Diagnosis and Management of IUGR

Kingdom, John; Smith, Graeme N.

doi:10.1007/978-1-4471-0735-4_13

Cited by 13 publications

(12 citation statements)

References 74 publications

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“…After delivery, the case records of each woman were independently reviewed by two of the authors (AE, EMW), blinded to the activin results and the pregnancy was grouped into one of three groups: constitutionally small fetus, IUGR fetus or IUGR fetus and maternal pre‐eclampsia (IUGR–pre‐eclampsia). A fetus was determined as constitutionally small if subsequent fetal surveillance and pregnancy outcome was normal; as IUGR if there was evidence of impaired placentation or fetal compromise at the time of presentation or subsequently (including abnormalities in umbilical artery Doppler flow studies, subsequent fetal growth patterns and/or biophysical assessments of fetal wellbeing 22 ) as IUGR–pre‐eclampsia if the woman had or developed pre‐eclampsia in association with a small for gestation fetus. Pre‐eclampsia was defined according to internationally agreed criteria: hypertension (systolic BP ≥140 mmHg and/or diastolic BP [Korotkoff V] ≥90 mmHg) arising after 20 weeks of gestation, proteinuria (≥300 mg/24 hours with or without additional features such as renal insufficiency, elevated liver transaminases and haematological disturbances) 23 .…”

Section: Methodsmentioning

confidence: 99%

Maternal serum activin A levels in association with intrauterine fetal growth restriction

Wallace

Schneider-Kolsky

Edwards

et al. 2003

BJOG

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Objective To assess maternal serum activin A as a potential marker of fetal growth restriction.Design A cohort study.Setting A maternal -fetal medicine unit, university teaching hospital.Population Fifty-seven women with a small fetus (less than 10th centile for gestation) referred for assessment of fetal size by ultrasound biometry. Methods At the time of presentation for fetal biometry, maternal blood was collected for activin A measurement. The case records of each woman were independently reviewed after delivery and the pregnancy grouped into one of three groups: constitutionally small fetus, intrauterine growth restricted (IUGR) fetus or IUGR fetus and maternal pre-eclampsia (IUGR -pre-eclampsia). Activin A levels in the three groups were compared. Main outcome measures Maternal serum activin A levels.Results Sixteen of the 57 pregnancies were classified as constitutionally small, 17 as IUGR and 24 as IUGR -pre-eclampsia. Expressed as multiples of a normal median (MoMs), the median (95% CI) activin A level in the constitutionally small pregnancies was 1.12 (0.72 -1.39) MoMs significantly lower than the level in both the IUGR pregnancies, 3.00 (1.84 -4.11) MoMs, and the IUGR -pre-eclampsia pregnancies, 7.96 (5.73 -10.62) MoMs ( P ¼ 0.002 and 0.0001 for IUGR vs constitutionally small and IUGRpre-eclampsia vs constitutionally small, respectively). Conclusions Maternal serum activin A may be useful in the assessment of the small for gestational age fetus.

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Section: Methodsmentioning

confidence: 99%

Maternal serum activin A levels in association with intrauterine fetal growth restriction

Wallace

Schneider-Kolsky

Edwards

et al. 2003

BJOG

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“…as IUGR if there was evidence of impaired placentation or fetal compromise at the time of presentation or subsequently (including abnormalities in umbilical artery Doppler flow studies, subsequent fetal growth patterns and/or biophysical assessments of fetal wellbeing 22 ) as IUGR -pre-eclampsia if the woman had or developed pre-eclampsia in association with a small for gestation fetus. Pre-eclampsia was defined according to internationally agreed criteria: hypertension (systolic BP !140 mmHg and/or diastolic BP [Korotkoff V] !90 mmHg) arising after 20 weeks of gestation, proteinuria (!300 mg/24 hours with or without additional features such as renal insufficiency, elevated liver transaminases and haematological disturbances) 23 .…”

Section: Methodsmentioning

confidence: 99%

Maternal serum activin A levels in association with intrauterine fetal growth restriction

Wallace

2003

BJOG: An International Journal of Obstetrics and Gynaecology

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“…Suboptimal fetal growth is likely to be a key factor underlying altered brain development. Specifically, fetal growth restriction (FGR), broadly describing the fetus that does not grow to its genetically destined potential (Kingdom & Smith, ; Resnik, ), is a critical pregnancy compromise that is strongly linked to neurodevelopmental deficits. Depending on the definition used, FGR complicates 3–9% of all pregnancies in high‐income countries, but the incidence is reportedly sixfold greater in low‐income countries such that worldwide FGR may affect up to 30 million infants per year (de Onis et al .…”

Section: Introductionmentioning

confidence: 99%

“…This is unfortunate, as it does not allow appropriate consideration of the distinction between poor fetal growth due to pathological compromise (true FGR), and those infants who are constitutionally small. Traditionally, the diagnosis of FGR described an infant with birth weight below the 10th percentile for their sex and gestational age (Kingdom & Smith, ), with more recent definitions incorporating measure of placental pathology with abnormal umbilical artery Doppler flow velocimetry during pregnancy (Figueras & Gratacos, ). Abnormality of Doppler flow in the umbilical arteries is clinically significant as it reflects placental compromise, where placental insufficiency is considered the principal cause of FGR (Cetin & Alvino, ; Figueras & Gardosi, ; Story et al .…”

Section: Introductionmentioning

confidence: 99%

The consequences of fetal growth restriction on brain structure and neurodevelopmental outcome

Miller

Hüppi

Mallard

2016

The Journal of Physiology

457

412

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Fetal growth restriction (FGR) is a significant complication of pregnancy describing a fetus that does not grow to full potential due to pathological compromise. FGR affects 3–9% of pregnancies in high‐income countries, and is a leading cause of perinatal mortality and morbidity. Placental insufficiency is the principal cause of FGR, resulting in chronic fetal hypoxia. This hypoxia induces a fetal adaptive response of cardiac output redistribution to favour vital organs, including the brain, and is in consequence called brain sparing. Despite this, it is now apparent that brain sparing does not ensure normal brain development in growth‐restricted fetuses. In this review we have brought together available evidence from human and experimental animal studies to describe the complex changes in brain structure and function that occur as a consequence of FGR. In both humans and animals, neurodevelopmental outcomes are influenced by the timing of the onset of FGR, the severity of FGR, and gestational age at delivery. FGR is broadly associated with reduced total brain volume and altered cortical volume and structure, decreased total number of cells and myelination deficits. Brain connectivity is also impaired, evidenced by neuronal migration deficits, reduced dendritic processes, and less efficient networks with decreased long‐range connections. Subsequent to these structural alterations, short‐ and long‐term functional consequences have been described in school children who had FGR, most commonly including problems in motor skills, cognition, memory and neuropsychological dysfunctions.

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Diagnosis and Management of IUGR

Cited by 13 publications

References 74 publications

Maternal serum activin A levels in association with intrauterine fetal growth restriction

Maternal serum activin A levels in association with intrauterine fetal growth restriction

Maternal serum activin A levels in association with intrauterine fetal growth restriction

The consequences of fetal growth restriction on brain structure and neurodevelopmental outcome

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