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Intrauterine Growth Retardation (Restriction)

Intrauterine Growth Retardation (Restriction). Jignesh Patel, MD Texas Tech University HSC Department of Pediatrics. Definitions. IUGR : Failure of normal fetal growth caused by multiple adverse effects on the fetus.

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Intrauterine Growth Retardation (Restriction)

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  1. Intrauterine Growth Retardation (Restriction) Jignesh Patel, MD Texas Tech University HSC Department of Pediatrics

  2. Definitions • IUGR: Failure of normal fetal growth caused by multiple adverse effects on the fetus. • SGA: Infant with wt < 10% ile for GA, or > 2 SDs below mean for GA.

  3. Easiest way to think about these terms are • IUGR: is a term used by OB to describe a pattern of growth over a period of time. • SGA: is a term used by Peds to describe a single point on a growth curve.

  4. Incidence • 3 - 10 % of all pregnancies. • 20 % of stillborns are growth retarded. • 30 % of infants with SIDS were IUGR. • 1/3 of infants with BW < 2800 gms are growth retarded and not premature. • 9 - 27 % have anatomic and/or genetic abnormalities. • Perinatal mortality is 8 - 10 times higher for these fetuses.

  5. Types of IUGR • Symmetric IUGR: weight,length and head circumference are all below the 10 th percentile. (33 % of IUGR Infants) • Asymmetric IUGR: weight is below the 10 th percentile and head circumference and length are preserved. (55 % of IUGR) • Combined type IUGR: Infant may have skeletal shortening, some reduction of soft tissue mass. (12 % of IUGR)

  6. Ponderal Index • Way of characterizing the relationship of height to mass for an individual. • PI = 1000 x • Typical values are 20 to 25. • PI is normal in symmetric IUGR. • PI is low in asymmetric IUGR. 3 Mass (kgs) Height (cms)

  7. Normal Intrauterine Growth pattern • Stage I (Hyperplasia) - 4 to 20 weeks - Rapid mitosis - Increase of DNA content • Stage II (Hyperplasia & Hypertrophy) - 20 to 28 weeks - Declining mitosis. - Increase in cell size.

  8. Normal Intrauterine Growth pattern • Stage III ( Hypertrophy) - 28 to 40 weeks - Rapid increase in cell size. - Rapid accumulation of fat, muscle and connective tissue. • 95% of fetal weight gain occurs during last 20 weeks of gestations.

  9. Etiology • Growth inhibition in stage I: - Undersized fetus with fewer cells. - Normal cell size. Result in symmetric IUGR. Associated conditions: - Genetic - Congenital anomalies - Intrauterine infections - Substance abuse - Cigarette smoking - Therapeutic irradiation

  10. Etiology • Growth Inhibition in Stage II/III -Decrease in cell size and fetal weight - Less effect on total cell numeric, fetal length, head circumferance. Result in asymmetric IUGR. Associated Conditions: - Uteroplacental insufficiency. • Combination above associated mixed type IUGR.

  11. Pathophysiology 1) Fetal factors: • Genetic Factors: - Race, ethnicity, nationality - sex ( male weigh 150 -200 gm more than female ) - parity ( primiparous, weigh less than subsequent siblings) -genetic disorders ( Achondroplasia, Russell - silver syn.) • Chromosomal anomalies: - Chromosomal deletions - trisomies 13,18 & 21

  12. Pathophysiology • Congenital malformations: examples:Anencephaly, GI atresia, potter’s syndrome, and pancreatic agenesis. • Fetal Cardiovascular anomalies • Congenital Infections: mainly TORCH infections. • Inborn error of metabolism: - Transient neonatal diabetes - Galactosemia - PKU

  13. Pathophysiology 2) Maternal Factors: • Decrease Uteroplacental blood flow: - Pre eclampsia / eclampsia - chronic renovascular disease - Chronic hypertension • Maternal malnutrition • Multiple pregnancy • Drugs - Cigarettes, alcohol, heroin, cocaine - Teratogens, antimetabolites and therapeutic agents such as trimethadione, warfarin, phenytoin

  14. Pathophysiology • Maternal hypoxemia - Hemoglobinopathies - High altitudes • Others - Short stature - Younger or older age (<15 and >45) - Low socioeconomic class - Primiparity - Grand multiparity - Low pregnancy weight - Previous h/o preterm IUGR baby - Chronic illness ( DM, renal failure, cyanotic heart disease etc.)

  15. Pathophysiology 3) Placental Factors: • Placental insufficiency ( most imp in 3rd trimester) • Anatomic problems: • Multiple infarcts • Aberrant cord insertions • Umbilical vascular thrombosis & hemangiomas • Premature placental separation • Small Placenta

  16. Postnatal Assessment • Growth parameters: weight, height, HC • Assess GA with Ballard score. • Plotted growth parameters in growth chart

  17. Physical Appearance

  18. Physical appearance: • Heads are disproportionately large for their trunks and extremities • Facial appearance has been likened to that of a “wizened old man”. • Long nails. • Scaphoid abdomen

  19. Signs of recent wasting - soft tissue wasting - diminished skin fold thickness - decrease breast tissue - reduced thigh circumference • Signs of long term growth failure - Widened skull sutures, large fontanelles - shortened crown – heel length - delayed development of epiphyses • Comparison to premature infants,IUGR has brain and heart larger in proportion to the body weight, in contrast the liver, spleen, adrenals and thymus are smaller.

  20. Complication • Hypoxia - Perinatal asphyxia - Persistent pulmonary hypertension - meconium aspiration • Thermoregulation - Hypothermia due to diminished subcutaneous fat and elevated surface/volume ratio

  21. Complications • Metabolic - Hypoglycemia - result from inadequate glycogen stores. - diminished gluconeogenesis. - increased BMR - Hypocalcemia - due to high serum glucagon level, which stimulate calcitonin excretion

  22. Complications • Hematologic - hyperviscosity and polycythemia due to increase erythropoietin level sec. to hypoxia • Immunologic - IUGR have increased protein catabolism and decreased in protein, prealbumin and immunoglobulins, which decreased humoral and cellular immunity.

  23. Management • Antenatal diagnosis and management is the key to proper management of IUGR • Delivery and Resuscitation - appropriate timing of delivery - skilled resuscitation should be available - prevention of heat loss • Hypoglycemia - close monitoring of blood glucose - early treatment ( IV dextrose, early feeding )

  24. Management • Hematological Disorder - central Hct to detect polycythemia - CBC with diff to r/o leukopenia or thrombocytopenia • Congenital infection - infant should be examined for signs of congenital infection (eg.rash, microcephaly hepatosplenomegaly, lymphadenopathy, cardiac anomalies etc….) - TORCH titer screening - Viral cx of urine, nasopharynx - Head CT to r/o calcification

  25. Management • Genetic anomalies - screening as indicated by physical exam - chromosomal analysis (infant with dysmorphic features) • Others - serum calcium to r/o hypocalcemia - fractionated bilirubin sec to polycythmia, congenital infection - urine, meconium tox for substance abuse

  26. Management • Early feeding and caloric intake should be 100-120 kcal/kg/d • Developmental and growth f/u in all IUGR infants

  27. Outcome • Symmetric vs. Asymmetric IUGR - symmetric has poor outcome compare to asymmetric • Preterm IUGR has high incidence of abnormalities • IUGR with chromosomal disease has 100% incidence of handicap • Congenital infection has poor outcome - handicap rate > 50% • IUGR has higher rate of learning disability.

  28. Thank You

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