intrauterine growth retardation (restriction)

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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. - PowerPoint PPT Presentation

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Intrauterine Growth Intrauterine Growth Retardation (Restriction)Retardation (Restriction)

Jignesh Patel, MD

Texas Tech University HSC

Department of Pediatrics

DefinitionsDefinitions

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.

Easiest way to think about these Easiest way to think about these terms areterms 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.

IncidenceIncidence

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.

Types of IUGRTypes 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)

Ponderal IndexPonderal 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.

Mass (kgs) Height (cms)

3

Normal Intrauterine Growth patternNormal Intrauterine Growth pattern

Stage I (Hyperplasia)

- 4 to 20 weeks

- Rapid mitosis

- Increase of DNA contentStage II (Hyperplasia & Hypertrophy)

- 20 to 28 weeks

- Declining mitosis.

- Increase in cell size.

Normal Intrauterine Growth patternNormal 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.

EtiologyEtiology 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

EtiologyEtiology

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.

PathophysiologyPathophysiology1) 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

PathophysiologyPathophysiology 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

PathophysiologyPathophysiology2) Maternal Factors:Decrease Uteroplacental blood flow:

- Pre eclampsia / eclampsia- chronic renovascular disease- Chronic hypertension

Maternal malnutritionMultiple pregnancyDrugs

- Cigarettes, alcohol, heroin, cocaine- Teratogens, antimetabolites and therapeutic

agents such as trimethadione, warfarin, phenytoin

PathophysiologyPathophysiology 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.)

PathophysiologyPathophysiology

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

Postnatal AssessmentPostnatal Assessment

Growth parameters: weight, height, HCAssess GA with Ballard score.Plotted growth parameters in growth chart

Physical AppearancePhysical Appearance

Physical appearance: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

• 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.

ComplicationComplicationHypoxia

- Perinatal asphyxia- Persistent pulmonary hypertension- meconium aspiration

Thermoregulation- Hypothermia due to diminished subcutaneous fat and elevated surface/volume ratio

ComplicationsComplications

Metabolic - Hypoglycemia

- result from inadequate glycogen stores.

- diminished gluconeogenesis.

- increased BMR

- Hypocalcemia

- due to high serum glucagon level, which stimulate calcitonin excretion

ComplicationsComplications

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.

ManagementManagement

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 )

ManagementManagement 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

ManagementManagementGenetic 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

ManagementManagement

Early feeding and caloric intake should be 100-120 kcal/kg/d

Developmental and growth f/u in all IUGR infants

OutcomeOutcome

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.

Thank YouThank You

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