Abstract
Background:
Fetal macrosomia is associated with negative outcomes, although less is known about how severities of macrosomia influence these outcomes. Planned community births in the United States have higher rates of gestational age-adjusted macrosomia than planned hospital births, providing a novel population to examine macrosomia morbidity.
Methods:
Maternal and neonatal outcomes associated with grade 1 (4000–4499 g), grade 2 (4500–4999 g), and grade 3 (≥5000 g) macrosomia were compared to normal birthweight newborns (2500–3999 g), using data from the MANA Statistics Project—a registry of planned community births, 2012–2018 (n = 68 966). Outcomes included perineal trauma, postpartum hemorrhage, cesarean birth, neonatal birth injury, shoulder dystocia, neonatal respiratory distress, neonatal intensive care unit (NICU) stay >24 hours, and perinatal death. Logistic regressions controlled for parity and mode of birth, obesity, gestational diabetes, and preeclampsia.
Results:
Sixteen percent of the sample were grade 1 macrosomic, 3.3% were grade 2 macrosomic, and 0.4% were grade 3 macrosomic. Macrosomia grades 1–3 were associated in a dose-response fashion with higher odds of all outcomes, compared to non-macrosomia. The adjusted odds ratios and 95% confidence intervals for postpartum hemorrhage for grade 1, grade 2, and grade 3 macrosomia vs normal birthweight were 1.75 (1.56–1.96), 2.12 (1.70–2.63), and 5.18 (3.47–7.74), respectively. Other outcomes had similar patterns.
Discussion:
The adjusted odds of negative outcomes increase as grade of macrosomia increases in planned community births; results are comparable with the published literature. Pre-birth fetal weight estimation is imprecise; prenatal supports and shared decision-making processes should reflect these complexities.
Keywords: birthing centers, fetal macrosomia, home childbirth, pregnancy complications
1 |. BACKGROUND
Fetal macrosomia is defined as birthweight of at least 4000 g, although classifications of >4500 g and >5000 g are also used.1–4 Higher birthweight newborns are associated with a number of negative labor and birth outcomes in planned hospital births, including prolonged labor, genital tract lacerations, postpartum hemorrhage, neonatal birth trauma including fractures, birth asphyxia, respiratory distress syndrome, neonatal intensive care unit (NICU) admission, and perinatal death.1–7 Outcomes of care for pregnant individuals who begin labor intending to birth in the community setting (ie, at home or in a birth center) with a macrosomic fetus have not been reported in the published literature.
Planned community births have increased steadily in the United States (US), from 0.9% of all births in 2007 to 1.6% of all births in 2017.8 Since both preterm labor and fetal growth restriction are contraindications for planned community birth, mean birthweight in this population is substantially higher than the United States average. In a large study of planned home births in the United States, the proportion of newborns weighing 4000 g or greater was 22.6%9(p16)—higher than the general United States prevalence of 7.9%.10 Higher rates of macrosomia in the community setting may be attributed solely to the lack of preterm and growth restricted newborns; however, it is possible that elevated rates of macrosomia are observed even when the absence of preterm and growth restriction is taken into account. Macrosomia may be contributing to elevated rates of morbidity resulting from commonly reported negative sequelae of larger than average babies born in the community setting. However, it is also possible that aspects of the Midwives Model of Care11 are protective, contributing to better than expected outcomes for pregnant individuals with macrosomic infants. Thus, the purposes of this study were as follows: (a) to examine the relationship between fetal macrosomia and selected maternal and neonatal outcomes; and (b) to examine the extent to which the known adverse effects of fetal macrosomia are mitigated when considering fetal macrosomia as an effect modifier in a sample of planned, singleton community births attended by midwives in the United States.
2 |. METHODS
2.1 |. Data source
This retrospective cohort study used data from the Midwives Alliance of North America Statistics Project (MANA Stats).12 All midwives, regardless of credentials or location of practice (ie, hospital vs community), are invited to participate in MANA Stats; membership in the organization is not required to use the data collection system.12 In practice, the majority of MANA Stats data are entered by midwives practicing in the United States who attend births at home or in freestanding birth centers. The system employs a convenience sampling method in which participating midwives in most states voluntarily enroll in the project. In a small number of US states, participation is or was required during some years of data collection (eg, required in Oregon beginning in 2012). All enrolled midwives then obtain verbal informed consent to submit data for all clients. They log consenting clients (>97%)13 early in care before the outcome of the birth is known and enter medical records data on pregnant individuals and their newborns over the course of care through 6–8 weeks postpartum.13 These analyses were approved by the IRB at Oregon State University.
2.2 |. Study population
This analysis used MANA Stats data from birth years 2012–2018, with low-risk, pregnant individual-newborn dyads planning a midwife-attended community birth at labor onset. The current version of MANA Stats began with birth year 2012; the most recent data available at time of analysis were birth year 2018. We excluded individuals who transferred care to another provider prior to labor onset, births that occurred outside of the United States, breech presentation at birth, non-singleton pregnancies, and term newborns with birthweights ≤2500 g. We also excluded preterm births (<37 weeks’ gestation). Although preterm birth is a contraindication for community birth, estimated due dates are occasionally incorrect, and the newborn is diagnosed as preterm via clinical examination by the attending midwife. After these exclusions, the final sample size available for analysis was n = 68 966.
2.3 |. Variable definitions
Fetal macrosomia is defined as neonatal birthweight of at least 4000 g. For this analysis, macrosomia was categorized into four levels: non-macrosomia (2501–3999 g), grade 1 macrosomia (4000–4499 g), grade 2 macrosomia (4500–4999 g), and grade 3 macrosomia (≥5000 g), as is common in the literature.2,14
Outcomes included perineal trauma (third- or fourth-degree perineal tear), postpartum hemorrhage (blood loss ≥ 1000 mL), cesarean birth (cesarean births would occur following intrapartum transfer of care to a hospital), neonatal birth injury (including skeletal fractures, peripheral nerve injury, and/or soft tissue/solid organ hemorrhage that required intervention), shoulder dystocia, neonatal respiratory distress, NICU stay of at least 24 hours, and perinatal death (including intrapartum fetal demise [stillbirth after onset of labor but before birth] and neonatal death within 28 days after live birth). All outcomes were dichotomous.
Covariables included maternal race (White, Black, American Indian/Alaska Native, Asian/Pacific Islander, Latina, Multiracial), advanced maternal age (>35 years), maternal education (less than high school, completed high school, completed some college, completed at least 4 years college), marital status (married/partnered, not married/partnered), parity and mode of birth (primiparous, multiparous without cesarean history, multiparous with cesarean history), gestational diabetes of current pregnancy (yes, no), preeclampsia of current pregnancy (yes, no), pre-gravid body mass index (BMI) (obese: ≥30 kg/m2, non-obese: <30 kg/m2; calculated from maternal self-reported height and pre-pregnancy weight), and neonatal sex (male, female).
2.4 |. Statistical analyses
Frequencies and percentages were calculated for each co-variable by fetal macrosomia status. Bivariable associations between fetal macrosomia status and all outcomes were calculated with chi-square tests. We then adjusted for confounders using unconditional logistic regression models. The exposure of interest, the four-level fetal macrosomia variable, was entered into the models as a nominal variable, with non-macrosomia as the reference group. Primiparity, pre-gravid BMI, preeclampsia, and gestational diabetes were treated as potential confounders; these confounders were chosen using directed acyclic graph (DAG) causal models.15 The DAG for this analysis is available from the authors on request. Adjusted odds ratios (AOR) and 95% confidence intervals (CI) were calculated for each outcome. For analyses involving perineal trauma, postpartum hemorrhage, and shoulder dystocia, vaginal births only (excluding cesareans) were used as the denominator.
Finally, to assess fetal macrosomia as a potential effect modifier, selected predictor variables were analyzed for association with each outcome using unconditional logistic regression models, separately for each subset of fetal macrosomia status. For these models, grades 2 and 3 macrosomia were grouped together to increase statistical power. The intent of this set of analyses was to explore whether the associations between known predictors of adverse birth outcomes (eg, primiparity) are associated with those outcomes (eg, cesarean) differently, depending on the grade of macrosomia involved. Analyses were performed using SAS Studio 3.8 (SAS Institute Inc).
3 |. RESULTS
Pregnant individuals in this analysis were mostly white, college-educated, and married or partnered; nearly 17% were older than 35 years of age (Table 1). A very small percentage had pregnancy complications of preeclampsia (0.1%) or gestational diabetes (1.6%); these are usually contraindications to planned community birth and are not expected to appear in the sample in large numbers (Table 1). Sixty-three percent were multiparous without cesarean history, and 11.9% had a pre-gravid BMI of 30 or greater (Table 1). Sixteen percent of newborns were grade 1 macrosomic, 3.3% were grade 2 macrosomic, and 0.4% were grade 3 macrosomic (Table 1).
TABLE 1.
Characteristics of pregnant individuals by fetal macrosomia status in Midwives Alliance of North America Statistics Project, birth years 2012–2018
| Characteristic,a n (%) | Total N = 68 966 (100) | Non-macrosomia n = 55 378 (80.3) | Grade 1 macrosomia n = 11 033 (16.0) | Grade 2 macrosomia n = 2256 (3.3) | Grade 3 macrosomia n = 299 (0.4) |
|---|---|---|---|---|---|
| Maternal race, n (%) | |||||
| White | 59 529 (86.6) | 47 268 (85.6) | 9919 (90.2) | 2066 (91.7) | 276 (92.3) |
| Non-Whiteb | 9234 (13.4) | 7945 (14.4) | 1080 (9.8) | 186 (8.3) | 23 (7.7) |
| Maternal age, n (%) | |||||
| ≤35 y | 57 466 (83.4) | 46 388 (83.8) | 9041 (82.0) | 1803 (80.0) | 234 (78.5) |
| >35 y | 11 480 (16.7) | 8975 (16.2) | 1989 (18.0) | 452 (20.0) | 64 (21.5) |
| Maternal education, n (%) | |||||
| Less than high school | 4426 (6.5) | 3671 (6.7) | 630 (5.8) | 114 (5.1) | 11 (3.7) |
| Completed high school | 9781 (14.3) | 7818 (14.3) | 1599 (14.6) | 314 (14.1) | 50 (17.0) |
| Completed some college | 19 778 (29.0) | 15 691 (28.6) | 3274 (30.0) | 719 (32.2) | 94 (32.0) |
| Completed at least 4 y of college | 34 276 (50.2) | 27 626 (50.4) | 5427 (49.7) | 1084 (48.6) | 139 (47.3) |
| Marital status, n (%) | |||||
| Married/partnered | 65 517 (95.0) | 52 443 (94.7) | 10 596 (96.0) | 2185 (96.9) | 293 (98.0) |
| Not married/partnered | 3437 (5.0) | 2923 (5.3) | 437 (4.0) | 71 (3.2) | 6 (2.0) |
| Parity and mode of birth, n (%) | |||||
| Primiparous | 21 875 (31.7) | 19 187 (34.7) | 2311 (21.0) | 335 (14.9) | 42 (14.1) |
| Multiparous w/o cesarean history | 43 487 (63.1) | 33 523 (60.1) | 8008 (72.6) | 1734 (76.9) | 222 (74.3) |
| Multiparous w/ cesarean history | 3590 (5.2) | 2658 (4.8) | 710 (6.4) | 187 (8.3) | 35 (11.7) |
| Gestational diabetes,c n (%) | 1088 (1.6) | 835 (1.5) | 188 (1.7) | 59 (2.7) | 6 (2.1) |
| Preeclampsia,c n (%) | 63 (0.1) | 50 (0.1) | 13 (0.1) | 0 (0) | 0 (0) |
| Pre-gravid BMI, kg/m2, n (%) | |||||
| Obese ≥ 30 | 7701 (11.9) | 5436 (10.4) | 1707 (16.6) | 466 (22.1) | 92 (33.8) |
| Non-obese < 30 | 57 070 (88.1) | 46 664 (89.6) | 8585 (83.4) | 1641 (77.9) | 180 (66.2) |
| Neonatal sex, n (%) | |||||
| Male | 33 688 (48.9) | 28 607 (51.7) | 4264 (38.7) | 723 (32.1) | 94 (31.4) |
| Female | 35 240 (51.1) | 26 747 (48.3) | 6758 (61.3) | 1530 (67.9) | 205 (68.6) |
| Median gestational age, days (interquartile range) | 281 (277–287) | 281 (276–286) | 285 (280–289) | 286 (281–291) | 286 (282–291) |
n missing for each characteristic (missing not included in percentage calculations): maternal race = 203, maternal age = 20, maternal education = 705, marital status = 12, parity = 14, gestational diabetes = 1485, preeclampsia = 1485, pre-gravid BMI = 4195, neonatal sex = 38, median gestational age = 0.
Black, American Indian/Alaska Native, Asian/Pacific Islander, Latina, Multiracial.
Refers to complication of the current pregnancy only.
Among those with non-macrosomia, 1.4% had shoulder dystocia, compared to 6.3% with grade 1 macrosomia, 15.2% with grade 2 macrosomia, and 26.0% with grade 3 macrosomia (Table 2). Additionally, among those with non-macrosomia, 2.7% experienced postpartum hemorrhage, compared to 4.2% with grade 1 macrosomia, 5.2% with grade 2 macrosomia, and 10.3% with grade 3 macrosomia (Table 2). Most outcomes follow a similar pattern: The outcome rate rises as fetal weight rises. The perinatal death rate for non-macrosomic newborns was 1.6/1000; the rates for grade 1, grade 2, and grade 3 macrosomic newborns were 1.6/1000, 2.7/1000, and 3.3/1000, respectively (Table 2). There was no statistically significant difference in perinatal death rates between macrosomia groups (Table 2), though small numbers of events limited statistical power for assessing perinatal death.
TABLE 2.
Outcomes by fetal macrosomia status in Midwives Alliance of North America Statistics Project, birth years 2012–2018
| Outcome variablea | Non-macrosomia n = 55 378 | Grade 1 macrosomia n = 11 033 | Grade 2 macrosomia n = 2256 | Grade 3 macrosomia n = 299 | P-valueb |
|---|---|---|---|---|---|
| Perineal trauma,c n (%) | 665 (1.3) | 188 (1.8) | 45 (2.1) | 7 (2.4) | <.0001 |
| Postpartum hemorrhage,c n (%) | 1443 (2.7) | 439 (4.2) | 111 (5.2) | 30 (10.3) | <.0001 |
| Cesarean birth, n (%) | 1680 (3.0) | 446 (4.0) | 107 (4.7) | 9 (3.0) | <.0001 |
| Neonatal birth injury, n (%) | 114 (0.2) | 59 (0.6) | 12 (0.5) | 7 (2.4) | <.0001 |
| Shoulder dystocia,c n (%) | 719 (1.4) | 652 (6.3) | 323 (15.2) | 74 (26.0) | <.0001 |
| Neonatal respiratory distress, n (%) | 893 (1.6) | 227 (2.1) | 75 (3.3) | 20 (6.7) | <.0001 |
| NICU stay >24 h, n (%) | 1041 (1.9) | 215 (2.0) | 68 (3.0) | 25 (8.4) | <.0001 |
| Perinatal death, n (rate/1000) | 91 (1.6/1000) | 18 (1.6/1000) | 6 (2.7/1000) | 1 (3.3/1000) | .356d |
n missing for each outcome (missing not included in percentage calculations): perineal trauma = 686, postpartum hemorrhage = 3561, cesarean birth = 1, neonatal birth injury = 1481, shoulder dystocia = 1012, neonatal respiratory distress = 0, NICU stay > 24 h = 0, perinatal death = 73.
P-value for chi-square test of independence between fetal macrosomia status and each outcome.
Denominator of vaginal births only.
Monte Carlo estimate for Fisher’s exact test.
A dose-response relationship was observed between increasing macrosomia and perineal trauma, postpartum hemorrhage, shoulder dystocia, neonatal respiratory distress, and NICU stay >24 hours. For example, the AORs for neonatal respiratory distress increase from grade 1 (AOR: 1.42 [95% CI: 1.21–1.66]), to grade 2 (2.56 [2.00–3.29]), to grade 3 macrosomia (5.53 [3.43–8.91]) (Table 3). Interestingly, this dose-response relationship is not observed for cesarean birth. Grade 2 macrosomia showed a stronger association with cesarean birth (2.54 [2.04–3.18]) than grade 1 macrosomia (1.88 [1.67–2.12]), while grade 3 macrosomia was not statistically significantly associated with cesarean birth (Table 3). Of all outcomes in this analysis, fetal macrosomia was most strongly associated with shoulder dystocia (grade 1:4.99 [4.46–5.60], grade 2:12.80 [11.02–14.87], grade 3:28.54 [21.32–38.21]) (Table 3).
TABLE 3.
Adjusted odds ratios of outcomes by fetal macrosomia status compared to non-macrosomia in Midwives Alliance of North America Statistics Project, birth years 2012–2018
| Adjusteda odds ratio (95% confidence interval) | ||||
|---|---|---|---|---|
| Outcome variable | Non-macrosomia | Grade 1 macrosomia | Grade 2 macrosomia | Grade 3 macrosomia |
| Perineal traumab,c | ref | 2.16 (1.81–2.57) | 3.00 (2.15–4.18) | 3.84 (1.77–8.35) |
| Postpartum hemorrhageb,c | ref | 1.75 (1.56–1.96) | 2.12 (1.70–2.63) | 5.18 (3.47–7.74) |
| Cesarean birthb | ref | 1.88 (1.67–2.12) | 2.54 (2.04–3.18) | 1.34 (0.67–2.69) |
| Neonatal birth injuryb | ref | 2.75 (1.96–3.86) | 2.67 (1.38–5.16) | 14.42 (6.53–31.82) |
| Shoulder dystociab,c | ref | 4.99 (4.46–5.60) | 12.80 (11.02–14.87) | 28.54 (21.32–38.21) |
| Neonatal respiratory distressb | ref | 1.42 (1.21–1.66) | 2.56 (2.00–3.29) | 5.53 (3.43–8.91) |
| NICU stay >24 hb | ref | 1.15 (0.98–1.35) | 1.96 (1.51–2.54) | 5.70 (3.68–8.83) |
Adjusted for parity (primiparous, multiparous with no history of cesarean, multiparous with history of cesarean), obesity (≥30 BMI, <30 BMI), gestational diabetes (yes, no), preeclampsia (yes, no).
Sample size for each model: perineal trauma = 60 707, postpartum hemorrhage = 61 342, cesarean birth = 63 384, neonatal birth injury = 62 034, shoulder dystocia = 60 493, neonatal respiratory distress = 63 385, NICU stay >24 h = 63 385.
Denominator of vaginal births only.
When analyzing macrosomia as an effect modifier, such dose-response relationships are not consistently apparent. Both primiparas and multiparas with cesarean history had substantially increased adjusted odds of perineal trauma at non-macrosomia as well as grade 1, and grades 2 and 3 macrosomia. Primiparity was associated with postpartum hemorrhage at non-macrosomia (1.99 [1.77–2.23]), grade 1 (2.94 [2.36–3.67]), and grades 2 and 3 macrosomia (1.16 [1.01–1.33]) (Table 4). Advanced maternal age was associated with cesarean at non-macrosomia, grade 1, and grades 2 and 3 macrosomia. Obesity was associated with cesarean at non-macrosomia (2.03 [1.74–2.35]), grade 1 (1.91 [1.48–2.47]), and grades 2 and 3 macrosomia (2.05 [1.81–2.33]) (Table 4). Despite the strong association between increasing macrosomia and shoulder dystocia, there were no obvious patterns between the selected predictor variables and shoulder dystocia when treating macrosomia as an effect modifier. Gestational diabetes was associated with shoulder dystocia at non-macrosomia (2.11 [1.35–3.28]), grade 1 (2.03 [1.25–3.29]), and grades 2 and 3 macrosomia (1.97 [1.48–2.63]) (Table 4).
TABLE 4.
Adjusted odds ratios of outcomes by selected predictors, separately for each subset of fetal macrosomia status in Midwives Alliance of North America Statistics Project sample, birth years 2012–2018. Each subset of macrosomia can be interpreted as an effect modifier in the association between each predictor variable and outcome
| Perineal traumaa | ||||
|---|---|---|---|---|
| Adjustedb odds ratio (95% confidence interval) | ||||
| Predictor variable | Total sample n = 60 071 | Non-macrosomia n = 48 417 | Grade 1 macrosomia n = 9477 | Grades 2 and 3 macrosomia n = 2177 |
| Gestational diabetesc | 1.53 (0.97–2.41) | 1.60 (0.94–2.70) | 0.71 (0.17–2.97) | 1.53 (0.97–2.41) |
| Advanced maternal aged | 0.94 (0.76–1.17) | 1.06 (0.83–1.35) | 0.65 (0.38–1.12) | 0.94 (0.76–1.17) |
| Obesitye | 0.87 (0.67–1.12) | 0.69 (0.49–0.98) | 1.01 (0.64–1.60) | 0.87 (0.67–1.12) |
| Primiparousf | 9.81 (8.12–11.86) | 9.93 (7.90–12.49) | 14.25 (9.54–21.30) | 9.81 (8.12–11.86) |
| Multiparous with cesarean historyf | 7.27 (5.43–9.73) | 6.60 (4.55–9.59) | 10.01 (5.79–17.30) | 7.27 (5.43–9.73) |
| Postpartum hemorrhagea | ||||
| Adjustedb odds ratio (95% confidence interval) | ||||
| Predictor variable | Total sample n = 60 687 | Non-macrosomia n = 48 927 | Grade 1 macrosomia n = 9567 | Grades 2 and 3 macrosomia n = 2202 |
| Gestational diabetesc | 1.38 (1.00–1.89) | 1.44 (0.99–2.09) | 1.35 (0.65–2.80) | 1.40 (1.04–1.88) |
| Advanced maternal aged | 1.00 (0.87–1.14) | 0.99 (0.84–1.16) | 0.98 (0.74–1.31) | 1.07 (0.95–1.21) |
| Obesitye | 1.15 (1.00–1.33) | 1.06 (0.88–1.27) | 1.03 (0.78–1.37) | 1.16 (1.01–1.33) |
| Primiparousf | 2.00 (1.81–2.21) | 1.99 (1.77–2.23) | 2.94 (2.36–3.67) | 2.14 (1.94–2.35) |
| Multiparous with cesarean historyf | 1.62 (1.32–1.99) | 1.61 (1.25–2.07) | 1.41 (0.92–2.18) | 1.76 (1.46–2.12) |
| Cesarean birth | ||||
| Adjustedb odds ratio (95% confidence interval) | ||||
| Predictor variable | Total sample n = 62 675 | Non-macrosomia n = 50 412 | Grade 1 macrosomia n = 9966 | Grades 2 and 3 macrosomia n = 2297 |
| Gestational diabetesc | 1.13 (0.83–1.54) | 1.07 (0.74–1.55) | 1.54 (0.81–2.94) | 1.13 (0.83–1.54) |
| Advanced maternal aged | 1.88 (1.66–2.11) | 1.97 (1.72–2.26) | 1.60 (1.20–2.12) | 1.88 (1.66–2.11) |
| Obesitye | 2.05 (1.81–2.33) | 2.03 (1.74–2.35) | 1.91 (1.48–2.47) | 2.05 (1.81–2.33) |
| Primiparousf | 18.76 (16.09–21.87) | 20.05 (16.57–24.26) | 21.38 (15.83–28.88) | 18.76 (16.09–21.87) |
| Multiparous with cesarean historyf | 18.42 (15.27–22.22) | 19.59 (15.49–24.76) | 15.70 (10.95–22.53) | 18.42 (15.27–22.22) |
| Neonatal birth injury | ||||
| Adjustedb odds ratio (95% confidence interval) | ||||
| Predictor variable | Total sample n = 61 352 | Non-macrosomia n = 49 384 | Grade 1 macrosomia n = 9726 | Grades 2 and 3 macrosomia n = 2242 |
| Gestational diabetesc | 2.60 (1.26–5.34) | 2.89 (1.16–7.19) | 1.06 (0.14–7.84) | 2.60 (1.26–5.34) |
| Advanced maternal aged | 1.09 (0.72–1.64) | 1.25 (0.75–2.09) | 0.69 (0.29–1.66) | 1.09 (0.72–1.64) |
| Obesitye | 1.64 (1.10–2.47) | 1.30 (0.72–2.36) | 1.38 (0.69–2.75) | 1.64 (1.10–2.47) |
| Primiparousf | 2.26 (1.63–3.12) | 3.12 (2.03–4.78) | 2.14 (1.15–3.96) | 2.26 (1.63–3.12) |
| Multiparous with cesarean historyf | 2.41 (1.37–4.21) | 2.93 (1.35–6.34) | 1.96 (0.75–5.12) | 2.41 (1.37–4.21) |
| Shoulder dystociaa | ||||
| Adjustedb odds ratio (95% confidence interval) | ||||
| Predictor variable | Total sample n = 59 848 | Non-macrosomia n = 48 260 | Grade 1 macrosomia n = 9422 | Grades 2 and 3 macrosomia n = 2175 |
| Gestational diabetesc | 1.99 (1.49–2.65) | 2.11 (1.35–3.28) | 2.03 (1.25–3.29) | 1.97 (1.48–2.63) |
| Advanced maternal aged | 1.10 (0.97–1.26) | 1.13 (0.91–1.39) | 0.97 (0.78–1.21) | 1.09 (0.96–1.24) |
| Obesitye | 1.17 (1.02–1.36) | 0.87 (0.67–1.14) | 0.92 (0.73–1.16) | 1.14 (0.99–1.32) |
| Primiparousf | 0.78 (0.69–0.88) | 1.32 (1.12–1.56) | 0.93 (0.75–1.16) | 0.72 (0.64–0.81) |
| Multiparous with cesarean historyf | 1.49 (1.23–1.80) | 1.90 (1.40–2.57) | 1.32 (0.95–1.82) | 1.36 (1.12–1.64) |
| Neonatal respiratory distress | ||||
| Adjustedb odds ratio (95% confidence interval) | ||||
| Predictor variable | Total sample n = 62 676 | Non-macrosomia n = 50 413 | Grade 1 macrosomia n = 9966 | Grades 2 and 3 macrosomia n = 2297 |
| Gestational diabetesc | 1.73 (1.20–2.49) | 1.50 (0.94–2.38) | 2.42 (1.16–5.07) | 1.73 (1.20–2.49) |
| Advanced maternal aged | 1.02 (0.86–1.21) | 1.02 (0.83–1.24) | 1.18 (0.81–1.73) | 1.02 (0.86–1.21) |
| Obesitye | 1.12 (0.93–1.34) | 1.03 (0.81–1.30) | 0.90 (0.61–1.34) | 1.12 (0.93–1.34) |
| Primiparousf | 2.12 (1.87–2.40) | 2.23 (1.93–2.58) | 2.68 (1.98–3.63) | 2.12 (1.87–2.40) |
| Multiparous with cesarean historyf | 1.48 (1.13–1.93) | 1.62 (1.17–2.23) | 1.37 (0.77–2.46) | 1.48 (1.13–1.93) |
| NICU > 24 h | ||||
| Adjustedb odds ratio (95% confidence interval) | ||||
| Predictor variable | Total sample n = 62 676 | Non-macrosomia n = 50 413 | Grade 1 macrosomia n = 9966 | Grades 2 and 3 macrosomia n = 2297 |
| Gestational diabetesc | 1.41 (0.97–2.04) | 1.32 (0.85–2.05) | 1.79 (0.77–4.15) | 1.41 (0.97–2.04) |
| Advanced maternal aged | 1.18 (1.01–1.38) | 1.23 (1.03–1.47) | 1.31 (0.90–1.92) | 1.18 (1.01–1.38) |
| Obesitye | 1.27 (1.07–1.50) | 1.24 (1.01–1.52) | 1.04 (0.70–1.54) | 1.27 (1.07–1.50) |
| Primiparousf | 2.28 (2.02–2.57) | 2.38 (2.08–2.73) | 2.90 (2.13–3.94) | 2.28 (2.02–2.57) |
| Multiparous with cesarean historyf | 1.47 (1.14–1.90) | 1.61 (1.19–2.17) | 1.23 (0.66–2.32) | 1.47 (1.14–1.90) |
Denominator of vaginal births only.
Adjusted for all predictors, race, maternal education, neonatal sex, and marital status.
Refers to complication of index pregnancy only; reference group: no gestational diabetes.
Maternal age >35 y; reference group: maternal age ≤35 y.
Maternal body mass index (BMI) ≥30 kg/m2; reference group: BMI <30 kg/m2.
Reference group: multiparous without cesarean history.
4 |. DISCUSSION
This is the first study to examine outcomes of fetal macrosomia among midwife-attended, planned, singleton births in the community setting. Among pregnant individuals in this United States sample (68 966 births), 16% had grade 1 macrosomic newborns, 3.3% had grade 2 macrosomic newborns, and 0.4% had grade 3 macrosomia newborns. Comparatively, 2018 US Vital Records data for births at >37 weeks’ gestation yield 7.3% grade 1, 1.0% grade 2, and 0.1% grade 3 macrosomic newborns.16 In contrast, for planned midwife-attended home births, the 2018 US Vital Records data are 15.5%, 3.3%, and 0.4%, respectively,16 which are comparable with results from this study. This discrepancy in macrosomia rates between planned hospital and planned community births can likely largely be attributed to the later gestational ages at birth observed in the community birth sample.
By categorizing fetal macrosomia status as grade 1, 2, or 3, we were able to understand the nuanced risk of several maternal and neonatal outcomes associated with increasing neonatal birthweight. Macrosomia was associated with increased adjusted odds of perineal tear, postpartum hemorrhage, cesarean birth, neonatal birth injury, shoulder dystocia, neonatal respiratory distress, and NICU stay >24 hours, although most absolute rates of these outcomes were low. A dose-response relationship was observed for the majority of outcomes, with increasing birthweight associated with increasing risk. Unexpectedly, cesarean birth did not follow a dose-response relationship, with grade 2 macrosomia at greater odds than grade 3 macrosomia, though the low numbers in the grade 3 macrosomia group led to a wide CI.
In order to evaluate effect modification, the data were subset by macrosomia status and separate models were run to test the effect of selected predictors on each outcome. We hypothesized that a dose-response effect and substantial effect modification would be discernible; however, no consistent relationships were observed. Primiparity and multiparity with cesarean history were associated with most outcomes, compared to multiparity without cesarean history.
Our results are consistent with the recent systematic review and meta-analysis by Beta et al,17 which documents the links between fetal macrosomia and a number of maternal and fetal complications. The authors analyzed eight studies with the outcome of postpartum hemorrhage and calculated a pooled odds ratio of 3.15 (2.14–4.63) in newborns with birthweight >4500 g (grade 2 or 3 macrosomia), compared to non-macrosomic newborns.17 Similarly, the pooled odds ratio from six studies for shoulder dystocia was 15.64 (11.31–21.64) in newborns with birthweight >4500 g (grade 2 or 3 macrosomia), compared to non-macrosomic newborns.17
Two large studies, by Zhang et al1 and Boulet et al,2 linked live birth and infant death records in the United States and found increased odds of several similar outcomes, including cesarean, birth injury, and neonatal ventilation. These studies also found increasing risk of morbidity with increasing birthweight (grade 3 macrosomia at greatest risk, followed by grade 2, then grade 1). Additionally, Nesbitt et al18 found a positive association between increasing birthweight and shoulder dystocia both in the presence and absence of maternal diabetes. Our results are consistent with these studies (primarily using hospital birth populations) and corroborate them in a sample of planned community births in the United States.
Strengths of this study include the use of a dataset that includes exclusively planned physiologic labors. It is important to note that 80% of pregnant individuals in this sample had a non-macrosomic newborn, and 96.3% had a non-macrosomic or grade 1 macrosomic newborn. It is possible that the labor and birth interventions that have become commonplace in hospital birth settings19 either mitigate or exacerbate known adverse outcomes associated with fetal macrosomia. Because all pregnant people in this dataset planned a community birth, we were able to explore outcomes associated with macrosomia independent of hospital practices and hospital practitioners. Additionally, community birth midwives spend more time with women during prenatal visits (3–4 times the length of “normal,” hospital practice visits),20 and there is evidence that this extra prenatal care time is spent discussing individualized strategies for promoting healthy pregnancies.20 In this sample with very low prevalence of gestational diabetes and extra prenatal care emphasis on prevention and management of complications through a focus on holistic health, we still observe adverse outcome associations with macrosomia. This finding illustrates how difficult it may be in some cases to affect fetal growth patterns through disease management and personal health behaviors alone. Other studies of fetal macrosomia have involved data mostly from hospital births. This study corroborates those previous findings in a different, understudied sample in the United States, with a high prevalence of macrosomia.
Misdiagnosis of fetal macrosomia is common. In a study that used data from the Listening to Mothers III Survey, Cheng et al21 found that 31.2% of respondents were told by their provider that their baby was getting “quite large” toward the end of their pregnancy; yet only 9.9% had a baby weighing 4000 g or more (grade 1 macrosomia or higher). Since fetal macrosomia cannot accurately be determined before birth, prenatal supports to help keep the newborn’s weight within normal limits should be considered. For example, prenatal care should include discussions not only about dietary recommendations, individual food preferences, and exercise guidelines, but also concrete strategies and resources for accessing healthy, culturally acceptable foods and physical activity when barriers exist. Shared decision-making, along with other elements of midwifery models of care, can create the opportunity for providers and patient/clients to develop prevention plans that harness strengths-based approaches (eg, uplifting existing social and familial networks), but that also help to ameliorate structural conditions (eg, food deserts) and inequities (eg, systemic racism) that hinder the prevention and management of macrosomia.
While our results offer a novel contribution to this understudied area of pregnancy health, our sample is not necessarily generalizable to the United States population, nor is it necessarily generalizable to all United States pregnant people who plan a community birth. An estimated 20%–30% of active certified professional midwives and a smaller percentage of active certified nurse-midwives who participate in community births contribute data to MANA Stats.13 Standards of practice and integration of midwives in the larger health-care system vary substantially across the United States.22 It is possible that midwives who contribute to this registry either serve a different population or engage in practice patterns that differ from midwives who do not, although the fact that US Vital Records data on planned home births contain rates of macrosomia similar to those found in our sample mitigates this concern somewhat. Additionally, we cannot necessarily draw comparisons between community and hospital births; our results do not allow conclusions about whether macrosomia in a community birth setting is either more or less risky than macrosomia in a hospital setting.
In conclusion, this study further substantiates the known complications of fetal macrosomia. Prevention and management strategies during pregnancy remain the best options to mitigate the negative effects of macrosomia in the absence of accurate estimation of fetal weight before birth. Providers in both hospital and community birth settings should partner with pregnant individuals and their support networks to develop a balanced approach to the prevention and management of fetal macrosomia. Such an approach does not downplay or obscure the risks, yet also does not lose sight of the fact that a majority of those planning a community birth will give birth to normal weight infants. It is in this balanced approach that clinical outcomes and childbearing experiences are most likely to demonstrate positive effect.
Funding information
This work was supported by Oregon State University President’s Commission on the Status of Women and NICHD/NIH 5R03HD096094. MANA Stats data collection was funded by the Foundation for the Advancement of Midwifery.
DATA AVAILABILITY STATEMENT
The data that support the findings of this study are available from the Midwives Alliance Division of Research. Restrictions apply to the availability of these data, which were used under license for this study. Data are available at https://mana.org/research-main with the permission of the Midwives Alliance Division of Research.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data that support the findings of this study are available from the Midwives Alliance Division of Research. Restrictions apply to the availability of these data, which were used under license for this study. Data are available at https://mana.org/research-main with the permission of the Midwives Alliance Division of Research.