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IUGR.pptx

Intrauterine growth restriction (IUGR) refers to diminished fetal growth velocity documented by at least two growth assessments, whereas small for gestational age (SGA) describes an infant whose measurements fall below the 10th percentile. IUGR babies appear malnourished with poor fat stores compared to constitutionally small but normal SGA infants. IUGR is associated with 3-10% of pregnancies and carries risks of stillbirth, prematurity complications, and long term metabolic issues. Diagnosis involves identifying risk factors, serial ultrasounds assessing growth curves and Doppler flow, and management focuses on determining causes, monitoring fetal wellbeing, and timing of delivery to balance prematurity risks.

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INTRAUTERINE GROWTH RESTRICTION (IUGR)
Definition Although many use the terms “SGA” and “IUGR” interchangeably, they refer to two different concepts. SGA describes a neonate whose birth weight or birth crown–heel length is <10th percentile for GA or <2 standard deviations (SDs) below the mean for the infant’s GA. IUGR describes diminished growth velocity in the fetus as documented by at least two intrauterine growth assessments (e.g., a fetus that is “falling off” its own growth curve). After birth, IUGR babies appear malnourished, with poor subcutaneous fat, whereas SGA babies will look like small but normal babies. Babies who are constitutionally SGA are at an overall lower risk compared to those who are IUGR due to some pathologic process. Numerous “normal birth curves” have been published from different populations. The etiology and management of SGA and IUGR fetuses overlap considerably.
IUGR Facts IUGR associated with 3-10 % of all pregnancies Perinatal mortality rate is 5-20 times higher for growth retarded fetuses. 2nd leading contributor to the Perinatal mortality rate 20% of all stillbirths are IUGR Incidence of intrapartum asphyxia in cases ofIUGR has been reported to be 50%. Early and proper identification and management lowers this perinatal mortality and morbidity
Normal Fetal Growth Normal fetal growth is characterized by cellular hyperplasia followed by hyperplasia and hypertrophy and lastly by hypertrophy alone. Fetal Growth From 8 to 40 Weeks
Classification of Inrauterine Growth Restriction 1. Symmetrical IUGR 2. Asymmetrical IUGR
Symmetrical IUGR Head circumference, length, and weight are all proportionally reduced for grstational age (below 10 percentile). It is due to either decreased growth potential of the fetus or extrinsic conditions that are active in pregnancy. Asymmetrical IUGR Fetal weight is reduced out of proportion to length and headcircumference. The usual causes are uteroplacental insufficiency, maternal malnutrition, or extrinsic conditions appearing late in pregnancy.
Diagnosis of IUGR Identifying mothers at risk poor maternal nutrition Poor BMI at conception Pre-eclampsia Renal disorders Diseases causes vascular insufficiency Infections (TORCH) Poor maternal wt. Gain during pregnancy
Diagnosis Clinical Palpation of uterus Serial measurement is important Fundal height Liqour volume Fetal mass Maternal weight gain- stationary or falling during second half of pregnancy SFH(symphysis fundal hieght) Closely correlates with gestational age after 24weeks Lag of 4 cm or more- IUGR Fairly sensitive (30-80%) Abdominal girth- stationary or falling
Biophysical First examination (16-20 weeks) should confirm gestational age, anomalies USG- 2-3 weekly Diagnosis of IUGR, type Head circumference/ Abdominal circumference ratios >1- before 32 weeks Elevated- asymmetrical IUGR =1-32-34 weeks Normal-asymmetrical IUGR <1- after 34 weeks 85% IUGR fetuses are detected AC-Single most sensitive parameter
Serial measurements of AC and estimation of fetal weight are more diagnostic Femur length Not affected in asymmetric IUGR FL/AC =22 from 21 weeks to term FL/AC> 23.5-IUGR Amniotic fluid volume Vertical pocket of amniotic fluid <1 cm suggests IUGR Four quadrant technique-measuring vertical diameter of largest pockets of fluid found in each of 4 quadrants of uterus. The sum of results is AFI AFI 5 to 25 cm-normal AFI< 5 cm- oligohydramnios Anatomical survey: To exclude fetal abnormalities Bi-parietal diameter
Ultrasound doppler parameters Doppler velocimetry Elevated uterine artery S/D ratio (>2.6) presence of diastolic notch Diastolic notch suggests incomplete invasion of placental trophoblasts to uterine spiral arteries Also predicts possible development of pre-eclampsia Normally, diastolic flow increases as pregnancy progresses. Reduced/absent/reversed diastolic flow in umbilical artery indicates fetal jeopardy and poor perinatal outcome
Middle cerebral artery Increased diastolic velocity(brain sparing effect) in compromised fetus Cerebro-Placental Doppler ratio [RI (mca)/ RI (umb. A.)] is decreased The normal ratio is > 1. PI Degree of fetal wasting judged (birth weight/Crown-heel length 3) <10 th percentile –IUGR Reduction of fetal facial fat stores- IUGR
Biochemical markers Elevated levels of MSAFP and hCG level in second trimester are markers of abnormal placentation and risks of IUGR
Complications Fetal Antenatal- chronic fetal distress, fetal death, diminished amniotic fluid volume increases the likelihood of cord compression Intranatal –hypoxia, acidosis After birth- immediate -late
Immediate Asphyxia, bronchopulmonary dysplasia and RDS Hypoglycemia due to shortage of glycogen reserve in liver because of chronic hypoxia Meconium aspiration syndrome Microcoagulation leading to DIC Hypothermia Pulmonary haemorrhage Polycythaemia, anaemia, thrombocytopenia Hyperviscosity thrombosis Necrotising enterocolitis due to reduced intestinal blood flow IVH
Electrolyte abnormalities, hyperphosphataemia, hypokalemia due to impaired renal function Multiorgan failure Increased perinatal mortality and morbidity
Late Symmetrical growth retarded baby is likely to grow slowly after birth Asymmetrical- catch up growth in early infancy 1. retarded neurologic and intellectual development in infancy Worst prognosis- congenital infection, congenital abnormalities, chromosomal defects 2. Increased risk- metabolic syndrome in adult life: obesity, hypertension, diabetes, coronary heart disease
3. altered orexigenic mechanism that causes increased appetite and reduced satiety 4. Reduced no of nephrons- renal vascular hypertension
Management of Small for Gestational Age/Intrauterine Growth Restriction Pregnancy a. Attempt to determine the cause of SGA/IUGR by searching for relevant factors by history, laboratory, and ultrasonic examination. Treat any underlying cause when possible. Chronic fetal hypoxemia is encountered in about 30% of SGA/IUGR fetuses. b. Monitor fetal well-being, including nonstress test, a biophysical profile, fetal movement counts, amniotic fluid volume evaluation, and serial ultrasonic examinations. Doppler evaluation of placental flow may be used to evaluate uteroplacental insufficiency. c. Consider the effects of prematurity if early delivery is contemplated.
Delivery. Early delivery is necessary if the risk of intrauterine fetal demise still is considered greater than the risks of preterm birth. A. Generally, indications for delivery are an arrest of fetal growth and/or fetal distress, especially closer to term. b. Acceleration of pulmonary maturity with glucocorticoids administered to the mother should be considered at 24 to 34 weeks pregnancy. C. If there is poor placental blood flow, the fetus may not tolerate labor and may require a cesarean delivery. D. Infants with extreme SGA/IUGR are at a risk for perinatal complications and often require specialized care in the first few days of life. Therefore, if possible, delivery should occur at a center with a NICU or special care nursery. The delivery team should be prepared to manage perinatal depression, meconium aspiration, hypoxia, hypoglycemia, and heat loss.
Management of new born Delivery Resuscitation Prevention of heat loss Hypoglycemia Hematologic disorders Congenital infections Genetic anomalies
Potential complications related to SGA/IUGR i. Congenital anomalies ii. Perinatal depression iii. Meconium aspiration, persistent pulmonary hypertension iv. Hypoglycemia from depletion of glycogen stores v. Hypothermia from depletion of subcutaneous fat vi. Polycythemia vii. Neutropenia viii. Thrombocytopenia ix. Hypocalcemia
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