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.

Elevated NRBCs and FTV were associated with higher illness severity during the first 24 h after birth in preterm infants. Ascending intrauterine infection was not associated with high illness severity.

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Background: Placental lesions are associated with neurological morbidity but the mechanism leading to morbidity is unclear. To provide insight into such a possible mechanism, we determined whether placental lesions were associated with regional cerebral tissue oxygen saturation (r c SO 2 ) and fractional tissue oxygen extraction (FTOE) in preterm infants during their first 5 d after birth. We hypothesized that as a result of cerebral hypoperfusion, r c SO 2 would be lower and FTOE would be higher. Method: In a prospective, observational study of 42 preterm infants (gestational age <32 wk), the infants' placentas were examined for histopathology. We measured r c SO 2 and transcutaneous arterial oxygen saturation (SpO 2 ) on days 1-5. FTOE was calculated as FTOE = (transcutaneous SpO 2 − r c SO 2 )/transcutaneous SpO 2 . results: Only three placentas showed no pathology. Ascending intrauterine infection (AIUI) (n = 16) was associated with lower r c SO 2 and higher FTOE values on days 2, 3, and 4 (P ≤ 0.05). Other placental lesions were not associated with r c SO 2 and FTOE. conclusion: AIUI is associated with lower r c SO 2 , and higher FTOE shortly after birth. The effect it has on cerebral oxygenation might be the mechanism leading to neurodevelopmental problems. t he placenta is the link between mother and fetus during pregnancy and as such it is an essential organ for the development of the fetus. It is the only organ that enables the exchange of nutrients and oxygen from mother to fetus and removes fetal waste products (1). Placental lesions carry the risk of fetal hypoxia, neonatal morbidity, and even perinatal death (2-6). Moreover, such lesions are associated with several neurological problems including intraventricular hemorrhage, white matter injury, cerebral palsy, and long-term neurodevelopmental problems (7-13).To date, the mechanism whereby placental lesions lead to cerebral damage is unclear. One study hypothesized that chronic placental insufficiency could induce fetal hypoxia that in turn could result in cerebral hypoperfusion, which leads to cerebral damage (14). Long-standing placental hypoperfusion can result in a non-optimal intrauterine environment. The placental underperfusion can lead to a reduction of perfusion surface and, as a consequence, nonoptimal oxygen delivery to the fetal circulation. This might result in some degree of intrauterine cerebral underperfusion, and as a consequence to a (transitional) effect on postnatal cerebral blood flow. On the other hand, cerebral hyperperfusion could also lead to cerebral damage (15). Understanding the mechanism of placental lesions leading to neurodevelopmental problems is necessary to provide possible clues for early interventions aiming to improve neurological outcome. To determine whether the disturbances in hemodynamics shortly after birth could be a possible mechanism underlying cerebral damage caused by placental lesions, it would be useful if we could measure cerebral tissue oxygen saturation and extraction. A noninvasive method of doing...

Background: Induced hypothermia is the only therapy with proven efficacy to reduce brain damage after perinatal asphyxia. While hypothermia downregulates global protein synthesis and cell metabolism, low temperature induces a small subset of proteins that includes the RNA-binding protein RBM3, which is transcriptionally induced also in response to hypoxia and has recently been implicated in cell survival.

Background:Little is known about the association of placental pathology and neurological morbidity shortly after birth in preterm infants. Neurological condition during this period can be evaluated by the quality of general movements (GMs).