ABSTRACT
BACKGROUND: In newborns, propofol anesthesia is commonly utilized. Propofol is increasingly being shown to be effective and safe in treating procedural sedation and anesthesia in neonates. This research aims to evaluate the efficacy and safety of propofol in neonates using systematic review and meta-analysis methodologies. METHODS: A thorough review and meta-analysis of studies on propofol anesthesia in neonates will be conducted. Conduct comprehensive searches in Web of Science, PubMed, Cochrane Library, EMBASE database, WanFang database, and Chinese biomedical literature database before May 25, 2021, to obtain published and qualified research. Two reviewers will assess the quality of the included papers and extract the data independently. Then, for meta-analysis, we will utilize RevMan 5.3 software. RESULTS: This study will pool the data of separate trials to analyze the efficacy and safety of propofol in the treatment of procedural sedation/anesthesia in neonates. CONCLUSION: Our findings will give strong data for determining whether propofol is an effective treatment for procedural anesthesia in neonates.
Subject(s)
Clinical Protocols , Patient Safety/standards , Propofol/pharmacology , Self Efficacy , Humans , Hypnotics and Sedatives/adverse effects , Hypnotics and Sedatives/pharmacology , Hypnotics and Sedatives/therapeutic use , Infant, Newborn , Meta-Analysis as Topic , Patient Safety/statistics & numerical data , Pediatrics/methods , Propofol/adverse effects , Propofol/therapeutic use , Systematic Reviews as Topic , Treatment OutcomeABSTRACT
OBJECTIVE: This study was performed to investigate the management of general anesthesia in an unusual case involving a patient with a broken tracheostomy tube presenting as an airway foreign body. METHODS: We herein describe the anesthetic management of a patient with a broken tracheostomy tube. A 77-year-old Chinese man who had been involved in a car accident underwent a tracheostomy. One year later, he presented with cough and bleeding at the tracheostomy site. Preoperative evaluation revealed that the metal tracheostomy tube was lodged in his left main bronchus. General anesthesia was induced to maintain spontaneous breathing, and adequate topical anesthesia of the airway was administered. RESULTS: The metal tracheostomy tube was successful removed, and a new tracheal tube was put in place. CONCLUSIONS: General anesthesia to maintain spontaneous breathing and adequate topical anesthesia of the airway can be safely used when removing broken tracheostomy tubes.
Subject(s)
Anesthetics/therapeutic use , Tracheal Stenosis/drug therapy , Tracheostomy/adverse effects , Aged , Disease Management , Humans , Male , Prognosis , Tracheal Stenosis/etiologyABSTRACT
BACKGROUND: Epidemiologic studies suggest the possibility of a modestly elevated risk of adverse neurodevelopmental outcomes in children exposed to anesthesia during early childhood. Sevoflurane is widely used in pediatric anesthetic practice because of its rapid induction and lower pungency. However, it is reported that sevoflurane leads to the long-term cognitive impairment. Some evidence revealed that the selective α2-adrenoreceptor agonist dexmedetomidine (DEX) exerts neuroprotective effects in various brain injury models of animals. But the role of DEX on sevoflurane-induced neuro-damage remains elusive. MATERIALS AND METHODS: In our study, we isolated the hippocampal neuron cells from newborn neonatal rats and verified the purity of neurons by immunocytochemistry. We employed the flow cytometry and western blot to examine the effect of sevoflurane, DEX and α2-adrenergic receptor antagonist yohimbine on cell cycle distribution. RESULTS: Immunocytochemistry results showed the purity of neurons > 94%, which provided a good model for neural pharmacology experiments. The exposure of sevoflurane-induced cell cycle arrest at S phase and suppressed the expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB). The addition of DEX suppressed sevoflurane-induced cell cycle arrest and the inhibitory of BDNF and TrkB expression. But the function of DEX was partly blocked by a α2 adrenergic receptor blocker yohimbine. CONCLUSION: Sevoflurane suppressed neuron cell proliferation via inhibiting the expression of BDNF and TrkB, and DEX relieved the neurotoxicity induced by sevoflurane via α2 adrenergic receptor. These findings provided new evidence that DEX exerted as a neuroprotective strategy in sevoflurane-induced neuro-damage, and provided new basis for the clinical application of DEX.
