Abstract
Objective
To compare the independent risk of neonatal morbidity between the offspring of obese and non-obese women without hypertension or diabetes.
Methods
This is a secondary analysis of a prospective single-center cohort study of singleton deliveries at or beyond 37 weeks of gestation from 2010–2014. Women with diabetes (pre-gestational or gestational) and hypertensive disorders were excluded. The primary outcomes were: 1) a composite neonatal morbidity including death, mechanical ventilation, respiratory distress, meconium aspiration, suspected sepsis, confirmed, sepsis, hypoxic ischemic encephalopathy, therapeutic hypothermia, or seizures and 2) a composite of neonatal neurologic morbidity including hypoxic ischemic encephalopathy, therapeutic hypothermia, or seizures. The primary outcomes were compared between the offspring of obese (BMI ≥ 30 kg/m2) and non-obese women. Adjusted odds ratios were estimated using multivariable logistic regression.
Results
Of 6,458 women without diabetes or hypertensive disorders, 3,311 (51%) were obese. After adjusting for race, neonates of obese patients were at significantly increased risk for the composite neonatal morbidity (9.2% vs 7.2%, (adjusted odds ratio [aOR] 1.39, 95% CI 1.15–1.67) and neurologic neonatal morbidity (0.7% vs 0.3%, aOR 2.84, 95% CI 1.22–6.65). Specifically, neonates of obese patients were more likely to have hypoxic ischemic encephalopathy (0.5% vs 0.2%, aOR 2.80, 95% CI 1.02–7.68), hypothermia treatment (0.6% vs 0.2%, aOR 2.92 95% CI 1.17–7.30]), and suspected sepsis (7.6% vs 5.8%, aOR 1.45, 95% CI 1.18–1.79).
Conclusion
In patients who labor, maternal obesity is an independent risk factor for significant neonatal morbidity, even in the absence of hypertensive disorders or diabetes.
Introduction
Among reproductive age women, 58.5% are defined as overweight or obese, making obesity the most common health care condition for this population1,2. Despite increasing prevalence, obesity’s implications for pregnancy and neonatal outcomes are often underappreciated and unrecognized3,4. Pregnancy in this population of women is considered high risk, mostly due to associated comorbidities such as hypertension and diabetes and their obstetric sequelae5,6.
Obese mothers have poor health outcomes including an increased risk for cardiac dysfunction7 and venous thrombosis, as well as higher rates of cesarean sections, failed trial of labor, endometritis, and wound complications8,9. Furthermore, obesity and the comorbidities of hypertension and diabetes have long been associated with adverse neonatal outcomes including congenital anomalies10,fetal growth restriction, stillbirth11, and death11. However, current literature suggests that between 65–85% of obese mothers do not have diabetes or hypertension at the time of delivery3,12,13.
Few studies have examined the independent risk of maternal obesity on neonatal outcomes in the absence of these comorbidities. Current data suggests that obesity may be as important, if not more important, than hypertension and diabetes as a potentially modifiable risk factor for clinicians to target in order to improve neonatal outcomes14,15. As obesity alone has been found to be a pro-inflammatory, pathophysiologic state16,17, it is possible that this condition may alter the intrauterine environment of the developing fetus leading to adverse neonatal outcomes3,18. We tested the hypothesis that obese women without hypertension or diabetes who labor are at increased risk of delivering neonate who suffer morbidity.
Materials and Methods
This is a secondary analysis of a prospective cohort study of singleton deliveries at 37 weeks or beyond from 2010–2014 from one large academic hospital19. The Washington University School of Medicine Human Research Protection Office approved of this study prior to enrollment (identification number 201102438). Women with diabetes (pre-gestational or gestational), hypertension (chronic, gestational, pre-eclampsia, and eclampsia), scheduled cesarean deliveries, and fetal anomalies were excluded from our cohort.
The primary outcomes were: 1) a composite of neonatal morbidity including death, mechanical ventilation, respiratory distress, meconium aspiration, suspected sepsis, confirmed sepsis, hypoxic ischemic encephalopathy, therapeutic hypothermia, or seizures and 2) a composite of neonatal neurologic morbidity including hypoxic ischemic encephalopathy, therapeutic hypothermia, or seizures. Information regarding maternal demographics, antenatal care, labor outcomes, and neonatal diagnoses were collected from medical records by trained research staff. Hypoxic ischemic encephalopathy was defined using American College of Obstetricians and Gynecologists (ACOG) and American Academy of Pediatrics (AAP) definitions20,21. Therapeutic hypothermia was based on institution specific indications for treatment (i.e. pH <7.1, base deficit >12 mmol/L, Apgar <5 at 10 minutes, acute perinatal event and/or neurologic exam demonstrating moderate to severe encephalopathy). Suspected sepsis was defined by pediatrician documentation of such in the medical records. At our institution, neonates with suspected sepsis are managed by AAP guidelines20.
The primary outcomes were compared between the offspring of patients with and without obesity (BMI ≥ 30 kg/m2) using standard World Health Organization obesity definitions at the time of delivery4. Baseline clinical characteristics between women with obesity and without obesity were compared using the X2 or Fisher exact test for categorical variables and Mann-Whitney U test or Student t test for continuous variables, as appropriate. Odds ratios (OR) and 95% confidence intervals (CI) were calculated for each of the outcomes of interests. Multivariable logistic regression was used to adjust for pertinent confounding variables, which were identified by those variables that had at least a 10% effect size on the OR or were clinically relevant as confounders. Normality of distribution of the continuous variables was evaluated using the Kolmogorov-Smirnov test. Final models were tested with the Hosmer-Lemeshow goodness of fit test. We assessed the trend in neonatal morbidity across increasing classes of obesity using the Cochrane Armitage test. We also performed additional analyses of neonatal outcomes among those with suspected sepsis. All patients from the primary study who met inclusion criteria were included; no a priori sample size estimation was performed. All analyses were performed using SAS software, Version 9.4 for Windows (Cary, North Carolina).
Results
A total of 8,580 patients were enrolled in the primary study19. Of these 1,585 were excluded for hypertension, 246 for diabetes, 135 with both hypertension and diabetes, 98 due to missing BMI data, and 58 who developed pre-eclampsia with severe features in labor and received magnesium, leaving a final cohort of 6,458 women. Of these, 3,147 (49%) were non-obese and 3,311 (51%) were obese. Of the women with obesity, 1,736 were class I, 947 were class II, and 628 were class III (Figure 1).
Figure 1.
Participant study flowchart. BMI, body mass index.
Several clinical characteristics differed between obese and non-obese pregnant women in our cohort. Women with obesity were older, more likely to be African American, deliver at a greater gestational age, have a prior cesarean section and undergo a cesarean delivery for the index pregnancy. Obese mothers were also more likely to be induced, have a prolonged 1st stage of labor, prostaglandin, foley bulb, and oxytocin during labor. Women with obesity also delivered neonates with a higher birthweight and lower mean umbilical artery pH. Rates of chorioamnionitis, maternal fever at delivery, and post-partum fever were higher in women with obesity, but these differences were not statistically significant (Table 1).
Table 1.
Clinical characteristics among pregnant women with obesity (BMI ≥ 30) and without obesity (N= 6,458)*
| Clinical Characteristics | Obese (n= 3311) | Non-Obese (n= 3147) | P† |
|---|---|---|---|
| Maternal Age, years | 25.7 ± 5.6 | 25.2 ± 5.9 | <0.01 |
| Maternal age ≥ 35, years | 257 (7.8) | 240 (7.6) | 0.84 |
| Race | <0.01 | ||
| African American | 2288 (69.1) | 1813 (57.6) | |
| Caucasian | 683 (20.6) | 825 (26.2) | |
| Latina | 246 (7.4) | 238 (7.6) | |
| Gestational age at delivery, weeks | 39.1 ± 1.2 | 38.9 ± 1.1 | <0.01 |
| Body mass index, kg/m2 | 36.2 ± 5.8 | 26.2 ± 2.5 | <0.01 |
| Nulliparous | 1252 (37.8) | 1420 (45.1) | <0.01 |
| Prior cesarean | 344 (10.4) | 231 (7.3) | <0.01 |
| Prostaglandin | 519 (15.7) | 390 (12.4) | <0.01 |
| Foley bulb | 326 (9.9) | 244 (7.8) | <0.01 |
| Oxytocin | 2227 (67.3) | 1870 (59.4) | <0.01 |
| Labor Type | |||
| Induction | 1325 (40.0) | 1069 (34.0) | <0.01 |
| Spontaneous and/or Augmented | 1986 (60.0) | 2078 (66.0) | |
| 1st Stage of Labor >95%tile | 159 (4.8) | 106 (3.4) | <0.01 |
| Mode of delivery | <0.01 | ||
| Vaginal | 2546 (76.9) | 2605 (82.8) | |
| Operative vaginal | 154 (4.7) | 172 (5.4) | |
| Cesarean | 611 (18.5) | 370 (11.8) | |
| Maternal fever | |||
| At delivery | 168 (5.1) | 129 (4.1) | 0.06 |
| Post-partum | 131 (3.9) | 97 (3.1) | 0.06 |
| Infant gender | 0.63 | ||
| Female | 1591 (48.1) | 1550 (49.2) | |
| Male | 1719 (51.9) | 1596 (50.8) | |
| Arterial pH | 7.2 ± 0.07 | 7.3 ± 0.06 | <0.01 |
| Acidemia pH ≤ 7.10 | 55 (1.7%) | 51 (1.6%) | 0.90 |
| Elevated lactate ≥ 4 | 819 (24.7) | 811 (25.8) | 0.32 |
| Birthweight, grams | 3331 ± 454 | 3173 ± 442 | <0.01 |
| Birthweight > 4000, grams | 242 (7.2) | 102 (3.2) | <0.01 |
| Chorioamnionitis | 162 (4.9) | 122 (3.9) | 0.16 |
Data are presented as number (percent) or mean ± standard deviation
Excludes women with diabetes (pre-gestational and gestational), hypertension (chronic, gestational, pre-eclampsia and eclampsia), and intra-partum magnesium
P values based on Student t test and X2
Of the neonates, 532 (8%) had the composite neonatal morbidity and 31 (0.5%) had the composite neurologic morbidity. After adjusting for race, neonates of women with obesity had increased odds of overall morbidity (9.2% vs 7.2% adjusted odds ratio [aOR] 1.39, 95% CI 1.15–1.67) and neurologic morbidity (0.7% vs 0.3%, aOR 2.84, 95% CI 1.22–6.65). Among the individual components of the composites, neonatal morbidity was largely driven by higher rates of suspected sepsis (7.6% vs 5.8%, aOR 1.45, 95%CI 1.18–1.79). Neonatal neurologic morbidity was driven by higher rates of hypoxic ischemic encephalopathy (0.5% vs 0.2%, aOR 2.80, 95% CI 1.02–7.68) and hypothermia treatment (0.6% vs 0.2%, aOR 2.92 95% CI 1.17–7.30). (Table 2). A supplementary analysis of neonates born to women with diabetes or hypertension comorbidities who were obese compared to non-obese demonstrated no differences in neonatal morbidity (Table 3).
Table 2.
Associations of neonatal outcomes among pregnant women with obesity (BMI ≥ 30) and without obesity (N= 6,458)*
| Neonatal Outcomes | Total | Obese (n= 3311) | Non-Obese (n= 3147) | cOR† (95% CI) | aOR‡ (95% CI) |
|---|---|---|---|---|---|
| Composite neonatal morbidity§ | 532 (8.2) | 305 (9.2) | 227 (7.2) | 1.31 (1.09–1.56) | 1.39 (1.15–1.67) |
| Neonatal death | 3 (0.05) | 2 (0.1) | 1 (0.03) | 1.90 (0.17–20.98) | 1.84 (0.16–20.48) |
| Respiratory distress | 228 (3.5) | 118 (3.6) | 100 (3.2) | 1.13 (0.86–1.48) | 1.12 (0.85–1.49) |
| Mechanical ventilation | 30 (0.5) | 15 (0.5) | 15 (0.4) | 0.95 (0.46–1.95) | 0.87 (0.41–1.83) |
| Meconium aspiration syndrome | 16 (0.2) | 11 (0.3) | 5 (0.2) | 2.09 (0.73–6.04) | 1.73 (0.59–5.10) |
| Suspected sepsis | 437 (6.8) | 253 (7.6) | 184 (5.8) | 1.33 (1.19–1.62) | 1.45 (1.18–1.79) |
| Confirmed sepsis | 7 (0.1) | 3 (0.1) | 4 (0.1) | 0.71 (0.16–3.19) | 0.61 (0.14–2.73) |
| Hypoxic-ischemic encephalopathy | 21 (0.3) | 16 (0.5) | 5 (0.2) | 3.05 (1.17–8.34) | 2.80 (1.02–7.68) |
| Therapeutic hypothermia | 27 (0.4) | 20 (0.6) | 7 (0.2) | 2.73 (1.15–6.46) | 2.92 (1.17–7.30) |
| Seizures | 14 (0.2) | 10 (0.3) | 4 (0.2) | 2.38 (0.75–7.60) | 2.65 (0.73–9.64) |
| Composite neurologic morbidity|| | 31 (0.5) | 23 (0.7) | 8 (0.3) | 2.74 (1.23–6.15) | 2.84 (1.22–6.65) |
| Hypoxic-ischemic encephalopathy | 21 (0.3) | 16 (0.5) | 5 (0.2) | 3.05 (1.17–8.34) | 2.80 (1.02–7.68) |
| Therapeutic hypothermia | 27 (0.4) | 20 (0.6) | 7 (0.2) | 2.73 (1.15–6.46) | 2.92 (1.17–7.30) |
| Seizures | 14 (0.2) | 10 (0.3) | 4 (0.2) | 2.38 (0.75–7.60) | 2.65 (0.73–9.64) |
Data are presented as number (percent)
Excludes women with diabetes (pre-gestational and gestational), hypertension (chronic, gestational, pre-eclampsia and eclampsa), and intra-partum magnesium
Crude odds ratios
Adjusted for race
Includes death, mechanical ventilation, respiratory distress, meconium aspiration syndrome, seizures, suspected sepsis, confirmed sepsis, hypoxic-ischemic encephalopathy, therapeutic hypothermia, and seizures
Includes hypoxic-ischemic encephalopathy, therapeutic hypothermia, seizures
Table 3.
Associations of neonatal outcomes among pregnant women with diabetes or hypertension with obesity (BMI ≥ 30) and without obesity (N=2,024)*
| Obese (n= 1416) | Non-Obese (n= 608) | cOR (95% CI) | aOR† (95% CI) | |
|---|---|---|---|---|
| Composite neonatal morbidity‡ | 162 (11.4) | 57 (9.4) | 1.25 (0.91–1.72) | 1.04 (0.75–1.44) |
| Neonatal death | 1 (0.1) | 0 (0.0) | -- | -- |
| Respiratory distress | 83 (5.9) | 27 (4.4) | 1.34 (0.86–2.09) | 1.10 (0.69–1.73) |
| Mechanical ventilation | 16 (1.1) | 3 (0.5) | 2.30 (0.67–7.94) | 2.12 (0.61–7.40) |
| Meconium aspiration syndrome | 6 (0.4) | 0 (0.0) | -- | -- |
| Suspected sepsis | 132 (9.3) | 46 (7.6) | 1.26 (0.89–1.78) | 1.05 (0.73–1.50) |
| Hypoxic-ischemic encephalopathy | 13 (0.9) | 1 (0.2) | 5.62 (0.73–43.09) | 4.00 (0.51–31.08) |
| Therapeutic hypothermia | 13 (0.9) | 2 (0.3) | 2.81 (0.63–12.48) | 2.26 (0.50–10.19) |
| Seizures | 4 (0.3) | 0 (0.0) | -- | -- |
| Composite neurologic morbidity§ | 17 (1.2) | 2 (0.3) | 3.68 (0.85–15.99) | 2.78 (0.63–12.25) |
| Hypoxic-ischemic encephalopathy | 13 (0.9) | 1 (0.2) | 5.62 (0.73–43.09) | 4.00 (0.51–31.08) |
| Therapeutic hypothermia | 13 (0.9) | 2 (0.3) | 2.81 (0.63–12.48) | 2.26 (0.50–10.19) |
| Seizures | 4 (0.3) | 0 (0.0) | -- | -- |
Data are n (%)
Includes women with diabetes (pre-gestational and gestational), hypertension (chronic, gestational, pre-eclampsia and eclampsia), and intra-partum magnesium
Includes death, mechanical ventilation, respiratory distress, meconium aspiration syndrome, seizures, suspected sepsis, hypoxic-ischemic encephalopathy, therapeutic hypothermia, and seizures
Includes hypoxic-ischemic encephalopathy, therapeutic hypothermia, seizures
Adjusted for mode of delivery
When stratified by degree of obesity, there was an increasing trend of the composite neonatal morbidity (7.2% for non-obese, 8.6% for class I obesity, and 10.4% for class II obesity, and 9.2% for class III obesity, p-trend=0.01) and the composite neurologic morbidity (0.3% for non-obese, 0.8% for class I obesity, 0.5% for class II obesity, and 0.8% for class III obesity, p-trend=0.04) with increasing class of obesity.
In the analysis of laboratory and clinical data among neonates with suspected sepsis, neonates born to obese mothers had lower absolute neutrophil counts at <6 hours and >12 hours. Neonates born to obese mothers had similar durations of antibiotic treatment (59.7 [interquartile range 59.3, 149.8] hours vs 59.7 [57.8, 72.1] hours, p=0.16). Obese mothers who delivered neonates with suspected sepsis were more likely to screen positive for group beta streptococcus on vaginal cultures. Maternal risk factors for sepsis as well as other clinical neonatal data did not differ between groups. The rate of bacterial proven sepsis in neonates with suspected sepsis was not significantly different with 3 (1.2%) neonates born to women with obesity and 4 (2.1%) neonates of non-obese women (Table 4).
Table 4.
Maternal and neonatal characteristics used by the American Academy of Pediatrics’ guidelines for suspected or bacterial proven neonatal sepsis among pregnant women with obesity (BMI ≥ 30) and without obesity (N=444)*
| Laboratory and Clinical Data | Obese(n= 256) | Non-Obese(n= 188) | P† |
|---|---|---|---|
| Maternal and neonatal risk factors for suspected and/or bacterial proven sepsis | |||
|
| |||
| Gestational Age | 39.2 ± 1.2 | 39.0 ± 1.2 | 0.11 |
| Induction | 105 (41.2) | 75 (39.9) | 0.82 |
| Rupture of Membranes > 18 hours | 179 (69.9) | 123 (65.4) | 0.36 |
| Maternal WBC | |||
| Leukopenia <3.8 k/cumm | 0 (0.0) | 0 (0.0) | -- |
| Leukocytosis >30 k/cumm | 1 (0.4) | 2 (1.1) | 0.58 |
| Chorioamnionitis | 129 (50.4) | 94 (47.8) | 0.57 |
| Maximum Temperature (Celsius) | 38.1 ± 0.75 | 38.2 ± 0.80 | 0.40 |
| Antibiotics Given during labor | 194 (75.8) | 133 (70.7) | 0.23 |
| Length of Antibiotics, hours | 0.0 (0.0, 16.2) | 0.0 (0.0, 15.5) | 0.41 |
| Maternal Vaginal Group B Streptococci Culture | 75 (29.3) | 35 (18.6) | 0.03 |
| White blood cell count | |||
| < 6 hours | 15.5 ± 5.9 | 16.8 ± 6.1 | 0.03 |
| 6 to 12 hours | 16.6 ± 7.7 | 21.6 ± 10.8 | 0.09 |
| >12 hours | 15.3 ± 5.5 | 17.02 ± 5.4 | 0.02 |
| Absolute neutrophil count | |||
| < 6 hours | 8379 (5616, 11160) | 9834 (6527, 13680) | <0.01 |
| 6 to 12 hours | 11552 (5704, 16236) | 14096 (7540, 21594) | 0.44 |
| >12 hours | 8178 (5618, 12052) | 10335 (7692, 13452) | 0.01 |
| Immature to mature neutrophil ratio | |||
| < 6 hours | 0.07 (0.04, 0.10) | 0.05 (0.03, 0.10) | 0.07 |
| 6 to 12 hours | 0.08 (0.03, 0.17) | 0.08 (0.01, 0.18) | 0.72 |
| >12hours | 0.08 (0.04, 0.13) | 0.04 (0.02, 0.09) | 0.02 |
| Neonatal C-reactive protein | |||
| < 6 hours | 4.0 (3.0, 14.0) | 4.0 (3.0, 27.5) | 0.94 |
| 6 to 12 hours | 16.5 (9.5, 29.5) | 10.0 (3.0, 14.7) | 0.29 |
| >12hours | 22.4 (8.0, 33.0) | 21.0 (11.5, 33.2) | 0.95 |
| Maximum Temperature (Celsius) | 36.9 ± 8.5 | 36.0 ± 14.0 | 0.40 |
| Minimum Temperature (Celsius) | 21.1 ± 4.5 | 20.8 ± 4.5 | 0.54 |
| Bacterial Culture Positive | 3 (1.2) | 4 (2.1) | 0.47 |
| Antibiotics Given | 241 (94.1) | 177 (94.2) | 0.99 |
| Length Antibiotic, hours | 59.7 (59.3, 149.8) | 59.7 (57.8, 72.1) | 0.16 |
| Lumbar Puncture | 43 (16.8) | 28 (14.9) | 0.61 |
| Cerebral Spinal Fluid Culture | 2 (0.8) | 0 (0.0) | 0.52 |
| Length of Neonatal Intensive Care or Specialty-Care Unit Stay, days | 3.0 (2.0, 7.0) | 3 (2.0, 6.0) | 0.20 |
Data are presented as number (percent), mean ± standard deviation, or median (interquartile range)
Excludes women with diabetes (pre-gestational and gestational), hypertension (chronic, gestational, pre-eclampsia and eclampsia), and intra-partum magnesium
Chi-square, Fisher’s exact test, Student’s t-test or Mann Whitney
Discussion
The results of this cohort study suggest that the offspring of women with obesity have a small but statistically significantly increased risk of neonatal and neurologic neonatal morbidity compared to the offspring of women without obesity. There is an obesity class-dependent trend towards increased neonatal morbidity. Specifically, neonates of women with obesity were more likely to have hypoxic ischemic encephalopathy, hypothermia treatment, and suspected sepsis. Among neonates with suspected sepsis, there were objective data that differed between women with and without obesity. However, bacterial culture proven sepsis was not different between groups.
The association between maternal obesity and neonatal morbidity is biologically plausible. Obesity is a pro-inflammatory, pathophysiologic disease state which alters the environment for the developing fetus16,17,22. Maternal fat deposition results in inflammation leading to oxidative stress and endothelial dysfunction in maternal and placental tissues3,18. Schmatz et. al propose that unique clinical manifestations are seen in neonates as the result of the pro-inflammatory state of obesity22. This has been validated at the molecular and tissue level using animal models17,22. Teo et. al found that maternal obesity exacerbated the severity of damage caused by hypoxic-ischemic brain injury with evidence of enhanced pro-inflammatory mediators (e.g. TNF-alpha) and tissue-specific damage in the brain17. Furthermore, this pro-inflammatory state may be further exacerbated by the additive effects of maternal obesity on labor such as prolonged first stage of labor4,9,23. Our findings suggest that neonates born to women with obesity may have clinical manifestations of this pro-inflammatory state.
Neonatal neurologic morbidity was an important but infrequent outcome in our study. The association between maternal obesity and neonatal neurologic morbidity has been previously demonstrated24–26. A recently published nationwide cohort study of 3,029 children in Sweden demonstrated that maternal obesity was associated with an increased rate of cerebral palsy in term neonates25. Additionally, our results are further in agreement with the growing body of literature which suggest that maternal obesity is as important for neonatal outcomes as obesity-related comorbidities14,15,27. In a retrospective study of 24,505 singleton pregnancies in Denmark, Kristensen et. al showed that increased pre-pregnancy weight doubled the risk of stillbirth and neonatal death after excluding hypertensive disorders or diabetes14. Furthermore, in a retrospective study of 109,488 singleton deliveries, Rastogi et. al used ICD-9 data to demonstrate increased neonatal morbidity including sepsis (aOR 1.91 95% CI 1.45, 2.50) in neonates born to women with obesity, both with and without disease comorbidities27. Our study is unique in that it includes a sample of women with obesity without comorbidities in a country with a wide prevalence of obesity and uses validated data abstracted from medical records.
The strengths of our study include the large sample size which allowed us to detect rare neonatal outcomes, prospective design, and unique cohort with the ability to use BMI in a class-dependent manner.
Our study has potential limitations to consider. Neonatal morbidity was largely driven by suspected sepsis. Although this was not culture proven sepsis, suspected sepsis is a clinically relevant outcome. The AAP guidelines for the management of suspected or early bacterial proven sepsis includes objective laboratory and clinical data pediatricians use to triage and risk stratify the neonate20. Our analysis demonstrated differences in these variables between women with and without obesity. Our study suggests that maternal obesity alone may be an important factor for clinicians to consider when interpreting AAP data. Additionally, the rate of culture-proven sepsis was not different between groups but was consistent with the rate of 0.77 to 1 per 1,000 reported in the literature28–30. Moreover, even after adjusting for race and the higher rate of maternal group B streptococci (GBS) culture in women with obesity, suspected sepsis remained statistically significant aOR 1.46 (1.17–1.82). Abnormal labor processes which may clinically impact neonatal morbidity including higher rate of induction, prolonged first stage of labor, and difference in mode of delivery in women with obesity were not significant covariates in our analysis.
The use of a composite morbidity may be considered a limitation. However, this was necessary for adequate statistical power to perform detailed analyses in what are otherwise infrequent individual outcomes.
In conclusion, obesity is an independent risk factor for neonatal morbidity, in the absence of maternal hypertension or diabetes. The results of this study highlight specific neonatal outcomes with long term sequelae that physicians should consider when counseling women with obesity. Future studies are needed to corroborate and identify strategies to reduce neonatal morbidity with the increasing number of women with obesity.
Acknowledgments
Supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD061619-01, PI Cahill). Dr Cahill was a Robert Wood Johnson Foundation Faculty Physician Scholar, which partially supported this work. The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official view of the NIH or Robert Wood Johnson Foundation.
The authors thank Tracy Burger for her help with the collection of data.
Footnotes
Presented at the Society for Maternal-Fetal Medicine Annual Meeting, January 29–February 3, 2018, Dallas, Texas.
Financial Disclosure:
The authors did not report any potential conflicts of interest.
Each author has indicated that he or she has met the journal’s requirements for authorship.
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