To document trends and covariates of creatinemia (Scr) in extremely low birth weight (ELBW, < 1,000 g) neonates, maternal characteristics [betamethasone, premature preterm rupture of membranes (PPROM), pre-eclampsia, maternal Scr], characteristics at delivery [gestational age (GA), birth weight (BW), small for GA (SGA), Apgar, intubation] and during neonatal stay [ventilation, oxygen, parenteral nutrition, ibuprofen, steroids, intraventricular hemorrhage, retinopathy of prematurity (ROP), phototherapy] were linked with Scr observations. Data were reported by median and range or incidence. Characteristics in ELBW neonates with raised peak Scr (>P75) were compared to controls (P75 (112.3 μmol/l), Scr remained elevated until day 28. Mothers of cases received less betamethasone, neonates had a lower GA, lower BW, lower Apgar, and needed more often intubation. Postnatal ventilation, oxygen, parenteral nutrition, ibuprofen, steroids, ROP, and intraventricular hemorrhage were different. GA and ventilation or Apgar were independent factors for raised peak Scr. ELBW neonates display trends similar to heavier neonates, but peak Scr is higher, and the subsequent decrease slower. Raised creatinemia in ELBW neonates reflects immaturity (GA) and morbidity (ventilation, Apgar).

Thrombocytopenia (platelet count &lt;150 × 109/L) regularly occurs in newborns but is especially observed in critically ill neonates. We describe the case of a small for gestational age (SGA) neonate, who showed an unexpected, severe thrombocytopenia (8 × 109/L) at day 5 of life. The thrombocytopenia recovered completely after cessation of ranitidine (0.5 mg/kg/6 hr), which was started in a context of feeding difficulties. Other causes of neonatal thrombocytopenia were ruled out. Besides a brief report on a cimetidine-induced thrombocytopenia over 25 years ago, no other neonatal or pediatric cases of H2 antagonist-induced thrombocytopenia have been reported to date, although being widely used in routine care. Moreover, several adult cases have been published. In general, neonatal thrombocytopenia, although one of the most frequent hematological conditions in newborns, is only rarely attributed to an adverse drug reaction. Clinicians should be aware of the risks for adverse reactions, especially in routinely used drugs and in critically ill patients.

Neonatal vitamin K prophylaxis is essential to prevent vitamin K deficiency bleeding (VKDB) with a clear benefit compared to placebo. Various routes (intramuscular (IM), oral, intravenous (IV)) and dosing regimens were explored. A literature review was conducted to compare vitamin K regimens on VKDB incidence. Simultaneously, information on practices was collected from Belgian pediatric and neonatal departments. Based on the review and these practices, a consensus was developed and voted on by all co-authors and heads of pediatric departments. Today, practices vary. In line with literature, the advised prophylactic regimen is 1 or 2 mg IM vitamin K once at birth. In the case of parental refusal, healthcare providers should inform parents of the slightly inferior alternative (2 mg oral vitamin K at birth, followed by 1 or 2 mg oral weekly for 3 months when breastfed). We recommend 1 mg IM in preterm <32 weeks, and the same alternative in the case of parental refusal. When IM is perceived impossible in preterm <32 weeks, 0.5 mg IV once is recommended, with a single additional IM 1 mg dose when IV lipids are discontinued. This recommendation is a step towards harmonizing vitamin K prophylaxis in all newborns.

Background: Method: Results: Conclusion: Bronchopulmonary dysplasia is an important cause of morbidity and mortality in premature infants. The aim of this study is to present a premature, extremely low birth weight infant with bronchopulmonary dysplasia. A review of the case records of a child with recurrent respiratory distress and the relevant literature. A preterm, extremely low birth weight baby (birth weight was 0.8 Kg), delivered by emergency caesarian section for previous caesarian section and prolonged rupture of fetal membranes at 27 weeks gestational age. She had spontaneous breathing at birth (APGAR scores were 8 in one minute and 10 in 5 minutes). She developed respiratory distress with cyanosis and became oxygen dependent from the second week of life. Examination revealed severe dyspnoea with grunting respiration, tachypnoea, cyanosis and crackles in the lung fields. Chest X-ray showed hyperinflation, right lower zone patchy consolidation with obliteration of the costophrenic angle. Echocardiography was however normal. She was successively managed with intermittent oxygen, dexamethasone, salbutamol and antibiotics (ceftriaxone). She was nursed in the incubator for 3 months. There was no episode of apneic attack throughout admission. She responded to treatment and was discharged home on intermittent oxygen therapy and nebulisation. The weight on discharge was 1.6kg. At 6 months of age, she is still having recurrent respiratory distress and supplemental oxygen at home. She is regular to follow up with recurrent episodes of wheeze requiring admissions. Bronchopulmonary dysplasia should be suspected in a premature extremely low birth weight infant with early recurrent respiratory distress.