ABSTRACT
PURPOSE: The purpose of this study was to examine the effects of parental presence on the incidence of emergence delirium (ED) of children in the postanesthesia care unit (PACU). DESIGN: A quasi-experimental pretest and post-test study with nonequivalent and nonsynchronized control groups. METHODS: About 93 children aged 3 to 6 years undergoing general anesthesia for tonsillectomy were divided into two groups: parental presence and absence. ED was recorded using the Pediatric Anesthesia Emergence Delirium Scale at 0, 10, 20, and 30 minutes after PACU admission. FINDINGS: ED score at each time point in the experimental group was lower than the control group, but not statistically significant. ED score in the experimental group significantly decreased over time (F = 6.98; P = .010). CONCLUSIONS: Parental visitation programs could be effective on the degree of ED in children in the PACU setting. This result may contribute to the establishment of PACU visitation program policy in South Korea.
Subject(s)
Anesthesia, General/methods , Emergence Delirium/epidemiology , Parents , Tonsillectomy/methods , Anesthesia Recovery Period , Child , Child, Preschool , Female , Humans , Incidence , Male , Recovery Room , Republic of Korea , Time FactorsABSTRACT
PURPOSE: Ca(2+) homeostasis plays an important role in myocardial cell injury induced by hypoxia-reoxygenation, and prevention of intracellular Ca(2+) overload is key to cardioprotection. Even though thiopental is a frequently used anesthetic agent, little is known about its cardioprotective effects, particularly in association with Ca(2+) homeostasis. We investigated whether thiopental protects cardiomyocytes against hypoxia-reoxygenation injury by regulating Ca(2+) homeostasis. MATERIALS AND METHODS: Neonatal rat cardiomyocytes were isolated. Cardiomyocytes were exposed to different concentrations of thiopental and immediately replaced in the hypoxic chamber to maintain hypoxia. After 1 hour of exposure, a culture dish was transferred to the CO(2) incubator and cells were incubated at 37 for 5 hours. At the end of the experiments, the authors assessed cell protection using immunoblot analysis and caspase activity. The mRNA of genes involved in Ca(2+) homeostasis, mitochondrial membrane potential, and cellular Ca(2+) levels were examined. RESULTS: In thiopental-treated cardiomyocytes, there was a decrease in expression of the proapoptotic protein Bax, caspase-3 activation, and intracellular Ca(2+) content. In addition, both enhancement of anti-apoptotic protein Bcl-2 and activation of Erk concerned with survival were shown. Furthermore, thiopental attenuated alterations of genes involving Ca(2+) regulation and significantly modulated abnormal changes of NCX and SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. Thiopental suppressed disruption of mitochondrial membrane potential (DeltaPsi(m)) induced by hypoxia-reoxygenation. CONCLUSION: Thiopental is likely to modulate expression of genes that regulate Ca(2+) homeostasis, which reduces apoptotic cell death and results in cardioprotection.
Subject(s)
Calcium/metabolism , Cell Hypoxia/physiology , GABA Modulators/pharmacology , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Thiopental/pharmacology , Animals , Apoptosis , Cell Survival/drug effects , Cells, Cultured , Homeostasis/drug effects , Immunoblotting , In Situ Nick-End Labeling , Membrane Potential, Mitochondrial/drug effects , Microscopy, Confocal , Rats , Rats, Sprague-Dawley , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
Intracellular Ca2+ overload induced by hypoxia-reoxygenation alters Ca2+ homeostasis, which plays an important role in myocardial cell injury. Even though propofol is known as a radical scavenger with Ca2+ channel blocking properties, little is known about cardioprotective effect associated with Ca2+ homeostasis in cardiomyocytes. In the present study, we showed that propofol protects cardiomyocytes against hypoxia-reoxygenation injury. In propofol-treated cardiomyocytes, we observed a decrease in the expression of pro-apoptotic protein Bax, cytochrome c, caspase-3 activation and intracellular Ca2+ content. We also found that propofol treatment enhanced expression of anti-apoptotic protein Bcl-2 and activation of ERK concerned with survival. Propofol attenuated alterations of genes involving Ca2+-regulatory mechanism and significantly modulated abnormal changes of SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. These results suggest that propofol modulates the expression of genes involved in Ca2+ homeostasis, thereby producing cardioprotective effects through a reduction in apoptotic cell death.
Subject(s)
Anesthetics, Intravenous/pharmacology , Calcium/metabolism , Cell Hypoxia/drug effects , Homeostasis/drug effects , Myocytes, Cardiac/drug effects , Propofol/pharmacology , Animals , Animals, Newborn , Apoptosis/drug effects , Blotting, Western , Calcium-Binding Proteins/biosynthesis , Calcium-Binding Proteins/genetics , Caspase 3/metabolism , Cell Survival/drug effects , Gene Expression/drug effects , In Situ Nick-End Labeling , Male , Microscopy, Confocal , Nerve Tissue Proteins/biosynthesis , Nerve Tissue Proteins/genetics , Rats , Rats, Sprague-Dawley , Reverse Transcriptase Polymerase Chain Reaction , Signal Transduction/drug effectsABSTRACT
After general anesthesia, peripheral nerve paralysis is a rare complication. The frequently damaged nerves including: branches of the brachial plexus, the ulnar, radial and common peroneal nerves, and sometimes the facial nerve. The radial nerve is the most infrequently damaged one, accounting for only 3% of nerve damage. We report a case of radial nerve paralysis due to self retractor during abdominal operation, its clinical findings, and review of the literature on peripheral nerve paralysis.
