Intrauterine Growth Restriction PDF

Intrauterine Growth Restriction Asena Ayar Madenli, M.D., Asst. Prof Istinye University Faculty of Medicine Department of Obstetrics and Gynecology Introduction IUGR:a fetus is unable to grow to its genetically determined potential size t...

Intrauterine Growth Restriction Asena Ayar Madenli, M.D., Asst. Prof Istinye University Faculty of Medicine Department of Obstetrics and Gynecology Introduction IUGR:a fetus is unable to grow to its genetically determined potential size to a degree that may affect the health of the fetus. SGA : refers to a fetus that has failed to achieve a specific biometric or estimated weight threshold by a specific gestational age. New terminology for IUGR is FGR (fetal growth restriction) Epidemiology Fetal growth restriction (FGR) is identified in about 3% to 7% of pregnancies. It is reported to be 6 times higher in the underdeveloped and developing countries compared to the developed ones. Approximately 20% of all infants are small for gestational age at birth in low-income countries, and one in four of such infants may encounter death. Asian continents account for 75% of all affected infants. Women with preeclampsia who have a prior history of growth-restricted fetuses demonstrate a recurrence rate of 20% in subsequent pregnancies. About 40 percent of the FGR cases are idiopathic, with no identifiable cause. Among the remaining 60% of cases with identifiable causes, 1/3 are due to genetic anomalies and the rest secondary to environmental factors Classification The severity of FGR is determined by the EFW. EFW between 3rd and 9th percentile - moderate FGR EFW less than the 3rd percentile - severe FGR Based on additional fetal biometric parameters, such as head circumference (HC), abdominal circumference (AC), femur length (FL), and biparietal diameter (BD), FGR can be categorized as SYMMETRICAL and ASYMMETRICAL. In symmetrical FGR, all growth parameters are proportionally reduced, whereas, in asymmetrical FGR, classically, the abdominal circumference is reduced below 10 percentile, while other measurements are relatively preserved and may be within normal limits. Depending on the time and duration of occurrence, severe fetal malnutrition can cause either symmetrical or asymmetrical FGR Symmetrical FGR This group constitutes 20% to 30% of all FGR cases. Poor placental function is a well-established cause of FGR. Adverse intrauterine conditions beginning in the early pregnancy (first trimester) that may cause fetal nutrient restriction, such as smoking, cocaine use, chronic hypertension, anemia, and chronic diabetes mellitus, may result in symmetrical FGR. Chromosome anomalies, such as aneuploidy, are a major cause of symmetrical FGR. TORCH infection (Toxoplasma gondii, cytomegalovirus, herpes simplex virus, varicella- zoster virus, Treponema, and others) contracted prenatally are present in 5% to 15% of cases with FGR and form an important group. Asymmetrical FGR In asymmetrical FGR, which constitutes about 70% to 80% of all FGR cases, the timing of intrauterine insult is at the late second or third trimester of pregnancy. The growth restriction is disproportionate, with relative preservation of head circumference (fetal brain) and reduced abdominal circumference (fetal liver), resulting in an increased brain to the liver ratio (BLR). Preeclampsia is a well-recognized cause of asymmetrical FGR. This condition, identified in about 8% of pregnancies in western countries, generally develops after 20 weeks of gestation and is characterized by hypertension and proteinuria.Chronic hypertension leads to placental vascular remodeling, vascular sclerosis, and ischemia, thus impeding blood flow to the fetus. As a result, the fetal liver glycogen and body adipose tissues are diminished while the brain continues to grow normally with a preferential blood supply. Etiology Clinically the etiology may be categorized into fetal, placental, or maternal causes. However, there is a significant overlapping of pathogenesis. Fetal causes: Fetal genetic anomalies are detected in 5% to 20% of FGR cases. These may be due to aneuploidy, uniparental disomy, single-gene mutations, partial deletions or duplications, ring chromosome, and aberrant genomic imprinting. The finding of symmetric FGR prior to 20 weeks of gestation suggests aneuploidy. Fetal infection is responsible for 5% to 10% of FGR cases, the most common being cytomegalovirus and toxoplasmosis. Other infectious agents implicated are varicella-zoster virus, malaria, syphilis, and herpes simplex. Fetuses with non-chromosomal congenital anomalies or specific syndromes may also be growth restricted. Etiology Maternal causes: Maternal morbidities can adversely interfere with uteroplacental-fetal blood flow and cause FGR. These conditions include chronic hypertension, gestational or pregestational diabetes mellitus, systemic lupus erythematosus, antiphospholipid syndrome, severe cardiopulmonary or renal diseases, severe anemia and malnourishment, sickle cell disease, substance abuse (alcohol, cocaine, nicotine, heroin, marijuana, and others), anti-neoplastic drugs or radiation exposure, chronic antepartum hemorrhage, low pre-pregnancy weight or poor gestational weight gain, extremes of maternal age, short interpregnancy interval, high altitude residency, multiple gestations, uterine malformations, and assisted conception. Maternal nutritional status can be responsible for almost a 10% variance in fetal weight. Mothers who were growth restricted carry twice the risk for delivering FGR neonates Etiology Placental/umbilical cord causes: Chromosomal placental mosaicism (CPM), presenting with placental trisomy (most commonly trisomy 21) and a chromosomally normal fetus, is identified in 10% of idiopathic cases of FGR and 33% of FGR with placental infarction and decidual vasculopathy. Placental anomalies (bilobate or circumvallate placenta, small placenta, placental mesenchymal dysplasia), umbilical cord anomalies (single artery, velamentous or marginal cord insertion) are other causes of FGR. Pathophysiology Pathologically, the body fat and muscle mass are reduced in the fetus, resulting in decreased subcutaneous fat, as well as body nitrogen and protein contents. The reduction in the maternal-fetal transfer of nutrients due to placental insufficiency, namely glucose, amino acids, and minerals, leads to lesser deposition of glycogen in the liver and muscles, and of minerals in the bones. As the fetus continues to be under stress, the blood flow is diverted away from less vital organs and redirected preferentially to the brain, heart, adrenal glands, and placenta History and Physical Examination History The maternal history of the following may suggest an increased risk of FGR. Previous pregnancy with FGR Previous pregnancy with preeclampsia History of smoking or substance abuse Multiple gestations Assisted conception Chronic illnesses Extremes of maternal age History and Physical Examination Physical Examination Maternal Findings The fundal height that estimates gestational age by measuring the distance between the pubic symphysis and the top of the uterus might be decreased. Neonatal Findings The neonate with FGR is less than 10 percentile for weight and typically looks emaciated with decreased muscle mass and subcutaneous fat at birth. The head may look proportionately large or small depending upon the pathogenic factor for intrauterine growth restriction. The facies may appear thin, and the umbilical cord shrunken. Due to the lack of proper bone mineralization and bone formation, the cranial suture may be wide and fontanels large. The Ponderal index [PI=weight (g) x100/height (cm)] is a good indicator of the severity of fetal malnutrition, especially in asymmetric FGR. PI less than the 10th percentile indicates malnutrition. Evaluation ACOG recommends performing serial fundal height during every prenatal visit.A serial ultrasonography study is warranted if the fundal height is less by 3 cm or more than the gestation in weeks. The ultrasound scan also serves to detect the presence of anatomical abnormalities in the fetus. An accurate assessment of the gestational age is of utmost importance for differentiating FGR from a misdated pregnancy. The guidelines also stress the need for early detection of high-risk pregnancies, such as those with a prior history of FGR, substance abuse (tobacco, alcohol, others), advanced maternal age, preeclampsia, or previous pregnancy complicated with preeclampsia among others. Serial ultrasonography is strongly indicated if risk factors are identified. If FGR is detected, amniotic fluid volume estimations and umbilical arterial Doppler blood flow velocimetry (UADV) studies should be performed. Treatment / Management Early detection is imperative for the optimization of neonatal outcomes. Ultrasonography is particularly useful in estimating fetal weight and for diagnosing FGR by utilizing biometric measures, such as head circumference (HC), abdominal circumference (AC), femur length (FL), and biparietal diameter (BD).[ AC is the single most sensitive biometry for FGR and yields the best results when done at 34 weeks of gestation, or closer to term, especially in the cases of asymmetric FGR. Other useful biometric studies are HC/AC and FL/HC ratios, which can differentiate between symmetrical and asymmetrical FGR. An interval of 3-4 weeks between scans is recommended in pregnancies with suspected FGR. Treatment / Management A distinction needs to be made between biometric tests (tests to measure size) and biophysical tests (tests to assess fetal wellbeing. the diagnosis of SGA would rely on biometric tests while abnormal biophysical tests are more indicative of FGR. Abdominal palpation has limited diagnostic accuracy to predict a SGA fetus. Symphyseal fundal height (SFH) measurement has limited diagnostic accuracy to predict an SGA neonate. Although early studies reported high sensitivity and specificity , a large study found the sensitivity and specificity to be 27% and 88%, respectively. Serial measurements may improve sensitivity and specificity A customised fundal height chart improves accuracy to predict a SGA fetus. A customised SFH chart is adjusted for physiological variables such as maternal height, weight, parity and ethnic group. Use of such charts was found to result in improvement in sensitivity. Treatment / Management Most prenatal interventions do not show any significant effects on perinatal outcome Aspirin oxygen therapy nutrient therapy hospitalization and bedrest Betamimetics calcium channel blockers hormonal therapy plasma volume expansion Not enough evidence Management of Early-onset FGR (