Intra uterine growth

retardation/restriction [ FGR]

/ DYSMATURITY/
SMALL FOR DATE/
CHRONIC PLACENTAL
INSUFFICIENCY
Definition

-It is said to be present in those babies

whose birth weight is below the tenth
percentile of the average for gestational
age.
-It can occur in preterm, term / post term
babies.
Incidence

■Dysmaturity comprises about one-

third of low birth weight babies.
Normal fetal growth

- Result of tissue growth, differentiation &

maturation in a sequential manner.
- Dependent on availability of adequate amount of
substrate in mother.
- Appropriate placental transfer to fetus & growth
potential determined by genetic make up.
-Normal rate of fetal growth are 5
gm/day at 15 weeks, 15-20 gm/
day at 24 weeks & 30-35 gm/ day
at 34 weeks.
Nomenclature

-SGA & IUGR are too often used

synonymously although there is a degree of
overlap.
-SGA is term for new born whose
birth weight is below 10 percentile
th

for their gestation.

-SGA may be due to IUGR
/constitutional small baby.
IUGR term is used in a fetus who fails to
reach its true genetic potential.
Etiology

Maternal
1.Constitutional
Small women. These babies are not at
increased risk.
2. Maternal nutrition before & during pregnancy
Under nutrition- glucose, amino acids &
oxygen.
3. Maternal diseases
-Anemia, hypertension, heart disease,
chronic renal disease are important causes.
4. Toxins
-Alcohol, smoking, cocaine, drugs.
Fetal

Failure of non-utilization due to

- Structural anomalies
- Chromosomal abnormality
- Infection TORCH agents
 -Multiple pregnancy

Mechanical hindrance to growth &

excessive fetal demand.
Placental

-Poor uterine flow-chronic placental

insufficiency with inadequate substrate
transfer.
-Placental pathology
Unknown
About 40%.
Types

-Based on clinical evaluation & ultrasound

examination small fetuses divide into
1. Fetuses –small & healthy.
-weight < 10th percentile
-normal ponderal index
-normal subcutaneous fat & uneventful
neonatal course.
Ponderal index [PI]

-Degree of fetal wasting is judged by

fetal PI.
[Weight (g)/length (cm3)] x 100
The normal value is 8.3. A value
of 7/ less strongly suggests fetal
malnutrition.
2. Fetus growth is restricted by
pathological process [true IUGR]
PI below 10th percentile taken as IUGR.
-

-Estimation of PI by fetal
ultrasonography.
-Reduction in fetal facial fat stores
associated with IUGR.
-Depending on relative size of head,
abdomen & femur. Fetuses sub divided
into
-Symmetrical/ Type I
-Asymmetrical /Type II
Symmetrical[20%]

-Noxious effect- early phase of cellular

hyperplasia.
-Total cell number is less.
-Caused by structural abnormalities/
congenital.
-Pathologic process is intrinsic to fetus &
involves all organs including head.
Asymmetrical [80%]

-Fetus affected during later phases of cellular

hypertrophy.
-Total cell number remains same but size is
smaller than normal.
-Maternal diseases are extrinsic to fetus.
SYMMETRICAL [EARLY ASYMMETRICAL
ONSET]/// [LATE ONSET]
Uniformly small Head larger than
abdomen

Ponderal index-normal Low

HC: AC & FL:AC ratios- Elevated

normal
SYMMETRICAL ASYMMETRICAL
Etiology: genetic Chronic placental
disease/infection [intrinsic to insufficiency-[extrinsic to
fetus] fetus]

Total cell number-less Normal

Cell size -normal Smaller

Neonatal course- Usually uncomplicated

complicated with poor having good prognosis.
prognosis.
Classification

-Classify patients with IUGR based

on presence/absence of symmetry
among different anatomic structures.
Morphological classification

Type I IUGR
-

Refers to a symmetrically small fetus with normal

head to abdomen ratio.
-Type II IUGR
Corresponds to a fetus has an abdominal
circumference smaller than head circumference & the
femur length.
-Type III IUGR
Refers to a fetus is symmetric
initially but becomes asymmetric later in
the pregnancy.
Etiological classification

INTRINSIC IUGR
Fetus is small because of chromosomal
abnormality/ intrauterine fetal infection.
EXTRINSIC IUGR
Growth failure is caused by an element outside
of fetus, such as placental/ maternal condition.
COMBINED IUGR
Both extrinsic & intrinsic factors acting in
conjunction to bring about growth failure.
IDIOPATHIC IUGR
Cause of fetal growth failure is unknown.
PHYSICAL FEATURES AT BIRTH
-Weight deficit at birth about 600gm below
minimum percentile standard.
-Length is unaffected.
-Head circumference larger than body in
asymmetric variety.
-Dry & wrinkled skin
-Scaphoid abdomen
-Thin meconium stained vernix
caseosa
-Thin umbilical cord.
-All these give baby an “ old man look”.
-Plantar creases are well defined.
-Baby is alert, active & having normal cry.
-Eyes are open.
-Reflexes normal
PATHOPHYSIOLOGY
1.
Pre-eclampsia/ etiological factors

Utero-placental insufficiency

Decreased placental transfer of nutrients[decreased

utilization of nutrients]
Decreased brain cell size[Asymmetry]

Decreased number of cells[Symmetry]

Small body mass related to surface area

-Decreased BAT [Brown adipose tissue] &
subcutaneous tissue

-Difficulty in temperature regulation

-Hypothermia
2.

-Decreased placental circulation

-Decreased blood supply to splanchnic

circulation[mesenteric, splenic & kidneys]
a.

-Liver shrinks with decreased glycogen

deposition

-hypoglycemia
b

-Blood flow to kidneys

-Reduction in urine output

-Decreased contribution to amniotic fluid

-Oligohydramnios
3.

-Decreased fetal body stores of lipids &

glycogen

-Hypoxemia

-Erythropoietin production
A. Hyperviscosity syndrome
B. Thrombocytopenia
C. Leukopenia
D. Pulmonary hemorrhage
E. Toxemia
4.

-Delayed introduction of feeds

-Diminished parathyroid hormone secretion

-Decreased calcium level

-Hypocalcemia
5.

-Hypoxia

-Injury to epithelium

-Leakage of plasma proteins

-Deficiency of surfactant
Decreased Lecithin Sphingomyelin ration

MAS

Pneumothorax & Bacterial pneumonia

6.

Hypoxia

Bowel under go tissue necrosis

Bacterial proliferation

Necrotizing enterocoilitis
7.

Perinatal asphyxia

Injury to brain

Intracranial bleeding[Non specific asphyxial

injuries]
HIE
DIAGNOSIS
a. CLINICAL METHODS
1.History

-Medical/obstetric problems
-Multiple pregnancy
-Previous history of IUGR
2.Weight gain

-Decreased maternal weight gain during

pregnancy is relatively insensitive sign of
inadequate fetal growth.
-Remains stationary/falling during 2 nd half of
pregnancy.
3.SFH

-In centimeters correlate with

gestational age after 24 weeks.
-A lag of 4 cm /more suggests growth
restriction.
4.Abdominal girth

-Showing stationary / falling values.

5.Fetal kick count

-Mother counts fetal movements & keeps a

daily record.
In cases of
-Poor maternal weight gain
-Diminished fetal movements
6.Clinical palpation

-Liquor volume
-Fetal mass
Less sensitive.
b. BIOPHYSICAL METHODS
a. USG

-Various USG parameters include

-PI
-BPD,TCD
-AC
-EFW
-Placental grading
-AFI
1.HC and AC ratios

HC & AC ratios in normal fetus

<36 weeks 1:1
>36 weeks ratio decreases as AC
increases
-Asymmetric IUGR- HC remains larger, HC/AC
then elevated.
-Symmetric IUGR- HC & AC reduced, HC/AC
remains normal.
- AC is the single most sensitive parameter to
detect IUGR.
2.Femur length

-Is not affected in Asymmetric IUGR

3.Amniotic fluid volume

-Reduced amniotic fluid volume –

Asymmetrical IUGR
-An AFI between 5-25/8-18 cm is normal
less than 5 indicated oligohydramnios.
-AFI is the score (expressed in cm) given
to the amount of amniotic fluid seen on
ultrasonography of a pregnant uterus.
- Measured by dividing the uterus into four
imaginary quadrants .
- Linea nigra is used to divide the uterus into
right and left halves.
- Umbilicus serves as the dividing point for the
upper and lower halves.
b. Doppler velocimetry

-Measures blood flow in fetal vessels

-Helps to detect fetus with hypoxia
-Fetal placental circulation assessed by
umbilical artery & measured by S/D
ratio.
-S/D ratio indirectly measures placental
resistance with in placental vessels.
-Peak systolic-maximum contraction of heart
-Peak diastolic-maximum relaxation of heart
-As placental resistance increases diastolic flow
decreases & S/D ratio increases.
-Normal S/D ratio at term is 1.8 to 2.
-In IUGR it is >2.6 with diastolic notch associated with
reduced/absent /reversed diastolic flow.[AEDF-
Absent end diastolic flow]
AEDF with diastolic notch indicates
fetal jeopardy & poor perinatal
outcome.
-Increased diastolic velocity in MCA
due to decreased placental perfusion
spares fetal brain.
-The fetal circulation is a parallel circuit
where the majority of the right ventricular
output is shunted through the ductus
arteriosus to the descending aorta, and the
left ventricle mainly supplies the upper body
and the brain.
-Vasodilation of the cerebral arteries
causes a decrease in left ventricular
afterload. These changes result in a
preferential shift of the cardiac output in
favor of the left ventricle, enhancing
blood supply towards the brain .
-The fetus redistributes its cardiac output
to maximize oxygen and nutrient supply
to the brain {brain-sparing}.
C. Biochemical markers

-Erythropoietin level in cord blood is

high in IUGR fetuses.
COMPLICATIONS
1.Fetal

-Antenatal
Chronic fetal distress, fetal death
-Intranatal
Hypoxia & acidosis
-After birth
Immediate & late
Immediate

-Asphyxia & RDS

-Hypoglycemia
-MAS
-DIC during first day of life/micro
coagulation
-Hypothermia
-Pulmonary hemorrhage
-Polycythemia
-Hyper viscosity syndrome
-NEC
-IVH
Late

-Symmetrical growth retarded baby grow

slowly after birth.
-Asymmetrical one catch up growth in early
infancy.
-IUGR with cardiovascular disease, type 2
diabetes & hyperlipidemia in adult hood.
2. Maternal

-Fetal growth restriction does not cause

any harm to mother.
-Underlying disease process like pre-
eclampsia, heart disease, malnutrition
may be life threatening.
MANAGEMENT
-To confirm presence of IUGR
-To exclude any congenital malformation
& genetic disorders.
-To treat the specific cause if found
1.General

-Bed rest in left lateral position

-Correct malnutrition[300 extra calories
per day]
-Appropriate therapy for associated
complicating factors.
-Avoidance of smoking & alcohol
-Maternal hyper oxygenation for short
term prolongation of pregnancy.
-Low dose aspirin 50 mg daily in selected
cases.
-Maternal volume expansion may be
helpful in improving placental perfusion.
-Maternal hyperalimentation by amino
acids can improve fetal growth if it was
due to malnutrition.
2.Antepartum evaluation

-Ultrasound examination [interval of 3-4

weeks]
-Fetal well being
-Doppler ultrasound parameters
3.Timing of delivery

Factors
-Fetal abnormality
-Duration of pregnancy
-Degree of growth restriction
-Associated complicating factor
-Results of antenatal fetal surveillance
-Facilities available at place of delivery
-Optimum time of delivery may be between
34 weeks & 37 weeks depending upon
presence of any additional risk factors.
A. Pregnancy > 37 weeks
Delivery should be done.
2.Pregnancy <37 weeks
1.Uncomplicated mild IUGR
-Treatment to improve placental function
may be employed.
-Pregnancy continued at least 37 weeks.
-There after delivery is done.
2.Severe degree of IUGR
-If lung maturation is achieved :
Evidenced by presence of PG & L:S
ratio [at least 2] from amniocentesis ,
termination is done.
-If the lung maturation not yet been
achieved:
a. Biophysical profile
b. Betamethasone therapy
To accelerate pulmonary maturation-
gestational age is <34 weeks.
-Betamethasone [Betnesol] 12mg IM
24 hours apart for 2 doses /
-Dexamethasone 6mg IM every 12
hours for 4 doses is given.
 [Reduce risk of neonatal HMD & IVH.]
C. Delivery is to be done before 32 weeks,
magnesium sulfate be given to mother for
fetal & neonatal neuroprotection.
4.Methods of delivery

-Low rupture of membranes followed by

oxytocin –as pregnancy beyond 34 weeks with
favorable cervix.
-Prostaglandin gel used when cervix is
unfavorable.
-Color of liquor to be noted.
5. Care during vaginal delivery

-Delivery be in an equipped
institution where intensive intranatal
monitoring is possible & facilities for
NICU.
6. Immediate care of the baby after birth

-A paediatrician be available at time

of delivery.
-Baby be placed preferably in NICU.