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Aim: To determine the incidence of post-phototherapy neonatal plasma total bilirubin (PTB) rebound. Methods: A prospective clinical survey was performed on 226 term and near-term neonates treated with phototherapy in the well baby nursery of the Shaare Zedek Medical Center from January 2001 to September 2002. Neonates were tested for PTB 24 hours (between 12 and 36 hours) after discontinuation of phototherapy, with additional testing as clinically indicated. The main outcome measure, significant bilirubin rebound, was defined as a post-phototherapy PTB >256 mmol/l. Phototherapy was not reinstituted in all cases of rebound, but rather according to clinical indications. Results: A total of 30 (13.3%) neonates developed significant rebound (mean (SD) PTB 287 (27) mmol/l, upper range 351 mmol/l). Twenty two of these (73%) were retreated with phototherapy at mean PTB 296 (29) mmol/l. Multiple logistic regression analysis showed significant risk for aetiological risk factors including positive direct Coombs test (odds ratio 2.44, 95% CI 1.25 to 4.74) and gestational age ,37 weeks (odds ratio 3.21, 95% CI 1.29 to 7.96). A greater number of neonates rebounded among those in whom phototherapy was commenced (72 hours (26/152, 17%) compared with .72 hours (4/74, 5.4%) (odds ratio 3.61, 95% CI 1.21 to 10.77). Conclusion: Post-phototherapy neonatal bilirubin rebound to clinically significant levels may occur, especially in cases of prematurity, direct Coombs test positivity, and those treated (72 hours. These risk factors should be taken into account when planning post-phototherapy follow up.

Objectives: Acute kidney injury in the critically ill pediatric population is associated with worse outcome. The aim of this study was to assess the prevalence, associated clinical variables, and outcomes of acute kidney injury in children admitted to the PICU with diabetic ketoacidosis. Design: Retrospective cohort. Setting: PICU of a tertiary, university affiliated, pediatric medical center. Patients: All children less than age 18 years with a primary diagnosis of diabetic ketoacidosis admitted to the PICU between November 2004 and October 2017. Interventions: None. Measurements and Main Results: Acute kidney injury was categorized into three stages using the Kidney Disease Improving Global Outcomes scale. Of the 82 children who met the inclusion criteria, 24 (30%) had acute kidney injury: 18 (75%) stage 1, five (21%) stage 2, and one (4%) stage 3. None needed renal replacement therapy. Compared with the patients without acute kidney injury, the acute kidney injury group was characterized by higher mean admission serum levels of sodium (143.25 ± 9 vs 138.6 ± 4.9 mmol/L; p = 0.0035), lactate (29.4 ± 17.1 vs 24.1 ± 10.8 mg/dL; p = 0.005), and glucose (652 ± 223 vs 542 ± 151 mg/dL; p = 0.01). There was no between-group difference in length of PICU stay (1.38 ± 0.7 vs 1.4 ± 0.7 d; p = 0.95) or hospitalization (6.1 ± 2.1 vs 5.8 ± 5.6 d; p = 0.45). Kidney injury was documented at discharge in four patients with acute kidney injury (16.7%), all stage 1; all had normal creatinine levels at the first clinical outpatient follow-up. All 82 patients with diabetic ketoacidosis survived. Conclusions: In this study, acute kidney injury was not uncommon in children with diabetic ketoacidosis hospitalized in the PICU. However, it was usually mild and not associated with longer hospitalization or residual kidney injury.

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