Hacer Yapıcıoğlu

Pseudomonas aeruginosa infections due to electronic faucets in a neonatal intensive care unit.

Aim:  To evaluate the role of electronic faucets in a newborn intensive care unit during a Pseudomonas aeruginosa outbreak.

Growth hormone and insulin‐like growth factor 1 levels and their relation to survival in children with bacterial sepsis and septic shock

Objectives:  Despite improved supportive care, the mortality of sepsis and septic shock is still high. Multiple changes in the neuroendocrine systems, at least in part, are responsible for the high morbidity and mortality. A reduced circulating level of insulin‐like growth factor and an elevated level of growth hormone are the reported characteristic findings early in the course of sepsis and septic shock in adults. The aim of this study was to evaluate the changes of growth hormone/insulin‐like growth factor 1 axis in sepsis and septic shock and investigate the relationship between these hormones and survival.

Sonographic measurements of the liver, spleen and kidney dimensions in the healthy term and preterm newborns

This study was conducted in order to assess normal liver, spleen and kidney dimensions in premature and term newborns and determine the acceptable range. A total of 253 (99 preterm and 154 term) healthy newborns were evaluated within the first week of life by sonography. Gestational age ranged from 24 to 41 weeks, weight ranged from 638 to 4800 g. Measurements were compared with gestational age, weight and height of the infants. Normal ranges for kidney, liver and spleen measurements according to gestational age and weight were obtained. We found that weight showed the best correlation with any one of the mentioned organ dimensions.

The use of surfactant in children with acute respiratory distress syndrome: efficacy in terms of oxygenation, ventilation and mortality

PURPOSE The aim of this prospectively designed study was to investigate the efficacy of surfactant (S) for acute respiratory distress syndrome (ARDS) in children. MATERIALS AND METHODS Children with ARDS were included in this study. Surfactant (Survanta, Abbott, USA) was given intratracheally at a dose of 150 mg/kg every 12 h for a total of two doses. During the study period none of the patients received permissive hypercapnia, high frequency ventilation, nitric oxide or ECMO. Peak inspiratory pressure (PIP), positive end expiratory pressure (PEEP), ventilation rate, mean airway pressure, tidal volume (TV), Murray index, PaO2/FiO2, ventilation index (VI), oxygen index (OI) and arterial oxygen tension difference (A-aDO2) were measured before and 48 h after surfactant treatment. Duration of mechanical ventilation therapy, duration in paediatric intensive care unit (PICU) and mortality rate were recorded. RESULTS Among the 36 children who met the inclusion criteria, 12 were treated with surfactant. The mean age was 72.5+/-56.2 months; 47% of children were male. Infants were ventilated by pressure-controlled ventilators whereas for older children volume-controlled ventilators were used. Sepsis (42%) was the main predisposing factor followed by pneumonia (25%) and malignancy (17%). The baseline characteristics including age, predisposing factors, gender, PIP, PEEP, A-aDO2, PaO2/FiO2, OI, TV, VI and Murray index were similar in the surfactant and non-surfactant (NS) group (p>0.05). There were significant improvements in PIP, PEEP, A-aDO2, PaO2/FiO2, OI, TV, VI and Murray index in the surfactant group after surfactant treatment compared with NS group (p<0.05). Duration of PICU stay and ventilator treatment was longer in NS group (14+/-3.7, 1.8+/-3.2 days vs. 9.2+/-3.1, 8.6+/-1.9 days), (p<0.05). Mortality rate was 42% in surfactant compared with 63% in the NS group, (p>0.05). Children in the surfactant group lived significantly longer (p<0.05). CONCLUSIONS Modified natural surfactant is an effective treatment option in children with ARDS for improving gas exchange, decreasing the use of ventilatory support and increasing survival time.

The effects of indomethacin on caspases, glutathione level and lipid peroxidation in the newborn rats with hypoxic-ischemic cerebral injury

Activation of phospholipase A(2), degradation of membrane phospholipids resulting in tissue accumulation of arachidonic acid, and the activation of cyclooxygenase that leads to the formation of prostaglandin and free radicals may occur after hypoxic-ischemic damage. The aim of this study was to investigate the effects of indomethacin, a nonselective cyclooxygenase inhibitor, on caspase activity, glutathione levels and lipid peroxidation in newborn rats with hypoxic-ischemic encephalopathy. The effects of indomethacin were evaluated by measuring caspase-3 and caspase-8 activities and glutathione levels. Lipid peroxidation was evaluated by measuring concentrations of malondialdehyde in rat brains. Seven-day-old rat pups with the Levine-Rice model of hypoxic-ischemic cerebral injury were randomly divided into three study groups. In the indomethacin-treated group, rats were administered three doses of indomethacin, at a dose of 2 mg/kg every 12 h. Sham and the hypoxic-ischemic group of rats were given physiologic saline. The sham group underwent all surgical procedures except for arterial ligation. After 72 hours, the rats were decapitated and brain tissues were evaluated. Caspase-3 and caspase-8 activities and glutathione and malondialdehyde levels were evaluated in all groups. There was an obvious decrease in caspase-3 and caspase-8 activities and depleted glutathione levels were reversed in the indomethacin-treated group compared to the hypoxic-ischemia group (p<0.001). As indomethacin was unable to prevent lipid peroxidation, malondialdehyde concentrations increased to ischemia-induced levels. In conclusion, indomethacin administration after hypoxic-ischemic encephalopathy injury has a neuroprotective effect since it inhibits caspase activity and reverses the depletion of glutathione. However, it also aggravates lipid peroxidation-induced ischemia.

Intraventricular streptokinase for the treatment of posthaemorrhagic hydrocephalus of preterm.

Posthaemorrhagic hydrocephalus following intraventricular haemorrhage is still one of the most serious complications of premature birth. Small premature babies are not suitable for shunt surgery because of high cerebrospinal fluid protein and risk of obstruction. For this reason there is a great need for alternative approaches for treatment of posthaemorrhagic hydrocephalus. The objective of this study was to investigate if intraventricular streptokinase treatment reduces the need for ventriculoperitoneal shunt in posthaemorrhagic hydrocephalus. A case-control trial was carried out in 12 premature babies with posthaemorrhagic hydrocephalus. Six of them were treated with intraventricular streptokinase and 6 premature babies were in the control group. While 5 babies in the study group needed ventriculoperitoneal shunt, 3 of the control patients needed shunt surgery. There were no rebleeding, ventriculitis or meningitis in either groups. In conclusion on the basis of our results we do not recommend routine use of intraventricular streptokinase in posthaemorrhagic hydrocephalus.

Healthcare-associated infections in a neonatal intensive care unit in Turkey in 2008: incidence and risk factors, a prospective study.

In this study, we have prospectively recorded healthcare-associated infections (HAIs) in NICU and found incidence density as 18 infections per 1000 patient days. Of the infections, 51.3% was bacteriemia (BSI), and 45.1% was ventilator-associated pneumonia (VAP). Gram-negative microorganisms were predominant in VAP and Staphylococcus epidermidis was the leading microorganism (53.0% of BSIs) in BSIs. Multivariate logistic regression analysis showed the importance of hood O(2) use in days (RR: 1.3) and total parenteral nutrition use in days (RR: 1.09) for BSIs. Umbilical arterial catheterization in days (RR: 1.94), ventilator use in days (RR: 1.05), chest tube (RR: 12.55), orogastric feeding (RR: 3.32) and total parenteral nutrition in days (RR: 1.05) were found to be significantly associated with VAP. In conclusion, incidence density in our unit is high and Gram-negative rods are predominant similar to developing countries. These results strongly suggest improving measures of prevention and control of HAIs in the unit.

A 6-year prospective surveillance of healthcare-associated infections in a neonatal intensive care unit from southern part of Turkey

Aim:  To report the incidence of healthcare‐associated infections (HAIs), site of infection and bacterial epidemiology in the Neonatal Intensive Care Unit in a university hospital in Adana, Turkey, between 2001 and 2006.

Barttin mutations in antenatal Bartter syndrome with sensorineural deafness

Case 1 The male patient had been born at 30 weeks of gestation (weight 1,360 g) to consanguineous parents. Pregnancy was complicated by severe polyhydramnios. Findings at his physical examination were normal except for a triangular face, large eyes, protruding ears, tachypnea and retractions. He rapidly developed renal salt wasting, hyper-reninemic hyperaldosteronism, hypokalemic metabolic alkalosis, and impaired renal function [creatinine (Crea) 1.5 mg/dl]. The diagnosis of antenatal Bartter syndrome (aBS) was suspected. On day 49 oral administration of indomethacin was started (2–3 mg/kg per day), which could not help to regulate serum potassium levels. Instead, upon indomethacin treatment, renal function further deteriorated (Crea 2.5 mg/dl). Therefore, indomethacin was stopped, and he was treated with spironolactone. Potassium need declined to 27 mEq/kg, and he was discharged after 140 days. He has unilateral sensorineural deafness detected by impaired brain stem evoked potentials and growth retardation. A homozygous mutation in the Barttin gene (BSND) leading to a loss of start codon was detected (Table 1). A similar mutation has been previously described [1].

Serum Insulin-Like Growth Factor 1 and Growth Hormone Levels of Hypoxic-Ischemic Newborns

A number of growth factors, their binding proteins, and their receptors have been shown to be induced in the hypoxic-ischemic (HI) brain. In this prospective study, we aimed at determining the levels of insulin-like growth factor 1 (IGF-1), growth hormone (GH), and cortisol in HI babies and at identifying whether they differ from the levels of control infants. The serum IGF-1 levels were measured after the first 12–24 h of life, and the measurements were repeated on the 5th and 10th days of life for babies with HI encephalopathy (n = 18) and on the 10th day of life for controls (n = 19). Blood samples for measurement of cortisol and GH from both HI and control groups were collected after the first 12–24 h of life. There were 11 babies in the mild-to-moderate (stages I and II) group and 7 babies in the severe (stage III) group according to Sarnat and Sarnat. The IGF-1 levels of the HI group measured after 12–24 h [78.5 ± 27.9 (range 9–123.4) ng/ml] and on the 10th day [72.2 ± 36.8 (range 29.7–159.2) ng/ml] of life were statistically significantly lower than the IGF-1 levels of the control group [121.5 ± 50.4 (range 74.4–280.5) ng/ml and 133.1 ± 34.4 (range 65.9–202) ng/ml, respectively] (p = 0.002 and p = 0.001, respectively). But there was no statistically significant difference between mild-to-moderate HI group and severe HI group in terms of IGF-1 levels after 12–24 h and 5 and 10 days of life (p > 0.05). Also there was no statistically significant difference in IGF-1 values after the first 12–24 h and after 10 days of life between HI subjects who died or survived (p > 0.05). The GH levels of the HI group after the first 12–24 h of life [34.6 ± 32.3 (range 0.1–120) mIU/l] were statistically significantly higher than those in the control group [10.4 ± 4.5 (range 3.7–16.9) mIU/l] (p = 0.005). There was no statistically significant difference in the serum cortisol levels between HI and control groups after the first 12–24 h of life [18.7 ± 17.0 (range 1.6–65.1) µg/dl vs. 10.8 ± 5.4 (range 3.0–23.2) µg/dl] (p > 0.05). No statistically significant correlation was found between IGF-1 levels and GH and cortisol levels of the HI encephalopathy group [r = –0.113 (p > 0.05) and r = 0.108 (p > 0.05), respectively]. In conclusion, this study showed decreased levels of serum IGF-1 and increased levels of GH which may be secondary to serum IGF-1 influx from the circulation to the brain as a protective mechanism or may be due to some cytokines which alter the GH/IGF axis, inhibit the action of IGF-1, and stimulate IGF-binding protein 1.