intra uterine growth retardation by dr shabnam naz

In the name of Allah, the beneficent. the merciful : 

In the name of Allah, the beneficent. the merciful

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IUGR DR. SHABNAM NAZ MBBS, MCPS,FCPS Assistant Professor OBGYN CMC & SMBBMU Larkana Intra Uterine Growth Retardation

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Fetal growth restriction 'wasted' and 'stunted' Intra Uterine Growth Retardation Intra Uterine Growth R estriction S mall for gestational age (SGA)

What is the difference between SGA and IUGR?: 

What is the difference between SGA and IUGR? Can these terms be used interchangeably?

SGA – Small For Gestational Age Infants: 

SGA – Small For Gestational Age Infants An infant whose weight is lower than the population norms Defined as weight below 10th percentile for gestational age or greater than 2 standard deviations below the mean Cause may be pathologic or nonpathologic

IUGR – Intrauterine Growth Retardation: 

IUGR – Intrauterine Growth Retardation defined as failure of normal fetal growth caused by multiple adverse effects on fetus due to process that inhibits normal growth potential of fetus

So what is the difference between SGA and IUGR?: 

So what is the difference between SGA and IUGR? These terms are related but not synonomous. Not all IUGR infants are small enough to fit the qualifications for SGA. Not all SGA infants are small because of a growth-restrictive process, and therefore, do not meet criteria for IUGR.

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SGA IUGR

INCIDENCE: 

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.

NORMAL INTRAUTERINE GROWTH: 

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

CLASSIFICATION : 

CLASSIFICATION Symmetrica l A symmetrical head=height, both > weight brain growth spared later in pregnancy: commonly due to uteroplacental insufficiency, maternal malnutrition, hypoxia, or extrinsic factors low ponderal index increased risk of asphyxia increased risk of hypoglycemia height, weight, head circ proportional early pregnancy insult: commonly due to congenital infection, genetic disorder, or extrinsic factors normal ponderal index low risk of perinatal asphyxia low risk of hypoglycemia Stage I growth inhibition Fewer cells but normal size Stage II/III growth inhibition - weight below 10th percentile, head and length preserved

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Newer Classification: - Normal Small Fetuses- have no structural abnormality, normal umbilical artery & liquor but wt., is less. They are not at risk and do not need any special care. Abnormal Small Fetuses- have chromosomal anomalies or structural malformations. They are lost cases and deserve termination as nothing can be done. Growth Restricted Fetuses- are due to impaired placental function. Appropriate & timely treatment or termination can improve prospects. CLASSIFICATION

PONDERAL INDEX: 

PONDERAL INDEX The ponderal index is used determine those infants whose soft tissue mass is below normal for their stage of skeletal development. Ponderal Index = birth weight x 100 crown-heel length Typical values are 20 to 25. Those who have a ponderal index below the 10th % can be classified as SGA PI is normal in symmetric IUGR. PI is low in asymmetric IUGR

DETERMINANT OF BIRTH WEIGHT: 

DETERMINANT OF BIRTH WEIGHT Sex term males 200 gm heavier and 0.9 cm longer than females Parity 1st born infants smaller effect loss after 3rd birth Race, ethnicity, nationality Altitude Denver population growth curves under estimate weights of infants born at sea level Maternal size( Height ,Weight) maternal pre-pregnancy weight and pregnancy weight gain correlate with fetus size

“MATERNAL CONSTRAINT”- NON-GENETIC: 

“MATERNAL CONSTRAINT”- NON-GENETIC Number of fetuses Reduced rate of fetal growth of multiples Small breed embryo transplanted into large breed uterus will grow larger

HORMONAL FACTORS: 

HORMONAL FACTORS Insulin Major hormone for in utero growth Produced by fetus Promotes fetal adipose deposition, glycogen stores

CAUSES OF IUGR: 

CAUSES OF IUGR Maternal factors Fetal factors Placental factors Environmental factors

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Medical disease Malnutrition  BMI < 19 twice the risk of IUGR Multiple pregnancy Smoking  (460 gm < then none smoker) Alcohol  12-fold increase risk of SGA, consumption of 120 gms (15 Units) of alcohol associated with 66 gm reduction in birth weight. Drugs  Beta- Blockers( Atenolol in second trimster , Anticoagulants, Anticonvulsants( phenytoin ) Hypoxemia Infections  UTI, Malaria, TB, Genital Infections MATERNAL FACTORS

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Small stature/ low pre-pregnancy weight Teen pregnancy Low SES Prima gravida Grand multiparity CONTINUE

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Pre- eclampsia / HELLP

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Mom with no prenatal care delivers undiagnosed twins at EGA 34 weeks Discordant twins

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Infant delivered at EGA 34 weeks to mom with no prenatal care and positive tox screen

FETAL FACTORS: 

FETAL FACTORS A Chromosome Defect - In second trimster 20% SGA fetuses have chromosomal abnormality In third trimster 1-2 %. Triploidy is most common under 26 wks. Trisomy - 18 is common after 26 wks . Other are 21(Down’s syndrome), 16, 13, xo (turner’s syndrome).

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Trisomy 13

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Trisomy 18 Turner syndrome

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Exposure to an infection - German measles ( rubella ), cytomegalovirus, herpes simplex, tuberculosis , syphilis, or toxoplasmosis, TB, Malaria, Parvo virus B19. A birth defects (cardiovascular , renal, anencephally , limb defect, etc ). A primary disorder of bone or cartilage. A chronic lack of oxygen during development (hypoxia). Developed outside of the uterus. Placenta or umbilical cord defects. CONTINUE

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Toxoplasmosis Rubella

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CMV

PLACENTAL FACTORS: 

PLACENTAL FACTORS Uteroplacental Insufficiency Resulting From -. Improper / inadequate trophoblastic invasion and placentation in the first trimester. Lateral insertion of placenta. Reduced maternal blood flow to the placental bed. Fetoplacetal Insufficiency Due To-. Vascular anomalies of placenta and cord. Decreased placental functioning mass-. Small placenta, abruptio placenta, placenta previa , post term pregnancy.

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An infant is delivered at 42 weeks via c- section due to NRHTs after induction - decreased subcutaneous fat - skin desquamation - wizened facies - large AF(diminished membranous bone formation) - meconium staining POST DATES

Neonate and Placenta in IUGR: 

Neonate and Placenta in IUGR Normal & IUGR Newborn babies Normal & IUGR Placentas

Environmental Causes of IUGR: 

Environmental Causes of IUGR High altitude - lower environmental oxygen saturation Toxins

PREDICTION OF IUGR: 

PREDICTION OF IUGR History risk factors last menstrual period - most precise size of uterus time of quickening (detection of fetal movements) Examination / c linical Assessments Fundal Height Measurement (FHM ) Maternal serum screening Ultra sound markers Scoring systems

MATERNAL SERUM SCREENING: 

MATERNAL SERUM SCREENING Alpha-fetoprotein (AFP) Oestriol (E3) Human placental lactogen (HPL) Human chorionic gonadotrophin (hCG) AFP if the level is 2.5 or more multiple of the median for gestation in the absence of fetal anomaly, there is a 5-10 fold increase in the risk of FGR

ULTRA SOUND MARKERS: 

ULTRA SOUND MARKERS Uterine Artery Doppler Velocimetry - Notching of the waveform /reduce EDF associated 3-fold increase in risk of FGR. Bright or echogenic fetal bowel in the second trimester is associated with increase risk of FGR. Combination of un-explain elevated maternal AFP and UADV is powerful predictor of adverse perinatal outcome (FGR) Increase AFP combine with echogenic bowel is strong predictor of FGR.

DIAGNOSIS OF IUGR (in utero): 

DIAGNOSIS OF IUGR (in utero ) IUGR can be difficult to diagnose . Presence of risk factors by taking detail history. Inadequate growth detected by serial measurement of Wt., abdominal girth and fundal Ht. Ultrasound to evaluate the fetal growth. - biparietal diameter abdominal circumference - best sensitivity ratio of head to abdominal circumference femur length Reduced AFI. - Placental calcification. Umbilical artery doppler velocity studies - REDF - AEDF

POSTNATAL ASSESSMENT: 

POSTNATAL ASSESSMENT Growth parameters: weight, height, HC Assess GA. Plotted growth parameters in growth chart

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

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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.

DIAGNOSIS ALGORITHM: 

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 tox screen no Unknown cause

PREVENTION OF IUGR: 

PREVENTION OF IUGR Strategies include prenatal care modalities, protein/energy supplementation, treatment of anaemia, vitamin/mineral supplementation, fish oil supplementation prevention and treatment of hypertensive disorders, foetal compromise Infection.

PREVENTION OF IUGR : 

PREVENTION OF IUGR Strong evidence of benefit only for the following interventions: balanced protein/energy supplementation, (Vit C, Vit E supplementation) strategies to reduce maternal smoking, antibiotic administration to prevent urinary tract infections and antimalarial prophylaxis. Avoid Somking CLASP trial (Collaborative low-dose aspirin studies in pregnancy) No benefit of prophylactic administration of low-dose aspirin in women with high risk for FGR

SURVEILLANCE OF IUGR : 

SURVEILLANCE OF IUGR Unless delivery occurs, once treatment begins the foetus must undergo surveillance. The purpose - to identify further progression of the disease process that would jeopardize the foetus to a point that it would be better to be delivered than to remain in utero .

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There are four testing modalities Non-Stress Test , Amniotic Fluid Index , Doppler of the Umbilical Artery Biophysical Profile , Each of which addresses different aspects of surveillance . C ombination of tests are better than an isolated test.

NON-STRESS TEST (NST): 

NON-STRESS TEST (NST) This simplest to perform test should b used first in the surveillance of IUGR foetuses. With the help of a heart rate monitor, the changes in the foetal heart rate with foetal movement are to be determined . The problem with this test is that it changes late in the course of the disease and is not an early predictor of adverse outcome .

NON-STRESS TEST (NST): 

NON-STRESS TEST (NST) If the heart rate increases more than 15 beats for more than 15 seconds, this is considered to be a reactive test . If the heart rate does not accelerate, remains flat, or decreases, then this is an abnormal test.

AMNIOTIC FLUID INDEX (AFI) : 

AMNIOTIC FLUID INDEX (AFI) The vertical depth of four pockets of amniotic fluid are measured by USG, to obtain a total AFI. This method allows for comparison of changes in amniotic fluid with time.

AMNIOTIC FLUID INDEX (AFI): 

AMNIOTIC FLUID INDEX (AFI) In the normal foetus the AFI remains relatively constant. In the foetus with IUGR, it may decrease slowly, or decrease abruptly with time. A decrease in AFI may occur before there are changes in the non-stress test.

AMNIOTIC FLUID INDEX (AFI) : 

AMNIOTIC FLUID INDEX (AFI) The current recommendations are that if the AFI decreases below 8 after 35 weeks, then delivery should occur.

DOPPLER OF THE UMBILICAL ARTERY: 

DOPPLER OF THE UMBILICAL ARTERY Reduced e nd diastolic flow. Absent end diastolic flow Reversed end diastolic flow( severe cases) Degree of abnormalities in UADW correlate well with risk of fetal hypoxia .

ADVANTAGE OF UADW : 

ADVANTAGE OF UADW It differentiate normal SGA from IUGR Use of UADW significantly improved several pregnancy outcome including Few induction of labor Decrease hospital admission Decrease perinatal mortality

BIOPHYSICAL PROFILE : 

BIOPHYSICAL PROFILE This test combines the NST and the AFI with foetal movement, breathing, and muscle tone. If each of the tests are normal they are given a score of 2. If abnormal, a score of 0. A score of 6 or less suggests the foetus is at risk for adverse outcome. While the biophysical profile is a n useful test, when it becomes abnormal the fetus may have already suffered some damage

TREATMENT OF IUGR: 

TREATMENT OF IUGR IUGR has many causes, therefore, there is no one treatment that always works.

TREATMENT OF IUGR: 

TREATMENT OF IUGR Either delivery Remaining in utero and improving blood flow to the uterus. When blood flow is improved, the delivery of oxygen and other nutrients to the foetus occurs. If the foetus is lacking in these substances, their increased availability may result in improved growth and development.

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If IUGR is caused by a problem with the placenta and the baby is otherwise healthy, early diagnosis and treatment of the problem may reduce the chance of a serious outcome. There is no treatment that improves foetal growth, but IUGR babies who are at or near term have the best outcome if delivered promptly. CONTINUE

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This is the initial approach for the treatment of IUGR . The benefit of bed rest is that it results in increased blood flow to the uterus. Studies have shown, however, that in most cases bed rest at home is just as effective as bed rest in the hospital environment. MATERNAL BED REST

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The use of aspirin to treat foetuses with IUGR is still controversial. If aspirin is used , it may be advantageous if given to patients before 20 weeks of gestation. It has limited benefit if given at the time of diagnosis (third trimester). At the present time it is not recommended as a form of prevention for low risk patients. ASPIRIN THERAPY

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Other forms of treatment that have been studied are nutritional supplementation, zinc supplementation , fish oil , hormones and oxygen therapy. Limited studies are available regarding the use of these modalities in the treatment of IUGR. Other Forms of Treatment

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RISK OF PREMATURITY DIFFICULT EXTRA UTERINE EXISTENCE RISK OF IUD HOSTILE INTRA UTERINE ENVIRONMENT Judge Optimum Time Of Delivery

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IUGR NEAR TERM Prompt delivery is likely to afford the best outcome for the IUGR fetus In the presence of significant oligohydraminos most fetus will be delivered if G.A has reached>34 wk.

Such often tolerate labor less than AGA and C/S is indicated for intra-partum fetal compromise.: 

Such often tolerate labor less than AGA and C/S is indicated for intra-partum fetal compromise. Unfortunately

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Importantly Uncertainly about the diagnosis of IUGR should preclude intervention until fetal lung maturity is assured.

IUGR REMOTE FROM TERM: 

IUGR REMOTE FROM TERM before 34 wk Normal Amniotic volume Normal fetal surveillance Observation Sono is repeated at interval 2-3 wk

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FGR is the result of insufficient placental function ↓ A.f cord compression breech presentation c/s

MANAGEMENT after birth: 

MANAGEMENT after birth Obtain history of risk factors Appropriate resuscitation Prevent heat loss Watch for hypoglycemia check glucoses early feeding parenteral dextrose Check hematocrit Screen for congenital infections Screen for genetic abnormalities Check calcium

SHORT TERM RISKS OF IUGR : 

SHORT TERM RISKS OF IUGR Increased perinatal morbidity and mortality. Intra uterine / Intrapartum death. Intrapartum fetal acidosis may occur in as many as 40 % of IUGR, leading to a high incidence of LSCS. IUGR infants are at greater risk of dying because of neonatal complications- asphyxia, acidosis, meconium aspiration syndrome, infection, hypoglycemia , hypothermia , sudden infant death syndrome. IUGR infants are likely to be susceptible to infections because of impaired immunity

Which CxR is more consistent with IUGR?: 

Which CxR is more consistent with IUGR? Decreased surfactant deficiency Increased M econium Aspiration

LONG TERM PROGNOSIS (Risks increase with the severity of the growth restriction): 

LONG TERM PROGNOSIS (Risks increase with the severity of the growth restriction) increased risk for death low blood sugar , low body temperature , abnormal development of the nervous system . Adult onset, degenerative disease s like maturity onset diabetes and cardiovascular diseases. Implication of IUGR can be life long affecting: Body size growth , composition and physical performance . Immunocompetence .

OUTCOME: 

OUTCOME Depends on cause of IUGR/SGA and neonatal course Symmetric IUGR - poor outcome because early insult Asymmetric IUGR - better outcome because brain spared Very bad if brain growth failure starts at < 26 weeks School performance influenced by social class 25-50% likelihood of neurodevelopmental problems

Moen Jo Daro Larkana Sindh: 

Moen Jo Daro Larkana Sindh THANKS