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ORIGINAL RESEARCH |
From the Division of Obstetrics and Gynecology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
Address reprint requests to: Dr. Marie Cedergren, Department of Obstetrics and Gynecology, University Hospital, SE-581 85 Linköping, Sweden; e-mail: marie.cedergren{at}lio.se.
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ABSTRACT |
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METHODS: In a prospective population-based cohort study, 3,480 women with morbid obesity, defined as a body mass index (BMI) more than 40, and 12,698 women with a BMI between 35.1 and 40 were compared with normal-weight women (BMI 19.8–26). The perinatal outcome of singletons born to women without insulin-dependent diabetes mellitus was evaluated after suitable adjustments.
RESULTS: In the group of morbidly obese mothers (BMI greater than 40) as compared with the normal-weight mothers, there was an increased risk of the following outcomes (adjusted odds ratio; 95% confidence interval): preeclampsia (4.82; 4.04, 5.74), antepartum stillbirth (2.79; 1.94, 4.02), cesarean delivery (2.69; 2.49, 2.90), instrumental delivery (1.34; 1.16, 1.56), shoulder dystocia (3.14; 1.86, 5.31), meconium aspiration (2.85; 1.60, 5.07), fetal distress (2.52; 2.12, 2.99), early neonatal death (3.41; 2.07, 5.63), and large-for-gestational age (3.82; 3.50, 4.16). The associations were similar for women with BMIs between 35.1 and 40 but to a lesser degree.
CONCLUSION: Maternal morbid obesity in early pregnancy is strongly associated with a number of pregnancy complications and perinatal conditions.
LEVEL OF EVIDENCE: II-2
It is already commonly known that maternal overweight and obesity are associated with adverse pregnancy outcome, such as maternal hypertension, preeclampsia, gestational diabetes, more frequent cesarean delivery, delivery of large-for-gestational-age (LGA) infants, and stillbirths.3–8 There are obvious signs in a few studies that pregnancies in morbidly obese women show even more complications and adverse outcomes,9–11 although low patient numbers limit their statistical power.
The objective of this study was to thoroughly assess, in a large prospective data set from the Swedish medical health register, whether morbid obesity, defined by a body mass index (BMI) 35.1–40 or BMI greater than 40, was associated with an increased risk of adverse perinatal outcome and if so to quantify this risk after adjustment for conceivable confounders.
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MATERIALS AND METHODS |
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ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Body mass index (kg/m2) was calculated from maternal weight and height data. Obese women were defined by a BMI greater than 29. Within this group, two subgroups of morbidly obese women were studied: BMI 35.1–40 and BMI greater than 40. The definition of morbid obesity may vary; therefore, we decided to evaluate the 2 groups separately. Obese women were compared with normal-weight women (BMI 19.8–26).
The unit of analysis was delivery. The possible impact of the fact that a woman may have more than one delivery during the study period was checked by only including the first delivery of each woman during the study period.
Primary outcomes were, antenatally, the occurrence of preeclampsia, abruptio placenta, placenta previa, and stillbirths after 28 weeks of gestation among singleton pregnancies. Around-term variables evaluated were the rate of cesarean delivery, labor inductions, pre- and postterm delivery, instrumental delivery, anal sphincter injury, shoulder dystocia, postpartum hemorrhage, and epidural anesthesia. Small-for-gestational age infants were defined as those with birth weights more than 2 standard deviations below the mean birth weight for gestational age according to a Swedish reference curve,14 and LGA infants were those with birth weight above 2 standard deviations. Estimated gestational age was in most cases based on second-trimester ultrasound screening.
Neonatal outcomes studied were as follows: meconium aspiration, fetal distress, low Apgar score (less than 7 at 5 minutes), and early neonatal death (less than 7 days after birth). The outcome variables are registered in the Swedish Medical Birth Registry by using the International Classification of Diseases. Women with insulin-dependent diabetes mellitus were excluded.
Maternal age, parity, smoking, and year of birth were thought to be potential confounding factors and were included as covariates in the adjusted analyses. Maternal education, as a marker of socioeconomic status, was also added (information only available for the years 1992–1995). Preexisting hypertension and gestational diabetes were not included as confounders in this analysis for 2 reasons. First, a true confounder affects both the exposure and the outcome. Exposure in this study was prepregnancy massive obesity. Second, our purpose was to address the outcome, not necessarily the path.
Adjusted odds ratios (ORs) were determined by using Mantel-Haenszel technique.15 The morbidly obese groups, BMI 35–40 and BMI greater than 40, were each compared with normal-weight women (BMI 19.8–26). Estimates of 95% confidence intervals (95% CI) were made with a test-based method, based on the Mantel-Haenszel 
2 (
Miettinen OS. Simple interval estimation of risk ratio [letter]. Am J Epidemiol 1974;100:515–6).
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RESULTS |
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ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The morbidly obese women were compared with normal-weight women with respect to maternal age, parity, maternal smoking in early pregnancy, and the number of multiple pregnancies (Table 1
). The women who were obese were slightly older, more often multiparous, and smokers. Multiple pregnancies occurred equally often across BMI strata.
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. The risk of preeclampsia among the morbidly obese women was increased almost 5-fold. The corresponding OR for women with BMIs between 35.1 and 40 was 3.90. Being morbidly obese carried an almost 3-fold increase in risk of antepartum stillbirths relative to normal-weight women, adjusted OR 2.79 (95% CI 1.94, 4.02). Abruptio placenta occurred equally often among normal-weight women and morbidly obese women. There was a decreased risk of placenta previa in the morbidly obese group, even more pronounced among the heaviest mothers.
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). The frequency was almost 3 times as high for morbidly obese women as it was for women of normal BMI. The risk of instrumental delivery was increased 18% in women with a BMI between 35.1 and 40 and increased 34% in women with a BMI greater than 40. When the analyses were restricted to only the first delivery of each woman during the study period, no significant change in OR was obtained. Shoulder dystocia occurred 3 times more often among the morbidly obese women.
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The prevalence of LGA infants was almost 4 times as high among morbidly obese women than among women with normal BMI (Table 4). The risk was also increased for having a small-for-gestational-age infant among the morbidly obese (greater than 40), although after removing women with preeclampsia, this increased risk was no longer statistically significant: adjusted OR 1.23 (95% CI 0.94, 1.60).
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. There was a more than 2-fold risk increase for fetal distress and low Apgar scores among infants of the morbidly obese women. Meconium aspiration occurred more often in infants of morbidly obese women than in women with normal BMI values: adjusted OR 2.85 (95% CI 1.60, 5.07). This variable was studied only when a vaginal delivery had been performed. The risk seems to be the same among women with a BMI between 35.1 and 40. For the years 1992–1995, information on maternal education was available. Adjustment for this factor reduced the estimated ORs only marginally.
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DISCUSSION |
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ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Perlow et al10 determined in the late 1980s the impact of massive obesity (weight more than 300 pounds = more than 136 kg) on perinatal outcome. The study included 111 women who fulfilled this definition. They found an increased risk for overall cesarean delivery (OR 2.9), Apgar score at 5 minutes less than 7 (OR 3.0), birth weight more than 4,500 g (OR 8.1), and intrauterine growth restriction (OR 9.3). More recently, in a study from the United Arab Emirates concerning 188 morbidly obese women, BMIs greater than 40 were presented.9 An increased risk for cesarean delivery (OR 2.3) and birth weight above 4,000 g (OR 3.9) was described.
When it comes to relatively rare complications, such as shoulder dystocia and stillbirth, sufficient patient numbers concerning the morbidly obese women have not previously been available. In a recent report from Sweden, the risk of stillbirth was doubled among obese women (BMI greater than 30).7 Our findings indicate an almost 3-fold increased risk of antepartum stillbirth in the group of morbidly obese women. Whatever mechanism is behind the association between maternal obesity and stillbirth, it seems to be influenced by the degree of obesity.
Massive obesity seems to be protective from placenta previa. The information on this condition comes to the register from the delivery units and therefore it is unlikely that the decreased risk is due to undetected cases by ultrasound among the massively obese.
In a large study from London, no increased risk of instrumental delivery was seen among women with a BMI greater than 30.3 That is in contrast with our findings because we found a slightly increased risk specifically for the massively obese women. Anal sphincter lacerations were surprisingly not over-represented in the group of morbidly obese women despite the increased prevalence of LGA infants, instrumental deliveries, and the use of epidural anesthesia. All of these are factors well documented to be associated with an increased risk of perineal lacerations.16,17 A possible explanation is that midline episiotomy is not practiced at all in Sweden. There were increased numbers of labor inductions. From a clinical point of view, this is relevant and warrants further evaluation, such as the reasons for induction of labor, which is beyond the scope of this study.
The advantage of register studies is that the large number of individuals available for evaluation gives higher statistical power and makes it possible to demonstrate associations with low-prevalence pregnancy outcome variables. The drawback is the sometimes-low validity of information.
Exposure information (weight and height) was recorded in early pregnancy and therefore prospective regarding the pregnancy outcome variables. Recall bias was thus avoided. Exposure information could be retrieved for 82.8% of all births registered during the study period. We evaluated the group of women with missing data on weight and height and no ORs concerning the outcome variables studied were increased compared with women with known BMI. The possibility of selection bias of extremely obese women in the group of women with missing data is thus less probable.
A number of potential confounding factors associated with maternal obesity were adjusted for in this study, such as maternal age, parity, and smoking in early pregnancy. A putative confounding factor, not stratified for in this study, is socioeconomic level that could have affected the results, but smoking during pregnancy is strongly correlated with socioeconomic level in Sweden.18 For part of the material, maternal education was added as a confounder. This reduced the estimated ORs marginally.
We did not exclude women with gestational diabetes diagnosed in late pregnancy. It is possible that our sample includes women with undetected or unreported non–insulin-dependent diabetes, which could explain the results, but these conditions can be regarded as intermediaries. The same is true for the inclusion of women with chronic hypertension. The purpose of this study was to evaluate the pregnancy outcome in the group of morbidly obese women and not to identify the mechanisms behind the associations. Earlier studies also found that stratifying for a number of potential factors that could influence the outcome did not substantially change the risk estimates.3
It is possible that a multiple-testing problem exists. Most effects found are strong and highly statistically significant, but some are moderate and show marginal statistical significance and may be the result of multiple testing, for example, the increased risk for postpartum bleeding.
Another problem concerning studies in this field is the definition of obesity and even more difficult the definition of morbid obesity. Different values for defining obesity were used in different studies, which make it difficult to compare risk estimates. To facilitate such comparisons, we present risk estimates for both women with BMIs between 35.1 and 40 and women with BMIs greater than 40. There seems to be overall slightly higher risk estimates in the group with BMIs greater than 40 as compared with the group with BMIs between 35.1 and 40, although ratios are not statistically significantly different.
This large study points out a strong association between maternal morbid obesity in early pregnancy and a number of threatening complications during pregnancy, delivery, and in the neonatal period. The importance of these findings could be examined from different views. It implicates the need of prepregnancy advice and counseling to young women and could be a convincing argument for weight reduction in this group. Pregnancies among morbidly obese women must be classified as high-risk pregnancies, and appropriate antenatal care should be provided. In addition, massive obesity among women of child-bearing age is associated with a number of health risks later in life.
Pregnancy is a life event in which women are inclined to behavioral changes. Is it possible that with appropriate management before and during pregnancy, the gestational weight gain could be reduced and maybe even contribute to persistent behavioral changes concerning nutrition and physical exercise postpartum?
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Footnotes |
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doi: 10.1097/01.AOG.0000107291.46159.00
Received August 25, 2003. Received in revised form October 9, 2003. Accepted October 17, 2003.
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REFERENCES |
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2. Lissner L, Johansson SE, Qvist J, Rossner S, Wolk A. Social mapping of the obesity epidemic in Sweden. Int J Obes Relat Metab Disord 2000;24:801–5.[Medline]
3. Sebire NJ, Jolly M, Harris JP, Wadsworth J, Joffe M, Beard RW, et al. Maternal obesity and pregnancy outcome: a study of 287,213 pregnancies in London. Int J Obes Relat Metab Disord 2001;25:1175–82.[Medline]
4. Cnattingius S, Bergstrom R, Lipworth L, Kramer MS. Prepregnancy weight and the risk of adverse pregnancy outcomes. N Engl J Med 1998;338:147–52.
5. Baeten JM, Bukusi EA, Lambe M. Pregnancy complications and outcomes among overweight and obese nulliparous women. Am J Public Health 2001;91:436–40.
6. Young TK, Woodmansee B. Factors that are associated with cesarean delivery in a large private practice: the importance of prepregnancy body mass index and weight gain. Am J Obstet Gynecol 2002;187:312–8.[Medline]
7. Stephansson O, Dickman PW, Johansson A, Cnattingius S. Maternal weight, pregnancy weight gain, and the risk of antepartum stillbirth. Am J Obstet Gynecol 2001;184: 436–9.
8. Jensen DM, Damm P, Sorensen B, Molsted-Pedersen L, Westergaard JG, Ovesen P, et al. Pregnancy outcome and prepregnancy body mass index in 2459 glucose-tolerant Danish women. Am J Obstet Gynecol 2003;189:239–44.[Medline]
9. Kumari AS. Pregnancy outcome in women with morbid obesity. Int J Gynaecol Obstet 2001;73:101–7.[Medline]
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11. Bianco AT, Smilen SW, Davis Y, Lopez S, Lapinski R, Lockwood CJ. Pregnancy outcome and weight gain recommendations for the morbidly obese woman. Obstet Gynecol 1998;91:97–102.[Abstract]
12. Cnattingius S, Ericson A, Gunnarskog J, Källén B. A quality study of a medical birth registry. Scand J Soc Med. 1990;18:143–8.[Medline]
13. The National Board of Health and Welfare. The Swedish medical birth register: a summary of content and quality. Available at: http://www.sos.se/FULLTEXT/112/2003-112-3/2003-112-3.pdf. Retrieved November 12, 2003.
14. Källén B. A birth weight for gestational age standard based on data in the Swedish Medical Birth Registry, 1985–1989. Eur J Epidemiol 1995;11:601–6.[Medline]
15. Mantel N, Haenszel W. Statistical aspects of the analyses of data from retrospective studies of disease. J Natl Cancer Inst 1959;22:719–48.
16. Handa VL, Danielsen BH, Gilbert W. Obstetric anal sphincter lacerations. Obstet Gynecol 2001;98:225–30.
17. Donnelly V, Fynes M, Campbell D, Johnsson H, O’Connell PR, O’Herlihy C. Obstetric events leading to anal sphincter damage. Obstet Gynecol 1998;92:955–61.[Abstract]
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