IUGR- INtra uterine growth retardation - iugr

monicadevanand1 216 views 29 slides Aug 01, 2024
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About This Presentation

iugr


Slide Content

IUGR Moderator : Dr.K.V . Shenoy

Overview Definition Incidence Types Normal intrauterine growth Clinical features Problems & management of IUGR infant Outcome Long term prognosis

Definition Low birth weight- Weight less than 2500gms at birth LBW Preterm-1/3rd IUGR- 2/3rd

IUGR- Clinical definition, neonates with clinical evidence of malnutrition SGA- Statistical definition, neonates whose birth weight is lower than population norm - less than 10 th percentile for the particular gestational age. IUGR/SGA babies can be either term/preterm Term SGA and IUGR not synonymous.

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.

Types of IUGR Symmetric IUGR : weight, length and head circumference are all below the 10th percentile. (33 % of IUGR Infants) Early onset Affect total cell number Decreased growth potential Lower risk for transitional problems Examples Genetic causes,chromosomal TORCH infections

Asymmetric IUGR : Head circumference is preserved relative to decreased weight, length. (55 % of IUGR) Late onset Due to redistribution of blood to vital organ Combined type IUGR : Infant may have skeletal shortening, some reduction of soft tissue mass.(12 % of IUGR)

Normal Intrauterine Growth Stage 1 Stage 2 Stage 3 Hyperplasia Hyperplasia/ hypertrophy Hypertrophy 4-20 weeks 20-28 weeks 28-40 weeks Rapid mitosis Declining mitosis Rapid hypertrophy Increasing DNA content Increasing cell size Rapid increasing cell size rapid accumulation of fat, muscle, connective tissue Symmetric Mixed- asymmetric Asymmetric

Clinical features Birth weight is below the 10 th percentile Heads are disproportionately large for their trunks and extremities Emaciated look- “OLD MAN” LOOK Lack of subcutaneous tissue- Loose skin folds, prominent over the buttocks and thighs. Alert, often plethoric Long nails Scaphoid abdomen Preterm IUGR babies have additional features of prematurity

Diminished skin fold thickness Decrease breast tissue 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.

Comparison of head and chest circumference Normal: Head size is bigger than chest by 2cm In IUGR babies HC exceeds chest circumference by more than 3cm

Ponderal Index Way of characterizing the relationship of height to mass for an individual. PI = Mass in kgs ( Height in m) 3 IF PONDERAL INDEX IS <2 =ASYMMETRIC IUGR IF PONDERAL INDEX IS >2= SYMMETRIC IUGR (ALSO IN TERM AGA)

Congenital infection - Infant should be examined for signs of congenital infection ( eg.rash , microcephaly , hepatosplenomegaly , lymphadenopathy , cardiac anomalies etc….) Genetic disorder

Diagnosis Algorithm IUGR yes TORCH stigmata  work-up? no yes Dysmorphic features  work-up? no yes Maternal/placental explanation work-up? no yes Maternal drug use toxicology screen no Unknown cause

Problems & management of IUGR infant

Perinatal asphyxia Hypothermia Hypoglycemia Polycythemia Jaundice These morbidities are common in severely growth restricted babies (<3 rd percentile)

Management Antenatal diagnosis and management is the key to proper management of IUGR Early delivery – arrest of fetal growth, lung maturity is satisfactory Delivery and Resuscitation - Emergency LSCS- Fetal hypoxia, meconium stained liquor Skilled resuscitation Ready to receive asphyxiated/depressed baby Ready to do endotracheal intubation and suctioning Prevention of heat loss Place the baby under radiant warmer Quick drying Remove wet linen Cover the baby

Criteria for admission to Nursery - All SGA infants < 2 SD (3rd percentile) - Infants with gestational age < 35 wks - Infants with birth asphyxia, respiratory distress etc.

Birth weight 3 rd -10 th percentile, gestation >35weeks No complications – managed with mother Skin to skin care Early initiation of breast feeding Monitoring for cold stress Monitored for hypoglycemia and polycythemia - 48-72hrs Prevent infection

Birth weight <3 rd percentile or gestational age <35wks Nurse in thermo neutral environment If stable, early initiation of feeds ( EBM). - Feed by orogastric tube or katori -spoon / paladai if gestation >32 wks - Initial intravenous fluids followed by orogastric or katori -spoon / paladai if gestation <32 wks Monitor blood sugar, hematocrit

Infants with absent or reversed en-diastolic blood flow At higher risk of development of NEC If preterm (gestation <32 weeks): Nil per oral or on minimal enteral nutrition for first 48-72 h of life followed by gradual advancement of feed volume

<30wks- IVF 30-34wks- OG / pallada feed 3 rd to 10 th percentile Breast feeding Term/ Borderline <35 wks IUGR Breast feeding Pallada feeding Admit to NICU Monitor with mother < 3 rd percentile NICU Monitoring- sugar, PCV, temperature

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.

The period from conception to birth is a time of rapid growth, cellular replication and differentiation, and functional maturation of organ systems. These processes are highly sensitive to alterations in the intrauterine milieu. The term  programming   describes the mechanisms whereby a stimulus or insult at a critical period of development has lasting or lifelong effects.

Barker’s hypothesis: Size at birth is related to the risk of developing disease in later life. Reduced birth weight and increased risk of coronary heart disease, diabetes, hypertension and stroke in adulthood. These relationships are modified by patterns of postnatal growth. Mechanisms underlying- fetal programming by nutritional stimuli or excess fetal glucocorticoid exposure

Fetal Origins of Adult Diseases ? Coronary artery disease correlates inversely with birth weight Rate of non-insulin dependent diabetes mellitus is highest in the “thinnest” babies at birth (low ponderal index) High serum cholesterol are linked to disproportionate size at birth (body smaller than head) Increased rate of hypertension in infants who were thin, short, &/or proportionately small at birth

Long term prognosis Syndrome X Diabetes mellitus Cardiovascular disease Hypertension Obesity

Catch up growth Asymmetric IUGR-Most have normal growth curves, slightly reduced adult size Early onset/ Symmetric IUGR- Continue to lag behind Small independent risk factor for CP Possible long term neurologic sequelae Depends on degree of IUGR, time of onset (earlier worse) and impact on head growth.
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