genetic

FETAL
GROWTH
placental

maternal

Introduction
Inheritance
Growth
potential

FETUS

Normal circumstances

HEALTHY NEWBORN
& APPR- SIZE

Introduction
Growth
potentia

Environment

Ability to
reach optimal
birth weight

Accelerating
Slow Growth
Growth

Maximum
Growth

Decelerating
Growth

0 to 15-16 weeks

10-17 to 26-27
weeks

26-27 to 37-38
weeks

37-38 to 44
weeks

Less than 10
grams/weeks

85 grams/weeks

200 grams/week

More than 70
grams/week

The normal rate of fetal growth in an ideal cases is limited by its internal constraints
(genetic in nature)

Introduction

Amino
Acids

Glucose

Oxygen
Fetal requirement

Simple Diffusion

Facilitated Diffusion

Active Transport

 Persistent decrease in availability of any of

these substrates limit the ability of the
fetus to reach its growth potential
Persistent and severe substrate deficiency
threaten the ability of the fetus to survive
So many factors associated with reducing
substrates supplies to the fetus

Intrauterine Growth
Retardation

Intrauterine Growth
Restriction

Abnormal Mental Function

Slow Growth or Ceases

Fetal weight 10th percentile for

gestational age and sex/SGA
Present of pathological process

SGA is defined as birth weight:

At 10th or less percentile, or
At 5th or less percentile, or
At 3rd or less percentile, or
2 SDs below the mean for gestational age

The lower cut-off incidence and morbidity

and mortality

Cut-off 10th percentile:

SGA : 37 %
IUGR: 1 quarter (failed to achieve its potential
growth)
Non-IUGR: 3 quarters (constitutionally small)

Risk factors
IUGR occurs when gas exchange and nutrient delivery
to the fetus are not sufficient
The process occur primariliy because of:
Maternal disease causing decreased oxygen-carrying
capacity
A dysfunctional oxygen delivery system secondary to
maternal vascular desease
Placental damage resulting from maternal disease
Many factors: fetoplacental fac tors and maternal
factors

Constitutionally small mother

Small women have smaller baby
Reduced intrauterine growth of mother reduced
intrauterine growth of her children
Environment more important than genetic contribution

Poor maternal weight gain and nutrition

Lack of weight gain in the second trimester associated with
fetal growth restriction

Social deprivation
Associated to lifestyle factors such as smoking, alcohol or other
substances abuse and poor nutrition

Fetal infections
Viral, bacterial, protozoon, and spirochaetal implicated on
fetal growth restriction
CMV direct cytolysis and loss functional cells
Rubella vascular deficiency
Another infection affect fetal growth : hepatitis A and B,
Listeriosis, TB, Syphilis, Toxoplasmosis and Congenital Malaria

Congenital malformations
More severe malformation more likely fetus to be small
Espescially with chromosomal abnormalities or serious
cardiovascular malformations

Chromosomal abnormalities
Autosomal trisomies related togrowth restriction
Trisomy 18, 13 and 21
Not seen in Turner or Klinefelter Syndrome

Trisomi 16
Patches of trisomy 16 confined placental mosaicism
placental insufficiency fetal growth restriction

Primary disorders of cartilage and bone

Osteogenesis imperfecta
Various chondrodystrophies

Chemical teratogens
Anticonvulsants (phenitoin, trimethadione)
Cigarette
Narcotics
Alcohol
Cocaine

Vascular disease
Chronic vascular disease especially when further complicated by
superimposed preeclampsia

Chronic renal disease

Renal disease maybe accompanied by restricted fetal growth

Chronic hypoxia
Women in high altitude
Cyanotic heart disease

Maternal anemia
Anemia does not cause growth restriction (in most
cases)
Except :
sickle cell disease
inherited anemia with serious maternal disease
deficient total blood volume early in pregnancy

Placental and cord abnormalities

Chronic partial placental separation
Extensive infarction
Chorioangioma
Marginal insertion of the cord
Velamentous insertion of the cord

Multiple fetuses
Two or more fetuses more likely complicated by
diminished growth of one or both fetuses compared
with normal singleton

Antiphospholipid antibody syndrome

Two classes of antiphospholipid antibodies :
Anticardiolipin antibodies
Lupus anticoagulant
Pathophysiological mechanism maternal platelet
aggregation & placental thrombosis

Extrauterine pregnancy
Fetus gestated outside uterus is usually growth
restricted
Also some maternal uterine malformations

Pathogenesis & Categories

There are standards and averages in weight
according to gestational age (weeks)
Using a fetal growth curve derived from one
population and applyng to another over- or
underestimation of true incidence of SGA
A population of smaller individual will have smaller
babies the difference lies in genetic growth
potential

Normal intrauterine growth pattern:

1st stage: 420 weeks gestation, rapid cell division and
multiplication (hyperplasia)
2nd stage: 2028 weeks gestation, cell division
(hyperplasia) and cells increase in size (hypertrophy)
3rd stage: 2840 weeks gestation, rapid increase in cell
size, rapid accumulation of fat, muscle and connective tissue

95% offetal weight gain occurs during the last 20 weeks

If development and weight gain is disturbed or
interrupted restricted growth

Fetal weight below tenth percentile

Pathological process present

IUGR

First Stage

Hyperplactic Stage

Symmetric

Stage 2
Hyperplastic and
Hypertrophic Stage

Stage 3

Hypertrophic Stage

Asymmetric

Pathogenesis & Categories

Symmetrical Growth Restriction

Growth inhibition during first stage undersized
fetus with fewer cells but normal size
Weight, head and length < 10th percentile
proportionally small
Condition associated include genetic
(constitutional, chromosomal and single gene
defect, deletion disorders and inborn error of
metabolism), congenital anomalies, intrauterine
infections, and therapeutic iradiation

Asymmetrical Growth Restriction

Growth inhibition during stage 2 and 3
decreased of cell size and fetal weight with less
effect on total cell number fetal length and fetal
head circumference
Implies fetus who is undernourished and
directing most of its energy to maintainaning
growth of vital organs such as brain and heart
at the expensive of the liver, muscle and fat
role of brain sparing effect (redistribution
mechanism)

Asymmetrical Growth Restriction

Normal head but small abdominal
circumference, scrawny limbs and thinned skin
Condition associated include uteroplacental
insufficiency (chronis hypertension or
preeclampsia), chronis renal disease, cyanotic
heart disease, hemoglobinopathies, placental
infarcs, abruptio placenta, multiple gestation,
velamentous insertion, cirmcumvallate placenta
and high altitude

Antepartum Complications
Stillbirth
Oligohydramnios
Intrapartum fetal
acidosis

Neonatal Complications
Meconium aspiration syndrome
Persistent fetal circulation
Hypoxic-ischemic encephalopathy
Hypoglicemia
Hypocalcemia
Hyperviscosity syndrome
Deficient temperature controle

IUGR is a part of SGA with present of pathological process

Growth restricted fetus have a great chance to suffer from
many prenatal and/or neonatal complications

Many factors should be recognized

Impaired substrates supply may reduce cellular process
resulting in symmetrical or asymmetrical IUGR