The effects of intranasal dexmedetomidine premedication in children: a systematic review and meta-analysis

Purpose

Intranasal dexmedetomidine premedication is a newly introduced method for reducing stress and anxiety before general anesthesia in children. We performed a meta-analysis to identify the effects of intranasal dexmedetomidine premedication in children.

Source

We conducted a systematic review to find published randomized-controlled trials using intranasal dexmedetomidine as premedication. We searched databases in EMBASE?, MEDLINE®, and the Cochrane Controlled Trials Register using the Ovid platform. This study was conducted based on the Cochrane Review Methods.

Principal findings

This review included 1,168 participants in 13 studies. Intranasal dexmedetomidine premedication provided more satisfactory sedation at parent separation (relative risk [RR], 1.45; 95% confidence interval [CI], 1.19 to 1.76; P = 0.0002; I² = 80%) than other premedication regimes. In addition, it reduced the need for rescue analgesics (RR, 0.58; 95% CI, 0.40 to 0.83; P = 0.003; I² = 0%). Nevertheless, there were no differences in sedation at mask induction (RR, 1.25; 95% CI, 0.98 to 1.59; P = 0.08; I² =71%) or in the incidence of emergence delirium (RR, 0.52; 95% CI, 0.24 to 1.13; P = 0.10; I² = 67%). Intranasal dexmedetomidine was associated with a significantly lower incidence of nasal irritation (RR, 0.05; 95% CI, 0.01 to 0.36; P = 0.003; I² = 0%) and postoperative nausea and vomiting (RR, 0.63; 95% CI, 0.40 to 0.99; P = 0.04; I² = 0%) than other premedication treatments. It also showed significantly lower systolic blood pressure (weighted mean difference [WMD], ?6.7 mmHg; 95% CI, ?10.5 to ?2.9; P = 0.0006; I² = 96%) and heart rate (WMD, ?6.8 beats·min^?1; 95% CI, ?11.3 to ?2.6; P = 0.002; I² = 98%).

Conclusions

Intranasal dexmedetomidine provided more satisfactory sedation at parent separation and reduced the need for rescue analgesics and the incidence of nasal irritation and postoperative nausea and vomiting when compared with other premedication treatments.

     

Expression of Vimentin and Cytokeratin in Eutopic and Ectopic Endometrium of Women with Adenomyosis and Ovarian Endometrioma

PROBLEM: To determine the expression of vimentin and cytokeratin in eutopic and ectopic endometrium of women with both adenomyosis and ovarian endometrioma and to evaluate their cyclic changes during the menstrual cycle. METHOD OF STUDY: Twenty patients requiring hysterectomy with salpingo-oophorectomy were studied by immunohistochemistry according to their menstrual cycles. RESULTS: Cyclic expression of vimentin was noted in eutopic endometrium and adenomyosis, but not in endometrioma. Cytokeratin expression did not change during the menstrual cycles. The mean intensities of epithelial vimentin were significantly different from each other, being the lowest in endometrioma, intermediate in adenomyosis, and the highest in eutopic endometrium. There was no significant difference in intensities of cytokeratin between adenomyosis and endometrioma, but these intensities were significantly lower than that of eutopic endometrium. CONCLUSIONS: Lower intensities of cytokeratin in adenomyosis and endometrioma than in eutopic endometrium suggest that the ectopic endometria may have a lower degree of differentiation regardless of the site. The lower intensity of epithelial vimentin in endometrioma than in adenomyosis during the proliferative phase may reflect decreased functional activity, probably because of a pressure effect on the lining epithelium within the endometrioma.     

Role of p38 MAPK and pro-inflammatory cytokines expression in glutamate-induced neuronal death of neonatal rats

Pro-inflammatory cytokines TNF-, IL-1β and IL-6 rises significantly during neuronal damage and activate the signaling p38 MAPK pathway, which is involved in the apoptotic (AP) neuronal death. Systemic administration of glutamate as monosodium salt (MSG) to newborn animals induces neuronal death, however whether neurons die by AP or necrosis through MAPK p38 pathway activation it is unknown. In this study, TNF-, IL-1β and IL-6 expression levels, AP neuronal death and cellular type that produces TNF- was also identified in the cerebral cortex (CC) and striatum (St) of rats at 8, 10, and 14 days of age after neonatal exposure to MSG. TNF- production and AP neuronal death was significantly increased in the CC at PD8–10, and in the St in all ages studied by excitotoxicity effect induced with MSG. This effect was completely inhibited by SB203580 (p38 inhibitor) in both regions studied. TNF-, IL-1β and IL-6 RNAm increased after MSG administration, whereas SB203580 did not modify their expression. These data indicates that neuronal death induced by excitotoxicity appears to be mediated through p38 signaling pathway activated by TNF- and their inhibition may have an important neuroprotective role as part of anti-inflammatory therapeutic strategy.     

Reduction of Squalene Epoxidase by Cholesterol Accumulation Accelerates Colorectal Cancer Progression and Metastasis

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Plasma adiponectin level and sleep structures in children with Prader–Willi syndrome

Adiponectin, an adipose tissue-derived hormone, has been negatively related to obstructive sleep apnea syndrome. Besides sleep apnea, children with Prader–Willi syndrome (PWS) may have excessive daytime sleepiness and rapid eye movement (REM) sleep abnormality. The aim of this study is to determine whether changes in sleep structures are related to plasma adiponectin levels in PWS. Correlations between adiponectin level and sleep variables were analyzed in 28 children with PWS and 18 controls. Overnight polysomnography was performed. The fasting plasma adiponectin levels were higher in the children with PWS than in the controls ( P  =   0.0006). In the PWS, Epworth sleepiness scale was significantly higher ( P  =   0.002); sleep latency ( P  =   0.003) and REM latency ( P  =   0.001) were significantly shortened; the apnea–hypopnea index (AHI) was significantly increased ( P  =   0.0001); and the duration of non-rapid eye movement (NREM) sleep stages 3 and 4 was decreased ( P  =   0.005). Multiple regression analysis revealed correlations between the adiponectin level and the total sleep time ( β  = 0.688, P  =   0.009), AHI ( β  = 1.274, P  =   0.010), REM latency ( β  = −0.637, P  =   0.021) and the percentage of NREM sleep ( β  = −7.648, P  =   0.002) in PWS. In children with PWS, higher plasma adiponectin levels were independently associated with several sleep variables, which was not observed in the control group. These results suggest a potential influence of elevated adiponectin level on the sleep structures in PWS.     

Effects of melatonin on the Harderian gland of lipopolysaccharide-treated rats: morphological observations.

Melatonin is a free radical scavenger and antioxidant. This indol is reported to efficiently scavenge both hydroxyl and peroxyl radicals and it also reduces both in vitro and in vivo tissue damage due to oxidants which generate oxygen toxic radicals. Lipopolysaccharide (LPS) administration induces oxidative damage in various tissues mainly due to its ability to increase reactive oxygen species. In the present work, we studied the morphological changes and lipid peroxidation in the Harderian gland after LPS administration and the effects of melatonin in preventing the induced changes. Hyperchromasia, vesicular degeneration, necrosis and infiltration with macrophages, monocytes and neutrophils were observed in the LPS-treated group (10 mg/kg, intraperitonally [i.p.]). Also, a typical structure of the glandular acini of the gland exhibited diffuse damage. In the LPS rats treated with melatonin (10 mg/kg, i.p.), a diminished number of infiltrative cells was seen, and cloudy swelling was reduced, as was nuclear hyperchromasia. Neither necrosis nor vesicular degeneration were noted in the melatonin-treated rats, and in general, glandular structure was preserved. Lipid peroxidation products increased significantly within six hours after LPS administration, and melatonin treatment decreased the LPS-dependent lipid peroxidation products. These data together suggest that melatonin protects the Harderian gland against LPS toxicity in terms of morphological damage.     

Clinical study using novel endoscopic system for measuring size of gastrointestinal lesion

AIM:To verify the performance of a lesion size measurement system through a clinical study.METHODS:Our proposed system,which consists of a conventional endoscope,an optical device,an optical probe,and a personal computer,generates a grid scale to measure the lesion size from an endoscopic image.The width of the grid scale is constantly adjusted according to the distance between the tip of the endoscope and lesion because the lesion size on an endoscopic image changes according to the distance.The shape of the grid scale was corrected to match the distortion of the endoscopic image.The distance was calculated using the amount of laser light reflected from the lesion through an optical probe inserted into the instrument channel of the endoscope.The endoscopist can thus measure the lesion size without contact by comparing the lesion with the size of the grid scale on the endoscopic image.(1)A basic test was performed to verify the relationship between the measurement error eM and the tilt angle of the endoscope;and(2)The sizes of three colon polyps were measured using our system during endoscopy.These sizes were immediately measured by scale after their removal.RESULTS:There was no error atα=0°.In addition,the values of eM(mean±SD)were 0.24±0.11 mm(α=10°),0.90±0.58 mm(α=20°)and 2.31±1.41mm(α=30°).According to these results,our system has been confirmed to measure accurately when the tilt angle is less than 20°.The measurement error was approximately 1 mm in the clinical study.Therefore,it was concluded that our proposed measurement system was also effective in clinical examinations.CONCLUSION:By combining simple optical equipment with a conventional endoscope,a quick and accurate system for measuring lesion size was established.     

Trichoblastoma in a Child

Abstract:   A trichoblastoma is a benign adnexal neoplasm composed of follicular germinative cells. It most commonly presents as a solitary nodule on the scalp, face, or perineum and occurs equally in males and females. It is diagnosed most commonly between the fourth and the sixth decades, and it is extremely rare in childhood. To our knowledge there is no prior case report of a primary trichoblastoma occurring outside the setting of a nevus sebaceous of Jadassohn in a child before adolescence. Herein we report a case of trichoblastoma of the right cheek in an 11-year-old Korean girl.