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Intrauterine Growth Restriction: Obstetric and Neonatal Aspects. Intervention Strategies

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Neonatology

Abstract

Normal fetal growth can be altered by several pathological processes, including genetic diseases, infections, congenital anomalies, maternal hypoxia, and inadequate placental exchanges. The impossibility to reach the fetal genetic growth potential because of placental malfunction is defined intrauterine growth restriction (IUGR). IUGR causes slowing fetal growth, so that fetal biometry shifts from a higher to a significantly lower percentile during gestation, and it progressively leads to fetal hypoxia, acidemia, multiorgan damage, and death. Indeed, IUGR is associated with an excess of perinatal mortality and short- and long-term morbidity as well as metabolic syndrome in the adulthood. Prenatal diagnosis and appropriate timing of delivery improve neonatal outcomes.

When a fetus is found to be small for gestational age (SGA) at prenatal ultrasound, every effort has to be made to differentiate IUGR from other causes of impaired fetal growth. In case of IUGR, the clinical management is critically dependent on gestational age at onset. In early onset IUGR, the timing of delivery has to take into account the risks of prolonged intrauterine hypoxia versus the complications associated with preterm birth. In late onset IUGR, early induction of labor is probably the most cost-efficient method to prevent perinatal mortality and morbidity. In intermediate-onset IUGR there is a lack of clear evidence about the best tool to identify the fetuses that would benefit of timely delivery.

At birth, neonatal weight, length, and head circumference are indicators of the quality and quantity of intrauterine growth. SGA newborns, both preterm and term, have increased perinatal mortality risk and short-term complications such as birth asphyxia, infections, hypothermia, hypoglycemia, feeding difficulties, respiratory distress syndrome, bronchopulmonary dysplasia, retinopathy of prematurity, and necrotizing enterocolitis.

Even if most term children born SGA experience catch-up growth and achieve a normal adult height, approximately 10% of them remain shorter than peers born appropriate for gestational age. Preterm SGA infants can take four or more years to achieve heights in a normal range and the majority of them show a postnatal growth deficit at the time of hospital discharge (Extra Uterine Growth Restriction, EUGR).

Being born SGA is associated with long-term unfavorable outcomes such as learning difficulties, behavior problems, and development of metabolic syndrome.

The recognition of intrauterine malnutrition and the monitoring of early postnatal growth are of utmost importance for optimum survival and long-term outcomes of SGA infants.

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Abbreviations

AGA:

Appropriate for gestational age

BMI:

Body mass index

BPD:

Broncopulmonary displasia

EUGR:

Extra uterine growth restriction

GA:

Gestational age

GH:

Growth hormone

INR:

International mormalized ratio

IUGR:

Intrauterine growth restriction

LGA:

Large for gestational age

NEC:

Necrotizing enterocolitis

PI:

Ponderal index

PT:

Protrombin time

RDS:

Respiratory distress syndrome

ROP:

Retinopathy of prematurity

SD:

Standard deviation

SGA:

Small for gestational age

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Bertino, E., Oggè, G., Di Nicola, P., Giuliani, F., Coscia, A., Todros, T. (2018). Intrauterine Growth Restriction: Obstetric and Neonatal Aspects. Intervention Strategies. In: Buonocore, G., Bracci, R., Weindling, M. (eds) Neonatology. Springer, Cham. https://doi.org/10.1007/978-3-319-29489-6_158

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