BackgroundThe placenta plays a crucial role during pregnancy for growth and development of the fetus. Less than optimal placental performance may result in morbidity or even mortality of both mother and fetus. Awareness among pediatricians, however, of the benefit of placental findings for neonatal care, is limited.ObjectivesTo provide a systematic overview of the relation between placental lesions and neonatal outcome.Data sourcesPubmed database, reference lists of selected publications and important research groups in the field.Study appraisal and synthesis methodsWe systematically searched the Pubmed database for literature on the relation between placental lesions and fetal and neonatal mortality, neonatal morbidity and neurological outcome. We conducted three separate searches starting with a search for placental pathology and fetal and neonatal mortality, followed by placental pathology and neonatal morbidity, and finally placental pathology and neurological development. We limited our search to full-text articles published in English from January 1995 to October 2013. We refined our search results by selecting the appropriate articles from the ones found during the initial searches. The first selection was based on the title, the second on the abstract, and the third on the full article. The quality of the selected articles was determined by using the Newcastle-Ottawa Quality Assessment Scale.ResultsPlacental lesions are one of the main causes of fetal death, where placental lesions consistent with maternal vascular underperfusion are most important. Several neonatal problems are also associated with placental lesions, whereby ascending intrauterine infection (with a fetal component) and fetal thrombotic vasculopathy constitute the greatest problem.ConclusionsThe placenta plays a key role in fetal and neonatal mortality, morbidity, and outcome. Pediatricians should make an effort to obtain the results of placental examinations.

INTRODUCTION: hydrocortisone (hc) and dexamethasone (DXM) are used to treat preterm infants at risk for bronchopulmonary dysplasia (BPD). This may, however, affect their longterm neurological development. We aimed to determine the effect of hc and DXM therapy in preterm infants on neurological functioning as assessed by the quality of general movements (GMs) until 3 months after term. RESULTS: We found no difference in the quality of GMs between hc and DXM infants until term age. at 3 months, hc infants had a higher median motor optimality score (MOs) than DXM infants (25 vs. 21, P = 0.015). In the DXM group, MOs on the first day of treatment was lower than before treatment (10 vs. 11, P = 0.030). DISCUSSION: MOs decreased in DXM infants on the first day following treatment and at 3 months after term. This was not the case in hc infants. Our study suggests that neurological functioning at 3 months after term is better in infants treated with hc than in infants treated with DXM. METHODS:We performed a longitudinal, observational study including 56 preterm infants (n = 17 hc, n = 17 DXM, n = 22 controls). GM quality, videoed before and after treatment, was assessed. In addition, a MOs was assigned to details of the GMs.

Background: High-dose dexamethasone (DXM) treatment of preterms at risk of bronchopulmonary dysplasia leads to a deterioration in quality of their general movements (GMs). It is unknown whether low-dose DXM affects GM quality similarly. Objectives: To assess the effect of low-dose DXM treatment on the quality of GMs and fidgety GMs (FMs). Methods: A prospective study of preterms admitted to our NICU between 2010 and 2012, and treated with DXM (starting dose 0.25 mg/kg/day). We assessed GM/FM quality and calculated their motor optimality score (MOS) before, during, and after treatment up to 3 months postterm. Neurological follow-up was performed between 12 and 36 months. We related risk factors with infants' GM trajectories and MOSs. At 3 months we compared the MOSs of low-dose DXM infants and a historical cohort of infants treated with high-dose DXM or hydrocortisone. Results: 17 infants were included. GM/FM quality improved in 9 out of 13 initially abnormal infants (p = 0.004). Shorter periods of mechanical ventilation and higher birth weights were associated with better GM trajectories (p = 0.032 and p = 0.042, respectively). Infants starting treatment later had higher MOSs on day 7 (p = 0.047). Low-dose DXM infants had higher MOSs than high-dose DXM infants (β = -0.535; 95% CI -0.594 to -0.132; p = 0.003). Out of 17 infants, 2 died, 14 developed normally, and 1 developed with mild neurodevelopmental impairments. Infants whose GMs/FMs remained normal or improved had better outcomes than infants whose GMs/FMs remained abnormal (p = 0.019). Conclusions: Out of the 17 infants treated with low-dose DXM, 2 died. Of the surviving infants, neurological functioning improved with the majority having normal neurodevelopment at the age of 12-36 months.