- Intrauterine Monitoring of the growth-restricted fetus.

 

Intrauterine Monitoring of the growth-restricted fetus

The fetus with IUGR is at risk from intrauterine hypoxia/intrauterine death and asphyxia during labor and delivery.

The growth-restricted fetus should be monitored closely to determine the optimal time for delivery.

Progressive uteroplacental failure results in:

o  Reduced growth in femur length and abdominal circumference (<10th centile)

o  Reduced amniotic fluid volume

o  Abnormal umbilical artery Doppler waveforms due to increased placental impedance – absent and then reversed end-diastolic flow velocity.

o  Redistribution of blood flow in the fetus – increased to the brain, reduced to the gastrointestinal tract, liver, skin and kidneys

o  Abnormal ductus venosus Doppler waveform denoting diastolic cardiac dysfunction

o  Reduced fetal movements

o  Abnormal CTG (cardiotocography)

o  Intrauterine death or hypoxic damage to the fetus.

- Neonatal clinical Assessment for IUGR newborn.

 Neonatal clinical Assessment for IUGR newborn

1.  Reduced birthwight for gestational age.

2.  Physical appearance:

When infants with congenital malformation syndromes and infections are excluded, the remaining groups of FGR infants have a characteristic physical appearance:

-        These infants, in general, are thin with loose, peeling skin because of loss of subcutaneous tissue, a scaphoid abdomen (must be distinguished from infants with diaphragmatic hernias), and disproportionately large head.

-        Senile face.

-        Cranial sutures may be widened or overriding, and the anterior fontanelle may be larger than expected, representing diminished membranous bone formation.

-        Vernix caseosa frequently is reduced or absent as a result of diminished skin perfusion during periods of fetal distress or because of depressed synthesis of estriol, which normally enhances vernix production. In the absence of this protective covering, the skin is continuously exposed to amniotic fluid and will begin to desquamate.

-        Sole creases appear more mature due to increased wrinkling from increased exposure to amniotic fluid.

-        Breast tissue formation also depends on peripheral blood flow and estriol levels and will be reduced.

-         female external genitalia will appear less mature because of the absence of the perineal adipose tissue covering the labia.

-        Ear cartilage also may be diminished.

-        The umbilical cord often is thinner than usual. When meconium has been passed in utero, the cord is yellow-green stained, as are the nails and skin.

-        Cerebral cortical convolutions, renal glomeruli and alveolar maturation all relate to gestational age and are not delayed with IUGR.

- Diagnosis Of IUGR.

 Diagnosis Of  IUGR

A.    Establishing gestational age.

B.    Fetal assessment:

                        I. Ultrasonography (may be as often as 1– 2 times per week).

1.     Estimated fetal weight:  4 biometric measures are commonly used: biparietal diameter, head circumference, abdominal circumference, and femur length. The biometric measurements can be combined to generate an EFW. The estimate may deviate from the birthweight by up to 20%. The liver is the first organ to suffer the effects of growth restriction due to redistribution of ductus venosus blood flow to the heart and a decrease in glycogen deposition in the liver. Reduced growth of the abdominal circumference (<5 mm/wk) is the earliest sign of asymmetric growth restriction and diminished glycogen storage.

2.     Ratio of head circumference to abdominal circumference. This ratio normally changes as pregnancy progresses. In the second trimester, the head circumference is greater than the abdominal circumference. At about 32 to 36 weeks’ gestation, the ratio is 1:1, and after 36 weeks, the abdominal measurements become larger. Persistence of a head-to-abdomen ratio <1 late in gestation is predictive of late-onset FGR.

3.     Femur length: Serial measurements of femur length are as effective as head measurements for detecting early-onset FGR.

4.     Placental volume measurements may be helpful in predicting subsequent fetal growth. Placental weight and/or volume is decreased before fetal growth decreases. FGR with decreased placental size is more likely to be associated with fetal acidosis. Placental volume correlates with placental flow indices.

- Neonatal complications of fetal growth restriction

 

Neonatal complications of fetal growth restriction

1.  Preterm labor: 

Pathophysiologic processes causing the IUGR also can lead to preterm labor and preterm delivery. Thus, IUGR frequently occurs with a variety of maternal conditions that are associated with preterm delivery.

2.  Hypoxia may be due to:

a.  Perinatal asphyxia:

-   FGR fetuses are at risk of hypoxia-ischemia at birth because Transient diminished placental blood flow during labor is poorly tolerated by growth-restricted fetuses.

-   A large proportion of stillborn infants had FGR in utero.

-   Intrauterine chronic hypoxia and limited carbohydrate reserves caused by placental insufficiency are more likely to predispose to perinatal hypoxic ischemia in SGA neonates than AGA newborns with an increased risk of all clinical sequelae of perinatal asphyxia.

b.  PPHN. Many FGR infants are subjected to chronic intrauterine hypoxia → abnormal thickening of the smooth muscles of the small pulmonary arterioles → ↓ pulmonary blood flow → results in varying degrees of pulmonary artery hypertension.

c.  RDS: It is controversial whether FGR results in accelerated fetal pulmonary maturation due to chronic intrauterine stress. Respiratory distress syndrome may be seen less frequently in FGR infants; however, these infants are at higher risk of pulmonary morbidities such as bronchopulmonary dysplasia compared to appropriately grown infants.

d.  Meconium aspiration. Post-term FGR infants are particularly at risk for meconium aspiration.

e.  PDA. Conflicting data suggest that hemodynamically significant patent ductus arteriosus (PDA) may be bigger and occur earlier in FGR infants compared to AGA infants; nevertheless, spontaneous closure of PDA is more frequent in FGR infants with <1000 g birthweight. FGR infants with PDA are at greater risk for pulmonary hemorrhage, intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), and renal failure.

Fetal Endocrine and Autocrine/Paracrine-Acting Growth Factor Effects on Fetal Growth In IUGR.

 Fetal Endocrine and Autocrine/Paracrine-Acting Growth Factor Effects on Fetal Growth In IUGR.

Fetal hormones promote growth (and development) in utero by altering both the metabolism and gene expression of fetal tissues.

A.    Insulin:

Insulin has direct mitogenic effects on cellular development and cell number. It also enhances glucose consumption and limits protein breakdown. The latter effects are associated with reduced fetal growth when insulin concentration is low.

Thus, insulin deficiency, directly and indirectly, results in a decrease in fetal nutrient supply.

 

B.    Insulin-Like Growth Factor-I:

IGF-1 is a major anabolic hormone in fetal development. IGF-I is positively regulated by glucose supply in the fetus.

IGF-I probably can regulate metabolic processes that affect fetal protein balance and growth, but these have been difficult to measure.

Human IUGR fetuses have decreased plasma IGF-I concentrations.

Mutations in the Igf1 and Igf1r genes in humans cause both intrauterine and postnatal growth restriction.

C.    Thyroid Hormones:

In all species, fetal thyroid hormone deficiency or reduced free thyroxine (T4) produces developmental abnormalities in certain tissues and reduced growth.

Fetal hypothyroidism decreases oxygen consumption and oxidation of glucose, thereby potentially decreasing fetal energy supply for growth. Hypothyroidism also can decrease circulating and tissue concentrations of IGF-I.

FETAL NUTRIENT UPTAKE AND METABOLISM AND REGULATION OF FETAL GROWTH IN IUGR.

 FETAL NUTRIENT UPTAKE AND METABOLISM AND REGULATION OF FETAL GROWTH  In IUGR .

1. Glucose Uptake, Metabolism:

First, relative fetal hypoglycemia is an important and natural compensatory mechanism that helps to maintain the maternal-to-fetal glucose concentration gradient and thus the transport of glucose across the placenta to the fetus.

Despite this compensation, fetal hypoglycemia limits tissue glucose uptake directly by diminished mass action and indirectly by limiting fetal insulin secretion and thus the effect of insulin to promote tissue glucose uptake by skeletal muscle, heart, adipose tissue, and liver.

Reduced glucose supply alone decreases fetal growth rate and oxygen consumption rate (metabolic rate) proportionally.

Insulin also normally suppresses hepatic glucose production and release, and it acts as an anabolic hormone that increases net protein balance by inhibiting protein breakdown. Thus, a decrease in fetal plasma insulin concentration initially may allow fetal glucose production to take place, thereby providing glucose for both fetal and placental needs, but subsequently, combined with hypoglycemia, results in increased protein breakdown and decreased protein accretion.

Circulating concentrations and tissue-specific expression of growth factors such as IGF-I also are decreased during fetal hypoglycemia, which may contribute to increased fetal protein breakdown and decreased rates of fetal growth.

Thus, fetal hypoglycemia in response to a decrease in maternal glucose supply acts to maintain fetal glucose supply, but it also leads to lower anabolic hormone concentrations, which limit the rate of fetal growth, thereby decreasing fetal nutrient needs.