Effect of ice popsicle treatment on emergence agitation in children undergoing oral surgery with sevoflurane anaesthesia: A prospective randomized controlled study.

PURPOSE: Emergence agitation is a common postoperative complication during recovery in children. The purpose of this study is to explore whether the use of ice popsicle could prevent emergence agitation in children undergoing oral surgery with sevoflurane anaesthesia. DESIGN AND METHODS: In this prospective randomized controlled study, 100 children undergoing oral surgery were randomly assigned to Group 1 which received ice popsicle after emergence (intervention, n = 50) or Group 2 which received verbal encouragement from their parents (control, n = 50). The primary outcome was the 2-hour postoperative incidence of EA. RESULTS: Group 1 had a significant lower incidence of emergence agitation (22% vs 58%, P < 0.001) compared with Group 2. The mean agitation score was significantly lower in Group 1 vs Group 2 at 10  minutes (1.64 vs 2.12, P = 0.024) and 20 min (1.60 vs 2.14, P = 0.004) after emergence. The peak agitation and pain scores were significantly lower in Group 1 than in Group 2 (P < 0.001). CONCLUSIONS: Findings from this study suggest that ice popsicle is an effective, cheap, pleasurable, and easily administered method for alleviating emergence agitation in paediatric patients after oral surgery under general anaesthesia. These results are worthy of confirmation in other surgeries. PRACTICE IMPLICATIONS: This approach is highly accepted by both children and their parents, and our findings support the effectiveness of ice popsicle in relieving emergence agitation and pain after oral surgery in children. CLINICAL TRIALS REGISTRATION: Chinese Clinical Trial Registry, ChiCTR1800015634.

Efficacy of different doses of intranasal dexmedetomidine in preventing emergence agitation in children with inhalational anaesthesia: A prospective randomised trial.

BACKGROUND: Emergence agitation is a common paediatric complication after inhalational anaesthesia. Intranasal dexmedetomidine can prevent emergence agitation effectively, but the optimal dose is uncertain. OBJECTIVE: The aim of our study was to investigate the 95% effective dose (ED 95 ) of intranasal dexmedetomidine for the prevention of emergence agitation after inhalational anaesthesia for paediatric ambulatory surgery. DESIGN: A prospective, randomised, placebo-controlled, double-blind, clinical trial. SETTING: The study was conducted in Guangzhou Women and Children's Medical Center in China from August 2017 to December 2018. PATIENTS: Three hundred and eighteen children scheduled for ambulatory surgery were enrolled into two age groups of less than 3 years and at least 3 years. INTERVENTIONS: The children in each age group were randomised into five equal subgroups to receive either intranasal dexmedetomidine 0.5, 1.0, 1.5 or 2.0 µg kg -1 (Groups D 0.5 , D 1.0 , D 1.5 and D 2.0 ), or intranasal isotonic saline (group C) after induction. MAIN OUTCOME MEASURES: The primary outcome was the ED 95 dose of intranasal dexmedetomidine for preventing emergence agitation after inhalational anaesthesia for paediatric ambulatory surgery. RESULTS: The incidences of emergence agitation for Groups C, D 0.5 , D 1.0 , D 1.5 and D 2.0 were 63, 40, 23, 13 and 3% in children less than 3 years, and 43, 27, 17, 7 and 3% in children at least 3 years. The ED 95 of intranasal dexmedetomidine for preventing emergence agitation was 1.99 µg kg -1 [95% confidence interval (CI), 1.83 to 3.80 µg kg -1 ] in children less than 3 years, and 1.78  µg kg -1 (95% CI, 0.93 to 4.29 µg kg -1 ) in children at least 3 years. LMA removal time for groups D 1.5 and D 2.0 was 9.6 ±â€Š2.2 and 9.7 ±â€Š2.5 min, respectively, for children less than 3 years, and 9.4 ±â€Š2.0 and 9.9 ±â€Š2.7 min in children at least 3 years, respectively. Length of stay in the postanaesthesia care unit for Groups D 1.5 and D 2.0 was 34.3 ±â€Š9.6 and 37.1 ±â€Š11.2 min, respectively, in children less than 3 years, and 34.7 ±â€Š10.2 and 37.3 ±â€Š8.3 min in children at least 3 years, respectively. These times were longer in the D 1.5 and D 2.0 subgroups than in the control subgroup in the two age groups of less than 3 years and at least 3 years, respectively: 7.2 ±â€Š1.9 min in children less than 3 years and 7.3 ±â€Š2.5 min in children at least 3 years for LMA removal time, 22.2 ±â€Š7.9 min in children less than 3 years and 22.0 ±â€Š7.7 min in children at least 3 years for PACU stay time in control subgroup, respectively ( P  < 0.05). CONCLUSION: Intranasal dexmedetomidine prevented emergence agitation after paediatric surgery in a dose-dependent manner. The optimal dose of intranasal dexmedetomidine for preventing emergence agitation was higher in younger children. TRIAL REGISTRY: chictr.org.cn: ChiCTR-IOR-17012415.

The impact of height on the spread of spinal anesthesia and stress response in parturients undergoing caesarean section: a prospective observational study.

BACKGROUND: The spread of spinal anesthesia was influenced by many factors, and the effect of body height on spinal anesthesia is still arguable. This study aimed to explore the impact of height on the spread of spinal anesthesia and the stress response in parturients. METHODS: A total of ninety-seven parturients were allocated into two groups according to their height: the shorter group (body height was shorter than 158 cm) and taller group (body height was taller than 165 cm). Spinal anesthesia was performed with the same amount of 12 mg plain ropivacaine in mothers of different heights. The primary outcome of the study was the success or failure of the spinal anesthesia. The secondary outcomes of the study were stress response, time to T6 sensory level, the incidence of hypotension, the satisfaction of abdominal muscle relaxation and patient VAS scores. RESULTS: The rate of successful spinal anesthesia in the shorter group was significantly higher than that in the taller group (p = 0.02). The increase of maternal cortisol level in the shorter group was lower than that in the taller group at skin closure (p = 0.001). The incidence of hypotension (p = 0.013), time to T6 sensory block (p = 0.005), the quality of abdominal muscle relaxation (p <  0.001), and VAS values in stretching abdominal muscles and uterine exteriorization (p <  0.001) in the shorter group were significantly different from those in the taller group. Multivariate analysis showed that vertebral column length (p <  0.001), abdominal girth (p = 0.022), amniotic fluid index (p = 0.022) were significantly associated with successful spinal anesthesia. CONCLUSIONS: It's difficult to use a single factor to predict the spread of spinal anesthesia. Patient's vertebral column length, amniotic fluid index and abdominal girth were the high determinant factors for predicting the spread of spinal anesthesia. TRIALS REGISTRATION: ChiCTR-ROC-17012030 ( Chictr.org.cn ), registered on 18/07/2017.

Effect of caudal ketamine on minimum local anesthetic concentration of ropivacaine in children: a prospective randomized trial.

BACKGROUND: Caudal ketamine has been shown to provide an effective and prolonged post-operative analgesia with few adverse effects. However, the effect of caudal ketamine on the minimum local anesthetic concentration (MLAC) of ropivacaine for intra-operative analgesia is unclear. METHODS: One hundred and sixty-nine children were randomized to five groups: Group C (caudal ropivacaine only), Group K0.25 (caudal ropivacaine plus 0.25 mg/kg ketamine), Group K0.5 (caudal ropivacaine plus 0.5 mg/kg ketamine), Group K0.75 (caudal ropivacaine plus 0.75 mg/kg ketamine), and Group K1.0 (caudal ropivacaine plus 1.0 mg/kg ketamine). The primary outcome was the MLAC values of ropivacaine with/without ketamine for caudal block. RESULTS: The MLAC values of ropivacaine were 0.128% (0.028%) in the control group, 0.112% (0.021%) in Group K0.25, 0.112% (0.018%) in Group K0.5, 0.110% (0.019%) in Group K0.75, and 0.110% (0.020%) in Group K1.0. There were no significant differences among the five groups for the MLAC values (p = 0.11). During the post-operative period the mean durations of analgesia were 270, 381, 430, 494, and 591 min in the control, K0.25, K0. 5, K0.75, and K1.0 groups respectively, which shown that control group is significantly different from all ketamine groups. Also there were significant differences between K0.25 and K0.75 groups, and between K1.0 groups and the other ketamine groups. CONCLUSIONS: Adding caudal ketamine to ropivacaine prolong the duration of post-operative analgesia; however, it does not decrease the MLAC of caudal ropivacaine for intra-operative analgesia in children. CLINICAL TRIAL REGISTRATION: ChiCTR-TRC-13003492. Registered on 13 August 2013.

The Incidence of and Risk Factors for Postoperative Fever after Cleft Repair Surgery in Children.

PURPOSE: The characteristics of postoperative fever after cleft repair surgery in children are unknown. Thus, the purpose of this study was to determine the incidence of and risk factors for postoperative fever. DESIGN AND METHODS: We retrospectively assessed 328 children who underwent cleft surgery at our hospital between March 2016 and April 2017 and were followed up for at least 3 days postoperatively. Fever was defined as a body temperature ≥38.0 °C. RESULTS: Seventy-one percent (n = 233) of patients developed fever within 72 h postoperatively, and most cases of postoperative fever were benign. Patients most frequently developed fever within 24 h postoperatively, and the occurrence of fever significantly decreased between 24 and 72 h postoperatively (p < 0.001). The incidence of fever with temperatures between 38.0 °C and 39.0 °C was higher than that of fever with temperatures ≥39.0 °C (p < 0.001). The mean duration of an episode of fever was 4 h. The type of surgery, method of anesthesia, and duration of anesthesia and surgery were found to be correlated with postoperative fever after cleft surgery. CONCLUSIONS: Most cases of postoperative fever after cleft surgery were benign occurrences. Postoperative fever after cleft repair surgery was characterized by a low grade, an early onset and a short duration in children. The method of anesthesia, duration of surgery and duration of anesthesia were risk factors for postoperative fever. PRACTICE IMPLICATIONS: Our results could help healthcare providers to gain increased knowledge of the risk factors for fever and when and how to treat postoperative fever.

Relationship Between Body Mass Index and Spread of Spinal Anesthsia in Pregnant Women: A Randomized Controlled Trial.

BACKGROUND The effect of body mass index (BMI) on the spread of spinal anesthesia is not completely clear. The aim of this study was to determine the dose requirements of ropivacaine and the incidence of hypotension in pregnant women with different BMIs during cesarean delivery. MATERIAL AND METHODS In this double-blind study, 405 women undergoing elective cesarean delivery were allocated to group S (BMI <25), group M (25 ≤BMI <30), or group L (BMI ≥30). Women in each group were further assigned to receive 7, 8, 9, 10, 11, 12, 13, 14, or 15 mg of spinal ropivacaine. RESULTS The ED50 and ED95 values of ropivacaine were 9.487 mg and 13.239 mg in Group S, 9.984 mg and 13.737 mg in Group M, and 9.067 mg and 12.819 mg in Group L. There were no significant differences among the 3 groups (p=0.915). Group L had a higher incidence of hypotension and a greater change in MAP after spinal anesthesia compared to the other 2 groups, and also required more doses of ephedrine than the other 2 groups when a dose of 15 mg ropivacaine was used. The incidence of hypotension had a positive correlation with the dose of ropivacaine (OR=1.453, p<0.001) and gestational age (OR=1.894, p<0.001). CONCLUSIONS Spinal ropivacaine dose requirements were similar in the normal BMI range. However, higher doses of spinal ropivacaine were associated with an increased incidence and severity of hypotension in obese patients compared with that in non-obese patients.

Effect of a bolus dose of fentanyl on the ED50 and ED95 of sevoflurane in neonates.

BACKGROUND: The minimum alveolar concentration (MAC) of sevoflurane in neonates is 3.3%, but this value has not been verified in Chinese neonates and the effect of different doses of fentanyl on MAC in neonates has not been investigated. This study was designed to determine the ED50 and ED95 values of sevoflurane in Chinese neonates with and without fentanyl. MATERIAL AND METHODS: Ninety-three neonates were randomly assigned to receive sevoflurane alone (control group, n=30), 1 µg/kg sevoflurane (group fent1, n=29), or 2 µg/kg fentanyl (group fent2, n=32). Following inhalational induction and tracheal intubation, the end-tidal concentration of sevoflurane was adjusted to achieve the designated concentration, which was determined using the modified Dixon's up-and-down method starting with 3.0% in each group, with a 0.25% step size. Success was defined as no motor response within 60 s of skin incision. RESULTS: The MAC (standard deviation) values of sevoflurane were 2.91% (0.27) in the control group, 2.53% (0.31) in the fent1 group, and 2.34% (0.33) in the fent2 group according to Dixon's up-and-down method. Logistic probit regression analysis revealed that the ED50 and ED95 (95% CI) of sevoflurane in neonates were 2.82% (2.66-2.98) and 3.39% (2.89-3.89), respectively, in the control group; 2.44% (2.19-2.68) and 3.30% (2.51-4.09), respectively, in the fent1 group; and 2.21% (1.97-2.45) and 3.11% (2.35-3.88), respectively, in the fent2 group. CONCLUSIONS: The MAC value of sevoflurane in Chinese neonates was lower than previously reported and was reduced by the addition of fentanyl.

Caudal dexmedetomidine decreases the required concentration of levobupivacaine for caudal block in pediatric patients: a randomized trial.

BACKGROUND AND OBJECTIVES: Dexmedetomidine (D) can prolong the duration of local anesthetics, but the effect of caudal dexmedetomidine on the potency of levobupivacaine (L) for caudal block has not been investigated. This study was designed to determine the effect of caudal dexmedetomidine on levobupivacaine for caudal block in pediatric patients. METHODS: Eighty-nine children scheduled for elective inguinal hernia repair or hydrocele were randomly assigned to one of the three groups: Group L (caudal levobupivacaine), Group LD1 (levobupivacaine plus 1 µg·kg(-1) dexmedetomidine), or Group LD2 (levobupivacaine plus 2 µg·kg(-1) dexmedetomidine). The primary endpoint was the minimum local anesthetic concentration (MLAC), which was determined using the Dixon up-and-down method. The secondary endpoints were the duration of analgesia and sedation. RESULTS: The MLAC values (sd) of caudal levobupivacaine were 0.103 (0.01)%, 0.068 (0.02)%, and 0.055 (0.03)% in Groups L, LD1, and LD2, respectively. The values of EC50 and EC95 (95% CI) of caudal levobupivacaine from logistic regression analysis were 0.094 (0.083-0.105)% and 0.129 (0.1-0.159)%, 0.058 (0.044-0.072)% and 0.106 (0.067-0.144)%, and 0.046 (0.033-0.059)% and 0.091 (0.055-0.127)% in Groups L, LD1, and LD2, respectively. The mean durations of analgesia in the postoperative period were 141, 378, and 412 min in Groups L, LD1, and LD2, respectively (L vs LD1 or LD2, P < 0.001). The mean durations of sedation in both Groups LD1 and LD2 also were significantly prolonged, compared with Group L (P < 0.01). CONCLUSIONS: Caudal dexmedetomidine reduces the MLAC values of levobupivacaine and improves postoperative analgesia in children without any neurological side effects.

Calpain-TRPC6 signaling pathway contributes to propofol-induced developmental neurotoxicity in rats.

Growing animal studies suggest a risk of neuronal damage following early childhood exposure to anesthesia and sedation drugs including propofol. Inhibition of transient receptor potential canonical 6 (TRPC6) degradation has been shown to protect neurons from neuronal damage induced by multiple brain injury models. Our aim was to investigate whether calpain-TRPC6 pathway is a target in propofol-induced neurotoxicity. Postnatal day (PND) 7 rats were exposed to five bolus injections of 25 mg/kg propofol or 10 % intralipid at hourly intervals. Neuronal injury was assessed by the expression pattern of TUNEL staining and cleaved-caspase-3. The Morris water maze test was used to evaluate learning and memory functions in later life. Pretreatments consisting of intracerebroventricular injections of a TRPC6 agonist, TRPC6 inhibitor, or calpain inhibitor were used to confirm the potential role of the calpain-TRPC6 pathway in propofol-induced neurotoxicity. Prolonged exposure to propofol induced neuronal injury, downregulation of TRPC6, and enhancement of calpain activity in the cerebral cortex up to 24 h after anesthesia. It also induced long-term behavioral disorders, manifesting as longer escape latency at PND40 and PND41 and as fewer platform-crossing times and less time spent in the target quadrant at PND42. These propofol-induced effects were attenuated by treatment with the TRPC6 agonist and exaggerated by the TRPC6 inhibitor. Pretreatment with the calpain inhibitor alleviated the propofol-induced TRPC6 downregulation and neuronal injury in the cerebral cortex. In conclusion, our data suggest that a calpain-TRPC6 signaling pathway contributes to propofol-induced acute cortical neuron injury and long-term behavioral disorders in rats.

Ketamine modulates neural stem cell differentiation by regulating TRPC3 expression through the GSK3ß/ß-catenin pathway.

Ketamine, a popular anesthetic, is often abused by people for its hallucinogenic effect. Thus, the safety of ketamine in pediatric populations has been called into question for potential neurotoxic effects. However, ketamine also has neuroprotective effects in many brain injury models. The differentiation of neural stem cells (NSCs) was influenced significantly by ketamine, but the molecular mechanism is still unclear. NSCs were extracted from the hippocampi of postnatal day 1 rats and treated with ketamine to induce NSCs differentiation. Our results found that ketamine promoted neuronal differentiation of NSCs dose-dependently in a small dose range (P < 0.001). The main types of neurons from NSCs were cholinergic (51 ± 4 %; 95 % CI: 41-61 %) and glutamatergic neurons (34 ± 3 %; 95 % CI: 27-42 %). Furthermore, we performed RNA sequencing to promise a more comprehensive understanding of the molecules regulated by ketamine. Finally, we combined bioimaging and multiple molecular biology techniques to clarify that ketamine influences NSC differentiation by regulating transient receptor potential canonical 3 (TRPC3) expressions. Ketamine dramatically repressed TRPC3 expression (MD [95 % CI]=0.67 [0.40-0.95], P < 0.001) with a significant increase of phosphorylated glycogen synthase kinase 3ß (p-GSK3ß; MD [95 % CI]=1.00 [0.74-1.27], P < 0.001) and a decrease of ß-catenin protein expression (MD [95 % CI]=0.60 [0.32-0.89], P = 0.001), thereby promoting the differentiation of NSCs into neurons and inhibiting their differentiation into astrocytes. These results suggest that TRPC3 is necessary for ketamine to modulate NSC differentiation, which occurs partly via regulation of the GSK3ß/ß-catenin pathway.

[Retracted] miR­218 suppresses tumor growth and enhances the chemosensitivity of esophageal squamous cell carcinoma to cisplatin.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Fig. 6 and the tumor images shown in Fig. 7A were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 33: 981­989, 2015; DOI: 10.3892/or.2014.3657].

A prospective study comparing the onset and analgesic efficacy of different concentrations of levobupivacaine with/without dexmedetomidine in young children undergoing caudal blockade.

STUDY OBJECTIVE: To investigate the onset and analgesic effect of adding dexmedetomidine to levobupivacaine for caudal block in young children. DESIGN: Randomized, prospective, double-blind study. SETTING: Women and Children Medical Center and university hospital. PATIENTS: Two hundred twelve children, American Society of Anesthesiologists physical status I or II, aged between 1 and 3 years and weighing between 8 and 18 kg, who were scheduled for elective inguinal hernia repair or hydrocele. INTERVENTIONS: Children were randomly allocated, using a computer-generated sequence of numbers, into 1 of 3 groups: caudal 0.25% levobupivacaine (Group L(0.25)), caudal 0.20% levobupivacaine (Group L(0.20)), or caudal 0.20% levobupivacaine plus 2 µg/kg dexmedetomidine (Group LD). MEASUREMENTS AND MAIN RESULTS: The primary end point of the study was the onset time of caudal levobupivacaine in children. The secondary end points of the study were the duration of analgesia and the degree of motor block in children. The 50% and 95% effective onset time (95% confidence interval) values of levobupivacaine were 8.19 minutes (7.30-9.08) and 11.17 minutes (9.44-12.91) in Group L(0.25), 10.16 minutes (8.90-11.41) and 15.85 minutes (13.14-18.57) in Group L(0.20), and 9.91 minutes (8.55-11.28) and 16.39 minutes (13.32-19.46) in Group LD, respectively. The mean durations of analgesia in these children were 7.23, 5.84, and 19.6 hours in Groups L(0.25), L(0.20), and LD, respectively. There were no significant differences in postoperative residual motor block among the 3 groups. CONCLUSIONS: Dexmedetomidine added to levobupivacaine does not have a significant effect on the onset time; however, it prolongs the duration of analgesia during caudal block in children.

miR-218 suppresses tumor growth and enhances the chemosensitivity of esophageal squamous cell carcinoma to cisplatin.

A growing body of evidence suggests that microRNA-218 (miR-218) acts as a tumor suppressor and is involved in tumor progression, development and metastasis and confers sensitivity to certain chemotherapeutic drugs in several types of cancer. However, our knowledge concerning the exact roles played by miR-218 in esophageal squamous cell carcinoma (ESCC) and the underlying molecular mechanisms remain relatively unclear. Thus, the aims of this study were to detect the expression of miR-218 in human ESCC tissues and explore its effects on the biological features and chemosensitivity to cisplatin (CDDP) in an ESCC cell line (Eca109), so as to provide new insights for ESCC treatment. Here, we found increased expression of miR-218 in the ESCC tissues compared with that in the matched non-tumor tissues, and its expression level was correlated with key pathological characteristics including clinical stage, tumor depth and metastasis. We also found that enforced expression of miR-218 significantly decreased cell proliferation, colony formation, migration and invasion, induced cell apoptosis and arrested the cell cycle in the G0/G1 phase, as well as suppressed tumor growth in a nude mouse model. In addition, our results showed that miR-218 mimics increased the sensitivity to the antitumor effect of CDDP in the human Eca109 cells. Importantly, this study also showed that miR-218 regulated the expression of phosphorylated PI3K, AKT and mTOR, which may contribute to suppressed tumor growth of ESCC and enhanced sensitivity of ESCC cells. These findings suggest that miR-218 is a potential therapeutic agent for the treatment of ESCC.

Hyperbaric oxygen treatment at various stages following chronic constriction injury produces different antinociceptive effects via regulation of P2X4R expression and apoptosis.

PURPOSE: The aims of this study were to investigate the effect of hyperbaric oxygen (HBO) treatment at various stages following chronic constriction injury (CCI) and to explore the underlying mechanisms of HBO treatment. METHODS: Forty adult male Sprague-Dawley rats were randomly assigned to five groups (n = 8 for each group): the sham group, CCI group, HBO1 group, HBO2 group, and HBO3 group. Neuropathic pain was induced by CCI of the sciatic nerve. HBO treatment began on postoperative days 1, 6, and 11 and continued for 5 days. The mechanical withdrawal threshold and thermal withdrawal latency were tested on preoperative day 3 and postoperative days 1, 3, 5, 7, 10, 14, and 21. The expression of P2X4R was determined by immunohistochemistry and western blot analysis. Cell apoptosis was measured using TUNEL staining. The expression of caspase 3 was measured using reverse transcription polymerase chain reaction (RT-PCR). Electron microscopy was used to determine the ultrastructural changes. RESULTS: Early HBO treatment beginning on postoperative day 1 produced a persistent antinociceptive effect and inhibited the CCI-induced increase in the expression of P2X4R without changing CCI-induced apoptosis. In contrast, late HBO treatment beginning on postoperative day 11 produced a persistent antinociceptive effect and inhibited CCI-induced apoptosis and upregulation of caspase-3 without changing the expression of P2X4R. In addition, late HBO treatment reduced CCI-induced ultrastructural damage. However, HBO treatment beginning on postoperative day 6 produced a transient antinociceptive effect without changing the expression of P2X4R or CCI-induced apoptosis. CONCLUSION: HBO treatment at various stages following CCI can produce antinociceptive effects via different mechanisms. Early HBO treatment is associated with inhibition of P2X4R expression, and late HBO treatment is associated with inhibition of cell apoptosis.