History
Fetal macrosomia has been defined to include birth weight greater than 4000 g or greater than 4500 g. [1] Macrosomia may place the mother and fetus or neonate at risk for adverse outcomes. Identification of pregnancies with antenatal risk factors for macrosomia may allow intervention to reduce the risk, to provide appropriate counseling, and to implement appropriate plans for monitoring and follow-up care during pregnancy and after delivery.
Note the following:
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Maternal diabetes is a strong risk factor associated with giving birth to an infant that is considered large for gestational age. Pregestational and gestational diabetes result in fetal macrosomia in as many as 50% of pregnancies complicated by gestational diabetes and in 40% of those complicated by type 1 diabetes mellitus. Studies of macrosomic infants of diabetic mothers reveal a greater amount of total body fat, thicker upper-extremity skin fold measurements, and smaller ratios of head to abdominal circumference than macrosomic infants of nondiabetic mothers. [10]
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Gestational age is associated with macrosomia. Birth weight increases as gestational age increases. Prolonged pregnancies (>41 wk) are associated with an increased incidence of macrosomia. Macrosomic infants account for about 1% of term deliveries and 3-10% of postterm deliveries. [5] See the Gestational Age from Estimated Date of Delivery (EDD) calculator.
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Multiparity and grand multiparity increase the risk of macrosomia. [29] Parity has been reported to be associated with 100-150 grams of weight gain at birth. [30] The risk increases with women with parity greater than three. Multiparity is not a major maternal risk factor, but it contributes to the risk of diabetes and obesity. [28]
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A history of macrosomia can influence future pregnancies. Women who previously delivered a macrosomic fetus are 5-10 times more likely than women without such a history to deliver a baby considered large for gestational age the next time they become pregnant. [31] In a large study that controlled for BMI, excess weight gain, diabetes, race, parity, and age, a history of macrosomia was a strong individual risk factor for macrosomia. [32]
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Excessive amniotic fluid defined as greater than or equal to 60th percentile for gestational age has recently been associated with macrosomia. [34]
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Despite these so-called risk factors for macrosomia, much of the variation in birth weights remains unexplained. Most infants who weigh more than 4500 g have no identifiable risk factors. Kim et al found that 46.8-61.0% of the mothers with macrosomic infants assessed in their study had none of the three primary risk factors studied, which included maternal overweight, excessive gestational weight gain and GDM. [3]
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Certain genetic and congenital disorders are associated with an increased risk of macrosomia, including Beckwith-Weidemann syndrome, Sotos syndrome, fragile X syndrome, and Weaver syndrome. [35]
Physical Examination
Many physical examination findings help identify a pregnancy at risk for macrosomia.
Maternal obesity
Maternal obesity is associated with fetal macrosomia. [27] Maternal body mass index (BMI) is a good way of diagnosing obesity prior to pregnancy. The most widely accepted definition for obesity is based on the World Health Organization (WHO) criteria, which uses the BMI. Under this convention for adults, grade 1 overweight (commonly and simply called overweight) is a BMI of 25-29.9 kg/m2. Grade 2 overweight (commonly called obesity) is a BMI of 30-39.9 kg/m2. Grade 3 overweight (commonly called severe or morbid obesity) is a BMI greater than or equal to 40 kg/m2. A BMI greater than 30 kg/m2 is associated with larger infants at delivery.
Maternal obesity is associated with an increased risk of diabetes. Increased concentration of glucose in diabetic mothers leads to fetal hyperinsulinemia, which contributes to increased fetal growth. [35]
Pregnancy weight gain
The recommendations for weight gain in pregnancy have been based on the Institute of Medicine (IOM) guidelines which were updated in 2009. The suggested weight gain is 28-40 lbs for BMI < 18.5, 25-35 lbs for BMI 18.5 – 24.9, 15-25 lbs for BMI 25.0-29.9, and 11-20 lbs for BMI ≥ 30.0. [19] The slowest weight gain occurs in the first trimester and the fastest in the second trimester. Most of the weight gained in the first trimester is fat. Later in pregnancy, the weight is from fetal weight, extravascular fluid, and maternal fat stores. Women with obesity require less weight gain in pregnancy owing to increased fat deposits; therefore, the energy expenditure associated with pregnancy is much less than in normal-weight women. [36]
Half of the weight gained in pregnancy is from the fetus, placenta, amniotic fluid, and gravid uterus. A quarter is from increased blood volume, extravascular volume, and breast tissue. The rest is associated with increased maternal accumulation of cellular water, fat, and protein. Other weight gain is attributable to maternal fat deposition. Increased weight gain in pregnancy is associated with an elevated risk of increased fetal growth, preterm delivery, cesarean delivery, gestational diabetes, hypertensive disorders, and infant mortality. [36]
Fundal height measurements and Leopold maneuvers
Fundal height measurements are an inaccurate way of estimating fetal size. A large retrospective cohort study, which used the perinatal database at Washington University Medical Center from 1990 to 2009, reviewed patients referred for a third-trimester ultrasound scan for “size unequal to dates” (both size less than dates and size greater than dates). These patients were further compared across various maternal BMI categories. There was a low detection rate of fetal growth abnormalities for those referred for an ultrasound scan based on clinical examination (ie, fundal height measurements). Only 15.8% of patients referred for size greater than dates actually had an estimated fetal weight of >90th percentile for gestational age. The sensitivity and specificity for detecting birth weight of >90th percentile were 9.7% and 96.6%, respectively. As maternal BMI increased, the sensitivity increased and the specificity and negative predictive value decreased. Interestingly, about 11.1% of patients in the study who had a normal fundal height delivered a neonate weighing >90th percentile for gestational age. [37]
Another retrospective cohort study, by Sparks et al, had similar findings, with a sensitivity and specificity of 16.6% and 95.4%, respectively, for detection with fundal heights of birth weight of >90th percentile for gestational age. [38] Fundal heights are influenced by maternal size, the amount of amniotic fluid, the status of the bladder, the presence of pelvic masses (eg, fibroids), fetal position, and many other factors.
Leopold maneuvers are techniques developed to determine fetal presentation, lie, and size. They are also limited by many factors, as mentioned previously for fundal height measurements. However, these maneuvers provide the clinician with a general appreciation of fetal size and other important information. Prospective studies designed to evaluate Leopold maneuvers with fundal height measurement for the prenatal diagnosis of possible macrosomia report sensitivities of 10-43%, specificities of 99-99.8%, and positive predictive values of 28-53%. [39, 40] However, discrepancy between fundal height and estimated gestation age is often used to screen women for referral for evaluation of possible large for gestational age fetus by growth ultrasound.
Complications
Morbidity/mortality
Morbidity and mortality associated with macrosomia can be divided into maternal, fetal, and neonatal categories.
Maternal morbidity
Macrosomia is associated with a higher incidence of cesarean delivery (double that of control subjects) and with birth canal lacerations associated with vaginal delivery. Mulik et al reviewed the outcomes of 8617 deliveries over a period of 11 years. [24] In that population, 666 neonates were born with a birth weight of 4000-4499 g and 97 neonates were larger than 4500 g. In their study, Mulik et al found maternal morbidity to be associated with a birthweight of 4500 g or higher compared with a birth weight of less than 4000 g. Postpartum hemorrhage occurred in 3.1% of mothers with newborns weighing 4500 g or more compared with 1.5% in mothers with newborns weighing less than 4000 g. Blood transfusions occurred in 15.4% of mothers with newborns weighing 4500 g or more compared with 3.1% in mothers with newborns weighing less than 4000 g.
Neonatal morbidity
Macrosomic neonates are at risk for shoulder dystocia and birth trauma. This risk is directly related to neonatal birth weight and begins to increase substantially when birth weight exceeds 4500 g and particularly when it exceeds 5000 g. [6] Brachial plexus injury is rare, with an incidence of fewer than two cases per 1000 vaginal deliveries. This risk is approximately 20 times higher when the birth weight is more than 4500 g. [12] Mulik et al reported a higher incidence of NICU admissions for neonates with a birth weight higher than 4500 g compared with newborns with a birth weight of less than 4000 g (9.3% vs 2.7%). Risk of shoulder dystocia was 10 times higher in the larger babies (4.1% vs 0.4%).
In a large study by Raio et al, 3356 newborns who weighed more than 4500 g at birth were studied. Shoulder dystocia occurred in 310 of the newborns, and brachial plexus injuries occurred in 94 of the newborns (about 10% and 3%, respectively). In this population, gestational diabetes increased the risk of shoulder dystocia by a factor of two, while preexisting diabetes increased the risk four-fold. [41]
Fetal morbidity/mortality
Mondestin et al investigated the effects of birth weight on fetal mortality and demonstrated that higher fetal mortality rates are associated with a birth weight of greater than 4250 g in nondiabetic mothers and a birth weight of 4000 g in diabetic mothers. [13] Stillbirth rates in macrosomic infants are twice as high as those in control subjects, irrespective of diabetes. However, for a birth weight of 4500-5000 g, the fetal death rate is fewer than two deaths per 1000 births for nondiabetic women and is approximately eight deaths per 1000 births for diabetic women. For a birth weight of 5000-5500 g, this rate is five to 18 deaths per 1000 births for nondiabetic women and is approximately 40 deaths per 1000 births for diabetic women. [13]
A retrospective cohort analysis designed to demonstrate the link between SGA and perinatal demise showed a “reverse J-shaped relationship” between birth weight percentile and risk of fetal and neonatal death. This means that the greatest risk of perinatal death is at birth weights ≤3rd percentile and ≥98th percentile. A great deal of research and management guidance has gone into surveillance for SGA infants, and this study would suggest that more investigation is warranted to examine the perinatal risks and optimal surveillance of the fetus with accelerated growth. [42]
This is supported by a study by Boulet et al that showed increased risk of neonatal death with increasing birth weight, most notable and statistically significant for infants with birth weights greater than 5000 g, or “grade 3 macrosomia” according to the model in their study. [6]
A large retrospective cohort study by Linder et al included singleton, full-term newborns with a birth weight of ≥4000 g at a tertiary care center, who were matched with healthy newborns with a birth weight of 3000-4000 g. The results showed that macrosomic infants had higher rates of hypoglycemia, transient tachypnea of the newborn, hyperthermia, and birth trauma. There were no differences between the two groups in low 5-minute Apgar scores, metabolic acidosis, infection, loss of >10% of body weight, meconium aspiration syndrome, or cyanotic episodes. Two additional studies that examined infants of diabetic mothers suggested that in utero exposure to hyperglycemia leads to disproportionate growth and higher rates of neonatal complications, such as hypoglycemia, hyperbilirubinemia, polycythemia, and metabolic acidosis. [43]
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Photograph of a macrosomic newborn soon after birth.
