Fetal growth restriction (FGK) is defined as the ultrasound-estimated fetal weight (EFW) below the 10th percentile for gestational age and sex. Doppler hemodynamic evaluation among FGC fetuses enables to distinguish fetuses with higher perinatal morbi-mortality risk. Therefore, the definition of fetal growth restriction includes doppler hemodynamic evaluation to distinguish fetuses with placental involvement from these non-affective fetuses. These unaffected fetuses have a better prognosis and are known as small for gestational age fetuses (SGA).
Fetal weight estimation is based on Hadlock’s formula including biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC), and femur length (FL). However, there is controversy in the medical literature regarding fetal weight percentage estimation. Percentage privatization according to maternal or paternal characteristics is one of the main sources of heterogeneity in the definition of growth retardation (IUGR). The usefulness of customized percentages is somewhat limited because the factors used for customization are not strong predictors of birthweight. The mother’s height, weight, ethnicity or race are related to fetal size, but this does not explain the significant variation in birth weight. Therefore, the limitations of these parameters limit their usefulness for IUGR definition. Therefore, the Fetal Growth Longitudinal Study, part of the Intergrowth-21st Project, aimed to develop international tabulated standards for fetal growth.
These curves have the advantage of using fetal growth standards derived from healthy populations. This reduces the underdiagnosis that can occur when compared with references, including fetal growth, high-risk mothers. In various study regions, these curves have proven to be similar for all fetal and neonatal measurements showing the same growth potential regardless of breed. Thus, the reported differences are likely to be related to nutritional issues rather than geographic location or ethnicity. However, several subsequent studies have shown that individualized fetal growth charts improve identification of patients at risk of adverse perinatal outcomes.
Differences Between Intrauterine Growth Retardation (IUGR) and Small Fetus by Gestational Age (SGA)
As small fetus is associated with worse obstetric outcomes, two groups of small fetuses are distinguished as the least intrauterine growth retardation (IUGR) and small for gestational age (SGA). The term intrauterine growth retardation (IUGR) refers to small fetuses with a higher risk of intrauterine fetal deterioration, stillbirth, and generally worse perinatal outcome than those with normal growth. These fetuses have a true growth retardation, usually associated with histological and biochemical manifestations of placental disease and doppler ultrasound findings showing hemodynamic redistribution due to adaptation to fetal malnutrition / hypoxia. Intrauterine growth retardation (IUGR) is also associated with an increased risk of preeclampsia.
Definition of Intrauterine Growth Retardation (IUGR) and Small for Gestational Age (SGA)
Available evidence suggests that there is no superior parameter to distinguish intrauterine growth retardation (IUGR) from small for gestational age (SGA). Looking at the individual doppler ultrasound study, the best candidate is the cerebroplacental ratio (CPR) calculated by dividing the middle cerebral artery (MCA) doppler pulsatility index (PI) (MCA-PI) by the umbilical artery (UA) doppler PI. This ratio reflects small decreases in fetal cerebral vascular resistance combined with slight increases in placental resistance. This relationship appears to be more susceptible to hypoxia than its individual components and is better associated with a possible negative outcome.
Also, uterine artery (UtA) PI (UtA-PI) is an indicator of worse perinatal outcomes in small fetuses. Another poor outcome prediction factor is a very small EFW independent of CPR and UtA-PI values. An EFW below the 3rd percentile indicates a much higher risk of reverse perinatal outcome. Therefore, when any of the three specified parameters (CPR, UtA-PI and / or EFW <3rd percentile), the risk of reverse perinatal outcome increases. Therefore, the definition of growth retardation IUGR should include these three parameters.
Severe Early Onset and Moderate Late Onset Intrauterine Growth Retardation (IUGR)
Intrauterine growth retardation (IUGR) is presented in two different phenotypes according to the onset of the disease in pregnancy: early onset and late onset. In general, there is a correlation between early onset and more severe forms of IUGR, so two types of intrauterine growth retardation (IUGR) are defined as severe early onset and moderate late onset. It was determined as the limit point for these forms at 32 weeks.
Early Onset Intrauterine Growth Retardation (IUGR)
Severe early onset IUGR represents 20-30% of all cases. It is associated with severe placental insufficiency and chronic fetal hypoxia, so UA doppler is often pathological. In this context, this type of growth retardation is associated with early preeclampsia in up to 50% of cases and severe damage or stillbirth before term. In addition, clinical management is a challenge due to the need to balance complications arising from prematurity with intrauterine permanence risks.
Without treatment, fetal well-being deteriorates progressively to hypoxia and acidosis, reflected in the sequence of changes in UA doppler and ductus venosus (DV) PI. The lag time to severe fetal deterioration is variable, but usually lasts for weeks and depends on the severity of placental compromise. The order of change is relatively constant, especially in the symptoms of advanced stages, except in cases where there is an associated preeclampsia that may distort the natural history. In such cases, fetal deterioration may appear unexpectedly. These changes in fetal doppler allow the progression of fetal deterioration to be monitored and delivery to be planned electively.
Moderate Late Onset Intrauterine Growth Retardation (IUGR)
While these fetuses represent 70-80% of cases, the placental change is mild and therefore UA is usually normal and has a low association with preeclampsia (10%). Diagnostic rates are low in these cases, which means that late (undiagnosed) IUGR causes the majority of late stillbirth. There is a high rate of CPR change in moderately late-onset IUGR. In addition, in 25% of cases of late-onset intrauterine growth retardation, a cerebral vasodilation may occur, reflecting the chronic state of hypoxia. In addition, signs of advanced fetal deterioration are almost never observed with changes in the ductus venosus.
Therefore, the sequential fetal deterioration cascade as previously described does not occur. These fetuses can undergo rapid deterioration that can result in serious injury or death. The explanation behind this fact may be a combination of factors such as the low tolerance of preterm fetuses to hypoxia (compared to preterm fetuses), higher frequency of uterine contractions in term pregnancies, and some cases of acute placental insufficiency. Despite the benign nature of this type of fetus, the risk of acute fetal deterioration before birth is significantly associated with late stillbirth, intrapartum fetal distress and neonatal acidosis.
Intrauterine Growth Retardation (IUGR) Common Problems
Both types of IUGR are associated with poorer long-term prognosis in neurological, cardiovascular, and metabolic development. This means that, regardless of its severity, chronic exposure to an unfavorable intrauterine environment is necessary to develop negative fetal programming. As might be expected, different stages of fetal maturation determine different adaptive programming responses.
Evidence suggests that both early and late onset IUGR are the result of a placental disease, but the extent to which they are the same type of pathology is unknown. Placental insufficiency of early onset intrauterine growth retardation is associated with histological changes in early implantation. However, it is not clear whether the late IUGR is a mildly abnormal form of placental implantation at the beginning of pregnancy, or if there is additional placental damage produced in the second half of pregnancy. The second option is supported by the fact that some of these patients had abnormal UtA doppler in the third trimester that were previously normal.
Author: Ozlem Guvenc Agaoglu