Simulation training for medical emergencies: Evaluation of dentists' long-term learning skills and confidence.

INTRODUCTION: As the population ages and more patients experience medical emergencies during dental treatments, dentists must competently and confidently manage these situations. We developed a simulation training course for medical emergencies in the dental setting using an inexpensive vital sign simulation app for smartphones/tablets without the need for an expensive simulator. However, the duration for which this effect is maintained is unclear. This study was performed to evaluate the long-term educational effect at 3, 6, and 12 months after taking the course. MATERIALS AND METHODS: Thirty-nine dental residents participated in this course. Scenarios included vasovagal syncope, anaphylaxis, hyperventilation syndrome, and acute coronary syndrome, each of which the participants had to diagnose and treat. The participants were evaluated using a checklist for anaphylaxis diagnosis and treatment skills immediately after and 3, 6, and 12 months after the course. The participants were also surveyed about their confidence in diagnosing and treating these conditions by questionnaire before, immediately after, and 3, 6, and 12 months after the course. RESULTS: The checklist scores for anaphylaxis were significantly lower at 3, 6, and 12 months after the course than immediately after the course. The percentage of participants who provided a correct diagnosis and appropriate treatment for vasovagal syncope, hyperventilation syndrome, and acute coronary syndrome was lower at all reassessments than immediately after the course. CONCLUSION: Because medical emergency management skills and confidence declined within 3 months, it would be useful to introduce a refresher course approximately 3 months after the initial course to maintain skills and confidence.

Simulation training for medical emergencies of dental patients: A review of the dental literature.

In recent years, due to the aging of the population, the number of dental patients with comorbidities such as hypertension and diabetes has increased. Although it has been reported that these patients are increasingly developing medical emergencies during their dental treatments, many dental providers still do not possess the skills to manage medical emergencies appropriately. Simulation training is essential to improve this situation however, there is no report describing how to conduct an effective simulation in detail for dental office medical emergencies. The purpose of this review is to provide information on simulations that is effective and practical. The authors will highlight the key characteristics for providing effective simulation trainings, such as the selection of simulators, simulation locations, instructors, debriefings, methods for evaluating educational effectiveness, and the use of telesimulation as a method for simulation training due to the global COVID-19 pandemic. In addition, this review provides recommendations on tailoring an ideal simulation training course for those who wish to create one. The authors hope that this review will promote the spread of effective simulation training and in turn, contribute to improving the medical safety of dental patients.

SARS-CoV-2 recombinant spike protein induces cell apoptosis in rat taste buds.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections can cause loss or alteration of taste and smell as early symptoms or sequelae, but the detailed mechanism behind this phenomenon remains unclear. Here, we investigated whether the SARS-CoV-2 spike protein induces taste cell apoptosis and expression of the apoptosis-related cytokine TNF-α in male Sprague-Dawley rats. Terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP)-fluorescein nick end labeling (TUNEL) assay results revealed a significantly higher apoptosis index for taste cells in the SARS-CoV-2 group than for those in the control group. An immunohistochemistry analysis indicated significantly more TNF-α-positive cells in the SARS-CoV-2 group compared with the control group. These data suggest that the SARS-CoV-2 spike protein promotes taste cell apoptosis and the release of apoptosis-related cytokine TNF-α, implicating its contribution to the taste malfunction caused by coronavirus disease 2019 (COVID-19).

Tracheal Bronchus Detected During General Anesthesia: A Case Report.

A tracheal bronchus is a congenital abnormality of the tracheobronchial tree in which a displaced or accessory bronchus arises from the trachea superior to its bifurcation. We herein report a case in which a tracheal bronchus was incidentally found after induction of general anesthesia, and we discuss the potential airway management problems that may have ensued. An 80-year-old man was scheduled for buccal mucosa resection and abdominal skin grafting for treatment of squamous cell carcinoma of the left buccal mucosa. Because of trismus and anticipated airway difficulty, an awake intubation was performed under sedation. A 3-branched structure was incidentally observed at the first branching site that was supposed to be the carina. The tip of the endotracheal tube was repositioned 3 cm above the tracheal trifurcation, and the rest of the procedure proceeded uneventfully. A flexible fiberoptic scope is not used in many anesthesia cases, making the identification of such tracheal or bronchial abnormalities more difficult. Therefore, it is important to carefully check the bronchial morphology on any available chest radiographs before surgery, listen to lung sounds after intubation, and assess thoracic lung compliance without neglecting routine safety checks.

SARS-CoV-2 recombinant proteins-induced degeneration of taste buds in rat circumvallate papillae.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections cause loss or alteration of taste and smell as early symptoms and sequelae, but the detailed mechanism remains unclear. This study investigated whether coronavirus disease 2019-induced taste disorders are caused by direct effects on taste bud cells. SARS-CoV-2 recombinant spike and nucleocapsid proteins were applied to circumvallate papillae of male Sprague-Dawley rats. Immunohistochemistry and image analysis were used to compare the number of taste buds, and taste bud cells and area, together with confirmation of angiotensin-converting enzyme 2 (ACE2) expression. Immunohistochemical analysis revealed ACE2 expression in the taste buds of rat circumvallate papillae. Decreases in the number of taste buds, taste bud cells, and their area were observed at 12 days after application of SARS-CoV-2 recombinant spike and nucleocapsid proteins. These data suggest that SARS-CoV-2 proteins induce degeneration of taste buds.

Unexpected Anesthetic Circuit Leak Attributed to Improper Use of a Tube Holder: A Case Report.

Leaks involving the anesthesia circuit can cause significant complications including hypoxia and hypoventilation. We present a case of a circuit leak caused by damage to the corrugated tubing attributed to improper use of the tube holder. A 58-year-old male was scheduled for resection of a palatal tumor under an intubated general anesthetic. After successful nasotracheal intubation, the anesthesiologist inserted the corrugated tubing of the anesthetic circuit into the tube holder. A leaking sound was heard and a tear in the corrugated tubing was promptly discovered. The corrugated tubing of the anesthetic circuit presumably tore because it was inserted into the groove of the tube holder at an inappropriate angle with excessive force. Anesthesiologists should be aware of potential leaks if the anesthesia circuit is damaged, which may be caused by improper use of tube holders.

Perivascular Hedgehog responsive cells play a critical role in peripheral nerve regeneration via controlling angiogenesis.

Hh signaling has been shown to be activated in intact and injured peripheral nerve. However, the role of Hh signaling in peripheral nerve is not fully understood. In the present study, we observed that Hh signaling responsive cells [Gli1(+) cells] in both the perineurium and endoneurium. In the endoneurium, Gli1(+) cells were classified as blood vessel associated or non-associated. After injury, Gli1(+) cells around blood vessels mainly proliferated to then accumulate into the injury site along with endothelial cells. Hh signaling activity was retained in Gli1(+) cells during nerve regeneration. To understand the role of Hedgehog signaling in Gli1(+) cells during nerve regeneration, we examined mice with Gli1(+) cells-specific inactivation of Hh signaling (Smo cKO). After injury, Smo cKO mice showed significantly reduced numbers of accumulated Gli1(+) cells along with disorganized vascularization at an early stage of nerve regeneration, which subsequently led to an abnormal extension of the axon. Thus, Hh signaling in Gli1(+) cells appears to be involved in nerve regeneration through controlling new blood vessel formation at an early stage.

Rapid elevation of brain-derived neurotrophic factor production in the bilateral trigeminal ganglia by unilateral transection of the mental nerve in mice.

OBJECTIVES: Previous spinal nerve injury studies have reported brain-derived neurotrophic factor (BDNF) mRNA upregulation in either the ipsilateral dorsal root ganglion (DRG) neurons or both the contralateral and ipsilateral DRG neurons from early period after peripheral nerve injury. This BDNF elevation induces hyperalgesia in the injured and/or uninjured sites, but this detailed mechanism remains unknown. This study aimed to investigate the BDNF mRNA expression in bilateral DRG neurons caused by unilateral nerve injury and to explore the possible mechanisms by which nitric oxide (NO) mediates BDNF production in the DRG, resulting in contralateral hyperalgesia. METHODS: Early changes in BDNF mRNA expression in the bilateral trigeminal ganglia, within 1 day after mental nerve transection, were examined. Additionally, the effects on BDNF production of the NO synthase inhibitor N(ω)-nitro-l-arginine methyl ester (L-NAME) were investigated in the bilateral trigeminal ganglia. The relationship between injured neurons and BDNF production in the trigeminal ganglia was then assessed using immunohistochemical and retrograde tracing methods. RESULTS: Reverse transcription-PCR analysis demonstrated that unilateral transection of the mental nerve induced a rapid elevation of BDNF mRNA expression, which was inhibited by the intracerebroventricular administration of L-NAME prior to nerve transection. This effect was observed in both the ipsilateral and contralateral sides to the nerve transection. BDNF immunostaining combined with FluoroGold retrograde tracing revealed two types of BDNF-reactive neurons, FluoroGold-labelled and non-FluoroGold-labelled neurons, in the ipsilateral and contralateral sides of the trigeminal ganglia. BDNF-positive cells were also observed in the trigeminal ganglia of other trigeminal nerve branches. CONCLUSIONS: Unilateral nerve injury upregulates BDNF production in the bilateral trigeminal ganglia by NO-mediated and/or indirect activation of afferent neurons, resulting in contralateral hyperalgesia.

Potentiation of Rocuronium Bromide by Lithium Carbonate: A Case Report.

Lithium carbonate is a medication used for the management of various mental disorders. The present report describes a case of prolongation of rocuronium bromide in a patient concurrently taking lithium carbonate. A 64-year-old woman was scheduled to undergo cystectomy under general anesthesia. The patient took lithium carbonate (600 mg/d) for treatment of bipolar affective disorder. General anesthesia was induced with propofol, fentanyl, remifentanil, and sevoflurane. After loss of consciousness, rocuronium bromide (50 mg) was administered, and the trachea was intubated. Approximately 1 hour after the administration of rocuronium, the degree of residual muscle relaxant was evaluated using a nerve stimulation device. No muscle contraction occurred with train-of-four (TOF) stimulation. Following administration of sugammadex (200 mg) the TOF ratio increased to 95%. The ionic size of lithium is similar to that of sodium; therefore, lithium is transported into the cell with sodium. The resting membrane potential decreases, leading to a reduction in the height of the action potential. Thus, the effect of the remaining lithium may have been superimposed on the rocuronium neuromuscular blockade. Evaluation with a nerve stimulation device in patients taking lithium is crucial before extubation because of the risk of rocuronium potentiation.

Gli3 is a Key Factor in the Schwann Cells from Both Intact and Injured Peripheral Nerves.

Hedgehog (Hh) signaling has been shown to be involved in regulating both intact and injured peripheral nerves. Therefore, it is critical to understand how Hh signaling is regulated in the peripheral nerve. One of the transcription factors of the Hh signaling pathway, Gli3, functions as both a repressor and an activator of Hh signaling activity. However, it remains unclear whether Gli3 is involved in controlling the intact and/or injured peripheral nerves. We found that Gli3 act as a repressor in the Schwann cells (SCs) of intact sciatic nerves. Although Dhh and Ptch1 expression were present, Hh signaling was not activated in these SCs. Moreover, heterozygous Gli3 mutation (Gli3-/+) induced ectopic Hh signaling activity in SCs. Hh signaling was thus suppressed by Gli3 in the SCs of intact sciatic nerves. Minor morphological changes were observed in the intact nerves from Gli3-/+ mice. Gli3 expression was significantly decreased following injury and ligand expression switched from Dhh to Shh, which activated Hh signaling in SCs from wild-type mice. Changes of these ligands was found to be important for nerve regeneration in which the downregulation of Gli3 was also involved. In fact, Gli3-/+ mice exhibited accelerated ligand switching and subsequent nerve regeneration. Both suppression of Hh signaling with Gli3 in the intact nerves and activation of Hh signaling without Gli3 in the injured nerve were observed in the SCs in an autocrine manner. Thus, Gli3 is a key factor in the control of intact peripheral nerve homeostasis and nerve regeneration.

Semaphorin 3A Inhibits Nerve Regeneration During Early Stage after Inferior Alveolar Nerve Transection.

Neuroma formation at sites of injury can impair peripheral nerve regeneration. Although the involvement of semaphorin 3A has been suggested in neuroma formation, this detailed process after injury is not fully understood. This study was therefore undertaken to examine the effects of semaphorin 3A on peripheral nerve regeneration during the early stage after injury. Immunohistochemistry for semaphorin 3A and PGP9.5, a general neuronal marker, was carried out for clarify chronological changes in their expressions after transection of the mouse inferior alveolar nerve thorough postoperative days 1 to 7. At postoperative day 1, the proximal stump of the damaged IAN exhibited semaphorin 3A, while the distal stump lacked any immunoreactivity. From this day on, its expression lessened, ultimately disappearing completely in all regions of the transected inferior alveolar nerve. A local administration of an antibody to semaphorin 3A into the nerve transection site at postoperative day 3 inhibited axon sprouting at the injury site. This antibody injection increased the number of trigeminal ganglion neurons labeled with DiI (paired t-test, p < 0.05). Immunoreactivity of the semaphorin 3A receptor, neuropilin-1, was also detected at the proximal stump at postoperative day 1. These results suggest that nerve injury initiates semaphorin 3A production in ganglion neurons, which is then delivered through the nerve fibers to the proximal end, thereby contributes to the inhibition of axonal sprouting from the proximal region of injured nerves in the distal direction. To our knowledge, this is the first report to reveal the involvement of Sema3A in the nerve regeneration process at its early stage.

Endotracheal Intubation Complicated by a Palatal Tooth in a Patient With Treacher Collins Syndrome.

We report a case of difficult endotracheal intubation in a patient with Treacher Collins syndrome. A sixteen-year-old female patient scheduled for general anesthesia had a displaced palatal tooth that interfered with laryngoscope insertion into the pharyngeal space. To address this problem, we successfully performed endotracheal intubation using a fiberscope while elevating the epiglottic vallecula using a King Vision™ video laryngoscope. A later operation was performed after tooth extraction without difficult laryngoscopy. Our experience stresses the importance of removing obstructions to laryngoscopic inspection prior to general anesthesia.

Vascularization via activation of VEGF-VEGFR signaling is essential for peripheral nerve regeneration.

Peripheral nerve injury has been suggested to up-regulate mRNA for the vascular endothelial growth factor (VEGF) which enhances nerve regeneration. VEGF is known to regulate angiogenesis by binding with a specific receptor, the vascular endothelial growth factor receptor (VEGFR). However, little is known about the involvement of VEGF-VEGFR signaling in the nerve regeneration at early stages though previous studies contained a lengthy observation. The present study examined that relationship between angiogenesis and peripheral nerve regeneration at the early stage after nerve transection by focusing on the chronological changes in the expression patterns of VEGF-VEGFR signaling. This study used our previously reported experimental model for nerve regeneration following the transection of the inferior alveolar nerve (IAN) in mice. In a double staining of PGP9.5 and CD31, respective markers for the nerve fibers and endothelial cells, CD31 immunoreactions first appeared in the injury site on postoperative (PO) day 2 when the transected nerve fibers had not been re-connected. The most intense immunoreaction for CD31 was found around the regenerating nerve fibers extending from the proximal stump on PO day 3, but it gradually lessened to disappear by PO day 7. The expression patterns of VEGFR1 and VEGFR2 showed similar chronological changes through the observation periods, with most intense immunoreaction found on PO day 3. Western blotting of total protein extracted from the injury site demonstrated the clear bands for VEGF-A and VEGF-B on PO day 2, indicating a time lag for the expression of ligands and receptors. A local administration of antibody to VEGF-A inhibited the elongation of the nerve fibers from the proximal stump. Furthermore, this administration of VEGF-A antibody inhibited the expression of CD31 in the gap between proximal and distal stumps. These results indicated that a nerve injury initiates productions in VEGF-A and VEFG-B, followed with the expression of VEGFR1 and VEGFR2 at early stages after the nerve injury. Taken these findings together, it is reasonable to postulate that immediate response of VEGF-VEGFR signaling to nerve injury plays a crucial role in local angiogenesis, resulting in a trigger for the regeneration of the nerve fibers in mouse IAN.

The Sonic Hedgehog signaling pathway regulates inferior alveolar nerve regeneration.

Activation of Shh signaling is known to be observed following injury of the peripheral nerves such as the sciatic nerve. However, the precise role of Shh signaling during peripheral nerve regeneration is not fully understood. The inferior alveolar nerve (IAN) is most commonly injured during oral surgery. Unlike the sciatic nerve, the IAN is isolated from other craniofacial tissues, as it resides in a long bony canal within the mandible. The IAN is thus an excellent experimental model for investigating peripheral nerve regeneration. In this study, the role of Shh signaling in peripheral nerve regeneration was investigated using the mouse IAN transection model. During regeneration, Shh signaling was activated within the entire distal region of the IAN and proximal stumps. Inhibition of Shh signaling by cyclopamine application at the transection site led to abnormal axon growth in random directions, a reduced number of macrophages, and an increase in myelin debris within the distal region. Shh signaling is thus involved in peripheral nerve regeneration via the regulation of myelin degradation.

Retropharyngeal Dissection by Parker Flex-Tip Nasal Endotracheal Tube.

Possible complications of nasotracheal intubation include injury to the nasal or pharyngeal mucosa. Dissection of the retropharyngeal tissue by the endotracheal tube is one of the rarer of the more severe complications. Previous studies have indicated that the Parker Flex-Tip (PFT) tracheal tube (Parker Medical, Highlands Ranch, Colo) reduces the incidence of mucosal injury. We experienced a case involving inadvertent retropharyngeal placement of a PFT tube in a 29-year-old patient during nasotracheal intubation under general anesthesia for elective dental treatment. Despite thermosoftening the PFT tube, expanding the nasal meatus, and ensuring gentle maneuvering, the tube intruded into the left retropharyngeal mucosa. However, the injury was not severe, and the only required treatment was the administration of antibiotics and corticosteroids. Even when a PFT tube is utilized, pharyngeal dissection is possible. When resistance is felt during passing of the PFT tube through the nasopharynx, an alternative method to overcome this resistance should be utilized.

Novel trigeminal slice preparation method for studying mechanisms of nociception transmission.

BACKGROUND: The trigeminal subnucleus caudalis (Vc) plays a critical role in transmission and modulation of nociceptive afferent inputs, and exhibits a similar layer construction to the spinal dorsal horn. However, afferent inputs enter the brainstem and project to a separately located nucleus. It has previously been difficult to record responses of the Vc to afferent fiber activation in a brainstem slice preparation. The aim of the present study was to establish a novel brainstem slice preparation method to study trigeminal nociceptive transmission mechanisms. NEW METHOD: Thirty adult 6-7-week-old C57/BL6J male mice were included in the study. Obliquely sliced brainstem sections at a thickness of 600µm, which included the Vc and the root entry zone to the brainstem, were prepared. The Vc response to electrical stimulation of afferent fibers was observed as a change in intracellular calcium concentration by fluorescence intensity response. RESULTS: Electrical stimulation of afferent inputs to the trigeminal nerve increased fluorescent intensity in the Vc, which was completely diminished by tetrodotoxin and significantly suppressed by the AMPA/kainate antagonist CNQX (paired t-test, P<0.001), although the non-competitive NMDA antagonist (+)-MK801 maleate resulted in no changes. These results suggested a glutamate receptor-mediated response. COMPARISON WITH EXISTING METHODS/CONCLUSION: This brainstem slice preparation will be useful for investigating nociceptive transmission mechanisms of the trigeminal nerve.