intra uterine fetal growth restriction

1
INTRA UTERINE FETAL GROWTH RESTRICTION/SMALL FOR
DATE.

• MARCH 2023
• S.P CHUWA

2
SMALL FOR GESTATION AGE.

• Small for gestational age (SGA) is defined as a
  birth weight of less than 10th percentile for
  gestational age.
• Small for gestation age have high morbidity and
  mortality during neonatal period and beyond.
• Growth restriction can occur in preterm, term or
  post-term babies.
• In developed countries the incidence is 11 in
  under developing countries estimated 32.5 million
  were born with Fetal growth restriction/small for
  gestation age.

3

• Newborns with FGR are at increased risk for
  other complications such as prematurity, neonatal
  asphyxia, hypothermia, hypoglycemia,
  hypocalcemia, polycythemia, sepsis, and death.
• NOMENCLATUREsmall for date and intrauterine
  fetal restriction are used synonymously but small
  for date is not necessarly growth retarted and
  those fetus are not at increased risk.

4
TYPES.

• TYPES Based on the clinical evaluation and
  ultrasound examination the small fetuses are
  divided into
• SMALL AND HEALTH -The birth weight is less than
  10th percentile for their gestational age.
• They have normal ponderal index, normal
  subcutaneous fat and usually have uneventful
  neonatal course.
• GROWTH RESTRICTED FETUS(TRUE IUGR)due to
  pathological process.Depends on the size of the
  head,abdomen and femur categorized into
  symmetrical(type I) and asymmetrical (Type II).

5

• Symmetrical (20 percent) fetus is affected from
  the noxious effect early in the phase of cellular
  hyperplasia.Less total cell number. Caused mostly
  by structural or chromosomal abnormalities or
  congenital infection (TORCH). The pathological
  process is intrinsic to the fetus and involves
  all the organs including the head.
• Asymmetrical (80 percent) Affects fetus in later
  months during the phase of cellular hypertrophy.
  Constant cell number but the size is small. The
  pathological processes that result in asymmetric
  growth retardation are maternal diseases
  extrinsic to the fetus. These diseases alter the
  fetal size by reducing utero placental blood flow
  or by restricting the oxygen and nutrient
  transfer or by reducing the placental size.

6
(No Transcript)
7
AETIOLOGY

• The cause can from Maternal,Fetal, Placental or
  unknown.
• MATERNAL.
• 1. ConstitutionalSmall women, maternal
  genetic and racial background are associated with
  small babies. These babies are not at increased
  risk.
• 2. Maternal nutrition before and during
  pregnancyCritical substrate requirement for
  fetal growth such as glucose, amino acids and
  oxygen are deficient during pregnancy.

8

• 3.Maternal diseases Anemia, hypertension,
  thrombotic diseases, heart disease, chronic renal
  disease, collagen vascular disease are the
  important causes.
• 4.ToxinsAlcohol, smoking, cocaine, heroin,
  drugs.
• FETAL FACTORS There is enough substrate in
  maternal blood and crosses the placenta but not
  utilized by the fetus
• Failure of utilization may be due to structural
  abnormalities cardiovascular or renal

9

• 1.Chromosomal abnormalities. The common
  abnormalities are triploidy and aneuploidy.
  Trisomies (13, 18, 21) and Turners syndrome.
• 2.INFECTIONSTORCH agents (toxoplasmosis,
  rubella, cytomegalovirus and herpes simplex) and
  malaria.
• 3.Multiple pregnancy mechanical hindrance to
  growth and excessive fetal demand

10

• PLACENTAL CAUSESThe causes include cases of poor
  uterine blood flow to the placental site for a
  long time. This leads to chronic placental
  insufficiency with inadequate substrate transfer.
  The placental pathology includes Placenta
  previa , Abruption, Circumvallate, Infarction and
  Mosaicism.
• UNKNOWN 40 Of IUGR remains unknown.

11
PATHOPHYSIOLOGY

• Basic pathology in small for gestational age is
  due to reduced availability of nutrients in the
  mother or its reduced transfer by the placenta to
  the fetus. It may also be due to reduced
  ultilization by the fetus. Brain cell size
  (asymmetricSGA) as well as cell numbers
  (symmetric-SGA) are reduced. Liver glycogen
  content is reduced. There is oligohydramnios as
  the renal and pulmonary contribution to amniotic
  fluid are diminished due to reduction in blood
  flow to these organs. The SGA fetus is at risk of
  intrauterine hypoxia and acidosis, which if
  severe, may lead to intrauterine fetal death.

12
DIAGNOSIS

• Diagnosis is through clinical, biophysical
  methods and biochemical method.
• Clinical-
• By palpation of the uterus for fundal
  height,liquor volume and fetal mass.
• Symphysial Fundal Height (SFH)-measurement in
  centimeters closely correlates with gestational
  age after 24 weeks. A lag of 4 cm or more
  suggests growth restriction. It is sensitive
  parameter (3080) but Serial measurement is
  important.

13

• MATERNAL WEIGHT GAIN-weight gain remains constant
  or falling.
• MEASUREMENT OF THE ABDOMINAL GIRTH-shows
  stationary or falling .
• BIOPHYSICAL
• In a normally growing fetus the Head
  circumference (HC) and abdominal circumference
  (AC) ratios e HC/AC ratio exceeds 1.0 before 32
  weeks. It is approximately 1.0 at 32 to 34 weeks.
  After 34 weeks, it falls below 1.0. If the fetus
  is affected by asymmetric IUGR, the HC remains
  larger. The HC/AC is then elevated.

14

• In symmetric IUGR,both the HC and AC are reduced.
  The HC/AC ratio remains normal. Using HC/AC
  ratio, 85 of IUGR fetuses are detected.
  Transcerebellar diameter correlates well with the
  gestational age. AC is the single most sensitive
  parameter to detect IUGR Serial measurements of
  AC and estimation of fetal weight are more
  diagnostic to fetal growth restriction.
• Femur length (FL) is not affected in asymmetric
  IUGR. The FL/AC ratio is 22 at all gestational
  ages from 21 weeks to term. FL/AC ratio greater
  than 23.5 suggests IUGR.

15

• Amniotic fluid volumeThe reduced amniotic fluid
  volume is too often associated with asymmetrical
  IUGR.A vertical pocket of amniotic fluid lt 1 cm
  suggests IUGR.
• The sum of the results is the amniotic fluid
  index (AFI). An AFI between 5 and 25 cm is normal
  and an AFI less than 5 indicates oligohydramnios.
• Anatomical survey To exclude fetal anomalies by
  sonography (Aneuploidy, structural defects).

16
ULTRASOUND DOPPLER PARAMETERS

• Doppler Velocimetry Elevated systolic/diastolic
  (S/D) ratio and/or presence of diastolic notch
  are associated with IUGR and intrauterine fetal
  hypoxia.
• Uterine artery The presence of diastolic notch
  suggests incomplete invasion of placental
  trophoblasts to the uterine spiral arteries This
  also predicts the possible development of
  pre-eclampsia. Normally, the diastolic flow
  increases as pregnancy progresses Reduced or
  absent or reversed diastolic flow in the
  umbilical artery indicates fetal jeopardy and
  poor perinatal outcome.

17

• Cerebral Placental Doppler ratio is decreased in
  IUGR.
• Ponderal index (PI) The degree of fetal wasting
  is judged by fetal PI. The index is determined by
  dividing the estimated fetal weight (g) by the
  third power of crown-heel length (cm) (weight
  (g)/length cm3).PI below 10th percentile is
  taken as IUGR. Reduction in fetal facial fat
  stores has been associated with IUGR.

18
BIOCHEMICAL MARKERS

• Elevated levels of MSAFP-(maternal serum alpha
  fetoprotein) and hCG (human chorionic
  gonadotrophic hormone)- level in the second
  trimester are the marker of abnormal placentation
  and risks of IUGR.
• PHYSICAL FEATURES AT BIRTH
• Weight deficit at birth is about 600 g below the
  minimum in percentile standard
• Length is unaffected.

19

• Head circumference -is relatively larger than the
  body in asymmetric IUGR
• Physical features show dry and wrinkled skin
  because of less subcutaneous fat, scaphoid
  abdomen,thin, meconium stained vernix caseosa and
  thin umbilical cord. All these give the baby an
  old man look. Pinna of ear has cartilaginous
  ridges. Plantar creases well defined
• The baby is alert, active and having normal
  cry.Eyes open

20
CONT.

• Reflexes are normal including Moro-reflex.

21
COMPLICATIONS

• Fetal (a) AntenatalChronic fetal distress,
  fetal death (b) IntranatalHypoxia and acidosis .
• After birth.
• Immediate (1) Asphyxia, bronchopulmonary
  dysplasia and RDS (2) Hypoglycemia due to
  shortage of glycogen reserve in the liver (3)
  Meconium aspiration syndrome (4)
  Microcoagulation leading to DIC (5) Hypothermia
  (6) Pulmonary hemorrhage (7) Polycythemia,
  anemia, thrombocytopenia (8) Hyperviscosity
  thrombosis.

22
CONT

• (9) Necrotizing enterocolitis due to reduced
  intestinal blood flow (10) Intraventricular
  hemorrhage (IVH) (11) Electrolyte abnormalities,
  hyper phosphatemia, hypokalemia due to impaired
  renal function (12)Multiorgan failure (13)
  Increased perinatal morbidity and mortality
• Late Asymmetrical IUGR babies tend to catch up
  growth in early infancy. The fetuses are likely
  to have(1) retarded neurological and
  intellectual development in infancy. The worst
  prognosis is for IUGR caused by congenital
  infection, congenital abnormalities and
  chromosomal defects.

23

• . Other long term complicationsare (2) Increased
  risk of metabolic syndrome in adult life
  obesity, hypertension, diabetes and coronary
  heart disease (CHD). (3) LBW infants have an
  altered orexigenic mechanism that causes
  increased appetite and reduced satiety. (4)
  Reduced number of nephronscauses renal vascular
  hypertension.
• MATERNAL Having baby with IUGR increase risk by
  2 fold of having another baby with IUGR.

24

• MORTALITYIncrease by six fold compared to normal
  infant. Most of the babies die within 24 hours.
  They are at higher risk for poor postnatal growth
  and adverse cognitive outcome.

25
MANAGEMENT

• Management depends on the diagnosis workup.
• Fetuses that are constitutionally small require
  no intervention.
• The fetuses that are symmetrically growth
  restricted, should
• be investigated to exclude fetal anomalies,
  infections and genetic syndromes
  there is no effective therapy for this group.
• Decision for early delivery has to balance the
  risk of neonatal deaths due to complications, on
  the other hand delay in delivery that may
  increase the risk of IUFD.

26
cont

• Majority of fetal deaths occur after the 36th
  week of gestation. So, correct diagnosis and
  timed intervention are essential.
• Perinatal outcome is poor with early onset of
  IUGR (lt34 weeks) compared to late onset of FGR
  (gt34 weeks). Decision for early delivery has to
  balance the risk of neonatal deaths due to
• complications,delay in delivery that may
  increase the risk of IUFD.
• GeneralCurrently, no proven therapy for growth
  restriction.
• PROPOSED MEASURES 1.Adequate bed rest especially
  in lt lateral position 2.Balanced diet increase
  extra 300calories/day.

27
Cont.

• 3.Avoid smoking,tobacco and alcohol .
• 4.low dose asprin (50MG OD) in women who had
  thrombotic events , preeclampsia, hypertension
  and recurrent IUGR.5.Maternal volume expansion
  may helpful in women who has placental
  insuffiency.
• Antepartum evaluation
• When diagnosiss have made fetal growth and well
  being should be serially examined.
• Ultrasound examination done 34 weeks for the
  assessment of BPD,HC/AC, fetal weight and AFI.

28
cont

• FETAL WELL BEING
• Assessed by fetal Kick count, NST, amniotic fluid
  volume ,breathing and cordocentesis for blood
  gases
• Doppler ultrasound should also be done.
• TIMING OF DELIVERY
• Factors to be considered are1) Presence of fetal
  abnormality (2) Duration of pregnancy (3)
  Degree of FGR (4) Associated complicating
  factor (5) Underlying pathology if known (6)
  Results of antenatal fetal surveillance and (7)
  Availability of neonatal intensive care unit
  (NICU).

29

• Optimum time of delivery for a growth restricted
  fetus may be between 34 weeks and 37 weeks
  depending upon the presence of any additional
  risk factor(s) (e.g. Oligohydramnios,
  preeclampsia,
• abnormal Doppler study).
• A.Pregnancy 37 weeks Delivery should be
  done.
• B. Severe degree of IUGR-
• Delivery should be planned on the basis of
  fetal surveillance report

30

• If the lung maturation is achieved as evidenced
  by presence of phosphatidylglycerol and L S
  ratio of 2 from the amniotic fluid study
  (amniocentesis), delivery is done.
• If the lung maturation has not yet been achieved,
  intrauterine transport to an equipped center in
  such a case Betamethasone therapy is given to
  accelerate pulmonary maturation when gestational
  age is less than 34 weeks Corticosteroids reduce
  the risk of neonatal HMD(Hyaline membrane
  disease) and intraventricular hemorrhage (IVH).

31
cont

• Delivery to be done at 34 0/7 weeks of gestation
  in cases of FGR with additional risk factors for
  adverse perinatal outcome (Preeclampsia,
  oligohydramnios).
• When delivery is to be done preterm, antenatal
  corticosteroids should be given.
• When delivery is to be done before 32 weeks,
  magnesium sulfate should be given to the mother
  for fetal and neonatal neuroprotection.
• Fetuses with aneuploidy or congenital infection
  have poor outcome irrespective of gestational age
  and timing of delivery.

32
Methods of delivery

• Low rupture of the membranes followed by oxytocin
  is employed in cases such as pregnancy beyond 34
  weeks with favorable cervix and the head is deep
  in the pelvis. Prostaglandin (PGE2)gel could be
  used when the cervix is unfavorable. The color of
  the liquor could be a guide for further
  management.
• Intrapartum monitoring by clinical, continuous
  electronic and scalp blood sampling is needed as
  the risk of intrapartum asphyxia is high.
• Cesarean delivery without a trial of labor is
  done when the risks of vaginal delivery are more
  (presence of fetal acidemia, absent or reversed
  diastolic flow in umbilical artery or unfavorable
  cervix).

33

• IMMEDIATE CARE OF BABY AT BIRTH.
• A pediatrician should be available at the time
  of delivery.
• The baby should be placed preferably in the
  neonatal intensive care unit.