[Neonatal skin care in tertiary Neonatal Intensive Care Units in Hungary]. / Borápolási gyakorlat a Neonatális Intenzív Centrumokban Magyarországon.

INTRODUCTION: Skin physiology of neonates and preterm infants and evidence-based skin care are not well explored for health care providers. AIM: The aim of our present study was to investigate the skin care methods of the tertiary Neonatal Intensive Care Units in Hungary. METHOD: A standardized questionnaire was distributed among the 22 tertiary Neonatal Intensive Care Units with questions regarding skin care methods, bathing, emollition, skin disinfection, umbilical cord care, treatment of diaper dermatitis, and use of adhesive tapes. RESULTS: The skin care methods of the centres were similar in several aspects, but there were significant differences between the applied skin care and disinfectant products. CONCLUSIONS: The results of this survey facilitate the establishment of a standardized skin care protocol for tertiary Neonatal Intensive Care Units with the cooperation of dermatologists, neonatologists and pharmacists.

Elevated morphine concentrations in neonates treated with morphine and prolonged hypothermia for hypoxic ischemic encephalopathy.

OBJECTIVES: Asphyxia and hypothermia may modify drug pharmacokinetics. We investigated whether analgesia with morphine in neonates with hypoxic ischemic encephalopathy undergoing prolonged moderate systemic hypothermia resulted in elevated serum morphine concentrations compared with normothermic infants. PATIENTS AND METHODS: Infants from 1 center participating in a multicenter randomized study of moderate whole-body hypothermia after perinatal asphyxia (the Total Body Hypothermia Study) were randomly selected for treatment with hypothermia (n = 10) or for standard care on normothermia (n = 6). Hypothermia (33 degrees C to 34 degrees C) was started before 6 hours of age and maintained for 72 hours. All of the infants were treated with a continuous infusion of morphine-hydrochloride, with the rate adjusted according to clinical status. Serum morphine concentrations were determined at 6, 12, 24, 48, and 72 hours after birth. RESULTS: Serum morphine concentrations at 24 to 72 hours after birth were (median [range]) 292 ng/mL (137-767 ng/mL) in the hypothermia-treated infants and 206 ng/mL (88-327 ng/mL) in the infants on normothermia, despite similar morphine infusion rates and cumulative doses. Morphine concentrations correlated with morphine infusion rate, cumulative dose, and treatment with hypothermia. Serum morphine concentrations reached a steady state after 24 hours in the normothermic infants but continued to increase throughout the assessment period in the hypothermia group. Morphine clearance was low in both groups: (median [range]) morphine clearance estimated from area under the curve was 0.69 mL/min per kg (0.58-1.21 mL/min per kg) in hypothermic group and 0.89 mL/min per kg (0.65-1.33 mL/min per kg) in infants on normothermia. Serum morphine concentrations >300 nL/mL occurred more often in the hypothermia group and when the morphine infusion rate was >10 microg/kg per h. CONCLUSIONS: Infants with hypoxic ischemic encephalopathy have reduced morphine clearance and elevated serum morphine concentrations when morphine infusion rates are based on clinical state. Potentially toxic serum concentrations of morphine may occur with moderate hypothermia and infusion rates >10 microg/kg per h.

Changes in laboratory parameters indicating cell necrosis and organ dysfunction in asphyxiated neonates on moderate systemic hypothermia.

AIM: Asphyxia is a major cause of morbidity and mortality in term infants. In addition to cerebral injury other organs are also distressed due to hypoxic-ischaemic insult. Systemic hypothermia has a beneficial effect on brain injury. We tested the impact of hypothermia on hypoxic damage of other internal organs. METHODS: Asphyxiated term neonates (n = 21) were randomised to groups treated with hypothermia (n = 12) and normothermia (n = 9). Hypothermia (33-34 degrees C) was initiated within 6 h of life, and maintained for 72 h. We determined serum transaminase, lactate dehydrogenase, creatine kinase, uric acid, creatinine levels and diuresis during 6, 24, 48 and 72 postnatal hours. RESULTS: Area under curve values of aspartate aminotransferase (ASAT), lactate dehydrogenase (LDH), uric acid and creatinine during the investigated period and alanine aminotransferase (ALAT) value at 72 h were lower in neonates on hypothermia than in those on normothermia. Renal failure and liver impairment affected less hypothermic than normothermic neonates (3/12 vs. 7/9, p = 0.03, 3/12 vs. 6/9 p = 0.08, respectively). Four of the 12 hypothermic and 6 of the 9 normothermic neonates developed multiorgan failure. CONCLUSIONS: These results suggest that systemic hypothermia may protect against cell necrosis and tissue dysfunction of internal organs after neonatal asphyxia.

[Whole body hypothermia for the treatment of hypoxic-ischaemic encephalopathy in term infants--a safety study in Hungary]. / A hypoxiás-ischaemiás encephalopathia kezelése mérsékelt, teljestest-hypothermia alkalmazásával érett újszülöttekben--biztonságossági vizsgálat Magyarországon.

UNLABELLED: Hypoxic-ischaemic encephalopathy is a major cause of long-term morbidity and mortality in term infants. Prolonged systemic hypothermia is a promising new approach for reducing brain damage in neonates. OBJECTIVE: The aim of the open cohort-series clinical study was to collect data about the safety and technical feasibility of the hypothermia treatment in Hungary before joining to a randomised efficacy trial. METHODS: The authors treated 28 asphyxiated term neonates with hypothermia between 2003 and 2005. Hypothermia (rectal temperature 33-34 degrees C) was maintained for 72 hours during continuous morphine analgesia. For historical control group 23 asphyxiated neonates were selected treated with standard therapy between 1996 and 2002. Entry criteria were the following: a 5-minute Apgar score 5 or less, the evidence of serious metabolic acidosis in the first hour of life (a BE of 15 mmol/l) and clinical sign of encephalopathy at the same time. Routine laboratory measurements of liver enzymes, renal functions, blood cell count, head ultrasound were performed daily. RESULTS: The anthropometric and clinical parameters (Apgar, pH, BE, neurological signs of encephalopathy) of the hypothermia and control infants were similar. There were no significant differences between the mortality of the hypothermia (10/28 36%) and the control (10/21 48%) groups. The clinical parameters (laboratory values, abnormality on the head ultrasound, incidence of serious hypotension, hypoglycaemia, bleeding, need for cardiovascular support, oliguria) and the neurological outcome after 1.5-2 year follow-up were also similar. CONCLUSIONS: This study demonstrated that prolonged whole body hypothermia of the asphyxiated neonate is safe and not associated with increased mortality and morbidity up to 18 month of age.

[Osteopenia of prematurity]. / Koraszülöttek osteopeniája.

The survival rate of premature infants has been significantly increased during the last decades. As a consequence, the problem of less imminent, slowly progressing, but also important disorders such as osteopenia of prematurity has been emerging. The diagnosis of osteopenia of prematurity is based evidence for less bone mineral density compared to fetuses or infants at the same gestational age in the absence of laboratory parameters and/or clinical signs for rachitis or other metabolic bone disease. The incidence of osteopenia among infants born before 28 weeks of gestational age are as high as 30%. The aim of this paper is to review the information regarding the prevention and treatment of osteopenia of prematurity and to summarize the preventive measures to avoid fractures or bone deformations and to achieve the genetically determined peak bone mass. The latter is essential for the prevention of osteoporosis in adulthood, a significant problem of public health.

Angiotensin II type 1 receptor A1166C polymorphism and prophylactic indomethacin treatment induced ductus arteriosus closure in very low birth weight neonates.

Altered pulmonary vascular resistance might be a factor for delayed closure of the ductus arteriosus (DA) in preterm infants. Angiotensin II plays a central role in the elevation of pulmonary vascular resistance. Angiotensin II exerts its vasoconstrictor effect on the angiotensin II type 1 receptor (AT1R). Homozygous carriers of the AT1R A1166C genetic variant present an exaggerated vasoconstrictor response to angiotensin II. We have investigated whether the presence of AT1R CC1166 influences the effect of prophylactic indomethacin treatment on the closure of DA until the fifth postnatal day in preterm infants. In this retrospective study detailed medical history of the first postnatal week was obtained in 159 infants born before the 33rd gestational week. All were treated by prophylactic indomethacin to induce permanent closure of the DA. On the sixth postnatal day the DA was still open in 56, whereas it was permanently closed in 103. The AT1R A1166C genotype of the infants was determined from Guthrie spots. Stepwise binary logistic regression analysis was used to assess the effect of medical conditions and genotype on the risk of patent DA (PDA). Birth weight, infantile respiratory distress, and severe hypotension were independent risk factors for PDA (p < 0.01, p < 0.05, p < 0.05, respectively). The carrier state of AT1R CC1166 was protective against PDA (p < 0.05; odds ratio, 0.067). AT1R AC1166 genotype was not associated with PDA. Our results indicate that the risk of PDA might be lower in infants of AT1R CC1166 than in those with AC or AA genotypes.