Intra Uterine Growth Retardation

1. Intra Uterine Growth Retardation Dr. Waffa Fageeh (Consultant and assistant professor King Abdulaziz University Hospital)

2. INTRODUCTION • Fetal growth restriction (FGR) is the term used to designate a fetus that has not reached its growth potential because of genetic or environmental factors. This term is an inaccurate label when used to describe the constitutionally small and otherwise healthy fetus. • FGR is a major focus of Prenatal care, because there is an inverse relationship between the fetal/neonatal weight percentile and parental morality.

3. DEFINITION • Intrauterine growth restriction (IUGR), fetal growth restriction (FGR), small for gestational age (SGA), and low birth weight (LBW) are all terms used to describe small babies. The most common definition of fetal growth restriction refers to a weight below the 10th percentile for gestational age. • As many as 70 percent of fetuses who are estimated to weigh below the 10th percentile for gestational age are small simply due to constitutional factors such as female sex or maternal ethnicity, parity, or body mass index; they are not at high risk of perinatal mortality and morbidity.

4. Normal Growth Is compromised of three consecutive and somewhat overlapping phases • The first phase is referred to as cellular hyperplasia (the first 16 weeks of gestation) • The second phase, known as the phase of concomitant hyperplasia and hypertrophy (between the 16th and 32nd weeks) increases in cell size and number. • The third phase, the phase of cellular hypertrophy (between the 32nd week and term) rapid increase in cell size.

5. Quantitatively, normal singleton fetal growth increases from approximately 5g/day at 14 to 15 week of gestation to 10g/day at 20 weeks and 30-35g/day at 32 to 34 weeks, after which the growth rate decreases. • The median growth rate in multiple gestations is lower than that of singletons during the 3rd trimester.

6. Abnormal growth • Abnormal growth • Symmetric FGR : comprises 30 percent of FGR, (all fetal organs are decreased proportionally) due to impairment of early fetal cellular hyperplasia. • Asymmetric FGR: comprises 70 percent of FGR is characterized by a relatively greater decrease in abdominal size (eg. Liver volume and subcutaneous fat tissue) then head circumference. It results from the capacity of the fetus to adapt to a hostile environment by redistributing blood flow in favor of vital organs (eg. Brain, heart, placenta) at the expense of non-vital fetal organs (eg. Abdominal viscera, lungs, skin, kidneys).

7. FETAL ETIOLOGIES • Genetic • Congenital anomaly • Multiple gestation

8. FETAL ETIOLOGIES • Genetic: contributes to approximately 40 percent of the variation in birth weight, most likely of symmetric type.

9. FETAL ETIOLOGIES • Congenital anomaly: 22 percent of anomalous infants were growth restricted.

10. FETAL ETIOLOGIES • Multiple gestations: fetal growth in multiple gestations has a direct relationship to the number of fetuses present; • The type of placentation also plays a role. • Growth is similar to that of singletons until 28-30 weeks • And then slows (15-20 percent less than that of singletons of the same gestational age)

11. PLACENTAL ETIOLOGIES • Placental size: which is a gross measure of placental capacity, is 24 percent lower in growth restricted infants than in normally grown infants when adjustments are made for gestational age • Gross placental structural anomalies: includes single umbilical artery, velamentous umbilical cord insertion, placental hemangioma, and possibly placenta previa. However, there is no single uteroplacental or villous pathalogical lesion that consistently results in FGR.

12. MATERNAL ETIOLOGIES • Poor nutrition • Hypoxia • Prothrombotic disorders • Hypertension and vascular disease • Infection • Substance abuse • toxin

13. MATERNAL ETIOLOGIES • Poor nutrition- severe maternal starvation during pregnancy ex (the Dutch population suffered severe famine during the winter of 1944-45; mean maternal {caloric intake fell from 750 to 450 kcal/day} average infant birth weight during this period decreased by 250 grams). Similarly, the average birth weight fell by more than 500 gramsin Leningrad during the world war 2 German siege, which resulted in a longer a more profound starvation period (down to 300 kcal of mostly carbohydrates and no proteins). • Modest degrees of nutritional deficiency also have an effect on birth weight, women who are underweight at the start of the pregnancy or have poor weight gain during the pregnancy are at higher risk of delivering an infant weighing less than 2500 grams.

14. MATERNAL ETIOLOGIES • Chronic maternal hypoxia due to pulmonary disease, cyanotic heart disease and sever anemia (as with sickle cell anemia) are often associated with FGR, as an example. • Residing at high altitudes also results in a chronic hypoxemia state and lower birth weight.

15. MATERNAL ETIOLOGIES • Hematological and immunological disorders: that cause thrombosis of the intervillous space and thus decreases uteroplacental perfusion (eg, antiphospholipid syndrome) • Hypotension and vascular disease: maternal medical disorders (eg, nephropathy, collagen vascular disease) and obstetrical complications (eg, preclampsia) associated with vasculopathy and diminished uteroplacental perfusion

16. MATERNAL ETIOLOGIES • Infection: viruses and parasites (eg, rubella, toxoplasmosis, cytomegalovirus, varicella-zooster, malaria) (to the fetus transplacentally or across the membranes) mainly early in pregnancy. There is less evidence implicating bacterial infection as an etiology for FGR, although maternal infection with listeria, TB, Chlamydia, and mycoplasma have been reported to increase the risk of FGR. • Substance abuse- including cigarette smoking, alcohol consumption and elicit drug abuse can cause FGR direct or indirectly from related variables such as inadequate nutrition. Smoking during the 3rd trimester appears to have the greatest impact on birth weight, and women who quit smoking by the 3rd trimester have birth weights similar to those of nonsmokers.

17. MATERNAL ETIOLOGIES • Toxins: • Toxic exposures, for various medications such as warfarin, anticonvulsants, antineoplastic agents, and folic acid antagonist, can produce FGR with specific dismorphic features, antihypertensive medications, high caffine consumption (>300 mg/day) unclear. • Environmental tobacco smoke (ETS) and infant birth weight. Most studies showed and increased risk of low birth weight in women with ETS

18. MATERNAL ETIOLOGIES • Sociodemographic variables: include race, pregnancy at the extremes of reproductive life, and previous FGR neonate. • Chronic maternal stress: is an active area of investigation. It is associated with elevated corticotrophin-releasing hormone (CRH) levels, which > FGR and preterm birth. • Paternal factors have less effects on birth weight than maternal.

19. Initial Diagnostic Evaluation • Diagnosis of FGR is based upon sonographic findings, which are discussed in details separately. • A complete hx and physical examination is performed to detect risk factors. • Fetal karyotyping is suggested if FGR is early (< 32 weeks), severe (> 3rd percentile), or accompanied by polyhydramnios (suggestive of trisomy 18) or structural.

20. Initial diagnosis and management • When there is a clinical suspection of viral infection maternal serum should be examined for evidence of seroconversion. Specific amniotic fluid viral DNA testing can also be performed, sonographic markers for viral infection are often non-specific but include echogenecity and classification of brain and liver and hydrops. • Assessment for congenital and acquired thrombophilic disorders maybe considered.

21. SUBSEQUENT OBSTETRICAL MANAGEMENT • Periodic asessment : once or twice weekly from the age of viability, using (BBP) and Doppler velocimentry is acceptable. To identify those fetuses who are at highest risk of utero demise and thus may benefit from intervention by preterm delivery. • Ultrasound evaluation of fetal growth. • Serial examinations should be performed with the frequency based upon the severity of findings (once to seven times per week) or fetal growth (ever 2-4 weeks).

22. Antenatal corticosteroids • The efficiency of antenatal corticosteroids in the management of the preterm growth restricted fetus remains controversial. • Fetal blood sampling- Antipartum fetal hypoxemia and acidemia are not associated with neonatal cerebral disfunction if fetal cardiovascular compensation with increased cerebral bloodflow occuring. However, if asphyxia persists, brain damage and death may occur • Fetal blood sampling (FBS) for in severly growth restrictesd fetuses to assist in the identification of the optimal timing for delivery. However, fetal loss may occur.

23. Medical interventions • Antenatal treatment for the growth restricted fetus is benifitial. Nutritional suplementation, plasma volume expansion, low-dose aspirin, heparin, bed rest, maternal oxygen therapy, and beta-mimetics/calcium channel blockers were used to improve blood flow to the placenta. None have consistantly been shown to be of value. • Antihypertensive therapy of hypertensive gravidus doesn't improve fetal growth

24. Intapratum management • Labour with careful intrapartum monitroing and vaginal delivery is a reasonable approach in the presence of normal antenatal testing. The clinician should be prepared for rapid intervention if there is any evidence of fetal intolerance to labour

25. Recurrence Risk • The tendancy to repeat SGA or low birth weight deliveries in succesive pregnancies are around 9 and 29 percent, respectively.