienced any side effects of mirogabalin.

  The present patient was suspected of having peripheral neuropathic pain caused by damage to the peripheral nerves of the superior alveolar nerve branches during a maxillary molar extraction. The efficacy of mirogabalin for the treatment of diabetic peripheral neuropathic pain and postherpetic neuralgia has been previously reported. The present case suggests that mirogabalin is also effective for peripheral neuropathic pain after tooth extraction.

  Myasthenia gravis (MG) is one of the autoimmune diseases which blocks and destroys the receptor sites for acetylcholine. Since the patient has varying sensitivity to non-depolarizing neuromuscular blocking agents, it should be carefully treated by titrating the muscle relaxing drug for anesthesia. The newly-development of the neuromuscular blockade provides the more precise information of the extent of muscle relaxation, thus, muscle relaxant can become safely used for even the patient with MG. Herewith, we report a case of MG anesthetized for extraction of the wisdom tooth.

  The patient is a 56-year-old woman. 157 cm, 50 kg. At the age of 52, she was diagnosed with MG. Since the wisdom teeth was deeply impacted, general anesthesia was indicated. It was planned to monitor muscle relaxation by using TOF-cuff^®, which is a type of Compressomyography : CMG. This monitor is built in the manchette for measurement of blood pressure. Thus, this monitor is feasible for a case of dental anesthesia because the monitoring condition is not affected by the position of the finger, and is not needed to align the position if necessary.

  General anesthesia was induced with remifentanil 0.5 μg/kg/min and propofol 70 mg. The rocuronium bromide was repeatedly administered by 5 mg, monitoring TOFcuff^®. We confirmed null TOF count by 20 mg, and the patient was intubated. The neuromuscular blocking condition was stable during the operation by titrating each 5 mg of rocuronium bromide as needed. After the surgery, 100 mg of the sugammadex successfully revered neuromuscular blockade, confirming the 100% recovery of the TOF ratio. The patient was postoperatively uneventful, no complication was confirmed.

  It is still controversial whether muscle relaxant should be used for the patient with MG. The precise monitoring of muscle relaxation could lead to safety usage of muscle relaxation even for MG. The compressomyography may become a useful monitor intraoperatively. This case report could be a reference to consider muscle relaxation for the patient with MG.

  Nasal high flow therapy (NHFT) is a non-invasive respiratory therapy used to maintain a high fraction of inspired oxygen (Fio₂) by delivering a mixture of high-flow oxygen and air. This technique has several physiological advantages compared with other standard oxygen therapies, including a reduced anatomical dead space, a positive end-expiratory pressure, and sufficient humidification. NHFT is attracting attention as an alternative respiratory support therapy for critically ill patients.

  Here, we report the maintenance of intravenous sedation using NHFT during a dental treatment in an intellectually disabled patient with tracheal stenosis. The patient was 148 cm tall, weighed 40 kg, and had a history of cardiac surgery for a double-outlet right ventricle. He suffered from tracheal stenosis caused by the long-term placement of a tracheal tube after an operation. No abnormalities were noted during a cardiac evaluation, including an echocardiogram and an electrocardiogram. Chest computed tomography showed the stenosis of the main bronchus, resulting in a diameter of only 6 mm at the narrowest point. For this reason, we considered that tracheal intubation during general anesthesia might carry a risk of airway stenosis, and we decided to maintain the intravenous sedation using NHFT without other active airway managements.

  The sedation was induced and maintained using midazolam and propofol. After an optimal sedation level was achieved, we inserted a nasal cannula for NHFT under an Fio₂ setting of 0.4 and a flow of 30 l/min. When an upper airway constriction occurred because of an increased anesthetic depth or the depression of the mandible, we increased the NHFT flow to 40 l/min and performed a jaw-lift maneuver. The Spo₂ remained stable under spontaneous respiration throughout the operation. A few minutes after the end of the use of the sedatives, voluntary movements were observed. Neither respiratory depression nor hemodynamic compromise was observed postoperatively. We suggest that intravenous sedation with NHFT could be a safe and effective method for preventing airway obstruction in patients with tracheal stenosis and might also be applicable for patients with intellectually disability.

  This article reviews the direct action of sevoflurane on contractile response to noradrenaline in canine mesenteric arteries and veins focusing on the influence of the endothelium. Second, our several observations concerning cardioprotective effects with sevoflurane are also introduced with some references.

  It is generally considered that sevoflurane is clinically vasodilator. However, studies in vitro have suggested that sevoflurane causes not only vasodilation but vasoconstriction, depending on the experimental situation. As results of our experiments, sevoflurane selectively impairs endothelium-dependent relaxation in canine mesenteric arteries by an oxygen free radical mechanism, mainly due to inactivation of EDRF/NO, and hypotension observed during sevoflurane anesthesia may due to its relaxing effect on veins and/or to inhibition of norepinephrine release from sympathetic nerve endings. It is also suggested that endothelium-intact arteries may protect against decreased arterial pressure by endothelium-dependent vasoconstriction, probably by inhibiting the release of basal EDRF/NO.

  Lethal injury to heart can be dramatically blunted by brief conditioning periods of ischemia/reperfusion : a phenomenon called ischemic preconditioning. And brief exposure to a volatile anesthetic agent such as isoflurane and sevoflurane also protects the heart against subsequent ischemia/reperfusion injury. This phenomenon has been recognized as anesthetic preconditioning. Ischemic preconditioning and sevoflurane-induced preconditioning exert infarct size limiting effects through opening of mitochondrial KATP channels. Recent investigations have also demonstrated that sevoflurane pre- and post-conditioning reduce myocardial infarct size to a degree comparable to that achieved with ischemic preconditioning. Sevoflurane post-conditioning may be clinically applicable in situations where the potential for ischemia/reperfusion injury is of concern.