Volume 198, Issue 5 , Pages 517.e1-517.e6, May 2008
How big is too big? The perinatal consequences of fetal macrosomia
Article Outline
Objective
The objective of the study was to examine the birthweight at which risks of perinatal death, neonatal morbidity, and cesarean delivery begin to rise and the causes and timing (antenatal, early or late neonatal, or postneonatal) of these risks.
Study Design
This was a cohort study based on 1999-2001 US-linked stillbirth, live birth, and infant death records. Singletons weighing 2500 g or larger born to white non-Hispanic mothers at 37-44 weeks of gestation were selected (n = 5,983,409).
Results
Infants with birthweights from 4000 to 4499 g were not at increased risk of mortality or morbidity vs those at 3500-3999 g, whereas those 4500-4999 g had significantly increased risks of stillbirth, neonatal mortality (especially because of birth asphyxia), birth injury, neonatal asphyxia, meconium aspiration, and cesarean delivery. Births at 5000 g or larger had even higher risks, including risk of sudden infant death syndrome.
Conclusion
Birthweight greater than 4500 g, and especially greater than 5000 g, is associated with increased risks of perinatal and infant mortality and morbidity.
Key words: birth asphyxia, birth injury, macrosomia, stillbirth, sudden infant death syndrome
From the early 1980s to the late 1990s, increases in mean birthweight, mean birthweight for gestational age, and the proportion of large-for-gestational-age (LGA; weight greater than the 90th percentile for gestational age) infants were described in several countries, including Canada,1 the United States,2 the United Kingdom,3, 4 and Norway.5 This trend was shown to be attributable to increases in maternal height, body mass, gestational weight gain, and diabetes; reduced maternal cigarette smoking; and changes in sociodemographic factors.6 Recent data from the United States, however, show a decline in macrosomia since the late 1990s.7
See Journal Club, page 603
No general consensus exists on the definition of fetal macrosomia; authors have variably defined it as a birthweight greater than 4000, greater than 4500, or greater than 5000 g, regardless of gestational age, or as LGA.8, 9 The birth prevalence of fetal macrosomia varies from 0.5% to 15%, depending on definition. The American College of Obstetricians and Gynecologists defines macrosomia as a birthweight greater than 4500 g, irrespective of gestational age.10 Maternal complications of fetal macrosomia include prolonged labor, cesarean delivery, postpartum hemorrhage, infection, third- and fourth-degree lacerations, thromboembolic events, and anesthetic accidents.8, 11, 12
Fetal macrosomia has also been associated with higher perinatal mortality9, 13 and neonatal morbidity.9, 11, 12 The birthweight-specific infant mortality curve has a well-described inverted-J shape, with a decline in mortality with increasing birthweight until a point at which the slope reverses (ie, increased mortality with rising birthweight).14, 15 The causes and timing (antenatal, early or late neonatal, or postneonatal) of the increased mortality are not fully understood, nor has the birthweight at which the risks begin to rise been clearly identified using data reflecting recent trends in birthweight and obstetric practice. This study attempts to fill these gaps.11, 12
Materials and Methods
We carried out a population-based, retrospective cohort study using US linked stillbirth–live birth–infant death files for the years 1999, 2000, and 2001. These files are compiled by the US National Center for Health Statistics (NCHS) and include information from the death certificate linked to information from the birth certificate for each infant born in the United States who dies before his or her first birthday. This information is provided to NCHS by the states under the Vital Statistics Cooperative Program. The data are coded according to uniform coding specifications, have passed rigid quality control standards, have been edited and reviewed, and are the basis for official US birth and death statistics.
The primary measure used to assess the gestational age of the newborn is the interval between the first day of the mother's last menstrual period (LMP) and the date of birth. If the length of gestation is not consistent with birthweight (normal-weight births of apparently short gestations and very low birthweight births reported to be full term), the clinical estimate of gestation is used instead. The clinical estimate is also used if the LMP date is not reported. The clinical estimate of gestation is recorded as a separate item on the US birth certificate, but no instructions (prior to the 2003 revision) are provided to specify the basis of the estimate. California does not report the clinical estimate. Gestational age is based on the clinical estimate of gestation for only a small percentage of births (about 5%), most of which (about 97%) are due to missing LMP.16, 17, 18
The main outcomes studied were fetal death, infant death (including neonatal and postneonatal mortality), and cause-specific mortality during each period. The NCHS does not collect data on causes of stillbirth. For infant mortality, we used International Classification of Diseases-10 codes to categorize underlying causes of death according to the categories recommended by the International Collaborative Effort (ICE) on Perinatal and Infant Mortality: immaturity-related conditions, congenital anomalies, asphyxia-related conditions, sudden infant death syndrome (SIDS), infectious diseases, and external causes.19 Multiple causes are converted to a single underlying cause of death by Automated Classification of Medical Entities, a computer software package developed by the NCHS that uses World Health Organization rules to select the underlying cause. Neonatal morbidity outcomes studied include Apgar score of less than 4 at 5 minutes, receipt of mechanical ventilation, neonatal seizures, birth injury, and meconium aspiration syndrome.
Birth injury was defined as any impairment of the infant's body function or structure because of adverse influences that occurred at birth.16, 17, 18 Nebraska and Texas did not report birth injury, New York City did not report assisted ventilation, and New Mexico did not report congenital anomalies.16, 17, 18 Finally, we also examined associations with instrumental (forceps or vacuum) vaginal or cesarean delivery.
Maternal risk factors in the linked data included maternal age, parity, marital status, education, diabetes, and cigarette smoking during pregnancy. Maternal age was defined as completed years at time of delivery and classified into 3 categories: younger than 20 years, 20-34 years, and 35 years or older. Missing information on maternal age or marital status was imputed by NCHS; these data items were missing for less than 0.1% of births.16, 17, 18 Missing maternal age was imputed according to the age of mother from the previous birth record of the same race and birth order (based on both fetal deaths and live births). Missing marital status was imputed as “married.” Parity was defined as the number of live births before the index pregnancy and dichotomized as primiparous vs multiparous. Maternal education was defined as the number of years of school completed and grouped into 5 categories: 0-8 years, 9-11 years, 12 years, 13-15 years, and 16 years or more. Diabetes includes juvenile-onset, adult-onset, and gestational diabetes. Maternal smoking was recorded as the average number of cigarettes per day during pregnancy and dichotomized for our analysis as any or none. Method of delivery was classified as noninstrumental vaginal, instrumental vaginal, or cesarean.
Because plurality and maternal ethnicity are associated with birthweight and perinatal mortality,20, 21 we restricted our analysis to singleton live births and stillbirths of white non-Hispanic mothers at 37-44 weeks of gestation with birthweight of 2500 g or greater. A total of 5,983,409 births were included. Because we observed no differences in adverse birth outcomes between birthweights of 3500-3999 g and those of 4000-4499 g, we used 3500-4499 g as our reference category (2,754,223 infants [46.0%]), with 107,511 (1.8%) classified as high birthweight (HBW; birthweight 4500-4999 g) and 11,018 (0.2%) as very high birthweight (VHBW; birthweight of 5000 g or greater). The remaining category contained births between 2500 and 3499 g, comprising 3,110,657 infants (52.0%).
χ2 tests for linear trend were used to compare proportions of demographic variables and maternal characteristics among the 4 birthweight groups, with 1-way analyses of variance used to compare gestational age. The rates of mortality (stillbirth, early neonatal [0-6 days], late neonatal [7-27 days], and postneonatal [28-364 days]), cause-specific mortality, and neonatal morbidity were calculated and compared among the birthweight groups. Unfortunately, the stillbirth data forwarded by the states to the NCHS do not include either the timing (antepartum vs intrapartum) or the cause of the stillbirths. Multiple logistic regression was used to estimate adjusted odds ratios and their 95% confidence intervals after controlling for maternal demographic and clinical variables. All data were analyzed using SAS version 9.1 (SAS Institute, Cary, NC).
Results
Table 1 shows the maternal demographic variables and clinical characteristics by birthweight category. Fetuses and infants in the HBW and VHBW categories were more likely than those of normal birthweight to be boys and of higher gestational age. Mothers of HBW and VHBW infants were more likely than those of normal birthweight infants to be married, older (35 years old or older), and multiparous. Larger proportions of mothers in the HBW and VHBW categories had a high educational level and diabetes, but lower proportions smoked during pregnancy.
TABLE 1. Sociodemographic and clinical characteristics by birthweight (g)
| 2500-3499 | 3500-4499 | 4500-4999 | 5000 or greater | |
|---|---|---|---|---|
Gestational age in completed weeks (mean ±SD) | 39.2±1.5 | 39.7±1.4 | 39.9±1.4 | 39.9±1.4 |
| Infant sex (% male) | 45.6 | 56.8 | 68.4 | 70.7 |
| Multiparous (%) | 55.3 | 61.8 | 68.6 | 71.2 |
| Mother's age 35 years or older (%) | 13.9 | 16.1 | 19.8 | 22.7 |
| Mother's education 13 years or more (%) | 53.8 | 61.6 | 63.0 | 61.6 |
| Marital status (% legally married) | 75.3 | 81.9 | 85.4 | 84.9 |
| Smoking (%) | 19.5 | 9.9 | 5.9 | 5.7 |
| Maternal diabetes (%) | 2.4 | 2.8 | 5.4 | 11.5 |
As shown in Table 2, HBW was associated with higher perinatal mortality; an even larger increase in risk was observed for VHBW. Table 2 also shows that the majority of deaths among HBW and VHBW infants occurred in the early neonatal period. HBW and (especially) VHBW infants were more likely to experience stillbirth (adjusted odds ratio [OR] 2.7 [95% confidence interval (CI) 2.2 to 3.4] and 13.2 [95% CI, 9.8 to 17.7], respectively) and early neonatal death (adjusted OR 1.8 [95% CI, 1.3 to 2.4] and 6.4 [95% CI, 3.9 to 10.4]). VHBW infants were also at increased risk of late neonatal death (OR 5.2 [95% CI, 2.9 to 9.4]). As expected, risks were also elevated in infants with birthweight of 2500-3499 g. Because the absolute infant mortality rates are very low, etiologic fractions (population attributable risks) for infant mortality because of fetal macrosomia were also very low. All etiologic fractions were less than 1%, except for 7.5% for stillbirth and birthweight of 5000 g or greater.
TABLE 2. Fetal and infant mortality by birthweight
| Birthweight (g) | Stillbirth | Early neonatal death | Late neonatal deatha | Postneonatal deathb |
|---|---|---|---|---|
| 2500-3499 | ||||
| n (%) | 3791(0.12) | 1611(0.05) | 1296(0.04) | 5221(0.17) |
| OR (95% CI) | 1.8(1.7to2.0) | 1.9(1.8to2.1) | 1.8(1.6to2.0) | 1.6(1.5to1.7) |
| 3500-4499 | ||||
| n (%) | 1479(0.05) | 732(0.03) | 598(0.02) | 2521(0.09) |
| OR (95% CI) | 1.0 | 1.0 | 1.0 | 1.0 |
| 4500-4999 | ||||
| n (%) | 139(0.13) | 55(0.05) | 15(0.01) | 74(0.07) |
| OR (95% CI) | 2.7(2.2to3.4) | 1.8(1.3to2.4) | 0.7(0.4to1.2) | 0.8(0.6to1.0) |
| 5000 or greater | ||||
| n (%) | 74(0.67) | 18(0.16) | 11(0.10) | 20(0.18) |
| OR (95% CI) | 13.2(9.8to17.7) | 6.4(3.9to10.4) | 5.2(2.9to9.4) | 2.3(1.5to3.5) |
aBased on infants who survived the first week after birth. |
bBased on infants who survived the neonatal period. |
The main causes of neonatal death, grouped according to the ICE classification, are shown in Table 3. Although the absolute numbers of deaths in the VHBW group were very low, the increases in risk were quite large and statistically significant. The leading cause of death in HBW and VHBW infants was asphyxia (0.2 and 1.1 per 1000, respectively). These rates were significantly higher than those of the reference group (adjusted OR 2.3 [95% CI, 1.5 to 3.5] and 10.5 [95% CI, 5.7 to 19.2], respectively). The majority of postneonatal deaths (51.8%) were caused by SIDS. VHBW infants were twice as likely to die of SIDS as normosomic infants, whereas HBW infants were not at an increased risk. In infants 2500-3499 g, the largest risk increase was due to congenital anomalies.
TABLE 3. Major causes of infant deaths by birthweight
| Birthweight (g) | Asphyxia | Congenital anomalies | Infection | Postneonatal SIDS |
|---|---|---|---|---|
| 2500-3499 | ||||
| n (%) | 353(0.01) | 1422(0.05) | 142(0.00) | 2230(0.07) |
| OR (95% CI) | 1.1(0.9to1.3) | 2.8(2.5to3.2) | 1.5(1.1to2.1) | 1.4 (1.3to1.6) |
| 3500-4499 | ||||
| n (%) | 295(0.01) | 448(0.02) | 70(0.00) | 1100(0.04) |
| OR (95% CI) | 1.0 | 1.0 | 1.0 | 1.0 |
| 4500-4999 | ||||
| n (%) | 26(0.02) | 12(0.01) | 4(0.00) | 32(0.03) |
| OR (95% CI) | 2.3(1.5to3.5) | 0.6(0.3to1.2) | 1.8(0.7to5.0) | 0.9(0.6to1.3) |
| 5000 or greater | ||||
| n (%) | 12(0.11) | 4(0.04) | 2(0.02) | 8(0.07) |
| OR (95% CI) | 10.5(5.7to19.2) | 2.3(0.9to6.3) | 8.9(2.2to36.6) | 2.3(1.1to4.6) |
Table 4 shows the results for neonatal morbidity. Both HBW and VHBW infants had significantly increased risks for all neonatal morbidity types, compared with the reference group. The largest increases were observed for birth injury and low 5-minute Apgar score. Infants 2500-3499 g were at slightly increased risk of asphyxic morbidities but at lower risk for both birth injury and meconium aspiration syndrome.
TABLE 4. Neonatal morbidity by birthweight
| Birthweight (g) | 5-minute Apgar score less than 4 | Neonatal seizures | Ventilation less than 30 min | Ventilation 30 minutes or more | Birth injury | Meconium aspiration syndrome |
|---|---|---|---|---|---|---|
| 2500-3499 | ||||||
| % | 0.12 | 0.06 | 2.01 | 0.41 | 0.24 | 0.15 |
| OR (95% CI) | 1.3(1.2to1.3) | 1.1(1.0to1.2) | 0.9(0.9to0.9) | 1.2(1.1to1.2) | 0.6(0.5to0.6) | 0.9(0.8to0.9) |
| 3500-4499 | ||||||
| % | 0.09 | 0.05 | 2.13 | 0.34 | 0.40 | 0.18 |
| OR (95% CI) | 1.0 | 1.0 | 1.0 | 1.0 | 1.0 | 1.0 |
| 4500-4999 | ||||||
| % | 0.17 | 0.08 | 2.87 | 0.57 | 0.91 | 0.26 |
| OR (95% CI) | 1.8(1.5to2.1) | 1.6(1.3to2.0) | 1.4(1.3to1.4) | 1.7(1.5to1.8) | 2.4(2.2to2.5) | 1.5(1.3to1.7) |
| 5000 or greater | ||||||
| % | 0.60 | 0.17 | 4.20 | 1.31 | 1.38 | 0.37 |
| OR (95% CI) | 6.4(4.9to8.4) | 3.3(2.1to5.3) | 2.0(1.8to2.2) | 3.7(3.1to4.5) | 3.5(3.0to4.2) | 2.1(1.5to2.9) |
Mothers who delivered a macrosomic infant were actually less likely to have an instrumental vaginal delivery (HBW 6.6%, VHBW 4.7%) than the reference group (8.3%) but far more likely to be delivered by cesarean (HBW 36.3%, VHBW 50.9%, reference group 22.1%). Adjusted ORs for cesarean delivery were 2.1 (95% CI, 2.0 to 2.1) for HBW infants and 3.6 (95% CI, 3.5 to 3.8) for VHBW infants.
Results were similar in separate analyses of diabetic and nondiabetic mothers. Because the rate of diabetes was only 2.6% in our study sample, however, statistical power was low for detecting differences in magnitude of associations between birthweight and fetal and infant outcomes.
Comment
Our findings of increased mortality and morbidity risks are in general agreement with those of previous studies2, 5, 9, 13, 21 and support the American College of Obstetricians and Gynecologists' definition of macrosomia as 4500 g or greater.10 We also observed markedly higher risks of fetal and infant mortality and neonatal morbidity associated with birthweights of 5000 g or greater. The major cause of early neonatal mortality in macrosomic infants was birth asphyxia. Of note, VHBW infants were also at elevated risk of postneonatal mortality, especially from SIDS. To our knowledge, no previous studies have focused on the association between fetal macrosomia and cause-specific infant mortality.
We observed lower risks of instrumental vaginal delivery in macrosomic infants. These results suggest some reluctance to use forceps or vacuum when the fetus is known (or strongly suspected) to be large. The risks of cesarean delivery were markedly increased with high birthweight, however, suggesting that obstetricians may have a lower threshold for operative delivery when faced with slow labor progress and a large fetus. The optimal route of delivery of macrosomic infants remains controversial. Although a recent population-based cohort study found that infants of 5000 g or greater have a slightly reduced risk of neonatal death when delivered by cesarean, the risks were increased for cesarean births 4000-4499 and 4500-4999 g.22 Moreover, neither ultrasound nor clinical prediction of macrosomia appears sufficiently accurate to serve as the basis for management decisions.7 Neither labor induction nor elective cesarean delivery in suspected cases of macrosomia has been demonstrated to do more good than harm.7, 23, 24, 25
Our study has several limitations. First, the NCHS files do not include information on the timing (ante- vs intrapartum) or causes of stillbirth. Thus, it is unclear whether the increased risk associated with macrosomia could be reduced by improved antepartum surveillance or earlier use of cesarean delivery once labor begins.
Second, high prepregnancy body mass index (BMI) is known to be associated with both macrosomia and adverse birth outcomes.26, 27 However, the linked NCHS data do not include information on maternal weight or height, and maternal prepregnancy BMI was therefore not available for analysis. Thus, we could not assess the extent to which the increased adverse outcomes were independently associated with macrosomia or could be partly explained by maternal obesity.
Third, coding errors are known to occur in administrative data. In particular, previous studies have demonstrated underreporting of medical risk factors, complications of labor and delivery, and neonatal morbidity.28 It is unlikely, however, that such underreporting would be differential with respect to birthweight and mortality or morbidity, and thus, the associations we observed are, if anything, likely to be conservative (biased toward the null). Another potential problem with the NCHS file is nonuniformity in reporting across the states. For example, as noted in Materials and Methods, Nebraska and Texas did not report birth injury, New York City did not report assisted ventilation, and New Mexico did not report congenital anomalies; we were therefore obligated to exclude these states from analyses of the corresponding outcomes.
Finally, the absence of information on postnatal factors such as breast- vs formula-feeding, sleep position, and day care attendance prevented us from controlling for confounding of associations between macrosomia and postneonatal mortality (and SIDS in particular) because of these factors.
Macrosomic infants constituted less than 2% of our cohort, and thus, their overall impact on adverse perinatal outcomes is small. The recent decline in macrosomia7 may be due to the induction or elective cesarean of large fetuses,29 but such a change in practice has not been shown to improve fetal or neonatal outcome.7, 23, 24, 25 The United States has experienced a 10-fold increment in the proportion of pregnant women weighing at least 300 lb at their initial perinatal visit,30 whereas gestational diabetes mellitus has increased between 7% and 10% per year over the last 12 years.31, 32, 33 Fetal macrosomia has been linked in other studies to long-term adverse consequences for the offspring, including obesity,34, 35, 36 hypertension,35 impaired glucose intolerance,37 and cancer.38
Efforts should be made to develop and test interventions aimed at reducing the incidence and/or sequelae of fetal macrosomia. In 2005 the American College of Obstetricians and Gynecologists issued a recommendation suggesting that obstetricians provide preconception assessment and counseling and encourage obese patients to undertake a weight reduction program.39 We are aware of no randomized trials, however, that assess the efficacy of interventions to encourage preconception weight loss.
With respect to screening and treatment of gestational diabetes, the evidence is mixed concerning prevention of macrosomia and its sequelae.40 A recent Cochrane review assessing the benefits of treatment of gestational diabetes found no difference in risks of cesarean delivery, neonatal admission to intensive care, macrosomia, or perinatal mortality.41 The Australian Carbohydrate Intolerance Study (ACHOIS) trial, which was published since the Cochrane review, reported that treatment of gestational diabetes reduced serious perinatal morbidity,42 although that finding has recently been challenged.41 Further studies are clearly required to determine safe and effective methods to reduce the risks of adverse perinatal outcomes among macrosomic fetuses.
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Cite this article as: Zhang X, Decker A, Platt RW, et al. How big is too big? The perinatal consequences of fetal macrosomia. Am J Obstet Gynecol 2008;198:517.e1-517.e6.
Reprints not available from the authors.
This study was supported by a grant from the Canadian Institutes of Health Research. R.W.P. is a Monat-McPherson Career Investigator of McGill University and a career investigator (chercheur-boursier) of the Fonds de la recherche en santé du Québec.
PII: S0002-9378(07)02270-3
doi:10.1016/j.ajog.2007.12.005
© 2008 Mosby, Inc. All rights reserved.
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Perinatal consequences of fetal macrosomia: Zhang et al
Volume 198, Issue 5 , Pages 517.e1-517.e6, May 2008
