Small For Gestational Age Infant

17/8/2014 Small for gestational age infant
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Author
George T Mandy, MD
Section Editor
Leonard E Weisman, MD
Deputy Editor
Melanie S Kim, MD
Small for gestational age infant
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2014. | This topic last updated: Apr 24, 2014.
INTRODUCTION Fetal growth restriction (FGR, also called intrauterine growth restriction [IUGR]) is the term
used to designate a fetus that has not reached its growth potential because of genetic or environmental factors.
FGR results in the birth of an infant who is small for gestational age (SGA). Mortality and morbidity are increased in
SGA infants compared with those who are appropriate for gestational age (AGA). (See "Fetal growth restriction:
Causes and risk factors".)
DEFINITION The most common definition of small gestational age (SGA) refers to a weight below the 10
percentile for gestational age (table 1) [1]. However, this definition does not make a distinction among infants who
are constitutionally small, growth-restricted and small, and not small but growth-restricted relative to their potential.
As an example, as many as 70 percent of fetuses who weigh below the 10 percentile for gestational age are small
simply because of constitutional factors such as female sex or maternal ethnicity, parity, or body mass index; they
are not at high risk of perinatal mortality or morbidity [1].
Moderate and severe fetal growth restrictions (FGR) are defined as birth weight in the 3 to 10 percentile and less
than 3 percentile, respectively. Normal term infants typically weigh more than 2500 g by 37 weeks gestation [2].
Ponderal index Ponderal index (PI) is a ratio of body weight to length expressed as [3]:
PI = [weight (in g) x 100] [length (in cm)]
With normal growth, the PI increases gradually from 30 to 37 weeks gestation and then remains constant.
Decreased growth of adipose tissue and skeletal muscle, the major contributors to body weight, results in a
reduced PI. Reductions in PI or other indices, such as the ratio of mid-arm to occipito-frontal circumference, can
identify growth restriction in newborns whose weight is greater than the 10 percentile [3]. PI of less than 10
percentile reflects fetal malnutrition; PI of less than 3 percentile indicates severe wasting [4].
GROWTH CURVES Anthropometric data from infants born at different gestational ages have been used to
generate cross-sectional growth curves [1,5-7]. These curves are not uniform and may vary by 100 to 200 g at any
gestational age. The following factors may contribute to these variations:
In general, a customized optimal growth curve developed for a specific fetus, which accounts for individual
differences (ie, maternal age and ethnicity), improves the detection of fetal growth restriction (FGR) [8-10]. In one
report, the use of customized growth curves in a cohort of 13,661 singleton deliveries improved the ability to detect
FGR and improved the ability to predict adverse neonatal outcome [8]. Ideally, separate growth curves should be
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Differences in maternal characteristics, including age, parity, race, ethnic background, socioeconomic status,
and body habitus.
Inaccurate measurements of body size and estimation of gestational age.

Because preterm birth is not a normal outcome, pathologic factors that result in prematurity may adversely
affect fetal growth.

used for each sex because male infants weigh more than females at each gestational age (table 1). In addition,
standards that incorporate birth weight of the mother and older siblings may improve classification of small
gestational age (SGA) infants [11]. Ethnic-specific growth curves have also been developed, and their use may
improve the identification of infants at risk for neonatal morbidity due to IUGR [12,13].
Curves derived from ultrasound measurements of fetuses of known gestational age who were subsequently born
healthy at term provide continuous normative values for fetal growth [14-16]. In preterm births, mean estimated fetal
weight is greater than the mean weight derived from live-born infants by gestational age because SGA infants are
more likely to be born prematurely than appropriate for gestational age (AGA) infants. As a result, estimated fetal
weight growth curves compared with birth weight-gestational standards will classify more infants as having
experienced FGR [17].
EPIDEMIOLOGY The incidence of fetal growth restriction (FGR) varies among populations and increases with
decreasing gestational age. Approximately 10 percent of term infants in developed countries are small for
gestational age (SGA) [18], compared with 23 percent of term infants in developing countries [19]. The values vary
in very low birth weight infants (<1500 g) depending upon whether data collection includes criteria for both birth
weight and gestational age. In the NICHHD Neonatal Research Network database, 22 percent of 4438 infants with
birth weight 500 to 1500 g were classified as SGA [20]. In a larger series of 20,000 very low birth weight infants in
which the gestational age was restricted to 25 to 30 weeks, the incidence of SGA was only 9 percent [21]. (See
"Fetal growth restriction: Causes and risk factors".)
CLASSIFICATION Small gestational age (SGA) infants have either symmetric or asymmetric fetal growth
restriction (FGR). Infants with symmetric FGR have reductions in both body and head growth. Symmetric FGR
begins early in gestation and usually is caused by intrinsic factors such as congenital infections or chromosomal
abnormalities. However, decreased nutrient supply early in development can restrict growth of all organs [18].
Infants with asymmetric FGR have reduced body weight and relatively normal length and head growth. Abnormal
growth typically begins in the late second or third trimesters and results from reductions in fetal nutrients that limit
glycogen and fat storage yet allow continued brain growth [18]. Mechanisms that spare brain growth are uncertain,
but may include increased cerebral blood flow.
Body composition Body composition is altered in SGA compared with appropriate for gestational age (AGA)
infants. Total body fat, lean mass, and bone mineral content are reduced [22]. Nitrogen and protein content are
lower because of reduced muscle mass [18]. Glycogen content is decreased in skeletal muscle and liver because
of lower fetal plasma glucose and insulin concentrations [18].
The concentrations of alpha-amino nitrogen and most essential amino acids are lower in umbilical blood obtained
by cordocentesis in FGR compared with normal fetuses [23]. In human studies, the fetal-maternal concentration
ratio of the essential amino acid leucine is reduced in FGR pregnancies with both normal and abnormal
oxygenation and acid-base status. This effect is caused by decreased placental transfer of leucine and/or increased
protein catabolism by the fetal-placental unit [24].
ETIOLOGY Fetal growth restriction (FGR) may be caused by maternal, placental, or fetal factors. Approximately
one-third of FGRs are due to genetic causes, and two-thirds are related to the fetal environment [25]. However, no
underlying etiology can be identified in at least 40 percent of small for gestational age (SGA) infants. This issue is
discussed in detail elsewhere but a brief listing is provided here. (See "Fetal growth restriction: Causes and risk
factors".)
Maternal factors (See "Fetal growth restriction: Causes and risk factors", section on 'Maternal factors'.)
Severe maternal starvation during pregnancy.
Maternal hypoxemia.
Hematologic and immunologic disorders that cause thrombosis of the intervillous space and decrease
Placental factors Any mismatch between fetal nutritional or respiratory demands and placental supply can
result in impaired fetal growth. FGR results from an accumulation of placental injuries, such as abnormal
uteroplacental vasculature, chronic inflammatory lesions, abruptio placenta, or thrombophilia-related uteroplacental
pathology, and gross placental structural anomalies, such as single umbilical artery, velamentous umbilical cord
insertion, and placental hemangioma. (See "Fetal growth restriction: Causes and risk factors", section on 'Placental
factors'.)
Neonatal factors
CLINICAL FEATURES Small gestational age (SGA) infants appear thin with loose, peeling skin and decreased
skeletal muscle mass and subcutaneous fat tissue. The face has a typical shrunken or "wizened" appearance, and
the umbilical cord often is thin (picture 1) [18]. Meconium staining may be present (picture 2). In newborns with
asymmetric fetal growth restriction (FGR), the head appears relatively large compared with the size of the trunk and
extremities.
Gestational age assessment The physical criteria used to assess gestational age are altered in SGA infants
[18]. (See "Postnatal assessment of gestational age".) As an example, decreased vernix production associated
with reductions in either estriol synthesis or skin perfusion leads to increased exposure of the skin to amniotic fluid.
This exposure results in increased desquamation and enhanced wrinkling (and more mature appearance) of the
soles of the feet. Other findings are diminished breast bud formation, less mature appearance of the female
genitalia, and reduced ear cartilage. The neurologic assessment is reliable in SGA infants without disorders
affecting the nervous system.
COMPLICATIONS Small gestational age (SGA) infants have a variety of associated clinical problems beginning
uteroplacental perfusion.
Maternal medical disorders (eg, nephropathy, collagen vascular disease) and obstetrical complications (eg,
preeclampsia) associated with vasculopathy.
Viruses and parasites (eg, rubella, toxoplasmosis, cytomegalovirus, varicella-zoster, malaria) that gain
access to the fetus transplacentally or across the intact fetal membranes.
Maternal substance abuse, including cigarette smoking, alcohol consumption, and illicit drug use.
Toxic exposures, including various medications such as warfarin, anticonvulsants, antineoplastic agents, and
folic acid antagonists.
High altitude.
Demographic variables including race, pregnancy at the extremes of reproductive life, maternal age at first
childbirth, nulliparity or grand multiparity, and previous delivery of a SGA newborn.
Karyotypic abnormalities, such as trisomies, autosomal deletions, ring chromosomes, uniparental disomy,
and confined placental mosaicism. The presence of a chromosomal abnormality often results in the
appearance of FGR early in pregnancy, most likely of the symmetric type.
Genetic syndromes, such as Bloom syndrome, dwarfism, and Russell-Silver syndrome. (See "Bloom
syndrome".)
Major congenital anomalies. In one study reviewing data from the National Birth Defects Prevention Study,
infants with congenital heart disease, in particular conotruncal and septal defects, were twice as likely to be
small for gestational age compared with those without a birth defect (15.2 versus 7.8 percent) [26].
Multiple gestation is related to fetal growth abnormalities in direct relationship to the number of fetuses
present. (See "Neonatal outcome, complications, and management of multiple births", section on 'Fetal
growth'.)

at birth. Severely affected term newborns deprived of oxygen and nutrients may have a difficult cardiopulmonary
transition with perinatal asphyxia, meconium aspiration, or persistent pulmonary hypertension.
Premature infants Infants with fetal growth restriction (FGR) who are delivered before term also may have
complications of prematurity.
In a study of approximately 20,000 very low birth weight infants (501 to 1500 g birth weight, 25 to 30 weeks
gestation), 9 percent were SGA [21]. The SGA infants had significantly greater rates of neonatal death, necrotizing
enterocolitis, and respiratory distress syndrome (RDS) (odds ratios 2.77, 1.27, 1.19, respectively) than did
appropriate for gestational age (AGA) infants. Administration of prenatal glucocorticoid reduced the risks of RDS,
severe intraventricular hemorrhage, and death in SGA infants (odds ratios 0.51, 0.50, 0.54, respectively), as it does
in AGA infants.
In a multicenter European study of infants born between 24 and 31 weeks gestation, the rate of bronchopulmonary
dysplasia (BPD) increased with decreasing birth weight percentiles [27]. However, there was no association with
birth weight percentiles and the risk of cystic periventricular leukomalacia or grade III and IV intraventricular
hemorrhage.
The increased risk of respiratory morbidity with SGA was demonstrated by a study of 797 preterm infants from the
United Kingdom Oscillation Study of preterm infants, which included 174 patients who were born SGA (22 percent)
[28]. Most patients in the entire cohort received routine administration of antenatal corticosteroids (92 percent) and
surfactant (97 percent). Patients born SGA had higher rates of BPD, pulmonary hemorrhage, and death, and were
more likely to receive postnatal corticosteroid therapy compared with AGA infants. After adjusting for infant and
respiratory morbidity risk factors, lower birth weight was associated with an increased risk for respiratory disease at
24 month follow-up (defined by admissions for respiratory conditions, cough and the use of bronchodilators, inhaled
steroids, or antibiotics).
In a study from the NICHHD Neonatal Research Network, patients who were SGA with a gestational age <27 weeks
compared with AGA controls were more likely to have received postnatal corticosteroid therapy and were at
increased risk for death, growth failure, and neurodevelopmental impairment at 18 to 22 months corrected age [29].
Impaired thermoregulation SGA infants have impaired thermoregulation because of increased heat loss and
reduced heat production [18]. The former is caused by reduced subcutaneous fat, whereas the latter results from
both depletion of catecholamines (needed for thermogenesis by brown fat) by intrauterine stress and reduced
availability of nutrient substrates. Affected infants should be cared for in a neutral thermal environment so that
oxygen consumption is minimized. In one report, SGA infants had significantly higher rates of hypothermia than
AGA controls (18 versus 6 percent) [30].
Hypoglycemia Glucose must be monitored in SGA infants because hypoglycemia is common [31,32]. The risk
of hypoglycemia correlates with the severity of growth restriction. In a large retrospective study, hypoglycemia
occurred in 2.4, 4.5, and 19.1 percent of infants with birth weight below 9.0, 4.3, and 1.7 percentiles, respectively
[31]. In another report, symptomatic hypoglycemia occurred in 5 percent of infants with birth weight below the 10
percentile, compared with 1 percent of those with birth weight 10 to 90 percentile [30].
SGA infants become predisposed to hypoglycemia in utero as low intrauterine insulin concentrations result in
decreased glycogen synthesis and reduced glycogen stores. After delivery, a poorly coordinated response of
counterregulatory hormones and peripheral insensitivity to these hormones may contribute to hypoglycemia in
some infants [33]. Hypoglycemia typically occurs within the first 10 hours after birth. (See "Neonatal
hypoglycemia".)
Polycythemia and hyperviscosity Polycythemia and hyperviscosity occur more frequently in SGA infants. In
one study, hyperviscosity was detected with a microviscometer in 18 percent of SGA infants; most had hematocrits
greater than 64 percent [34].
The risk of polycythemia increases with the severity of growth restriction. In one report, polycythemia occurred in
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9.5, 13.8, and 41.5 percent of infants with mild, moderate, and severe growth restriction, respectively, compared
with 7.5 percent of AGA infants [31]. Increased erythropoietin production resulting from fetal hypoxia is thought to
be responsible [35].
Impaired immune function Cellular immunity can be impaired in FGR infants in the newborn period and
through childhood. In a cross-sectional study, T and B peripheral lymphocytes were decreased at birth; T
lymphocyte numbers became normal in later childhood, but their proliferative capacity was reduced [36]. Delayed
cutaneous hypersensitivity to phytohemagglutinin was reduced in both newborns and children.
Approximately 50 percent of infants born to mothers with severe hypertension (a common cause of FGR) have
neutropenia that may increase their risk of infection [37]. In one study, nosocomial infection occurred more often in
neutropenic than in nonneutropenic infants (55 versus 12 percent), although data are conflicting [37,38].
MORTALITY Fetal, neonatal, and perinatal mortality are increased in small for gestational age (SGA) compared
with appropriate for gestational age (AGA) infants in both term and preterm infants [6,27,39-42].
Term infants Several studies have demonstrated that SGA is a risk factor for mortality in term infants [6,39-42].
In a systematic review of the literature, absolute birth weight correlated with neonatal mortality, with a birth weight
below 1.5 kg in term infants associated with the greatest risk of mortality (odds ratio [OR] 48.6, 95% CI 28.6-82.5)
[42].
Premature infants Mortality rates increase with decreasing gestational age and decreasing birth percentiles as
illustrated by the following studies:
MANAGEMENT If a fetus is known to be growth restricted, problems can be anticipated beginning at birth.
In the previously mentioned multicenter European study of premature infants with gestational ages between 24
and 31 weeks, mortality rate increased with decreasing birth percentiles except for infants who were large for
gestational age (>90 percentile) as follows [27]:
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<10 percentile 26 percent
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10 to 24 percentile 20 percent
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>90 percentile 16 percent
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Perinatal mortality increases as growth restriction becomes more severe, rising abruptly when birth
weight is below the 6 percentile (figure 1) [43]. Congenital malformations, perinatal asphyxia, and
transitional cardiorespiratory disorders contribute to the high mortality rate in term infants. Complications
of prematurity play a greater role as gestational age decreases [41].
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In the French EPIPAGE study that prospectively followed premature live births born in 1997, 536 of the 2846
infants born alive were SGA [44]. Mortality increased with decreasing gestational age and birth percentiles as
follows:
Among the infants born between 24 and 28 week gestation, the mortality was 30, 42, and 62 percent for
infants born AGA (birth weight >20 percentile), mild SGA (birth weight between the 10 and 19
percentile), and SGA (birth weight <10 percentile), respectively.
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Among the infants born between 29 and 32 weeks gestation, the mortality was 4.8, 4.2, and 10.5
percent for infants born AGA, mild SGA, and SGA, respectively.

Delivery of severely affected infants should be planned at a perinatal center. The etiology of fetal growth restriction
(FGR) should be investigated in affected infants when it is not known prior to delivery. In approximately 40 percent
of cases, no cause can be identified. Specific attention should be given to congenital malformations, chromosomal
abnormalities, and congenital infection, in addition to the many other factors listed above. (See 'Etiology' above.)
Because small gestational age (SGA) infants have impaired thermoregulation, heat loss should be avoided by
immediate drying and placement under a radiant warmer. Prompt resuscitation, including clearing the airway of
meconium if needed, should be instituted. Appropriate therapy is begun for disorders of transition, including
meconium aspiration pneumonia, myocardial dysfunction, or persistent pulmonary hypertension, that develop.
Enteral feeding should be started early in infants at volumes appropriate for the infant's weight, including premature
infants [45]. In infants who have severe perinatal asphyxia, are ill, or do not tolerate enteral feeds, feedings should
be withheld and intravenous nutrition provided.
Monitoring for hypoglycemia is initiated within one to two hours after birth. Samples are obtained before feedings.
Surveillance is continued in infants with low plasma glucose concentrations (less than 40 mg/dL, 2.2 mmol/L) until
feedings are well established and glucose values have normalized. (See "Neonatal hypoglycemia".)
SGA infants who are premature or have birth asphyxia are at risk for hypocalcemia. Ionized calcium concentrations
should be monitored starting at 12 hours after birth, and adequate calcium intake should be provided. (See
"Neonatal hypocalcemia".)
OUTCOMES Small gestational age (SGA) infants are at risk for impaired growth and neurodevelopment.
Subsequent disorders in adults may also result from fetal growth restriction (FGR).
Physical growth SGA infants have different patterns of growth depending upon the etiology and the severity of
growth restriction. In moderately affected infants, growth during the first 6 to 12 months after birth may be
accelerated, resulting in attainment of normal size in most children [46,47]. In one study, for example, 87 percent of
3650 term infants with birth length more than two standard deviations below the mean had normal height at one
year of age [47]. However, in a report of national survey data, SGA infants appeared to catch up in weight in the first
six months, but maintained a deficit in height of approximately 0.75 standard deviation units through 47 months
compared with appropriate for gestational age (AGA) infants [48].
In comparison, severely affected SGA infants frequently weigh less and are shorter than AGA infants throughout
childhood and adolescence. In one report, for example, body measurements at age 17 years in adolescents who
had birth weight less than the 3 percentile were compared with those who were AGA [49]. The average height was
significantly less in the SGA group (169 versus 175 cm and 159 versus 163 cm, for boys and girls respectively). In
addition, the adolescent height of SGA newborns was more likely to be less than the 10 percentile (odds ratio
[OR] 4.13 and 3.32, for boys and girls respectively).
The pathophysiology of growth restriction and the efficacy of growth hormone therapy are discussed separately.
(See "Growth hormone treatment for children born small for gestational age".)
Neurodevelopment SGA infants appear to be at increased risk for neurodevelopmental abnormalities and
decreased cognitive performance, although the data are conflicting. Most older studies of outcome are difficult to
interpret because of small sample sizes and inclusion of infants with underlying conditions and neonatal
complications that affect outcome.
Nevertheless, SGA due to FGR appears to affect neurodevelopment and behavior in adolescents and young adults,
as demonstrated by the following case series of individuals born at term or population-based studies:
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In one study, adolescents born at term with severe FGR (3 percentile) had intelligence test scores
comparable to those born AGA, but affected males were significantly more likely to have less than 12 years of
schooling or attend a vocational school (OR 2.4) [50].
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In another report, adolescents born SGA (3 percentile) at term were more likely to have learning difficulties
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Premature infants Cognitive and neurodevelopmental abnormalities are more common in survivors who were
growth restricted premature infants compared with those who were AGA and born at the same gestational age.
In comparison with AGA controls, children who were premature and growth restricted are more likely to have:
Other factors
Relationship to chronic disorders
(32 versus 18 percent) compared with those born AGA, although cognitive ability was not affected [51].
Learning difficulties were related to the severity of growth restriction, but not symmetry. Attentional problems
were more frequent in the SGA girls, but not boys.
In a population-based cohort study of young adult Swedish males evaluated at the time of military
conscription, multiple logistic regression analysis demonstrated low intellectual performance scores were
associated with birth weight <2 standard deviations (SDS) below the mean (OR 1.22, 95% CI 1.13-1.33), birth
length <2 SDS below the mean (OR 1.33, 95% CI 1.22-1.46), and birth head circumference <2 SDS below the
mean (OR 1.28, 95% 1.20-1.37) [52].
In a registry-based cohort Norwegian study of 36,604 term SGA singleton births, 104 patients died in the
neonatal period and 69 developed cerebral palsy [53]. Retrospective review of cases suggested that cerebral
palsy was due to an antenatal cause in about 90 percent of affected SGA children.
In a study of young adults born at term, IQ scores on the Wechsler Adult Intelligence Scale 3 edition were
lower in individuals who were born SGA compared with those who were born AGA (mean difference -6.3, 95%
CI -2.8 to -9.7) [54].
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Lower scores on cognitive testing [29,41,44,55]
School difficulties or require special education [41,44]
Gross motor and minor neurologic dysfunction [29,41]
Behavioral problems (attention deficit hyperactivity syndrome) [44]
Growth failure [29]
Perinatal factors Other perinatal factors that may affect neurodevelopmental outcome were evaluated in a
cohort of 282 SGA infants (mean gestational age and birth weight 36.5 weeks and 2095 g, respectively) born
in the mid 1990s in New Zealand and examined at 18 months of age [56]. The proportion of SGA infants with
low Mental Developmental Index (MDI) scores of the Bayley Scales of Infant Development was significantly
less when mothers had pregnancy-induced hypertension compared with normal blood pressure in pregnancy
(23 versus 44 percent). Although hypertension may be protective, a more likely explanation is that other
causes of SGA are associated with a greater risk of poor outcome. Factors associated with low Psychomotor
Development Index (PDI) scores were not being breastfed at three months, long hospital stay, and need for
mechanical ventilation. A low Behavioral Rating Scale (BRS) score was associated with small head
circumference at birth and increased arterial base deficit in cord blood. No relationship was found between
maternal demographic factors, including age, ethnicity, parity, smoking, education, or severe deprivation, and
abnormal MDI, PDI, or BRS scores.
Postnatal growth Excessive or poor postnatal weight gain during the first four months of life appears to have
a negative impact on neurodevelopmental outcome. This was illustrated in a study from the Collaborative
Perinatal Project (CPP) that evaluated the cognitive outcome of 463 children who were SGA at birth at seven
years of age using the Wechsler Scale of Children's Intelligence (WISC) [57]. Children who gained less than
1200 g or more than 5000 g during the first four months of life had lower WISC scores than children with
weight gains between these two extremes. In addition, body mass index at seven years of age correlated with
postnatal weight gain.

Ischemic heart disease Adults who were SGA infants may be at increased risk for ischemic heart disease
and related disorders. This proposed association (fetal origins of adult disease theory or Barker hypothesis)
between FGR and adult coronary and vascular disease is based upon the assumption that fetal undernutrition
results in changes in vascular development that predisposes to adult disease, such as hypertension, stroke,
diabetes, and hypercholesterolemia (Barker hypothesis) [58-60].
The association with SGA and adult ischemic heart disease was best illustrated in a cohort study of 6425 subjects
born SGA or preterm at four major Swedish delivery units between 1925 through 1949 [61]. At follow-up during the
time period from 1987 to 2002, the risk of ischemic heart disease was greater in subjects who were born SGA
compared with age- and gender-matched controls who were born AGA with gestational ages greater than 35 weeks
(adjusted hazard ratio 1.64, 95% CI 1.23-2.18). The negative association between poor fetal growth and risk of
ischemic heart disease was independent of gestational age.
Other studies demonstrated an increase in aortic wall thickness (a marker of early atherosclerosis) by
ultrasonography in infants with fetal growth restriction compared with infants with normal birth weight [62,63], and
increased aortic stiffness [64]. In addition, one postmortem study in children between 1 and 13 years of age
demonstrated an inverse relationship between birth weight and the extent and severity of aortic lesions [65].
Although these findings are suggestive of a fetal contribution to later cardiovascular risk, long-term longitudinal
studies are needed to more fully understand the clinical significance of these changes and whether they contribute
to atherosclerosis [66]. (See "Possible role of low birth weight in the pathogenesis of primary (essential)
hypertension".)
However, this hypothesis (fetal origins of the adult disease theory) is not universally accepted [67-70]. In a smaller
case cohort study, no significant differences in health quality outcomes were noted between 50-year old adults who
were born full term with a birth weight below the 10 percentile (defined as FGR) compared with controls with birth
weights greater than the 10 percentile [67].
Hypertension The association between birth weight and adult blood pressure is discussed separately. (See
"Possible role of low birth weight in the pathogenesis of primary (essential) hypertension".)
Chronic kidney disease There are data that suggest individuals who are born SGA are at risk for chronic
kidney disease (CKD) including end-stage renal disease (ESRD) [71]. This was illustrated in a large population-
based study from Norway of individuals born between 1967 and 2004 that reported individuals with a weight for
gestational age that was <10 percentile were more likely to develop ESRD than those born AGA after adjusting for
confounding variables such as congenital malformations, multiple delivery, maternal age, and prenatal eclampsia
(relative risk 1.5, 95% CI 1.2-1.9) [72]. A systematic review also reported an association between low birth weight
and CKD [73].
SUMMARY
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Small gestational age (SGA) is the result of fetal growth restriction (FGR) caused by genetic or fetal
environmental factors that result in the inability of the fetus to reach its growth potential. (See "Fetal growth
restriction: Causes and risk factors" and 'Etiology' above.)
The most common definition of SGA is a birth weight that is below the 10 percentile for gestational age
(table 1). (See 'Definition' above.)
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Mortality and morbidity are increased in SGA infants when compared with infants who have appropriate birth
weights (birth weight 10 percentile) for gestational age (AGA).
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Infants who are SGA typically appear thin with loose, peeling skin, and decreased skeletal muscle mass and
subcutaneous fat tissue. The face generally has a shrunken or "wizened" appearance, and the umbilical cord
often is thin (picture 1).
Complications associated with SGA during the neonatal period include prematurity, poor thermoregulation,
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hypoglycemia, polycythemia resulting in hyperviscosity, and impaired immune function. (See 'Complications'
above.)
Population-based data demonstrate a 20- to 30-fold increase in mortality between term infants born AGA
compared with those born SGA with birth weights of 1500 to 2500 g, and rises to 70- to 100-fold increase with
birth weights below 1500 g. The mortality rate also increases with decreasing gestation.
Management of infants with SGA includes (see 'Management' above):

Identifying and, if possible, treating the underlying cause of FGR. (See 'Etiology' above.)
Supportive care including avoidance of heat loss, initiation of enteral feeds as early as possible, and
monitoring for potential complications, such as hypoglycemia.
Long-term complications of patients who were born SGA include impaired growth and neurodevelopment. In
addition, individuals who were SGA infants may be predisposed to cardiovascular disease, hypertension, and
chronic kidney disease. (See 'Outcomes' above.)

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Topic 5062 Version 17.0
GRAPHICS
Tenth percentile of birth weight (g) for gestational age by gender:
United States, 1991, single live births to resident mothers
Gestational age, weeks Male Female
20 270 256
21 328 310
22 388 368
23 446 426
24 504 480
25 570 535
26 644 592
27 728 662
28 828 760
29 956 889
30 1117 1047
31 1308 1234
32 1521 1447
33 1751 1675
34 1985 1901
35 2205 2109
36 2407 2300
37 2596 2484
38 2769 2657
39 2908 2796
40 2986 2872
41 3007 2891
42 2998 2884
43 2977 2868
44 2963 2853
Reprinted with permission from the American College of Obstetricians and Gynecologists (Obstetrics and
Gynecology, 1996; 87:163).
Graphic 75060 Version 3.0
Small for gestational age (SGA) infant
The infant has the typical shrunken or "wizened" appearance of an
SGA infant.
Courtesy of George T Mandy, MD.
Meconium-stained small gestational age (SGA)
infant
The infant has the characteristic appearance of an SGA infant. Note
the loose, peeling skin, decreased subcutaneous tissue and muscle
mass, and meconium staining.
Courtesy of George T Mandy, MD.
Morbidity and mortality in 1560 small for gestational
age fetuses
Data from: Manning FA. Intrauterine growth retardation. In: Fetal Medicine:
Principles and Practice, Appleton & Lange, Norwalk, CT 1995. p.312.
Di scl osures: George T Mandy, MD Nothing to disclose. Leonard E Weisman, MD Consultant/Advisory Boards: Glaxo-Smith-Kline
[Malaria vaccine]. Patent Holder: Baylor College of Medicine [Ureaplasma diagnosis, vaccines and antibodies, process f or preparing
biological samples]. Equity Ownership/Stock Options: Vax-Immune (no product currently). Melanie S Kim, MD Employee of UpToDate,
Inc.
Contributor disclosures are reviewed f or conf licts of interest by the editorial group. When f ound, these are addressed by vetting through
a multi-level review process, and through requirements f or ref erences to be provided to support the content. Appropriately ref erenced
content is required of all authors and must conf orm to UpToDate standards of evidence.
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Small For Gestational Age Infant

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17/8/2014 Small for gestational age infant

Inaccurate measurements of body size and estimation of gestational age.

17/8/2014 Small for gestational age infant

17/8/2014 Small for gestational age infant

17/8/2014 Small for gestational age infant

17/8/2014 Small for gestational age infant

Management of infants with SGA includes (see 'Management' above):

17/8/2014 Small for gestational age infant

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