Systemic Lidocaine Infusion for Post-Operative Analgesia in Children Undergoing Laparoscopic Inguinal Hernia Repair: A Randomized Double-Blind Controlled Trial

Systemic lidocaine can provide satisfactory post-operative analgesia in adults. In this study, we assessed whether intravenous lidocaine is effective for post-operative analgesia and recovery in children undergoing laparoscopic inguinal hernia repair. A total of 66 children aged from six months to less than six years were classified in either the lidocaine (L) or control (C) groups. Children in Group L received a lidocaine infusion (a bolus dose of 1 mL kg-1, followed by a 1.5 mg kg-1 h-1 infusion), whereas Group C received the same volume of 0.9% saline. The primary outcome was the number of patients who presented face, legs, activity, crying and consolability (FLACC) scores of four or more, and therefore received rescue analgesia in the post-anesthesia recovery care unit (PACU). Secondary outcomes included the highest FLACC score in the PACU, FLACC, and the parents' postoperative pain measure (PPPM) score at 48 h post-operation, as well as side effects. The number of children who received rescue analgesia in the PACU was 15 (50%) in Group L and 22 (73%) in Group C (p = 0.063). However, the highest FLACC score in PACU was lower in Group L (3.8 ± 2.4) than in Group C (5.3 ± 2.7) (p = 0.029). In conclusion, systemic lidocaine did not reduce the number of children who received rescue analgesia in PACU.ope

Appropriate dose of dexmedetomidine for the prevention of emergence agitation after desflurane anesthesia for tonsillectomy or adenoidectomy in children: up and down sequential allocation

BACKGROUND: Dexmedetomidine can be used for the prevention of emergence agitation (EA) in children. However, an inadequate dose of dexmedetomidine can induce prolonged sedation and cardiovascular complications. The aim of this study was to evaluate the effective dose of dexmedetomidine for the prevention of EA after desflurane anesthesia for patients undergoing a tonsillectomy or adenoidectomy. METHODS: We enrolled 21 unpremedicated children, between 2 and 12 years, undergoing either a tonsillectomy or an adenoidectomy. General anesthesia was induced using sevoflurane and oxygen, and dexmedetomidine was administered before surgery. Anesthesia was maintained using desflurane resulting in a BIS range of 40-60. In the postanesthetic care unit (PACU), EA (agitation measured at level 4 or more at least once) was assessed on arrival in the PACU,15 min later, and 30 min later. The dose of dexmedetomidine for consecutive patients was determined by the response of the previous patient, using an increment or decrement of 0.1 μg/kg. RESULTS: The 50% effective dose of dexmedetomidine for prevention of EA was 0.25 μg/kg (95% confidence limits, 0.17-0.33 μg/kg), and the 95% effective dose was 0.38 μg/kg (95% confidence limits, 0.29-0.39 μg/kg). CONCLUSIONS: For prevention of EA after desflurane anesthesia for 50% and 95% of children undergoing tonsillectomies or adenoidectomies, 0.25 μg/kg or 0.38 μg/kg of dexmedetomidine is suggested. Further study is needed to validate the suggested dose of dexmedetomidine to prevent the EA that was identified in the present study.ope

Lipid Emulsion Inhibits Vasodilation Induced by a Toxic Dose of Bupivacaine via Attenuated Dephosphorylation of Myosin Phosphatase Target Subunit 1 in Isolated Rat Aorta

Lipid emulsions are widely used for the treatment of systemic toxicity that arises from local anesthetics. The goal of this in vitro study was to examine the cellular mechanism associated with the lipid emulsion-mediated attenuation of vasodilation induced by a toxic dose of bupivacaine in isolated endothelium-denuded rat aorta. The effects of lipid emulsion on vasodilation induced by bupivacaine, mepivacaine, and verapamil were assessed in isolated aorta precontracted with phenylephrine, the Rho kinase stimulant NaF, and the protein kinase C activator phorbol 12,13-dibutyrate (PDBu). The effects of Rho kinase inhibitor Y-27632 on contraction induced by phenylephrine or NaF were assessed. The effects of bupivacaine on intracellular calcium concentrations ([Ca(2+)]i) and tension induced by NaF were simultaneously measured. The effects of bupivacaine alone and lipid emulsion plus bupivacaine on myosin phosphatase target subunit 1 (MYPT1) phosphorylation induced by NaF were examined in rat aortic vascular smooth muscle cells. In precontracted aorta, the lipid emulsion attenuated bupivacaine-induced vasodilation but had no effect on mepivacaine-induced vasodilation. Y-27632 attenuated contraction induced by either phenylephrine or NaF. The lipid emulsion attenuated verapamil-induced vasodilation. Compared with phenylephrine-induced precontracted aorta, bupivacaine-induced vasodilation was slightly attenuated in NaF-induced precontracted aorta. The magnitude of the bupivacaine-induced vasodilation was higher than that of a bupivacaine-induced decrease in [Ca(2+)]i. Bupivacaine attenuated NaF-induced MYPT1 phosphorylation, whereas lipid emulsion pretreatment attenuated the bupivacaine-induced inhibition of MYPT1 phosphorylation induced by NaF. Taken together, these results suggest that lipid emulsions attenuate bupivacaine-induced vasodilation via the attenuation of inhibition of MYPT1 phosphorylation evoked by NaF.ope

Dexmedetomidine Inhibits Phenylephrine-induced Contractions via Alpha-1 Adrenoceptor Blockade and Nitric Oxide Release in Isolated Rat Aortae

The goal of this in vitro study was to examine the effect of the alpha-2 adrenoceptor agonist dexmedetomidine on phenylephrine (alpha-1 adrenoceptor agonist)-induced contraction in isolated rat aortae and to elucidate the associated cellular mechanisms, with a particular focus on alpha-1 adrenoceptor antagonism. Dexmedetomidine dose-response curves were generated in isolated endothelium-intact and endothelium-denuded rat aortae precontracted with phenylephrine or 5-hydroxytryptamine. Endothelium-denuded aortic rings were pretreated with either dexmedetomidine or the reversible alpha-1 adrenoceptor antagonist phentolamine, followed by post-treatment with the irreversible alpha-1 adrenoceptor blocker phenoxybenzamine. Control rings were treated with phenoxybenzamine alone. All rings were repeatedly washed with Krebs solution to remove all pretreatment drugs, including phenoxybenzamine, phentolamine and dexmedetomidine. Phenylephrine dose-response curves were then generated. The effect of rauwolscine on the dexmedetomidine-mediated change in phenylephrine-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells was examined using western blotting. The magnitude of the dexmedetomidine-mediated inhibition of phenylephrine-induced contraction was higher in endothelium-intact aortae than in endothelium-denuded aortae or endothelium-intact aortae treated with Nω-nitro-L-arginine methyl ester. However, dexmedetomidine did not significantly alter 5-hydroxytryptamine-induced contraction. In further experiments, prazosin attenuated dexmedetomidine-induced contraction. Additionally, pretreatment with either dexmedetomidine plus phenoxybenzamine or phentolamine plus phenoxybenzamine produced greater phenylephrine-induced contraction than phenoxybenzamine alone, suggesting that dexmedetomidine protects aortae from the alpha-1 adrenoceptor blockade induced by phenoxybenzamine. Rauwolscine attenuated the dexmedetomidine-mediated enhancement of phenylephrine-induced eNOS phosphorylation. Taken together, these results suggest that dexmedetomidine attenuates phenylephrine-induced contractions via alpha-1 adrenoceptor blockade and endothelial nitric oxide release in the isolated rat aorta.ope

Comparison of the Effects of Lumbar Spine Flexion on the Acoustic Windows Between Young and Elderly Patients

Background: The effects of lumbar flexion on posterior longitudinal ligament (PLL) length as an acoustic window for neuraxial block in older patients have not been fully elucidated. Objective: This study aimed to compare changes in PLL length during lumbar spine flexion in young and old patients. Study design: Observational cohort study. Setting: Tertiary University Hospital. Methods: Forty young and older adult patients were placed in the lateral decubitus position. To flex the lumbar spine, patients were asked to flex their hips and knees and then their neck and shoulder toward their knees as much as they could (fetal position). An assistant pushed the patients' abdomen to the back and held their neck and legs to help them maintain position. To obtain an optimal ultrasound view, lumbar spinal ultrasonography was performed from L5/S1 to L2/L3 using a paramedian oblique sagittal plane. PLL lengths were measured on the ultrasound image before fetal position, after unassisted fetal position, and after assisted fetal position. Results: PLL lengths increased after lumbar spine flexion in both young and older adult patients, except at the L3-L4 level in old patients. The change in PLL length during lumbar spine flexion was significantly lower in old patients than in young patients at the L5-S1 and L3-L4 levels (P = 0.0028 and P = 0.0134, respectively). After lumbar spine flexion, the PLL length was significantly different between the spinal levels in older patients (P = 0.0392). Limitations: First, we measured the PLL length as an acoustic window for neuraxial block using lumbar spinal ultrasonography. Second, the researcher who obtained the spinal ultrasound view was not blinded to the patient's group and position. However, the researcher who measured the PLL lengths on ultrasonography was blinded. Third, all participants had no history of surgery, trauma, or congenital abnormalities of the spine, regardless of age. Conclusion: Lumbar spine flexion can increase PLL length in young and old patients. However, lumbar spine flexion is less effective in increasing the PLL length in old patients than in young patients.ope

Pediatric characteristics and the dose of propofol for sedation during radiological examinations: a retrospective analysis

Objective: The present study aimed to investigate patients' characteristics that can affect the dose of propofol required to sedate children undergoing imaging. Methods: In this retrospective, observational study, we reviewed medical records of children aged 0 to 18 years who were classified as having American Society of Anesthesiologists status 1 or 2 and they underwent imaging under propofol sedation between January 2011 and August 2016. Collected data included patients' demographics, propofol doses, duration of sedation, and complications. Regression analysis was performed to determine patients' characteristics that may affect the dose of propofol required to induce sedation. Results: A total of 925 patients were included. Simple linear regression showed that the dose of propofol was correlated with age, height, weight, and body surface area. Using the results of multiple linear regression, the following formula was used to estimate the dose of propofol (mg) for sedation: 0.75 + 0.14 × age (months) + 45.82 × body surface area (m2). Conclusion: A child's age, height, and body surface area should be considered when deciding the induction dose of propofol. Additionally, the formula that we have proposed can be used to estimate the dose of propofol required to induce sedation in children undergoing imaging.ope

A Novel Propofol Dosing Regimen for Pediatric Sedation during Radiologic Tests

The dose of propofol for pediatric sedation during radiologic tests has been proposed as an equation of 0.75 + 0.14 × age (months) + 45.82 × body surface area (m2) based on results in a previous study. We compared this equation and the conventional dosing strategy for sedation in children undergoing radiologic tests. An amount of 180 children scheduled for magnetic resonance imaging (MRI) were randomized to experimental and control groups. The initial induction dose of propofol calculated using the equation was administered in the experimental group. In the control group, children received 1 mg/kg of the initial induction dose of propofol. Then, 0.5 mg/kg of the additional dose was followed to induce sedation in both groups. When awake or moving, a rescue injection of 0.5 mg/kg propofol was given. The total induction dose was more significant in the experimental group. The number of injections for induction in the experimental group was lesser. The dose and number of rescue injections in the experimental group were significantly less. The equation for the induction dose of propofol in a previous study could achieve quick induction of sedation and prevent a rescue injection during sedation. However, caution is needed when using the equation.ope

Factors affecting determination of the optimal ketamine dose for pediatric sedation

OBJECTIVE: Children are sedated before undergoing diagnostic imaging tests in emergency medicine or pediatric sedation anesthesia units. The aim of this study was to identify variables potentially affecting the dose of ketamine required for induction of sedation in pediatric patients undergoing diagnostic imaging. METHODS: This retrospective study included children aged 0 to 18 years who underwent sedation with ketamine for computed tomography or magnetic resonance imaging in the pediatric sedation anesthesia unit of a tertiary medical center between January 2011 and August 2016. The children's hemodynamic status and depth of sedation were monitored during the examination. We recorded data on demographics, categories of imaging tests, ketamine doses administered, adverse events, respiratory interventions, and duration of sedation. Data for patients who experienced adverse events were excluded. RESULTS: Sixty-six patients were included in the final analysis. Univariate linear regression analysis revealed that patient age, height, and body surface area (BSA) affected the sedative dose of ketamine administered. These three variables showed multicollinearity in multivariate linear regression analysis and were analyzed in three separate models. The model with the highest adjusted R-squared value suggested the following equation for determination of the dose of ketamine required to induce sedation: ketamine dose (mg)=-1.62+0.7×age (months)+36.36×BSA (m2). CONCLUSION: Variables such as age and BSA should be considered when estimating the dose of ketamine required for induction of sedation in pediatric patients.ope

A novel electromagnetic guidance ultrasound system on radial artery cannulation: a prospective randomized controlled trial

Background: Radial artery cannulation can cause complications such as haematoma formation or thrombosis due to its small diameter. Recently, a novel ultrasound device equipped with an electromagnetic guidance system was introduced, showing the path and alignment of the needle during the procedure. The aim of this study was to investigate the effects of this novel system on both success and complication rates during radial artery cannulation under ultrasound guidance. Methods: In this randomized controlled trial, 76 adults scheduled for neurosurgery requiring radial artery cannulation were recruited. In group E (n = 38), radial artery cannulation was performed using the electromagnetic guidance ultrasound system, whereas in group C (n = 38), the procedure was performed using conventional ultrasound guidance. The success rates of cannulation on the first attempt, cannulation times, number of attempts, and incidence of complications were compared between the two groups. Results: There was a significant difference in the success rates on the first attempt between the two groups (group C = 78.9% vs. group E = 94.7%, P = 0.042). Incidences of posterior wall puncture and haematoma formation (group C = 8 vs. group E = 1; P = 0.028) were significantly lower in group E than in group C. The median cannulation time for successful attempts was comparable between groups. Conclusions: Use of the novel electromagnetic guidance system resulted in a better success rate on the first attempt and a lower incidence of complications during radial artery cannulation. Trial registration: This study was registered at http://cris.nih.go.kr (registration number: KCT0002476 ).ope

Effect of upper respiratory infection on anaesthesia induced atelectasis in paediatric patients

Upper respiratory tract infection (URI) symptoms are known to increase perioperative respiratory adverse events (PRAEs) in children undergoing general anaesthesia. General anaesthesia per se also induces atelectasis, which may worsen with URIs and yield detrimental outcomes. However, the influence of URI symptoms on anaesthesia-induced atelectasis in children has not been investigated. This study aimed to demonstrate whether current URI symptoms induce aggravation of perioperative atelectasis in children. Overall, 270 children aged 6 months to 6 years undergoing surgery were prospectively recruited. URI severity was scored using a questionnaire and the degree of atelectasis was defined by sonographic findings showing juxtapleural consolidation and B-lines. The correlation between severity of URI and degree of atelectasis was analysed by multiple linear regression. Overall, 256 children were finally analysed. Most children had only one or two mild symptoms of URI, which were not associated with the atelectasis score across the entire cohort. However, PRAE occurrences showed significant correspondence with the URI severity (odds ratio 1.36, 95% confidence interval 1.10-1.67, p = 0.004). In conclusion, mild URI symptoms did not exacerbate anaesthesia-induced atelectasis, though the presence and severity of URI were correlated with PRAEs in children.Trial registration: Clinicaltrials.gov (NCT03355547).ope