Small for gestational age neonates - are we missing some by only using standard population growth standards and does it matter?

Narchi, Hassib; Skinner, Andrew C.; Williams, Bernadette

doi:10.1080/14767050903067352

Cited by 9 publications

(12 citation statements)

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“…Fetal growth restriction (FGR) is a leading cause of perinatal morbidity and mortality in humans. [1][2][3][4][5] Suboptimal uteroplacental perfusion is a commonly identified cause of FGR, and histologic evidence of placental ischemia and inflammation is commonly observed. Because the placental vasculature is not regulated by the autonomic nervous system, vasoactive mediators play a prominent role in the regulation of placental perfusion.…”

Section: Introductionmentioning

confidence: 99%

The Significance of Endothelin in Platelet-Activating Factor-Induced Fetal Growth Restriction

et al. 2012

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The significance of endothelin-1 (ET-1) in platelet-activating factor (PAF)-induced fetal growth restriction (FGR) was evaluated in timed-pregnant rats receiving intravenous carbamyl-PAF (c-PAF; 0.5, 1.0, or 2.5 µg/kg per h) or vehicle, with or without ET-1 receptor A (ET(A)) antagonist (10 or 20 mg/kg per d) for 7 days beginning on gestation day 14. Tissues were collected on day 21. Carbamyl-PAF reduced fetal weights dose dependently. Placental weights were significantly reduced but not dose dependently. ET(A) antagonism prevented FGR at the 0.5, but not the 1.0 and 2.5 µg/kg per h c-PAF doses. Correspondingly, placental, but not uterine, preproET-1 messenger RNA (mRNA) expression (determined by reverse transcription-polymerase chain reaction) was increased at 0.5 µg/kg per h but not at higher c-PAF doses. In summary, c-PAF infusion results in fetal and placental growth restriction in the rat. At low doses of c-PAF, ET-1 is central to the pathophysiology of PAF-induced FGR. At higher c-PAF doses, FGR is induced by mechanisms other than ET-1 action.

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Section: Introductionmentioning

confidence: 99%

The Significance of Endothelin in Platelet-Activating Factor-Induced Fetal Growth Restriction

et al. 2012

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“…Several studies have shown low birthweight to be a common feature in pregnancies of opioid‐dependent mothers 2–14,17 . However, we have recently described that there is no direct dose effect of opiates on size at birth 23 .…”

mentioning

confidence: 88%

“…Chronic opiate and/or amphetamine exposure in utero frequently leads to the neonatal abstinence syndrome. Both substances have been postulated to restrict fetal growth 3–17 . Individuals who are susceptible to addiction to illicit drug are frequently also addicted to nicotine 6,9 .…”

mentioning

confidence: 99%

The relationship between maternal opiate use, amphetamine use and smoking on fetal growth

Delsing¹,

Wittenboer²,

Liu³

et al. 2011

Australian and New Zealand Journal of Obstetrics and Gynaecology

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“…High risk newborns are children with gestational age less than 37 weeks, newborns who weigh more than 4 kg or less than 2 kg, large for gestational age (LGA) infants, small for gestational age (SGA) [23], and infants with intrauterine growth restriction. In addition high risk neonates are newborns with sepsis or born to a mother having chorioamnionitis, toxemic mothers, children born to insulin-dependent diabetic mothers or mothers with gestational diabetes.…”

Section: High Risk Newbornsmentioning

confidence: 99%

“…Newborns who have a high-risk of hypoglycemia and need of hypoglycemia screening in the first hour of life [22] are newborns who weigh more than 4 kg or less than 2 kg, large for gestational age (LGA) infants who are above the 90th percentile, small for gestational age (SGA), infants below the 10th percentile [23], and infants with intrauterine growth restriction [24][25][26][27][28][29][30][31]. In addition, high risk newborns are children with gestational age less than 37 weeks, children with sepsis [32] or born to a mother having chorioamnionitis or toxemia.…”

Section: High Risk Neonatesmentioning

confidence: 99%

Neonatal Hypoglycemia: A Continuing Debate in Definition and Management

Stomnaroska-Damcevski

Petkovska

Jancevska

et al. 2015

Prilozi

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Neonatal hypoglycemia (NH) is one of the most common abnormalities encountered in the newborn. Maintaining glucose homeostasis is one of the important physiological events during fetal-to-neonatal transition. Transient low blood glucose concentrations are frequently encountered in the majority of healthy newborns and are the reflections of normal metabolic adaptation processes. Nevertheless, there is a great concern that prolonged or recurrent low blood glucose levels may result in long-term neurological and developmental consequences. Strikingly, it was demonstrated that the incidence and timing of low glucose concentrations in the groups most at risk for asymptomatic neonatal hypoglycemia, did not find association between repetitive low glucose concentrations and poor neurodevelopmental outcomes. On the contrary, NH due to hyperinsulinism is strongly associated with brain injury. Fundamental issue of great professional controversy is concerning the best manner to manage asymptomatic newborns NH. Both, overtreating NH and undertreating NH are poles with significant potential disadvantages. Therefore, NH is one of the most important issues in the day-to-day practice. This article appraises the critical questions of definition (widely accepted blood glucose concentration: < 2.6 mmol/l or 47 mg/dl), follow-up ad management of NH.

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Small for gestational age neonates - are we missing some by only using standard population growth standards and does it matter?

Cited by 9 publications

References 0 publications

The Significance of Endothelin in Platelet-Activating Factor-Induced Fetal Growth Restriction

The Significance of Endothelin in Platelet-Activating Factor-Induced Fetal Growth Restriction

The relationship between maternal opiate use, amphetamine use and smoking on fetal growth

Neonatal Hypoglycemia: A Continuing Debate in Definition and Management

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