Small and large

for gestational
age baby.
 Gestational age is loosely defined
as the number of weeks between
the first day of the mother’s last
normal menstrual period and the
day of delivery. More accurately,
the gestational age is the
difference between 14 days
before the date of conception
and the date of delivery.
Gestational age is not the actual
embryologic age of the fetus, but
it is the universal standard among
obstetricians and neonatologists
for discussing fetal maturation.
Small for gestational age (SGA)
is a term used to describe a baby who is smaller than the usual amount
for the number of weeks of pregnancy. SGA babies usually have
birthweights below the 10th percentile for babies of the same
gestational age. This means that they are smaller than many other
babies of the same gestational age.

SGA babies may appear physically and neurologically mature but are
smaller than other babies of the same gestational age. SGA babies
may be proportionately small (equally small all over) or they may be of
normal length and size but have lower weight and body mass. SGA
babies may be premature (born before 37 weeks of pregnancy), full
term (37 to 41 weeks), or post term (after 42 weeks of pregnancy).
Etiology
Although some babies are small because of genetics (their
parents are small), most SGA babies are small because of fetal
growth problems that occur during pregnancy. Many babies with
SGA have a condition called intrauterine growth restriction (IUGR).
IUGR occurs when the fetus does not receive the necessary
nutrients and oxygen needed for proper growth and
development of organs and tissues. IUGR can begin at any time in
pregnancy. Early-onset IUGR is often due to chromosomal
abnormalities, maternal disease, or severe problems with the
placenta. Late-onset growth restriction (after 32 weeks) is usually
related to other problems.
 Factors that may contribute to SGA
and/or IUGR include the following:
 Maternal factors: •Factors involving the •Factors related to
 High blood pressure uterus and placenta: the developing baby
• Decreased blood (fetus):
 Chronic kidney disease flow in the uterus • Multiple
 Advanced diabetes and placenta gestation (for
• Placental abruption example, twins or
 Heart or respiratory
disease (placenta detaches triplets)
from the uterus) • Infection
 Malnutrition, anemia • Placenta previa • Birth defects
 Infection (placenta attaches • Chromosomal
low in the uterus) abnormality
 Substance use (alcohol,
drugs) • Infection in the
tissues around the
 Cigarette smoking fetus
 Pathophysiology
There is a compromise in the supply of nutrients reaching the fetus in SGA. In an attempt to
maximize the survival chance, the fetus responds to the reduction in its nutrient supply by
reducing its overall size but preserving certain functions like brain growth, lung maturation, and
increasing red blood cell production. The fetus prioritizes blood supply to more vital organs
such as the brain, heart, adrenals, and placenta. There is a decrease in the total body fat, lean
mass, and mineral contents in infants with severe SGA, giving the neonate a wasted
appearance.
SGA is divided into symmetric and asymmetric growth restriction. Infants with symmetric SGA
have a proportionate reduction in all organ systems, and the growth restriction typically begins
early in the gestation. The incidence of symmetric SGA ranges from 38% to 45%, and factors
such as first-trimester congenital infection and chromosomal abnormalities have been
implicated. In asymmetric SGA, which constitutes about 55% to 61% of SGA cases, the growth
in head circumference is preserved while the length and weight are affected.
The growth restriction in asymmetric SGA begins in the late 2nd or 3rd trimesters and usually
results from a reduction in fetal nutrients due to placental or maternal factors. Continued brain
growth is prioritized.
Symptoms of SGA newborn

Despite their size, small-for-gestational-age newborns usually look

and act similar to normal-sized newborns of similar gestational age.
Some neonates with SGA are thin, with loose peeling skin,
decrease muscle mass, and loss of subcutaneous fat tissues. The
face in these newborns is usually shrunken and wrinkled, and the
umbilical cord is thin. The membranous bone formation in these
infants is decreased, resulting in widened cranial sutures and larger
than normal anterior fontanelle. The head appears relatively larger
than the rest of the body in neonates with asymmetric SGA.
Evaluation

Evaluation begins during the antenatal period. Maternal medical history and
history of the index pregnancy are very important in directing the prenatal
diagnosis of SGA.

Antenatal Diagnosis: During antenatal care, symphysis-fundal height

measurement using a measuring tape is a simple, affordable, and common ways
of detecting SGA or other conditions that can cause size/date discrepancy.
Suspicion for SGA is raised when there is a discordance between the measured
fundal length and the expected size for gestational age. The measurement is said
to be discordant when the fundal height is at least 3 cm less than the gestational
age in weeks. However, there are controversies on the use of symphysis-fundal
height measurement for the diagnosis of SGA, as many studies have reported a
wide range of sensitivities between 13% to 86%.
The routine ultrasound examination is another method of screening for
SGA, but there is no agreement on the timing and number of screening
required. When two screening is obtained, the exams are usually
performed at 32 and 36 weeks of gestation, while for a single screening,
the exam is performed between 32 to 36 weeks of gestation.
In many countries, serial fundal height measurement, and risk assessment
for impaired fetal growth such as the history of maternal chronic disease,
substance use disorder, smoking, placental insufficiency are
recommended for each antenatal visit. In pregnancy with a high risk for
SGA, ultrasound is performed once or twice in the 3rd trimester or when a
lag in fundal height is detected. However, in SGA, low-risk pregnancies,
ultrasound is only performed in any of the following: a lag in fundal height,
inability to palpate fundal height, or fundal height not reliable as in the
case of a uterine mass
Postnatal Diagnosis: SGA is diagnosed in postnatal life when the birth
weight is less than the 10th percentile for gestational age. Other
features in support of SGA include physical evidence of malnutrition,
such as decreased skeletal muscles, subcutaneous fat tissues, and
loose peeling skin.

Accurate determination of gestational age is important in making a

reliable diagnosis of SGA. The two reliable methods used in assessing
the gestational age of the fetus are calculated using the date of the
last menstrual period or from the measurement from a prenatal
ultrasound performed before a gestational age of 20 weeks. In
situations where either the correct menstrual date and prenatal
ultrasound are not obtainable, gestational age can be determined
after birth using the physical and neuromuscular assessments of the
neonate using the Ballard exam.
 Ballard exam
Ballard Scale is a commonly used technique of gestational age assessment. It was
devised by Dr Jeanne L Ballard, Professor Emeritus of Pediatrics, Obstetrics and
Gynecology at the University of Cincinnati College of Medicine.
The assessment assigns a score to various criteria, the sum of all of which is then
extrapolated to the gestational age of the fetus. These criteria are divided into physical
and neurological criteria. This scoring allows for the estimation of age in the range of 26
weeks-44 weeks. The New Ballard Score is an extension of the above to include
extremely pre-term babies i.e. Up to 20 weeks.
The scoring relies on the intra-uterine changes that the fetus undergoes during its
maturation. Whereas the neurological criteria depend mainly upon muscle tone, the
physical ones rely on anatomical changes. The neonate (less than 37 weeks of age) is in
a state of physiological hypotonia. This tone increases throughout the fetal growth
period, meaning a more premature baby would have lesser muscle tone.
 The neuromuscular criteria
1. Posture:muscle tone is reflected in the infant’s preferred posture at rest. As maturation
progresses, the foetus gradually assumes increasing passive flexor tone at rest that
precedes in a centripetal direction with lower extremities slightly ahead of upper
extremities. Term newborn (flexed posture) and preterm newborn (extended posture).
2. Square window, assessing the flexibility of the wrist. Wrist flexibility and resistance to
extensor stretching are responsible for the resulting angle of flexion at the wrist. The
examiner strengthen the infant’s fingers and applies gentle pressure on the dorsum of the
hand, close to the fingers. From extremely preterm to post term, the resulting angle
between the palm of the infant’s hand and forearm is gradually diminished.
3. Arm recoil: Arm recoil examines the passive flexor tone of the biceps muscle by
measuring the angle of recoil following very brief extension of the upper extremity. With
the infant lying supine, the examiner places one hand beneath the infant’s elbow for
support taking the infant’s hand, the examiner briefly sets the elbow in flexion, then
momentarily extents the arm before releasing it. The angle of recoil, to which the forearm
springs back into flexion is noted.
 The neuromuscular criteria
4. Popliteal angle: This maneuver assesses the maturation of passive flexor tone of the knee
extensor muscles by testing for resistance to extension of the lower extremity. With the neonate lying
supine, the thigh is placed gently on the abdomen of the knee fully flexed. The examiner gently
grasps the foot at the sides with one hand while supporting the side of the thigh with the other.
Care is taken not to exert pressure on the hamstrings. The leg is extended until a definite resistance
to extension is appreciated. At this point the angle formed at the knee by the upper and lower leg
is measured.
5. Scarf sign: It is tests the passive tone of the flexors about the shoulder girdle. With infant lying
supine, the examiner adjusts the infant’s head to the midline and supports the infant’s hand across
the upper chest with one hand. The thumb of the examiner’s other hand is placed on the infant’s
elbow. The examiner tries to pull the elbow gently across the chest, feeling for the resistance.
6. Heel To ear: This measures the passive flexor tone of the posterior hip flexor muscles. The infant is
placed supine and the flexed lower extremity is brought to rest on the cot. The examiner supports
the infant’s thigh laterally alongside the body with the palm of one hand. The other hand is used to
grasp the infant’s foot at the sides and to pull it towards the ipsilateral ear. The examiner feels for the
resistance to extension of the posterior pelvic girdle flexors and notes the location of the heel where
significant resistance is appreciated.
Neuromuscular maturity
The physical criteria

1. Skin
2. Ear/eye
3. Lanugo
hair
4. Plantar
surface
5. Breast
bud
6. Genitals
 Scoring
Each of the above criteria are scored from 0 through 5, in the original Ballard Score. The
scores were then ranged from 5 to 50, with the corresponding gestational ages being 26
weeks and 44 weeks. An increase in the score by 5 increases the age by 2 weeks. The
New Ballard Score allows scores of -1 for the criteria, hence making negative scores
possible. The possible scores then range from -10 to 50, the gestational range extending
up to 20 weeks.
A simple formula to come directly to the age from the Ballard Score:

Age=((2 x score)+120)) / 5

maturity rating
 Treatment / Management
Management of SGA starts before birth. Prenatal fetal surveillance is performed using a biophysical
profile (BPP) to monitor fetal well-being and determine the timing of delivery. BPP variables include
nonstress test heart rate monitoring, fetal breathing movement, gross fetal movement, fetal tone, and
amniotic fluid volume, which are monitored using ultrasound. A score of 2 is assigned to a normal
variable and zero for an abnormal variable, and the total score ranges between 0 and 10. The lower
the total score, the higher the risk of fetal compromise and vice versa. In other studies, serial umbilical
artery Doppler studies have been recommended for monitoring and can be used for the timing of
delivery, as are cerebral Doppler studies and cardiotocography.
If delivery is felt to be indicated prematurely, administration of maternal corticosteroids for fetal lung
maturation before birth is indicated at <34 weeks’ gestation and should be considered for
pregnancies between 34 to 36 6/7 weeks gestation in some cases. The majority of the studies
recommend magnesium sulfate for neuroprotection before preterm delivery as well, generally < 32-
week gestation. There are variations in the surveillance approach and timing of birth in late-onset SGA
(gestational age > or =32 weeks) neonates across different countries. In addition, late-onset SGA
newborns with abnormal Doppler studies or estimated fetal weight of < 3rd percentiles, delivery is
recommended at 37-38 weeks gestational age. While with normal doppler studies, delivery is
recommended between 37-40 weeks gestational age.
As per the Neonatal Resuscitation Program, in preparation for delivery, every birth should be
attended by a dedicated, qualified individual whose only responsibility is the assessment and care
of the newborn. In the case of a delivery with suspected risk factors, two qualified individuals should
be present with a full team equipped for extensive resuscitation, including intubation and CPR,
immediately available if called. Care of the SGA infant after birth should begin as it does for any
infant with a quick assessment of the infant’s gestational age, tone, and breathing. If the infant
appears term with good tone and adequate breathing, initial steps of warming and drying,
positioning the airway, and clearing any secretions can be done on the mother’s chest or
abdomen; otherwise, the infant should be moved to the warmer for more extensive assessment and
resuscitation. Following stabilization, newborn care for the term SGA infant can typically be done in
the mother’s room or newborn nursery per institutional policy. However, preterm infants will need
admission and continuing care for issues related to their prematurity in the neonatal intensive care
unit.
Following initial stabilization of the term SGA infant, a thorough physical exam should be performed,
and measurements of head circumference, length, and weight should be obtained with care to
note if the SGA is symmetric or asymmetric. Special attention should be paid to thermoregulation
and feeding. Given their low-fat stores and increased area-to-body mass ratio, these infants are at
risk of hypothermia and subsequent poor feeding, increased calorie expenditure, and slow weight
gain. Keeping the mother’s room warm, encouraging skin-to-skin, and appropriate clothing and
swaddling are effective techniques to maintain euthermia, but additional support with an incubator
or radiant warmer may be needed if euthermia (36.5 to 37.5 degrees C) cannot be sustained.
Early establishment of enteral feeding should be a priority to avoid hypoglycemia.
Exclusive breastfeeding from birth until six months of age should be encouraged of
all infants, including preterm and term SGA infants, as per the World Health
Organization. In the SGA population, glucose should be checked every 3 hours until
stable with a pre-prandial goal of >25 mg/dL for asymptomatic infants in the first 4
hours of life, >35 mg/dL in hours 4 to 24 of life, and >45 mg/dL after 24 hours.
Supplementation with formula or dextrose-containing intravenous fluid may be
needed while breastfeeding or milk supply is established. Fortification of breastmilk or
formula for increased calories may be needed in the newborn period or into the first
year of life for adequate growth in the SGA population as well.

Finally, an investigation into the etiology of fetal growth restriction should be

undertaken if it remains unknown. Serum and urine testing for congenital infections
such as toxoplasmosis and Cytomegalovirus should be considered. Placental
pathology is often helpful for signs of prenatal infection or vasculopathy. If the infant
presents with dysmorphology, genetic testing should be considered as well.
Complications
The risk of complications is high in infants with SGA in the neonatal period, throughout childhood and
beyond. Complications in the perinatal period include prematurity, perinatal asphyxia, impaired
thermoregulation, hypoglycemia, polycythemia and hyperviscosity, impaired immune function, and
hypocalcemia. Infants with SGA are at increased risk of premature delivery and those with SGA who
are born preterm have increased risk for death and prematurity-related complications such as
necrotizing enterocolitis, respiratory distress syndrome, retinopathy of prematurity, and
bronchopulmonary dysplasia.
Infants with SGA are prone to additional hypoxic stress of uterine contraction during delivery and, with
impaired placenta function, there is an increased risk of hypoxic-ischemic encephalopathy, ischemic
heart failure, meconium aspiration, pulmonary hypertension, and kidney and gastrointestinal injury.
Early-onset hypoglycemia is common and the risk of hypoglycemia increases with increasing severity of
SGA due to depleted fat, protein, and glycogen storage.
Immunity is impaired for SGA infants as both T and B peripheral lymphocytes are found to be
decreased at birth in patients with SGA due to stress-induced erythropoiesis, although the number of T
lymphocyte normalized later in childhood but not its proliferative potential.
Infants born SGA are at higher risk of long-term complications including chronic kidney disease,
coronary heart disease, hyperlipidemia, and hypertension.
Prevention of SGA

Prenatal care is important in all pregnancies, and especially to

identify problems with fetal growth. Stopping smoking and use of
substances such as drugs and alcohol are essential to a healthy
pregnancy and can reduce the risk for sudden infant death
syndrome (SIDS) and other sleep-related infant deaths. Eating a
healthy diet in pregnancy may also help.
Large for gestational age (LGA)
Is a term used to describe babies who are born weighing more than the
usual amount for the number of weeks of pregnancy. LGA babies have
birthweights greater than the 90th percentile for their gestational age,
meaning that they weigh more than 90 percent of all babies of the same
gestational age.

The average baby weighs about 3500 grams at birth. About 9 percent of
all babies weigh more than 4,000 grams. Rarely do babies weigh over
5000 grams.

Although most LGA babies are born at term (37 to 41 weeks of

pregnancy), a few premature babies may be LGA.
 Etiology
Multiple factors have been shown to increase likelihood of infant macrosomia including: preexisting
obesity, diabetes, or dyslipidemia of the mother, gestational diabetes, post-term pregnancy, prior history of
a macrosomic birth, genetics, and other factors.

Risk factors
Diabetes of the mother
One of the primary risk factors of LGA births and macrosomia is poorly-controlled maternal diabetes,
particularly gestational diabetes (GD), as well as preexisting type 2 diabetes mellitus (DM).The risk of having
a macrosomic fetus is three times greater in mothers with diabetes than those without diabetes.

Obesity in the mother

Obesity prior to pregnancy and maternal weight gain above recommended guidelines during pregnancy
are another key risk factor for macrosomia or LGA infants. It has been demonstrated that while maternal
obesity and gestational diabetes are independent risk factors for LGA and macrosomia, they can act
synergistically, with even higher risk of macrosomia when both are present.
Genetics
Genetics can also play a role in having an LGA baby and it is seen that
taller, heavier parents tend to have larger babies. Genetic disorders of
overgrowth (e.g. Beckwith–Wiedemann syndrome, Sotos syndrome,
Perlman syndrome, Simpson-Golabi-Behmel syndrome) are often
characterized by macrosomia.

Other risk factors

Gestational age: pregnancies that go beyond 40 weeks increase
incidence of an LGA infant
Fetal sex: male infants tend to weigh more than female infants
Multiparity: giving birth to previous LGA infants vs. Non-LGA infants
Frozen embryo transfer as fertility treatment, as compared with fresh
embryo transfer or no artificial assistance
How each of these factors leads to excess fetal growth is complex and not
completed understood.

Traditionally, the Pedersen hypothesis has been used to explain the mechanism in
which uncontrolled gestational diabetes can lead to macrosomia, and many aspects
of it have been confirmed with further studies. This explanation proposes that
impaired glucose control in the mother leads to a hyperglycemic state for the fetus,
which leads to a hyperinsulinemia response, in turn causing increased glucose
metabolism, fat deposition, and excess growth.

It has also been shown that different patterns of excess fetal growth are seen in
diabetic associated macrosomia compared to other predisposing factors, suggesting
different underlying mechanisms. Specifically, macrosomic infants associated with
glucose abnormalities are seen to have increased body fat, larger shoulders and
abdominal circumference
Symptoms of LGA newborn

LGA infants are large, obese, and plethoric. The 5-

minute Apgar score may be low. These infants may be
listless and limp and feed poorly. Delivery complications
can occur in any LGA infant. Congenital anomalies and
some metabolic and cardiac complications are specific
to LGA infants of diabetic mothers.
Evaluation
During pregnancy, a baby’s birthweight can be estimated in different
ways. The height of the fundus (the top of a mother’s uterus) can be
measured from the pubic bone. This measurement, in centimeters, usually
corresponds with the number of weeks of pregnancy. If the measurement
is high for the number of weeks, the baby may be larger than expected.
Other diagnostic procedures may include the following:
Ultrasound (a test using sound waves to create a picture of internal
structures) is a more accurate method of estimating fetal size.
Measurements can be taken of the fetus’ head, abdomen, and femur to
estimate fetal weight.
A mother’s weight gain can also influence a baby’s size. Excessive
maternal weight gain in pregnancy may correspond with a big baby.
Complications
Because LGA babies are so large, delivery can be difficult. Delivery problems may include the following:
Prolonged vaginal delivery time
Difficult birth
Birth injury
Increased risk of cesarean delivery

Because many large babies are born to diabetic mothers, many problems of LGA babies are related to
problems with glucose regulation. These may include the following:
Hypoglycemia (low blood sugar) of baby after delivery
Increased incidence of birth defects
Respiratory distress (difficulty breathing)

Many babies with LGA also have hyperbilirubinemia (jaundice or yellowing of the skin, eyes, and mucous
membranes).
Treatment of LGA

There is no specific treatment for large-for-

gestational-age newborns, but underlying
conditions and complications are treated as
needed.
Prevention

LGA and fetal macrosomia associated with poor glycemic control can
be prevented by effective blood glucose management below a mean
blood glucose level of 100 mg/dl before and during pregnancy;
additionally, closely monitoring weight gain and diet during pregnancy
can help to prevent LGA and fetal macrosomia. Women with obesity
that undergo weight loss can greatly decrease their chances of having
a macrosomic or LGA infant. Additionally, regular prenatal care and
routine check-ups with one’s physician are important in planning
pregnancy, especially if one has obesity, diabetes, hypertension, or
other conditions before conception.