Thursday, August 10, 2017

Patterns of Intrauterine Growth Restriction.

 Patterns of Intrauterine Growth Restriction.

1.  Symmetric or non-symmetric:

 

Symmetric

Non-symmetric

Onset

Early

Late

Incidence

less common ≈ 30% of FGR cases

more common ≈ 70%–80% of cases

Pattern of retardation

Symmetric, Infants have reductions in all organ systems with the body, head, and length proportionally affected.

Asymmetric, Infants have disproportionate growth restriction in which head circumference is preserved, length is somewhat affected but may be spared, and weight is compromised to a greater degree.

The weight deficit is principally due to a reduction in fat deposition, particularly during the 3rd trimester of pregnancy. The disproportion is due to the redistribution of blood flow during fetal development with preferential perfusion of the brain, heart and adrenal glands at the expense of the kidney, GIT and liver, limbs and SC tissues.

Reduction in cell number.

Reduction of cell size.

Head size

Decreased

Normal

Ponderal index

Normal

Decreased

Catch up growth

Less

More

Genetic growth potential

Not attainable

Attainable

Amniotic fluid

typically accompanied by normal amniotic fluid volume but may be accompanied by polyhydramnios if there is reduced fetal swallowing of amniotic fluid, e.g. trisomy 21 or GIT anomalies.

often oligohydramnios, which is a

result of chronic stress on the fetus and reduced urine production.

Causes

usually is caused by intrinsic factors such as congenital   infections or chromosomal abnormalities, maternal drug and alcohol abuse or a chronic medical condition or malnutrition.

usually is caused by Extrinsic factors such as   disorders of the placenta or from maternal problems e.g uteroplacental dysfunction secondary to maternal pre-eclampsia, multiple pregnancy, maternal smoking or may be idiopathic.

Prognosis

poor prognosis, these infants are more likely to remain small permanently, decreased nutrient supply early in development can restrict growth of all organs.

good prognosis, these infants rapidly put on weight after birth.

2.  Early or late onset FGR.

Early detection of FGR identifies infants at risk of mortality in utero, but is difficult based on fetal anthropometry (by measuring crownrump length) alone. Estimation of fetal growth velocity with serial measurements may be useful to identify FGR. For example, a fetus with weight >10th percentile may be growth restricted if fetal growth velocity declines.

a)    Early onset FGR (<32 weeks’ gestation).

-   Early onset is associated with sequential changes in Doppler studies that parallel worsening placental function.

-   Typically, umbilical artery Doppler changes precede biophysical profile parameters.

-   Early FGR is associated with more severe placental disease, fetal hypoxia and undernutrition, systemic cardiovascular adaptation, increased risks of preeclampsia in the mother, and increased risks of fetal mortality and neonatal morbidity.

b)    Late onset (>32 weeks’ gestation).

Late FGR is more difficult to identify and has less characteristic Doppler changes.

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