Control of an Acinetobacter [corrected] baumannii outbreak in a neonatal ICU without suspension of service: a devastating outbreak in Diyarbakir, Turkey.

BACKGROUND: A nosocomial outbreak of Acinetobacter baumannii bloodstream infections (Ab-BSI) was identified in Diyarbakir Children's Hospital's (Diyarbakir, Turkey) 60-bed Neonatal Intensive Care Unit (NICU) in 2006 and 2007. METHODS: The investigation and control of the outbreak were based on case-control and epidemiological studies as well as multifaceted interventions. Sixty-four neonates (case patients) with Ab-BSI and 128 neonates (control patients) free of Ab-BSI, who had been hospitalized at the unit during the outbreak period, were included in the study. Case and control patients were compared for possible predisposing factors (e.g., gender, length of NICU stay, antibiotic use, intubation, etc.). An intervention program (cohorting, education, reinforcing hand hygiene, antibiotic restriction, improving processes of patient care, environmental cleaning, and barrier isolation) was implemented to control the outbreak. Surveillance cultures were collected from all possible sources, and the epidemiological investigation was supplemented by a pulsed field gel electrophoresis (PFGE) study. RESULTS: Fifty-three neonates (82.8%) died in the case group and 51 (39.8%) in the control group (P < 0.001). The duration of stay at the NICU [odds ratio (OR) 1.15; 95% confidence interval (CI) 1.07-1.23; P < 0.001] and re-intubation (OR 38.62; CI 12.66-117.87; P < 0.001) were found to be significant risk factors for Ab-BSI. Surveillance cultures showed a heavy contamination in the NICU, and the outbreak ended after a series multifaceted interventions. All A. baumannii isolates, both from the cases and environmental samples, had an identical PFGE fingerprint pattern. CONCLUSION: The control of Ab-BSI requires a multifaceted intervention program and complex efforts and implementations, especially if the ICU does not implement any suspension of care provision.

Renal function in children with sickle cell anemia.

BACKGROUND: Patients with sickle cell anemia have various forms of renal dysfunction. SUBJECTS, MATERIALS AND METHODS: The purpose of this study is to demonstrate the abnormalities of HbSS patients' renal function in childhood. Renal function studies were performed in 55 patients with homozygote sickle cell anemia and compared with 13 healthy children. The blood and timed urine samples were obtained for hematological and biochemical determinations. RESULTS: Mean serum creatinine, sodium, phosphorus and calcium levels were not statistically different between patients and controls. Mean serum potassium and uric acid levels were significantly higher in patients than in controls. Mean tubular phosphate reabsorption (p < 0.001) and fractional excretion of potassium (p < 0.05) were lower in patients than in the control. There were no significant differences in fractional excretion of sodium and uric acid between patients and controls. Patients had significantly higher urine pH and significantly lower specific gravity and osmolality than controls. Also, there were no significant differences in urinary protein/ creatinine, urinary N-acetyl-beta-D-glucosaminidase/creatinine and urinary malondialdehyde/creatinine between patients and controls. CONCLUSION: Thus, significant proximal tubular dysfunction is not a common feature but distal tubular abnormality is the most consistent renal functional derangement of patients with SCA in childhood.

Renal function in pediatric patients with beta-thalassemia major.

In patients with beta-thalassemia major, the most important cause of mortality and morbidity is organ failure due to deposits of iron. In this study, the nature of the kidney injury and possible pathogenetic factors were investigated. Seventy children with beta-thalassemia major and 14 age and sex-matched healthy children were involved in the study. Blood and timed urine samples were obtained for hematological and biochemical tests. The mean values of blood urea nitrogen (BUN), serum creatinine, creatinine clearance, serum sodium, urine osmolality, fractional excretion of sodium, potassium, and uric acid were not statistically different between the groups. Serum levels of potassium, phosphorus, and uric acid and the urine volume, high urinary protein to creatinine (UP/Cr), urinary N-acetyl-beta-D-glucosaminidase to creatinine (UNAG/Cr), and urinary malondialdehyde to creatinine, (UMDA/Cr) and the tubular phosphate reabsorption (TRP) values were statistically different between two groups (P<0.05). Increased serum levels of potassium, phosphorus, and uric acid in the patient group were attributed to the rapid erythrocyte turnover. The presence of high UP/cr, UNAG/Cr and UMDA/Cr ratios shows that in these patients with proximal renal tubular damage may be secondary to oxidative lipid peroxidation mediated by the iron overload.