2. FETAL GROWTH
• characterized by sequential patterns of tissue &
organ growth, differentiation, & maturation
• ability to growth restrict may be adaptive rather
than pathological
• determined by maternal provision of substrate,
placental transfer of substrates, & fetal growth
potential governed by the genome
• insulin & IGFs– important in regulation of fetal
growth and weight gain
• dependent on adequate supply of nutrients
3. FETAL GROWTH PHASES
HYPERPLASIA
• First 16 weeks
• Rapid increase
in cell number
• 5 g/day at 15
weeks’
gestation
HYPERPLASIA
AND
HYPERTROPHY
• Up to 32 weeks’
gestation
• 15-20 g/day at
24 weeks
HYPERTROPHY
• After 32 weeks
• Fetal fat and
glycogen are
accumulated
• 30-35 g/day at
34 weeks
4. NORMAL BIRTHWEIGHT
Normative data for fetal growth based on
birthweight vary with ethnicity and
geographic region.
Infants born to women who reside at high
altitudes are smaller than those born at
sea level.
Birthweight doesn’t define the rate of fetal
growth. Rate or velocity can be estimated by
serial sonographic anthropometry.
5. FETAL–GROWTH
RESTRICTION
• Low-birthweight newborns who
are small for gestational age
• BWs <10th percentile, are not
pathologically growth restricted,
but are small because of
normal biological factors.
• 25-60% SGA infants are
appropriately grown when
maternal ethnic group, parity,
weight, & height are considered
6. SYMMETRICAL VS
ASYMMETRICAL
• Campbell and Thoms (1977) described use of
sonographically determined head-to-abdomen
circumference ratio (HC/AC).
• Onset or etiology of fetal insult has been linked
to either type of growth restriction.
• Symmetrical growth restriction: early insult
decrease in cell number and size
• Asymmetrical growth restriction: late insult
(placental insufficiency from HPN)
7. SYMMETRICAL VS
ASYMMETRICAL
• Diminished glucose transfer and hepatic
storage would affect cell size and not number,
and fetal abdominal circumference—which
reflects liver size—would be reduced.
• Somatic-growth restriction shunting of oxygen
and nutrients to the brain
• Because of brain-sparing effects, asymmetrical
fetuses were thought to be protected from the
full effects of growth restriction.
8. PLACENTAL
ABNORMALITIES
• Rogers and coworkers (1999) observed that
implantation site disorders (incomplete
trophoblastic invasion) are associated with
fetal growth restriction & hypertensive disorders.
• Atrial natriuretic peptide converting enzyme
(corrin), has been shown to play critical role in
trophoblastic invasion and remodeling of the
uterine spiral arteries.
• Maternal rejection of the “paternal semiallograft”
9. LONG-TERM SEQUELAE
Fetal-growth restriction affect organ development,
particularly that of the heart. Individuals with low
birthweight demonstrate cardiac structural
changes and dysfunction persisting through
childhood, adolescence, and adulthood.
Deficient fetal growth is also associated with
postnatal structural and functional renal changes.
Association of low birthweight with disordered
nephrogenesis, renal dysfunction, chronic kidney
disease, and hypertension.
11. DIAGNOSIS
Effective screening for IUGR requires accurate dating,
review of the mother’s menstrual history, relevant
assisted reproductive technology information, and either
1st trimester or early 2nd trimester dating ultrasound.
Symphysis-fundal height determination is of limited
value in routine obstetrical care, but continues to be the
only physical examination screening test available.
Determining whether IUGR is symmetric or asymmetric
is of less clinical importance than careful re-evaluation
of fetal anatomy and uterine and umbilical artery
Doppler studies.
SOGC CLINICAL PRACTICE GUIDELINE, 2013
12. RECOGNITION OF FETAL-
GROWTH RESTRICTION
UTERINE FUNDAL
HEIGHT
• Between 18 and 30
weeks’ gestation,
uterine fundal height in
centimeters coincides
within 2 weeks of
gestational age.
• If the measurement is
>2-3 cm from expected
height, inappropriate
fetal growth is
suspected.
SONOGRAPHIC
MEASUREMENTS OF
FETAL SIZE
• Initial sonographic
examination: 16-20
weeks’ gestation,
• Increasingly in 1st tri—to
establish gestational
age & identify anomalies
• Femur length is the
easiest and the most
reproducible.
13. RECOGNITION OF FETAL-
GROWTH RESTRICTION
AMNIONIC FLUID
VOLUME
MEASUREMENT
• Association between
pathological fetal-growth
restriction and
oligohydramnios
• Hypoxia & diminished
renal blood flow has
been hypothesized as
explanation for
oligohydramnios.
DOPPLER
VELOCIMETRY
• Absent or reversed
end-diastolic flow—
been uniquely linked w/
fetal-growth restriction
• Improve clinical
outcomes
• Recommended in
management of fetal-
growth restriction as
adjunct to standard
surveillance techniques
14. PREVENTION
Before conception, w/ optimization of maternal
medical conditions, medications, & nutrition.
Smoking cessation
Antimalarial prophylaxis for women living in
endemic areas.
Accurate dating is essential in early pregnancy.
Serial sonographic evaluations are used.
15. MANAGEMENT
Patient counseling and prenatal diagnostic testing
are indicated.
Pregnancies complicated by fetal-growth
restriction and at risk for birth <34 weeks receive
antenatal corticosteroids for pulmonary maturation.
Near Term: Delivery between 34 and 37 weeks when
there are concurrent conditions such as
oligohydramnios.
Remote from Term: Nutrient supplementation,
plasma volume expansion, oxygen,
antihypertensives, heparin, & aspirin ineffective
17. SUMMARY
Fetal-growth restriction result of placental
insufficiency d/t faulty maternal perfusion and/or
reduction of functional placenta
Diminished amnionic fluid volume increases
likelihood of cord compression during labor.
Woman w/ growth-restricted fetus should
undergo “high-risk” intrapartum monitoring.
Frequency of cesarean delivery is increased.
Care for the newborn should be provided
immediately by an attendant who can skillfully
clear the airway and ventilate infant as needed.
18. MACROSOMIA
• birthweights that exceed certain
percentiles for a given population
• large-for-gestational age (LGA)
birthweight
• infants >90th percentile for a
given gestational week
• newborns who weigh ≥4500 g at
birth (ACOG 2013)
• excessive glycemia; excessive
transfer of lipids to fetus
19. RISK FACTORS FOR
FETAL OVERGROWTH
Obesity, Large size of parents
Diabetes—gestational and type 2
Post term gestation
Multiparity
Previous macrosomic infant
Advancing maternal age
Racial and ethnic factors
20. MATERNAL AND
PERINATAL MORBIDITY
Neonates with BW of at least 4500 g have
been reported to have cesarean delivery
rates >50%.
Shoulder dystocia reported to be as high
as 17% (BW of 4500 g) and 23% (BW of
5000 g).
Complications: Postpartum hemorrhage,
Perineal laceration, and Maternal
infection, Increased neonatal fat mass,
Morphological heart changes
21. DIAGNOSIS
Estimates provided by measurements
of the head, femur, and abdomen:
• REASONABLY ACCURATE in predicting the wt
of small, preterm fetuses
• LESS VALID in predicting the wt of large fetuses
Sonographic estimation of fetal wt is
UNRELIABLE, and its routine use to identify
macrosomia is NOT RECOMMENDED.
22. MANAGEMENT
PROPHYLACTIC
LABOR INDUCTION
• Nondiabetic women
• ACOG 2013, doesn’t
support a policy for
early labor induction
<39 weeks’ gestation
or delivery for
suspected
macrosomia.
ELECTIVE CESAREAN
DELIVERY
• ACOG 2013, doesn’t
recommend routine
cesarean delivery in
women w/o diabetes
when fetal wt <5000g.
• In diabetics with
overgrown fetuses,
elective cesarean
delivery is tenable.
23. MANAGEMENT
“Current guidelines state that planned cesarean delivery for
diabetic pregnant woman whose fetal weight estimates
exceed 4250-4500 gm may be reasonable.”
-ACOG Practice Patterns Number 7, October 1997
“With an estimated fetal weight >4500 gm, prolonged
second stage of labor or arrest of descent in the second
stage is an indication for cesarean delivery.”
-ACOG Practice Bulletin Number 22, November 2000
“For macrosomic pregnancies including diabetic mothers,
previous deliveries with shoulder dystocia, or considering
VBAC, expectant management with vigilance for fetopelvic
disproportion will have optimal results.”
-Zamorski and Biggs, American Family Physician 2001
24. PREVENTION OF
SHOULDER DYSTOCIA
ACOG (2012) notes that fewer than 10% of all shoulder
dystocia cases result in persistent brachial plexus
injury, and 4% of these follow cesarean delivery.
Ecker and coworkers (1997) concluded that excessive
no. of unnecessary cesarean deliveries would be
needed to prevent brachial plexus injury in neonates
born to women without diabetes.
Planned cesarean delivery may be a reasonable strategy
for diabetic women with an estimated fetal weight >4250
or >4500 g.
25. SUMMARY
When fetal overgrowth is suspected, the
obstetrician naturally seeks to balance the
risks to the fetus with maternal risks.
Elective delivery for the fetus that is to be
overgrown is inadvisable, particularly <39
weeks’ gestation.
Elective cesarean delivery is not indicated
when fetal weight is <5000 g (without
diabetes) and <4500 g (with diabetes).
26. REFERENCES
• Cunningham, F. G., Leveno, K. J., Bloom, S. L., Spong, C. Y.,
Dashe, J. S., Hoffman, B. L., . . . Sheffield, J. S. (2014). Williams
obstetrics (24th edition.). New York: McGraw-Hill Education.
• Fetal Macrosomia. ACOG Practice Bulletin Clinical Management
Guidelines for Obstetrician-Gynecologists. Number 22, November
2000.
• Kingdom, J., & Smith, G. (2000). Diagnosis and Management of
IUGR. Intrauterine Growth Restriction, 257-273. doi:10.1007/978-1-
4471-0735-4_13
• Practice Bulletin No. 134. (2013). Obstetrics & Gynecology, 121(5),
1122-1133. doi:10.1097/01.aog.0000429658.85846.f9
• Zamorski MA, Biggs WS. Management of Suspected Fetal
Macrosomia. American Family Physician 2001;63:302-6.
Editor's Notes
insulin-like growth factors (IGF)
Other hormones implicated in fetal growth, particularly hormones derived from adipose tissue. These are known as adipokines and include leptin, the protein product of the obesity gene.
Other adipokines under investigation include adiponectin, ghrelin, follistatin, resistin, visfatin, vaspin, omentin-1, apelin, and chemerin.
Term infants average 3400 g at sea level, 3200 g at 5000 feet, and 2900 g at 10,000 feet.
1st bullet: to differentiate growth-restricted fetuses… Those who were symmetrical were proportionately small, and those who were asymmetrical had disproportionately lagging abdominal growth.
3rd bullet: Global insults from chemical exposure, viral infection, or cellular maldevelopment with aneuploidy may cause a proportionate reduction of both head and body size.
2nd bullet: This allows normal brain and head growth, that is—brain sparing.
Ratio of brain weight to liver weight during the last 12 weeks—usually about 3 to 1—may be increased to 5 to 1 or more in severely growth restricted infants.
1st bullet: They concluded that implantation site disorders may be both a cause and consequence of hypoperfusion at the placental site.
ACCELERATED LUNG MATURATION: Fetus responds to a stressed environment by increasing adrenal glucocorticoid secretion
Risk factors and causes of impaired fetal growth centering on the mother, her fetus, and the placenta.
Infectious causes such as CMV and rubella may affect the fetus directly.
Bacterial infections such as TB and syphilis may have significant maternal effects that lead to poor fetal growth.
Malaria, a protozoal infection, possibly creates placental dysfunction.
Anticonvulsants; Antineoplastics; Some immunosuppressive drugs for organ transplantation maintenance are implicated in poor fetal growth; Cigarette smoking, opiates and related drugs, alcohol, and cocaine may cause growth restriction
trisomy 21, trisomy 18, Klinefelter syndrome (47,XXY), monosomy X or Turner syndrome
Society of Obstetricians and Gynecologists of Canada
Once surveillance of a fetus with intrauterine growth restriction is instituted, umbilical artery Doppler studies and biophysical profile scoring can be used as short-term predictors of fetal well-being.
Early establishment of gestational age, ascertainment of maternal weight gain, and careful measurement of uterine fundal growth throughout pregnancy will identify many cases of abnormal fetal growth in low-risk women.
In women with risks, serial sonographic evaluation is considered.
Initial early dating examination followed by examination at 32-34 weeks, or when otherwise clinically indicated, will identify many growth-restricted fetuses.
Doppler Velocimetry
Early changes in placenta-based growth restriction are detected in peripheral vessels such as the umbilical and middle cerebral arteries.
Late changes are characterized by abnormal flow in the ductus venosus and fetal aortic and pulmonary outflow tracts and by reversal of umbilical artery flow.
Standard surveillance techniques: nonstress testing and biophysical profile
ACOG (2013a), if growth is normal during a pregnancy following a prior pregnancy complicated by fetal-growth restriction, Doppler velocimetry and fetal surveillance are not indicated.
Prophylaxis with low-dose aspirin beginning early in gestation is not recommended because of its poor efficacy to reduce growth restriction (ACOG, 2013a; Berghella, 2007).
3rd: With reassuring fetal heart rate pattern, vaginal delivery is planned. However, some fetuses do not tolerate labor, necessitating cesarean delivery.
Algorithm for management of fetal-growth restriction
Risk of neonatal hypoxia or meconium aspiration is also increased.
The severely growth-restricted newborn is particularly susceptible to hypothermia and may also develop other metabolic derangements such as hypoglycemia, polycythemia, and hyperviscosity.
Low-birthweight infants are at increased risk for motor and other neurological disabilities.
Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) Study Cooperative Research Group (2008) found that elevated cord C-peptide levels, which reflect fetal hyperinsulinemia, have been associated with increased birthweight.
Free or nonesterified FAs in maternal plasma may be transferred to the fetus via facilitated diffusion or after liberation of fatty acids from triglycerides by trophoblastic lipases (Gil-Sánchez, 2012).
Many are interrelated and thus likely are additive.
Advancing age is usually related to multiparity and diabetes, and obesity is obviously related to diabetes.
Of these, maternal diabetes is an important risk factor for fetal overgrowth.
Incidence of maternal diabetes increases as BW > 4000 g increases.
Because there are no current methods to estimate excessive fetal size accurately, macrosomia cannot be definitively diagnosed until delivery.
Inaccuracy in clinical estimates of fetal weight by physical examination is often attributable, at least in part, to maternal obesity.
“To date, no management algorithm involving selective interventions based on estimates of fetal weight has demonstrated efficacy in reducing the incidence of either shoulder dystocia or brachial plexus injury…planned interventions based on estimates of fetal weight do not reduce the incidence of shoulder dystocia and do not decrease adverse outcomes attributable to fetal macrosomia.”
--Sacks and Chen, Obstetrical and Gynecological Survey 2000