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Approach to Intrauterine growth restriction

The document is a presentation on intrauterine growth restriction (IUGR) by Dr. Anurakkhi Barua and Dr. Habibur Rahman Bhuiyan, outlining its definition, epidemiology, pathophysiology, and complications. IUGR is identified as a condition where a fetus fails to achieve its genetically determined growth potential, significantly increasing risks of stillbirth and perinatal mortality. The presentation also discusses diagnostic methods, maternal and fetal risk factors, and the long-term consequences of IUGR on health.

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Seminar on IUGR Dr. Anurakkhi Barua Resident, year 3, neonatology Dr. Habibur Rahman Bhuiyan Resident, year 4, neonatology
Presentation Outline • Definition • Epidemiology • Classification • Pathophysiology • Diagnosis • Complications • Prognosis • Prevention
• A fetus with IUGR is one that has failed to achieve its genetically determined growth potential, owing to one or more pathological factors . • SGA: when its estimated fetal weight is below a specific percentile for its gestation (10th percentile) for a given population. Definition WHO
• SGA baby having a higher rate of adverse outcome than average for gestational age babies. • up to 70% of fetuses identified as SGA are ‘constitutionally small. • IUGR fetus has at least a 10-fold increased risk of perinatal mortality SGA vs IUGR
Epidemiology • IUGR is the commonest cause of stillbirth. • the second leading cause of perinatal mortality, after preterm birth. • recent reports shows undiagnosed IUGR associated with 50% of stillbirths in the UK. • 30% of babies born before 35 weeks have IUGR • 4.5% of babies born at term have IUGR • SGA is 6 times higher in babies born preterm than term
• At least 10% of singleton pregnancies are SGA. • SGA is 20% in dichorionic and 30% of monochorionic twins. • IUGR occurs in 30–40% of pregnancies affected by pre- eclampsia. • In women who had a previous IUGR pregnancy the recurrence rate is about 20% • This is increased to approximately 50% in women with previous early IUGR Incidence
• Nationwide data is not available. • At NICU, BSMMU 2021 • SGA 11.8% • IUGR 9.54% • Symmetrical IUGR 7% • Asymmetrical IUGR 2.54% Many IUGR cases remain undetected. Incidence at Bangladesh perspective
Classification According to symmetry of growth: 1. Symmetrical IUGR 2. Asymmetrical IUGR According to onset: 1. Early onset (onset before 32 weeks) 2. Late onset (onset after 32 weeks)
Symmetrical IUGR • Head circumference, length, and weight are all proportionally reduced for gestational age (below 10th percentile). • When insufficiency appearing early in pregnancy. • Fetal weight is reduced out of proportion to length and head circumference . • Head sparing IUGR. When insufficiency appearing late in pregnancy. Asymmetrical IUGR
Normal Fetal Growth • upto 16 weeks = Cellular hyperplasia • 16 to 32 weeks= Hyperplasia & hypertrophy • After 32 weeks = Hypertrophy • Two third of fetal weight gain occurs beyond 24 th week of pregnancy
Fetal Risk Factors • Chromosomal anomaly: triploidy, trisomies (21,18,13), Turner syndrome etc • Genetic abnormalities and syndromes • Congenital anomalies • Fetal infections: TORCHs, malaria, human immunodeficiency virus, Epstein–Barr virus • Multiple pregnancies: monochorionic gestation, twin- to-twin transfusion
Maternal Risk Factors • Past obstetric history: previous intrauterine growth restriction, stillbirth, preterm birth • Social/environmental/nutritional: • extreme reproductive age • short pregnancy interval • poor diet • anorexia nervosa • body mass index <20 • high altitude • active inflammatory bowel disease • Smoking, substance abuse • self-neglect and/or psychiatric illness • medication (β-blockers, overtreatment of hypertension)
Maternal Risk Factors (cont) • Vasculopathy: chronic hypertension, pre-eclampsia, sickle-cell disease, antiphospholipid syndrome, SLE • Hypoxia: severe anaemia, chronic lung disease, severe asthma, cyanotic heart disease, Reduced plasma volume expansion • Renal disease: glomerulonephritis, lupus nephritis, chronic renal failure • Thrombophilia
Placental Risk Factors • Abnormalities of the umbilical cord: single umbilical artery, velamentous insertion of the cord, overcoiled umbilical cord • Tumours: chorioangiomatosis, placental mesenchymal dysplasia • Vascular: vascular malformations, fetal thrombotic vasculopathy, placental abruption • Abnormal placental development: placenta praevia, circumvallate placenta, abnormal trophoblast invasion, recurrent bleeding, confined placental mosaicism
Other Risk Factors • Uterine factors • Uterine abnormality, uterine fibroids, assisted reproductive techniques • Endocrine factors • Vascular endothelial growth factor, placental growth factor, pregnancy-associated plasma protein A, insulin-like growth factor
Insulin • Anabolic hormone • It controls the cell number because of direct mitogenic effects. • It leads to glucose uptake and consumption by body tissues and decreases protein breakdown. • Fetal insulin acts as a signal of nutrient availability for growth and insulin deficiency will lead to IUGR. • In insulin deficiency, IUGR results because of reduced uptake and utilization of nutrients.
IGF-I • It has mitogenic properties inducing somatic cell growth and proliferation. • It influences the transport of glucose and amino acids across the placenta. • IGF-I also has positive effect on brain growth, 1. increase in oligodendrocytes 2. neuronal number and neuronal outgrowth, 3. increases dendritic branching 4. increases axon terminal fields.
Thyroid hormone Thyroid hormone triggers discrete developmental events in the fetal brain and somatic tissues from early in gestation. Fetal hypothyroxinaemia leads to developmental abnormalities such as- • decreased oxygen consumption and • decreased oxidation of glucose • leading to decreased fetal energy supply for growth.
Others • Glucocorticoid hormone- development and maturation of fetal organs. • Insulin-like growth factor-II (IGF-II) -intrauterine programming of adipose tissue • Insulin-like growth factor binding protein-2 (IGFBP-2) developmental Neurotropic and Regenerative Functions IN CNS - binds (IGFs) • Insulin-like growth factor binding protein-3 (IGFBP-3) • vasoactive intestinal polypeptide (VIP) signaling is critical for the modulation of appetite/satiety and body mass phenotype
Stress Primary adaptive response Secondary adaptive response Progressive decompensation Death Chronic respiratory and nutritional insufficiency Decrease fetal growth rate • Fetal energy conservation Decreased fetal movement Decreased fetal heart rate reactivity • Circular redistribution Falling cerebral flow impedance Rising umbilical and aortic impedence • Fetal growth preferred over placental growth • Increased efficiency of placental exchange • Polycythemia- Greater O2 carrying capacity • Hypoxia → metabolic acidosis • High impedance in fetoplacental circulation → absent end diastolic flow in umbilical arteries • Declining amniotic fluid volume → Oligohydroamnios • Loss of fetal movement • Loss of fetal heart rate activity • Further detoriation Pathophysiology
Adapted from Sharma D, Farahbakhsh N, Shastri S, Sharma P. Intrauterine growth restriction–part 2.
Diagnosis of IUGR 1. Proper history taking 2. Establishing gestational age 3. Fetal assessment A) Clinical diagnosis B) Ultrasonography -Estimated fetal weight -Ratio of head and abdominal circumference -Femur length -Placental morphology and amniotic fluid -Placental volume measurements C) Biophysical profile D) Doppler study
Clinical Diagnosis Symphysio Fundal height (SFH) Closely correlates with gestational age after 24 weeks Lag of 4 cm or more –IUGR Sensitivity 21-27% Specificity 80-90% Serial measurement is important.
Biophysical profile 8-10 Normal, 6 = equivocal, <4 abnormal - induction of labor
Biophysical profile score • BPP <2 is 100% sensitive to detect fetal acidemia • However, BPP is less sensitive to detect fetal detoriation • Cardiotocography (CTG). It is a component of BPP and is limited when used alone.
USG of Pregnancy profile • To assess for FGR, 4 biometric measures are commonly used: 1. abdominal circumference 2. biparietal diameter 3. head circumference 4. femur length • The liver is the first organ suffers due to redistribution of ductus venosus blood flow to the heart • a decrease in glycogen deposition in the liver. • Reduced abdominal circumference (<5 mm/wk) is the earliest sign
• In the second trimester, • the head circumference>abdominal circumference. • 32 to 36 weeks =1:1 • after 36 weeks, the abdominal circumference ↑↑ • If the ration is <1 suggestive of IUGR. • Femur length: Serial measurements of femur length are as effective as head measurements for detecting early-onset FGR. Ratio of head circumference to abdominal circumference
Placental morphology • Placental morphology and amniotic fluid assessment helps in differentiating a constitutional small fetus from a growth-restricted fetus. • Placental aging with oligohydramnios suggests FGR • Placental volume measurements FGR with decreased placental size is more likely to be associated with fetal acidosis.
Doppler study • used to detect, monitor, and optimize time of delivery • Doppler studies are more helpful in diagnosing moderate to severe FGR than mild FGR. • The various groups of vessels used are as follows: • Uterine artery Doppler • Umbilical artery Doppler • Middle cerebral artery Doppler • Cerebro-placental ratio (CPR) • Ductus venosus Doppler • Aortic isthmus Doppler.
• Uterine arteries > maternal circulation • Umbilical arteries > fetal circulation • Middle cerebral arteries > fetal compensation • Ductus venosus Doppler > reflects fetal cardiac status
Quantitive analysis: • Pulsatility index (PI) • Resistance Index (RI) • Systolic/diastolic ratio (SD ratio) Qualitative analysis • Uterine artery: presence or absence of early diastolic notch • Umbilical artery(UA): normal with reduced diastolic flow • Absent End diastolic flow • Reversed EDF
Pulsatility Index chart
• Uterine artery flow abnormalities • Used to predict FGR as early as 12 to 14 weeks. • A persistent abnormality at 23 to 24 weeks has an approximate 75% sensitivity in predicting early FGR.
Umbilical artery flow abnormalities • Normally, the umbilical artery resistance declines with pregnancy. • Increased pulsatility index (PI), • decreased end-diastolic velocity (EDV) • absent EDV (AEDV) • reversed EDV (REDV) • AEDV and REDV are associated with 20% to 68% mortality. • Decreased EDV is seen when 30% of placental flow is attenuated • AEDV/REDV is noted when 60% to 70% of placental flow is affected. • AEDV and REDV are associated with a 4.0- and 10.6-fold increased risk of mortality.
Fetal cerebaral arterial flow • Usually studied in the MCA as a Pulsatility index and MCA peak systolic velocity (MCA PSV). • With worsening FGR, MCA PSV increases. • decreased MCA resistance is associated with worse perinatal outcomes. • MCA Doppler changes better identify late-onset FGR
Cerebroplacental ratio The CPR quantifies the redistribution of cardiac output by dividing the Doppler PI of the MCA with that of the UA. CPR = MCA PI/UA PI. • Adverse outcomes = CPR ratio of <1 or <1.08. • CPR can be affected in about 25% of term SGA fetuses. A decrease in expected CPR measurement after 28 weeks gestation is highly sensitive in diagnosing late onset FGR.
FREQUENCY OF MONITORING IN EARLY AND LATE FGR BPP: biophysical profile; CPR, cerebroplacental ratio; CTG, cardiotocography; DV, ductus venosus; EDV, end-diastolic flow; FGR, fetal growth restriction; FHR, fetal heart rate; MCA, middle cerebral artery; PI, pulsatility index;
Decreased amniotic fluid index Increased uterine artery resistance with EDV Decreased MCA resistance (brain sparing) Absent UA EDV Increased resistance in DV-reversed EDV in UA Reversed flow in DV and pulsatile flow in Umbilical vein Early Changes (2-3 Weeks before nonreactive FHR) Initial changes Late changes (6 days before nonreactive FHR) Very late changes (24 hours before changes in BPP) Sequential changes of doppler studies in decompensating fetal growth restriction
Comparision between normal and abnormal uterine artery Doppler velocimetry
International Archives of Integrated Medicine, 2019; 6(1): 118-127 In the present study, PIH was found to be the commonest (50.9%) cause of IUGR. Abnormal Doppler Indices in Umbilical and MCA correlated statistically with lower birth weight, higher rates of caesarean delivery, oligohydramnios, lower Apgar scores, perinatal death, and higher admissions to NICU. AEDF/REDF was associated with highest perinatal loss, poor perinatal outcome.
Ponderal index • to diagnose impaired fetal growth • to identify soft tissue mass is below normal for skeletal development. • The higher the score, the higher the level of body fat. • Normal range: 2.2 to 3.0 g/cm3 . • A ponderal index of <2 or <10% is suggestive of asymmetrical FGR
Placental magnetic resonance imaging • severity of FGR can be assessed by placental thickness-to volume ratio. • Fetal demise can also be predicted by a • abnormal vasodilatation • mesenteric vasoconstriction • preferential shunting through the foramen ovale etc
stages condition findings Intervention Stage I mild placental insufficiency Abnormal Doppler studies Carefull monitoring Stage II severe uteroplacental insufficiency There is absent EDV in the UA after 34 weeks Stage III fetal deterioration, low suspicion of fetal acidosis Risks of stillbirth reversal of EDV in the UA or DV PI >95th percentile around 32 weeks Stage IV fetal acidosis reversal of atrial flow on DV Imminent risk of fetal demise Deliver immediately Timing of delivery
• Early Antenatal diagnosis • Early admission of mother • Mode of delivery • Antenatal Corticosteroid • Delivery and Resuscitation • Prevention of heat loss • Prevention of hypoglycemia • Feeding protocol • Infection control • Management of complications Management
Neonatal Assesment Anthropometry • Reduced birth weight for gestational age. • Appropriate growth charts should be used. • Ponderal index˂ 10th percentile. • Ballard scoring
• Heads are dis proportionately large for their trunks and extremities • Facial appearance has been likened to that of a “wizened old man”. • Thin loose, peeling skin • Long nails. • Scaphoid abdomen Physical appearance
Gestation < 35 weeks Gestation ≤ 29 weeks If tolerating well Start MEN * after 24 hours if no contraindication @10ml/kg/day Birth weight ≥1250g Birth weight <1250g increase feeds @10- 20 ml/kg/day increase feeds @ 20-30 ml/kg/day Start MEN on day 1 if no contraindication @10-20 ml/kg/day Gestation ≥ 29 weeks Continue MEN for 48 hours then increase feeds @10ml/kg/day Add fortification once baby tolerates 100ml/kg/day of feeds and increase feeds till 150-180ml/kg/day AIIMS protocol 2019 Feeding algorithm for absent or reverse end diastolic flow *MEN minimal entral neutrition
• Dysmorphic facies • Congenital anomalies • Features of infection • Microcephaly • Petechiae • cardiac defect • Hepatosplenomegaly • intracranial calcification • Chorioretinitis • Cataracts). Physical appearance cont
Nine parameters (hair, cheeks, neck and chin, arms, legs, back, buttocks, chest, and abdomen) The maximum score is 36 Each category ranges 1-4 marks <25 is considered to be malnourished. Clinical Assessment of Nutrition Score (CAN Score):
It is the ratio of the head circumference (HC) to body weight • higher cephalization index reflects greater degree of brain vulnerability and • increased risk of cerebral palsy and severe psychomotor retardation. Cephalization Index
1. Intrapartum: • Fetal death • Acute-on-chronic hypoxia • Metabolic acidosis • Meconium aspiration Consequences of intrauterine growth restriction
2. Neonatal: • Hypoxic–ischaemic encephalopathy • Seizures • Respiratory distress syndrome • Hypotension • Heart failure • Pulmonary haemorrhage • Pulmonary hypertension • Renal failure • Hypoglycaemia/Hyperglycaemia • Hypothermia • Polycythaemia •Hyperviscosity •Renal vein thrombosis •Thrombocytopenia •Hyperbilirubinaemia •Feeding intolerance •Necrotising enterocolitis •Coagulopathy •Infection •Congenital abnormality •Adrenal insufficiency •Retinopathy of prematurity •Neonatal death Consequences of IUGR
66 Long term: Bronchopulmonary dysplasia Cognitive delay Cerebral palsy dysplasia Consequences of intrauterine growth restriction cont
They found that, despite a median difference of 3 weeks in gestational age at birth between IUGR and AGA infants, neonatal mortality was 35% higher in neonates who had experienced fetal growth restriction, and that IUGR was five times more predictive of CLD than was AGA. Neonatology 2014;106:304–310
68 Adulthood: Diabetes Obesity Hypertension Dyslipidaemia Cardiac disease Stroke Bronchitis Early menopause Consequences of IUGR
Thrifty Phenotype (Barker Hypothesis) • This metabolic programming (epigenetic modification ie, those molecular mechanisms affecting gene expression patterns without causing alterations in DNA base sequence) occurs at the critical time window of fetal development • These epigenetic changes become permanent or “programmed” in the genes of the fetus.
Antenatal epigenetic changes •Postnatal mismatched (normal or excessive nutrition) •Suboptimal environment (sedentary life, less physical activity, and sedentary life habits) •Child’s genetics Developmental origin of health and diseases (DoHaD)
Prognosis • Mortality decreases by 48% for each week that the fetus remains in utero before 30 weeks’ gestation • At 24 to 26 weeks gestation, survival is around 50% • survival improves to >90% by 32 weeks. • The total brain volume is also reduced by 10% particularly in the hippocampal, parietal, and parietooccipital areas. • Infants with congenital rubella or cytomegalovirus infection with microcephaly have a poor outcome, with a disability rate >50%. • increased prevalence of elevated fasting glucose and metabolic syndrome in childhood and adolescence.
• Neurodevelopmental morbidities are 5 to 10 times more often in FGR • minimal brain dysfunction, including hyperactivity, short attention span, and learning problems. • shows early neurobehavioral functions, such as attention- interaction capacity and cognitive and memory dysfunction. • Increased risk of cerebral palsy, learning disabilities, mental retardation, and neuropsychiatric disorders. • Growth may be hampered, growth hormone therapy (started before 8 years of age and continued for >7 years) can augment growth parameters.
A higher incidence of almost 50% in poorer neurodevelopmental scores during early childhood ages (from 15 to 24 months) among infants born after a pregnancy complicated by IUGR. results showed that the developmental outcome for children with IUGR was not influenced by birth weight, GA, gender, or type of IUGR, suggesting that IUGR is an independent variable for poor neurodevelopmental outcome. 2018
Prevention of IUGR • Prepregnancy counselling and proper health education • Balanced protein energy and micronutrients supplementation with healthy life style. • Ensure planned pregnancy at right age • Ensure regular antenatal check up • Treating chronic disease and pregnancy-induced disorders accordingly • Development a strong surveillance system with skilled manpower at all level
Key Messages • IUGR is a major concern in worldwide. • Proper history, antenatal, natal and postnatal assessment in necessary for diagnosis. • Better to follow up with Doppler study and ensure proper mode and timing of delivery • Early diagnosis and prompt management may reduce complication and unexpected consequences • These infants need to be monitored for long time with appropriate intervention.
Thank You