- Prognosis and long-term outcome of IUGR.

Prognosis and long-term outcome of IUGR.

A. Mortality:

-        Mortality ↑ with decreasing gestational age when FGR is also present.

-        Mortality ↓ by 48% for each week that the fetus remains in utero before 30 weeks’ gestation.

B. Postnatal Growth Impairment:

-        usually, Term SGA have adequate catch-up growth during the first 12 months without pharmacologic intervention and in most cases catch-up growth is complete by two years.

-        However, it is having been suggested that SGA children aged 2−4 years with no evidence of catch-up growth and heights less than –2.5 SD should be referred for endocrine evaluation and eligibility for growth hormone (GH) treatment [for a minority, growth hormone therapy (started before 8 years of age and continued for >7 years) can augment growth parameters.

-        Preterm SGA infants can take 4 or more years to achieve heights in a normal range.

-        Many preterm infants show a postnatal growth deficit at the time of hospital discharge, so-called extrauterine growth restriction (EUGR), which is defined as a centile at discharge lower than the birth centile.

-        EUGR is largely due to an inadequate postnatal nutrient intake as well as postnatal morbidities, and it ↑ with decreased gestational age.

-        Premature infants with EUGR also have metabolic abnormalities similar to those observed in term SGA children and these occur irrespectively of whether they are SGA or AGA at birth.

-        SGA term infants suffer from an adverse fetal environment during the last trimester of pregnancy, whereas very preterm infants suffer from an adverse postnatal environment during the first three months, a time biologically equivalent to the third trimester of fetal life.

C. Neurological and developmental delay

-        Neurodevelopmental morbidities are seen 5 to 10 times more often in FGR infants compared with AGA infants and depend not only on the cause of FGR but also on the adverse events in the neonatal course (eg, perinatal depression or hypoglycemia).

-        Even without identified perinatal events, IUGR infants have a higher incidence of long-term neurologic or developmental handicaps.

-        Many studies reveal evidence of minimal brain dysfunction, including hyperactivity, short attention span, and learning problems.

-        Preterm FGR infants also show alterations in early neurobehavioral functions, such as attention-interaction capacity and cognitive and memory dysfunction, that persist.

-        Increased risk of cerebral palsy, a wide spectrum of learning disabilities, mental retardation, developmental delay, and neuropsychiatric disorders are seen in later years.

-        The most important predictor of subnormal performance is the absence of catch-up growth in height and/or head circumference.

-        Long-term exclusive breastfeeding could help to prevent some of the neurological sequelae of being born SGA. Overfeeding with an enriched formula could accelerate growth, but it does not seem to lead to an advantage for intellectual development and could increase metabolic and cardiovascular risks.

- Managment of IUGR

 Managment of IUGR

The initial management of a neonate with fetal growth restriction (FGR) is supportive and is focused on preventing or addressing any associated complications.

Antenatal management

1.  Bed rest: has been used but is now largely abandoned.

2.  Calcium channel blockers: used in pregnancy as tocolytics and to alter cerebral blood flow.

3.  Hormonal therapy: maternal estrogen administration may result in greater uterine blood flow allowing ↑ nutritional supply to improve fetal growth.

4.  Corticosteroid therapy: maternal glucocorticoid administration results in improved fetal doppler waveforms and better outcomes.

 

Perinatal management

A. Assessment of fetal well-being:

-        Fetal movement: All women with pregnancies with risk factors for adverse perinatal outcome should perform daily fetal movements counts and consult their physician if they notice a decrease or change in fetal movements.

-        Non stress test (NST): Frequency of regular NST to assess fetal well-being should be based on severity of IUGR.

-        Biophysical profile (BPP): In presence of decreased fetal movement, abnormal NST, suspicion or diagnosis of IUGR, a BPP or amniotic fluid assessment is warranted.

B. Delivery and resuscitation.

-        The optimal timing for delivery discussed before.

-        Outcomes are more favorable with cesarean delivery because the FGR fetus tolerates the stress of labor poorly and signs of fetal distress are common. In such cases, the already stressed, chronically hypoxic infant is exposed to the acute stress of diminished blood flow during uterine contractions.

-        Skilled resuscitation should be available because of possible complications for example perinatal depression .

A.    Prevention of heat loss.

- Staging of fetal growth restriction and optimal timing of delivery.

 

Staging of fetal growth restriction and optimal timing of delivery

 

The optimal timing of delivery with FGR is determined by the severity of

fetal compromise and the risk of stillbirth:

1.     Stage I (mild placental insufficiency): Abnormal Doppler studies including CPR ratios.

2.     Stage II (severe uteroplacental insufficiency): There is absent EDV in the UA. Delivery should be after 34 weeks with twice-a-week monitoring.

3.     Stage III (fetal deterioration, low suspicion of fetal acidosis): There is a reversal of EDV in the UA or DV PI >95th percentile. Risks of stillbirth and neurologic handicap are increased. Delivery should be around 32 weeks.

4.     Stage IV (fetal acidosis): Spontaneous fetal decelerations, reduced variability or reversal of atrial flow on DV. Imminent risk of fetal demise. Deliver immediately.

 

Also timing of delivery should be individualized and based on gestational age and fetal condition. The following principles may guide management of pregnancies complicated by IUGR:

·       Remote from term, conservative management to prolong pregnancy may be performed safely with serial antepartum surveillance as described earlier to achieve further fetal maturity.

·       The term or late preterm (>34 weeks) IUGR fetus should be delivered when there is evidence of maternal hypertension, poor interval growth (over 2- to 4-week intervals), nonreassuring antenatal testing (NST, BPP), and/or umbilical artery Doppler testing to demonstrate absence or reversal of flow.

·       When growth restriction is mild, no complicating maternal or fetal factors are present, and the umbilical artery Doppler and fetal testing are reassuring, delivery can be delayed until at least 37 weeks to minimize the risks of prematurity.

·       Each specific clinical scenario requires close consideration and an individualization of management plans.

- 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.