Intrauterine Growth Restriction (IUGR)

OTHER NAMES DYSMATURITY. SMALL FOR DATE. CHRONIC PLACENTAL INSUFFICIENCY.

Normal Fetal Growth Normal fetal growth is characterized by cellular hyperplasia followed by hyperplasia and hypertrophy and lastly by hypertrophy alone.

Definition Intrauterine growth restriction is defined as babies whose birth weight is below 10 th percentile of the average for the gestational age. Growth restriction can occur in preterm, term or post term babies.

Incidence About 2-8%. Among term babies (5%). Post term babies (15%).

Types of IUGR SYMMETRICAL IUGR ASYMMETRICAL IUGR INTERMEDIATE IUGR

Cont.,., Symmetrical IUGR:  Fetus is affected from the noxious effect very early in the phase of cellular hyperplasia.  Caused by: Structural or chromosomal abnormalities. Congenital infection (TORCH).  The pathological process is intrinsic to the fetus & involves all the organs including the head.

Cont.,., Asymmetrical IUGR:  The fetus is affected in later months during the phase of cellular hypertrophy.  Total cell number remains the same but SIZE is smaller than normal.  Alters the fetal size by reducing utero placental blood flow or by restricting the O2 & nutrient transfer or by reducing the placental size.

Cont.,., Intermediate IUGR: It is a combination of type 1 and type 2. Fetal growth restriction occurs during intermediate phase of growth affecting both hyperplasia and hypertrophy, resulting in decrease in cell no, as well as size. Causes include Chronic HT. Lupus nephritis. Maternal vascular diseases that are severe and have onset in early 2 nd trimester.

Cont.,.,.,

Features of IUGR Fetuses Symmetrical Uniformly small. Ponderal index(between wt/crown to heel)-Normal. Head circumference: Abdominal circumference. Femur length: AC –Normal. Etiology: Genetic disease or infection (Intrinsic to fetus). Asymmetrical Head- larger than abdomen. Low. Elevated. Chronic placental insufficiency (Extrinsic to fetus).

Cont.,.. Symmetrical Total cell no: less. Cell size: Normal. Neonatal Course: Complicated with poor prognosis. Asymmetrical Total cell no: Normal. Cell size: Smaller. Neonatal Course: Usually uncomplicated having good prognosis.

A comparison between normal and IUGR babies.

Normal and IUGR placenta

Etiology IUGR is a manifestation of maternal, fetal and placental disorders that affect fetal growth. Maternal Causes: 1.Maternal Characteristics: Those contributing to IUGR are- Extremes of maternal age. Grandmultiparity. History of IUGR in previous pregnancy. Low maternal weight gain in pregnancy.

Cont.,., 2.Maternal diseases: Uteroplacental insufficiency resulting from medical complications like: Hypertension. Renal disease. Autoimmune disease. Hyperthyroidism. Long term insulin dependent diabetes. Smoking. Alcohol & drugs.

Cont.,., Fetal Causes: 1.Chromosomal Disorders: Usually result in early onset IUGR. Trisomies 13, 18, 21 contribute to 5% of IUGR cases. Aneuploidy. Triploidy. Turner’s syndrome.

Cont.,., 2.Congenital Infections: The growth potential of fetus may be severely impaired by intrauterine infections. Viruses- rubella, CMV, varicella and HIV rubella is the most embryotoxic virus, it cause capillary endothelial damage during organogenesis and impairs fetal growth. CMV causes cytolysis and localized necrosis in fetus. Protozoa- like malaria, toxoplasma, have also been associated with growth restriction.

Cont.,., 3. Structural Anomalies: All major structural defects involving CNS,CVS,GIT, Genitourinary and musculoskeletal system are associated with increased risk of fetal growth restriction. If growth restriction is associated with polyhydramnios, the incidence of structural anomaly is substantially increased.

Cont.,., 4.Genetic Causes: Maternal genes have greater influence on fetal growth. Inborn errors of metabolism like agenesis of pancreas, congenital lipodystrophy, galactosemia, phenylketonuria also result in growth restriction of fetus.

Cont.,., Placental Causes: Placenta is the sole channel for nutrition and oxygen supply to the fetus. Single umbilical artery. Abnormal placental implantation. Velamentous umbilical cord insertion. placental haemangiomas have all been associated with fetal growth restriction.

Cont.,., Unknown Causes: About 40% of the causes remains unknown.

Pathophysiology

Signs & Symptoms PHYSICAL FEATURES AT BIRTH:  Weight deficit at birth is about 600 g below the minimum in percentile standard.  Length is unaffected.  H.C is larger than body.  Physical features: Dry & wrinkled skin because of less subcutaneous fat. Scaphoid abdomen.

Cont.,., Thin meconium stained vernix caseosa. Thin umbilical cord. Pinna of ear: cartilaginous ridges. Plantar creases: well defined. Baby looks like: “OLD MAN”. Baby is alert, active & having a normal cry. Reflexes are normal.

Diagnosis 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.

Cont.,.., Determination of gestational age is of utmost importance: – Can be calculated from the date of LMP- not reliable – Ultrasound dating before 21 wks of pregnancy provides more accurate estimation.

Cont.,., 1.Clinically- Serial measurement of fundal height and abdominal girth. NORMAL: Symphysio-fundal height normally increases by 1cm per wk b/w 14 and 32 wks. MODERATE: A lag in fundal ht. of 4 wks. SEVERE: A lag in fundal ht. of >6 wks.

Cont.,., 2.Sonographic evaluation: Most useful tool for diagnosis of IUGR. To differentiate between symmetrical and asymmetrical IUGR. To monitor the fetal condition.

Cont.,., 3. Biophysical:  H.C & A.C ratios: Asymmetrical IUGR: H.C/A.C is elevated. Symmetrical IUGR: Both H.C & A.C is reduced.  FEMUR LENGTH (FL): If FL/AC ratio greater than 23.5 suggests IUGR.  AMNIOTIC FLUID VOLUME: AFI: 5-25 cm (Normal). AFI: <5 ( Oligohydramnios).

Complications of IUGR IMMEDIATE Asphyxia, Broncho- pulmonary dysplasia & RDS. Hypoglycemia. MAS, DIC. Hypothermia. Polycythemia. Pulmonary hemorrhage. Thrombocytopenia, NEC. Hypokalemia. Hyperphosphatemia. LATE Retarded neurological & intellectual development in infancy. In adult life: Obesity, HT,DM,CHD. Reduced no of nephrons causes Renal vascular HT.

Management If pregnancy < 37 weeks. Severe IUGR Mild IUGR Equipped center sed rest Fetal surveillance Folic acid. Non assuring fetal status sed fluid intake. Assess lung maturity Fetal monitoring close upon 37wks.

Cont.,., Delivery. Not mature Mature Betamethasone therapy (Corticosteroids) Delivery. Delivery.

Cont.,., If pregnancy > 37 weeks. Delivery.