We investigated the hemodynamic and mortality effects of continuous ketamine infusion in critically ill pediatric patients. We conducted a retrospective cohort study in a tertiary pediatric intensive care unit (PICU). Patients who used continuous sedative from 2015 to 2017 for 24 hours or more were included. We compared blood pressure, heart and respiratory rates, vasogenic medications, and sedation and pain scores for 12 hours before and after initiation of continuous ketamine. The mortality rates for continuous ketamine and Non-ketamine groups were compared by multivariate logistic regression. A total of 240 patients used continuous sedation, and 82 used continuous ketamine. The median infusion rate of ketamine was 8.1 mcg/kg/min, and the median duration was 6 days. Heart rates (138 vs. 135 beat/minute, P = .033) and respiratory rates (31 vs. 25 respiration/minute, P = .001) decreased, but blood pressure (99.9 vs. 101.1 mm Hg, P = .124) and vasogenic medications did not change after ketamine infusion. Continuous ketamine was not a significant risk factor for mortality (hazard ratio 1.352, confidence interval 0.458–3.996). Continous ketamine could be used in PICU without hemodynamic instability. Further studies in randomized controlled design about the effects of continuous ketamine infusion on hemodynamic changes, sedation, and mortality are required.

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PurposeTo identify the effects of modified parenteral nutrition (PN) and enteral nutrition (EN) regimens on the growth of very low birth weight (VLBW) infants.MethodsThe study included VLBW infants weighing <1,500 g, admitted to Chungnam National University Hospital between October 2010 and April 2014, who were alive at the time of discharge. Subjects were divided according to 3 periods: period 1 (n=37); prior to the PN and EN regimen being modified, period 2 (n=50); following the PN-only regimen modification, period 3 (n=37); following both PN and EN regimen modification. The modified PN regimen provided 3 g/kg/day of protein and 1 g/kg/day of lipid on the first day of life. The modified EN regimen provided 3.5-4.5 g/kg/day of protein and 150 kcal/kg/day of energy. We investigated growth rate, anthropometric measurements at 40 weeks postconceptional age (PCA) and the incidence of extrauterine growth restriction (EUGR) at 40 weeks PCA.ResultsAcross the 3 periods, clinical characteristics, including gestational age, anthropometric measurements at birth, multiple births, sex, Apgar score, surfactant use and PDA treatment, were similar. Growth rates for weight and height, from time of full enteral feeding to 40 weeks PCA, were higher in period 3. Anthropometric measurements at 40 weeks PCA were greatest in period 3. Incidence of weight, height and head circumference EUGR at 40 weeks PCA decreased in period 3.ConclusionBeginning PN earlier, with a greater supply of protein and energy during PN and EN, is advantageous for postnatal growth in VLBW infants.

Abstract. KR-31378 is a newly developed K ATP -channel opener. To investigate the ability of KR-31378 to protect retinal ganglion cells (RGC), experiments were conducted using two retinal ischemia models. Retinal ischemia was induced by transient high intraocular pressure (IOP) for acute ischemia and by three episcleral vein occlusion for chronic retinal ischemia. KR-31378 was injected intraperitoneally and administered orally in the acute and chronic ischemia models, respectively. Under the condition of chronic ischemia, RGC density in the KR-31378-treated group was statistically higher than that in the non-treated group, and IOP was reduced. In the acute retinal ischemia model, 90% of RGC were degenerated after one week in non-treated retina, but, RGC in KR-31378-treated retina were protected from ischemic damage in a dosedependent manner and showed inhibited glial fibrillary acidic protein (GFAP) expression. Furthermore, the KR-31378 protective effect was inhibited by glibenclamide treatment in acute ischemia. These findings indicate that systemic KR-31378 treatment may protect against ischemic injury-induced ganglion cell loss in glaucoma.