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6. Foetal Growth Restriction as IUGR is Obsolete
6.1 Introduction
Foetal growth restriction (FGR) refers to a pathological condition in which the foetus is unable to grow to its genetically determined biological potential and is below the tenth percentile of the estimated foetal weight for that gestational age. The term FGR needs to be differentiated from the term small for gestational age (SGA) for a foetus in utero. Small for gestational age foetus refers to a foetus with an estimated weight less than tenth percentile on ultrasound. These foetuses may or may not be growth restricted. Majority of SGA foetuses (50–70%) are not growth restricted but are constitutionally small but are healthy and appropriate for the maternal height, weight, ethnic origin and foetal sex [1]. Small mothers give birth to small babies. Of the remaining, 10–15% are small due to inherent defect in the foetus, and the remaining 20–35% are due to chronic placental insufficiency. Physiological SGA babies or constitutionally small babies are healthy and have perinatal morbidity and mortality comparable to appropriate for gestational age babies, whereas FGR babies have higher perinatal mortality and morbidity [2]. Foetal growth restriction is more common in neonates with severe SGA that have a weight below the third percentile [3]. However, average for gestational age AGA foetuses may be growth restricted sometimes. Inspite of being above tenth percentile these foetuses have evident signs of chronic placental insufficiency and foetal compromise such as reduced abdominal circumference, oligohydramnios and abnormal Doppler studies in utero that often result in intrapartum stillbirth. The placenta in these cases is smaller than normal, calcified and meconium stained. These are often missed during antenatal examination.
The challenge to the obstetrician managing foetal growth restriction is to differentiate growth restricted foetuses from constitutionally small healthy foetuses and to monitor and optimally time the delivery of growth restricted foetuses and at the same time avoid inadvertent harm to the healthy foetuses by premature intervention. The aim is to minimize adverse sequelae in growth restricted foetuses due to suboptimal intrauterine environment and balance it against the risks of prematurity.
6.2 Aetiopathogenesis
Foetal growth restriction can be placental mediated or non-placental mediated. The placental-mediated growth restriction is secondary to conditions like hypertensive disorders of pregnancy, antiphospholipid syndrome and diabetes mellitus with vasculopathy. Non-placental-mediated growth restriction is due to intrinsic defects in the foetus like chromosomal abnormalities, structural anomalies, metabolic disorders or intrauterine foetal infections like cytomegalovirus, toxoplasma, malaria, syphilis, etc.
In placental-mediated causes, there is chronic placental insufficiency due to poor placentation and/or thrombosis compromising the blood flow and supply of nutrients and oxygen to the foetus. Conditions affecting the oxygen-carrying capacity of blood in the mother like haemoglobinopathies, cyanotic heart disease, high altitude, smoking, etc. can also result in foetal growth restriction.
Causes of foetal growth restriction
Maternal | Placental | Foetal |
|---|---|---|
• Smoking • Substance abuse: tobacco, alcohol cocaine, narcotics • Protein calorie malnutrition • Uterine malformation • Hypertensive disorders of pregnancy • Renal disease • Pre-gestational diabetes mellitus with vasculopathy • Cyanotic heart disease • Autoimmune disorders: SLE • Thrombophilia • Haemoglobinopathies | • Placental abnormalities: circumvallate placenta, chorioangioma • Placenta previa • Chronic placental abruption • Abnormal cord insertion: marginal or velamentous | • Multiple pregnancy: twin-to-twin transfusion syndrome, discordant twins • Structural anomalies: gastroschisis • Chromosomal/genetic anomalies: trisomy 13, 18 • Intrauterine infections: Cytomegalovirus, toxoplasma, rubella, malaria, syphilis • Inborn errors of metabolism • Exposure to teratogens like warfarin, valproic acid |
6.3 Diagnosis and Differential Diagnosis (Flow Chart 1)
Approach to a woman suspected with SGA foetus
FGR is also suspected on ultrasonographic examination by a lag in foetal biometry that is BPD, HC, AC, FL and estimated foetal weight for that gestational age. Of these parameters, foetal abdominal circumference (AC) or EFW of less than tenth percentile is the most reliable for diagnosis of SGA foetus [5]. Foetal abdominal circumference is the first to get affected due to depletion of liver glycogen and loss of subcutaneous fat in a foetus deprived of nourishment. However, it is important to have an accurate assessment of gestational age preferably by crown-rump length (CRL) in a first trimester ultrasound. Serial assessment of AC and/or EFW for growth velocity should be done at least 3 weeks apart to differentiate normally growing constitutionally small foetuses from growth restricted foetuses with reduced foetal growth velocity [5]. A detailed anatomical survey of the foetus to rule out any structural anomaly should be done in all foetuses with growth below the tenth centile.
The presence of advanced placental maturity or grading and reduced liquor suggests chronic placental insufficiency and foetal growth restriction [6]. Doppler flow studies are effective in diagnosing placental cause of foetal growth restriction. Umbilical artery Doppler flow study is done initially and is followed by middle cerebral artery and venous Doppler studies if required. As the pregnancy advances, the diastolic flow in umbilical artery increases with resultant decrease in the systolic to diastolic (S/D) flow ratio. Normally S/D ratio is less than three after 30 weeks of gestation. In patients with placental cause of FGR, this increase in flow is compromised and is reflected progressively as an increased S/D ratio, absent end-diastolic flow and reversed end-diastolic flow.
In women with evidence of chronic placental insufficiency, further workup for the cause should be initiated. The woman should be followed up for development of preeclampsia, subjected to investigations for the diagnosis of antiphospholipid syndrome, namely, antiphospholipid antibodies, anticardiolipin antibodies, lupus anticoagulant and anti-beta-2 glycoprotein 1 antibodies. The woman is screened for autoimmune disorders like systemic lupus erythematosus by testing for antinuclear antibodies or any infections caused by VDRL and TORCH profile.
In foetuses with normal Doppler flow studies and normal liquor amnii, serial ultrasound examinations are carried out to see the growth velocity, and if found normal, the foetus is likely to be constitutionally small. If the EFW or AC is less than third centile, it is suggestive of severe SGA and is likely to be FGR. Inherent foetal defects and chromosomal or genetic or intrauterine infections should be suspected in these women. Invasive testing in the form of amniocentesis for karyotyping or gene analysis may be offered in women with severe and/or early FGR, presence of normal or excessive liquor, structural anomalies and normal Doppler flow. It is not indicated in women with FGR due to chronic placental insufficiency.
6.4 Complications
Growth restricted foetuses are at an increased risk of stillbirth and neonatal mortality and morbidity. The risk is directly proportional to the severity of growth restriction and prematurity. The neonate is at an increased risk of hypoglycaemia, hypothermia, hyperbilirubinemia, respiratory distress syndrome, intraventricular haemorrhage, necrotizing enterocolitis, sepsis, seizures, NICU admission and neonatal death. These babies are also predisposed to long-term morbidity in the form of cognitive defects and diseases like type 2 diabetes mellitus, obesity, coronary heart disease, etc.
6.5 Management
6.5.1 Antepartum
6.5.1.1 Risk Assessment for Foetal Growth Restriction (Table 6.2)
Risk factors for FGR
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