[The Influence of Preoperative Oral Carbohydrate Administration on Perioperative Blood Sugar Levels and Patients' Satisfaction].

BACKGROUND: After introducing preoperative oral carbohydrate as a part of enhanced recovery after surgery (ERAS) protocols, we assessed the influence of carbohydrate administration on the perioperative blood sugar levels (BS), the variation of vital signs and patients' satisfaction. METHODS: After IRB's approval and obtaining patients' consent, patients were divided into two groups; taking carbohydrate (Group AW) or not (Group NAW). Anesthesia was induced and maintained with total intravenous anesthesia using propofol, remifentanil and rocuronium. We measured BS six times during perioperative period. We also compared blood pressures and heart rates during induction of anesthesia. Moreover, we carried out questionnaire surveys about degree of satisfaction for ERAS among patients and nurses. RESULTS: Heart rates were significantly higher in Group AW (P < 0.05), but there were no significant difference in blood pressures or BS between the groups. Patients in Group AW had more anxiety for surgeries (P = 0.003), but more than 85% of patients and nurses were satisfied with carbohydrates. CONCLUSIONS: The carbohydrate administration had little influence on the perioperative vital signs. However, we gained high reputations from patients and paramedics.

Phosphine-olefin ligands based on a planar-chiral (π-arene)chromium scaffold: design, synthesis, and application in asymmetric catalysis.

The NMR and X-ray crystallographic studies clarified that planar-chiral alkenylene-bridged (phosphino-π-arene)(phosphine)chromium complexes 3 were capable of coordinating to a rhodium(I) cation in a bidentate fashion at the (π-arene)-bound phosphorus atom and at the olefin moiety. The P-olefin chelate coordination of 3 constructs the effective chiral environment at the metal center, and thus, these rhodium complexes display high performances in various rhodium-catalyzed asymmetric 1,4- and 1,2-addition reactions with arylboron nucleophiles. The control experiments demonstrated that the (η(2)-olefin)-Rh interaction as well as the bridging structure in 3 played the pivotal roles in the high enantioselectivity of the Rh-catalyzed asymmetric reactions. To enhance the synthetic utilities of these phosphine-olefin ligands, an enantiospecific and scalable synthetic method was developed. The novel synthetic method is flexible in terms of the substituent variation, and a library of the planar-chiral (arene)chromium-based phosphine-olefin ligands was established by the combinatorial approach. Among the newly prepared ligand library, compound 3g, which is with a bis(3,5-dimethylphenyl)phosphino group on the η(6)-arene ring, was found to be a far better chiral ligand in the rhodium-catalyzed asymmetric reactions showing excellent enantioselectivity and high yields.

Effect of preconditioning on propofol-induced neurotoxicity during the developmental period.

At therapeutic concentrations, propofol (PPF), an anesthetic agent, significantly elevates intracellular calcium concentration ([Ca2 +]i) and induces neural death during the developmental period. Preconditioning enables specialized tissues to tolerate major insults better compared with tissues that have already been exposed to sublethal insults. Here, we investigated whether the neurotoxicity induced by clinical concentrations of PPF could be alleviated by prior exposure to sublethal amounts of PPF. Cortical neurons from embryonic day (E) 17 Wistar rat fetuses were cultured in vitro, and on day in vitro (DIV) 2, the cells were preconditioned by exposure to PPF (PPF-PC) at either 100 nM or 1 µM for 24 h. For morphological observations, cells were exposed to clinical concentrations of PPF (10 µM or 100 µM) for 24 h and the survival ratio (SR) was calculated. Calcium imaging revealed significant PPF-induced [Ca2+]i elevation in cells on DIV 4 regardless of PPF-PC. Additionally, PPF-PC did not alleviate neural cell death induced by PPF under any condition. Our findings indicate that PPF-PC does not alleviate PPF-induced neurotoxicity during the developmental period.

Negative-pressure wound therapy to treat thoracic empyema with COVID-19-related persistent air leaks: A case report.

The novel coronavirus disease (COVID-19) has resulted in a global pandemic. Recently, COVID-19-related pneumothorax has gained attention because of the associated prolonged hospital stay and high mortality. While most cases of pneumothorax respond well to conservative and supportive care, some cases of refractory pneumothorax with persistent air leaks (PALs) do not respond to conventional therapies. There is a lack of evidence-based management strategies to this regard. We describe the case of a 73-year-old man with COVID-19-related acute respiratory distress syndrome (ARDS) who developed delayed tension pneumothorax with PALs caused by alveolopleural fistulas. Despite chest tube drainage, autologous blood pleurodesis, and endoscopic procedures, the PALs could not be closed, and were complicated by thoracic empyema. Subsequent minimally invasive open-window thoracostomy (OWT) with vacuum-assisted closure (VAC) therapy helped successfully control the refractory PALs. Serial chest computed tomography monitoring was useful for the early detection of the pneumothorax and understanding of its temporal relationship with air-filled lung cysts. Our case provides a new perspective to the underlying cause of refractory pneumothorax with PALs, secondary to COVID-19-related ARDS, and underscores the potential of OWT with VAC therapy as a therapeutic alternative in such cases.

Intravenous anesthetic-induced calcium dysregulation and neurotoxic shift with age during development in primary cultured neurons.

Anesthetic-induced neurotoxicity in the developing brain is a concern. This neurotoxicity is closely related to anesthetic exposure time, dose, and developmental stages. Using calcium imaging and morphological examinations in vitro, we sought to determine whether intravenous anesthetic-induced direct neurotoxicity varies according to different stages of the days in vitro (DIV) of neurons in primary culture. Cortical neurons from E17 Wistar rats were prepared. On DIV 3, 7, and 13, cells were exposed to the intravenous anesthetics thiopental sodium (TPS), midazolam (MDZ), or propofol (PPF), to investigate direct neurotoxicity using morphological experiments. Furthermore, using calcium imaging, the anesthetic-induced intracellular calcium concentration ([Ca2+]i) elevation was monitored in cells on DIV 4, 8, and 13. All anesthetics elicited significant [Ca2+]i increases on DIV 4. While TPS (100 µM) and MDZ (10 µM) did not alter neuronal death, PPF (10 µM and 100 µM) decreased the survival ratio (SR) significantly. On DIV 8, TPS and MDZ did not elicit [Ca2+]i elevation or SR decrease, while PPF still induced [Ca2+]i elevation (both at 10 µM and 100 µM) and significant SR decrease at 100 µM (0.76 ± 0.03; P < 0.05), but not at 10 µM (0.91 ± 0.03). Such anesthetic-induced [Ca2+]i elevation and SR decrease were not observed on DIV 13-14 for any of the anesthetic drugs. Our study indicates that more caution may be exercised when using PPF compared to TPS or MDZ during development.

Thiopental sodium preserves the responsiveness to glutamate but not acetylcholine in rat primary cultured neurons exposed to hypoxia.

Although many in vitro studies demonstrated that thiopental sodium (TPS) is a promising neuroprotective agent, clinical attempts to use TPS showed mainly unsatisfactory results. We investigated the neuroprotective effects of TPS against hypoxic insults (HI), and the responses of the neurons to l-glutamate and acetylcholine application. Neurons prepared from E17 Wistar rats were used after 2weeks in culture. The neurons were exposed to 12-h HI with or without TPS. HI-induced neurotoxicity was evaluated morphologically. Moreover, we investigated the dynamics of the free intracellular calcium ([Ca(2+)]i) in the surviving neurons after HI with or without TPS pretreatment following the application of neurotransmitters. TPS was neuroprotective against HI according to the morphological examinations (0.73±0.06 vs. 0.52±0.07, P=0.04). While the response to l-glutamate was maintained (0.89±0.08 vs. 1.02±0.09, P=0.60), the [Ca(2+)]i response to acetylcholine was notably impaired (0.59±0.02 vs. 0.94±0.04, P<0.01). Though TPS to cortical cultures was neuroprotective against HI morphologically, the [Ca(2+)]i response not to l-glutamate but to acetylcholine was impaired. This may partially explain the inconsistent results regarding the neuroprotective effects of TPS between experimental studies and clinical settings.

Only extra-high dose of ketamine affects l-glutamate-induced intracellular Ca(2+) elevation and neurotoxicity.

The neurotoxic effects of anesthetics on the developing brain are a concern. Although most of the anesthetics are GABAA agonists or NMDA antagonists, the differences in these effects on prospective glutamate-neurotoxicity in the brain is not fully understood. We examined the degree of L-glutamate-induced intracellular calcium ([Ca(2+)]i) elevation and neurotoxicity in neurons exposed to anesthetics. Primary cortical neurons from E17 rats were preincubated with 1-100 µM of ketamine or thiopental sodium (TPS) for the first 72 h of culturing. Two weeks later, the neurons were exposed to L-glutamate. The extent of glutamate toxicity was evaluated using Ca(2+)-imaging and morphological experiments. Preincubation with 100 µM ketamine but not with other concentrations of ketamine and TPS for the first 72 h in culture significantly enhanced L-glutamate-induced [Ca(2+)]i elevation 2 weeks later. Morphology experiments showed that vulnerability to L-glutamate-mediated neurotoxicity was only altered in neurons preincubated with 100 µM ketamine but not with TPS. Although preincubation with high concentration of ketamine showed enhancement of L-glutamate-induced [Ca(2+)]i elevation 2 weeks later, long-term exposure to TPS or ketamine at clinical doses during developmental periods may not result in a dose-related potentiation of exogenous glutamate-induced neurotoxicity, once the intravenous anesthetics are discontinued.

Transversus abdominis plane block for bilateral orchiopexy in an 8-year-old patient with Eisenmenger's syndrome.

Non-cardiac surgery should only be performed in patients with Eisenmenger's syndrome if absolutely mandatory because these patients are at high risk of perioperative mortality. Proper anesthetic and perioperative pain management in these patients remains a controversial topic. Transversus abdominis plane (TAP) block provides safe and beneficial perioperative analgesia in adults and children; however, no report has described the performance of TAP block in a child with Eisenmenger's syndrome. Herein, we describe the performance of bilateral orchiopexy for cryptorchidism in an 8-year-old boy with Eisenmenger's syndrome due to an uncorrected muscular ventricular septal defect (mVSD). Anesthesia induction and maintenance were uneventful. Subsequently, the patient received ultrasound-guided bilateral TAP block by using 10 mL of 0.25 % levobupivacaine shortly before recovery from anesthesia. The TAP block provided pain relief and maintenance of stable hemodynamics during the postoperative period. We successfully used a TAP block in a child with Eisenmenger's syndrome to provide postoperative analgesia. No side effects were apparent during the perioperative period. TAP block can be considered a beneficial pain management technique for analgesia in children with Eisenmenger's syndrome.