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:
- 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.
3. Hypothermia: because of diminished subcutaneous fat insulation.
4. Metabolic:
a. Hypoglycemia: The risk of hypoglycemia is greatest during the first 3 days of life, but fasting hypoglycemia, with or without ketonemia can occur repeatedly up to weeks after birth.
Carbohydrate metabolism is seriously disturbed, and FGR infants are highly susceptible to hypoglycemia as a consequence of diminished glycogen reserves and decreased capacity for gluconeogenesis. Oxidation of free fatty acids and triglycerides is reduced in FGR infants, which limits alternate fuel sources. Hyperinsulinism, excess sensitivity to insulin, and deficient catecholamine release during hypoglycemia suggest abnormalities of counterregulatory hormonal mechanisms during periods of hypoglycemia in FGR infants. Hypothermia may potentiate the problem of hypoglycemia as well.
b. Hyperglycemia: FGR infants may have low insulin secretion, resulting in hyperglycemia.
c. Hypocalcemia: Hypocalcemia may occur in asphyxiated FGR infants.
d. Liver disease: FGR infants are at greater risk for developing cholestasis associated with parenteral nutrition. There is also an increased risk of non–fatty liver disease in children born SGA.
e. Other: Hypertriglyceridemia, increased sympathetic tone, and reduced concentrations of IGF-1 have been associated with increased aortic intimal thickness in FGR infants.
5. Hematologic disorders:
A. hyperviscosity and polycythemia: due to ↑ erythropoietin levels secondary to fetal hypoxia associated with FGR.
Polycythemia may also contribute to hypoglycemia and lead to hypoxia and cerebral injury.
There is an increased number of nucleated red cells secondary to extramedullary hematopoiesis. Persistent elevation of nucleated red cell counts is associated with worse prognosis.
B. The hepatic dysfunction that results from chronic intrauterine hypoxia may lead to hemostatic alterations, mainly concerning a reduction in vitamin-K dependent factors and thrombocytopenia. Such disorders are usually short-lived and respond to simple corrective measures.
c. Prolonged PT and INR were observed in full-term healthy SGA neonates, indicating a predisposition to hemorrhagic events e.g pulmonary Hge.
D. Neutropenia is also seen.
6. Altered immunity:
˗ FGR infants have decreased immunoglobulin G levels.
˗ In addition, the thymus is reduced in size by 50%, and peripheral blood lymphocytes are decreased.
˗ Reduction in total white cell count, neutrophils (neutropenia) , monocyte and lymphocyte subpopulations, and thrombocytopenia may occur, and selective suppression of helper and cytotoxic T cells can be seen.
˗ May be also due to Congenital infection (TORCH infections).
7. NEC:
- FGR infants are at increased risk of developing NEC, particularly when associated with an absent or reversed end-diastolic flow in UA Doppler.
8. Retinopathy of Prematurity (ROP):
˗ SGA infants are at increased risk of developing ROP
˗ Changes in organ development due to fetal hypoxemia, nutrient
restriction and an altered endocrine environment are all possible explanations.
˗ lower serum concentrations of insulin-like growth factor 1 in iugr infants and there is evidence of roles for this growth factor and for vascular endothelial growth factor in the pathogenesis of ROP.
9. Others:
- Preterm FGR infants are also at increased risk of more severe IVH, and renal failure.
- Sudden infant death syndrome may be more common after IUGR.
- An increased risk of chronic lung disease has also been reported in IUGR preterm infants
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