Intrauterine growth restriction

Intrauterine growth restriction

Micrograph of villitis of unknown etiology,

aplacental pathology associated with IUGR.H&E

stain.

Classification and external resources

Specialty pediatrics

ICD-10 P05.9

ICD-9-CM 764.9

DiseasesDB 6895

MedlinePlus 001500

eMedicine article/261226

Patient UK Intrauterine growth restriction

MeSH D005317

Intrauterine growth restriction (IUGR) refers to poor growth of a fetus while in the mother's

womb during pregnancy. The causes can be many, but most often involve poor maternal

nutrition or lack of adequate oxygen supply to the fetus.

At least 60% of the 4 million neonatal deaths that occur worldwide every year are associated

with low birth weight (LBW), caused by intrauterine growth restriction (IUGR), preterm

delivery, and genetic/chromosomal abnormalities,[1] demonstrating that under-nutrition is already

a leading health problem at birth.

Intrauterine growth restriction can result in baby being Small for Gestational Age (SGA), which

is most commonly defined as a weight below the 10th percentile for the gestational age.[2] At the

end of pregnancy, it can result in a low birth weight.

Contents

  [hide] 

1 Symmetrical vs. asymmetrical

2 Causes

o 2.1 Maternal

o 2.2 Uteroplacental

o 2.3 Fetal

3 Pathophysiology

o 3.1 Neurological Development Postpartum

3.1.1 Cerebral Changes

3.1.2 Neural Circuitry and Brain Networks

4 Outcomes and clinical significance

5 Sheep

6 References

Symmetrical vs. asymmetrical[edit]

There are 2 major categories of IUGR: symmetrical and asymmetrical.[3][4] Some conditions are

associated with both symmetrical and asymmetrical growth restriction.

Asymmetrical IUGR is more common (70%). In asymmetrical IUGR, there is restriction of

weight followed by length. The head continues to grow at normal or near-normal rates (head

sparing). A lack of subcutaneous fat leads to a thin and small body out of proportion with the

head. This is a protective mechanism that may have evolved to promote brain development. In

these cases, the embryo/fetus has grown normally for the first two trimesters but encounters

difficulties in the third, sometimes secondary to complications such as pre-eclampsia. Other

symptoms than the disproportion include dry, peeling skin and an overly-thin umbilical cord.

The baby is at increased risk of hypoxia and hypoglycaemia. This type of IUGR is most

commonly caused by extrinsic factors that affect the fetus at later gestational ages. Specific

causes include:

Chronic high blood pressure

Severe malnutrition

Genetic mutations, Ehlers–Danlos syndrome

Symmetrical IUGR is less common (20-25%). It is commonly known as global growth

restriction, and indicates that the fetus has developed slowly throughout the duration of the

pregnancy and was thus affected from a very early stage. The head circumference of such a

newborn is in proportion to the rest of the body. Since most neurons are developed by the 18th

week of gestation, the fetus with symmetrical IUGR is more likely to have permanent

neurological sequela. Common causes include:

Early intrauterine infections, such as cytomegalovirus, rubella or toxoplasmosis

Chromosomal  abnormalities

Anemia

Maternal substance abuse (prenatal alcohol use can result in Fetal alcohol syndrome)

Causes[edit]

Maternal[edit]

pre-pregnancy weight and nutritional status

poor weight gain during pregnancy

poor nutrition

anemia

alcohol and/or drug use

maternal smoking

recent pregnancy

pre-gestational diabetes

gestational diabetes

pulmonary disease

cardiovascular disease

renal disease

hypertension

Celiac disease  increases the risk of intrauterine growth restriction by an odds ratio of

approximately 1.5.[5]

Uteroplacental[edit]

preeclampsia

multiple gestation

uterine  malformations

Placental insufficiency

Fetal[edit]

chromosomal abnormalities

Vertically transmitted infections

Pathophysiology[edit]

If the cause of IUGR is extrinsic to the fetus (maternal or uteroplacental), transfer of oxygen and

nutrients to the fetus is decreased. This causes a reduction in the fetus’ stores

ofglycogen and lipids. This often leads to hypoglycemia at birth. Polycythemia can occur

secondary to increased erythropoietin production caused by the

chronic hypoxemia.Hypothermia, thrombocytopenia, leukopenia, hypocalcemia,

and pulmonary hemorrhage are often results of IUGR.

If the cause of IUGR is intrinsic to the fetus, growth is restricted due to genetic factors or as a

sequela of infection.

Neurological Development Postpartum[edit]

IUGR is associated with a wide range of short- and long-term neurodevelopmental disorders

Cerebral Changes[edit]

white matter effects – In postpartum studies of infants, it was shown that there was a decrease of

the fractal dimension of the white matter in IUGR infants at one year corrected age. This was

compared to at term and preterm infants at one year adjusted corrected age.

grey matter effects – Grey matter was also shown to be decreased in infants with IUGR at one

year corrected age.

Neural Circuitry and Brain Networks[edit]

Children with IUGR are often found to exhibit brain reorganization including neural circuitry.[6] Reorganization has been linked to learning and memory differences between children born at

term and those born with IUGR.[7]

Studies have shown that children born with IUGR had lower IQ. They also exhibit other deficits

that point to [frontal lobe] dysfunction.

IUGR infants with brain-sparing show accelerated maturation of the hippocampus which is

responsible for memory.[8] This accelerated maturation can often lead to uncharacteristic

development that may compromise other networks and lead to memory and learning

deficiencies.

Outcomes and clinical significance[edit]

IUGR affects 3-10% of pregnancies. 20% of stillborn infants have IUGR. Perinatal mortality

rates are 4-8 times higher for infants with IUGR, and morbidity is present in 50% of surviving

infants.

According to the theory of thrifty phenotype, intrauterine growth restriction

triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food

shortage. If the offspring actually develops in an environment rich in food it may be more prone

to metabolic disorders, such as obesity and type II diabetes.[9]

Sheep[edit]

In sheep, intrauterine growth restriction can be caused by heat stress in early to mid pregnancy.

The effect is attributed to reduced placental development causing reduced fetal growth.[10][11]

[12] Hormonal effects appear implicated in the reduced placental development.[12] Although early

reduction of placental development is not accompanied by concurrent reduction of fetal growth;[10] it tends to limit fetal growth later in gestation. Normally, ovine placental mass increases until

about day 70 of gestation,[13] but high demand on the placenta for fetal growth occurs later. (For

example, research results suggest that a normal average singleton Suffolk x Targhee sheep fetus

has a mass of about 0.15 kg at day 70, and growth rates of about 31 g/day at day 80, 129 g/day at

day 120 and 199 g/day at day 140 of gestation, reaching a mass of about 6.21 kg at day 140, a

few days before parturition.[14])

In adolescent ewes (i.e. ewe hoggets), overfeeding during pregnancy can also cause intrauterine

growth restriction, by altering nutrient partitioning between dam and conceptus.[15][16] Fetal

growth restriction in adolescent ewes overnourished during early to mid pregnancy is not

avoided by switching to lower nutrient intake after day 90 of gestation; whereas such switching

at day 50 does result in greater placental growth and enhanced pregnancy outcome.[16] Practical

implications include the importance of estimating a threshold for "overnutrition" in management

of pregnant ewe hoggets. In a study of Romney and Coopworth ewe hoggets bred to Perendale

rams, feeding to approximate a conceptus-free live mass gain of 0.15 kg/day (i.e. in addition to

conceptus mass), commencing 13 days after the midpoint of a synchronized breeding period,

yielded no reduction in lamb birth mass, where compared with feeding treatments yielding

conceptus-free live mass gains of about 0 and 0.075 kg/day.[17]

In both of the above models of IUGR in sheep, the absolute magnitude of uterine blood flow is

reduced.[16] Evidence of substantial reduction of placental glucose transport capacity has been

observed in pregnant ewes that had been heat-stressed during placental development.[18][19]

References[edit]

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2. Jump up^ Small for gestational age (SGA) at MedlinePlus. Update Date: 8/4/2009.

Updated by: Linda J. Vorvick. Also reviewed by David Zieve.

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