Acta Obstetricia et Gynecologica. 2010; 89: 924–930

MAIN RESEARCH ARTICLE

Maternal super-obesity (body mass index ‡ 50) and adverse pregnancyoutcomes

MARK CHRISTOPHER ALANIS1, WILLIAM H. GOODNIGHT2, ELIZABETH G. HILL3,CHRISTOPHER J. ROBINSON1, MARGARET S. VILLERS1 & DONNA D. JOHNSON1

1Department of Obstetrics and Gynecology, Medical University of South Carolina, Charleston USA, 2Department ofObstetrics and Gynecology, University of North Carolina, Chapel Hill, USA, and 3Department Biostatistics,Bioinformatics, and Epidemiology, Medical University of South Carolina, Charleston, USA

AbstractObjective. To determine if pregnancy complications are increased in super-obese (a body mass index (BMI) of 50 or more)compared to other, less obese parturients. Design. Cross-sectional study. Setting and population. All 19,700 eligible women,including 425 (2.2%) super-obese women with singleton births between 1996 and 2007 delivering at a tertiary referral center,identified using a perinatal research database. Methods. Bivariate and trend analyses were used to assess the relation betweensuper-obesity and various pregnancy complications compared to other well-established BMI categories. Adjusted odds ratios(ORs) were calculated using multivariable logistic regression techniques. Main outcome measures. Outcomes for adjusted andunadjusted analyses were small-for-gestational age (SGA) birth, large-for-gestational age (LGA) birth, preeclampsia,gestational diabetes mellitus (GDM), fetal death, preterm birth, placental abruption, cesarean delivery, and Apgarscores < 7. Results. Compared to all other obese and non-obese women, super-obese women had the highest rates ofpreeclampsia, GDM, LGA, and cesarean delivery (all p < 0.05 for trend test). Super-obesity was also associated with a44% reduction in SGA compared to all other women (OR 0.55, 95% confidence interval (CI) 0.40–0.76) and a 25% reductioncompared to other, less obese women (OR 0.75, 95% CI 0.54–1.03). Super-obesity was positively associated with LGA,GDM, preeclampsia, cesarean delivery, and a 5-minute Apgar score < 7 compared to all other women after controllingfor important confounders. Conclusion. Super-obesity is associated with higher rates of pregnancy complications comparedto women of all other BMI classes, including other obese women.

Key words: Obesity, super-obesity, pregnancy complications, cesarean, small-for-gestational age

Introduction

Obstetricians are increasingly concerned regarding theprevalence and morbidity associated with obesity inreproductive aged women (1). According to resultsfrom the 2004 National Health and Nutrition Exami-nation Survey (NHANES), the rate of obese reproduc-tive-aged women, defined by a body mass index (BMI)of ‡30, was 28.9% (2). Obesity during pregnancy isassociatedwith increasedmorbidity for both themotherand baby (3). In addition, obese women have a 3-foldrisk of death or near-death morbidity during pregnancy

compared to womenwith a normal BMI (4). In womenwith spontaneous conceptions, recurrent first or sec-ond trimester miscarriage is increased 3.5-fold com-pared towomenwith a normalBMI (5).The risk of fetaldeath after 20 weeks of gestation increases in adose-dependent fashion with BMI, with the highestrisk being in women with extreme obesity (‡ 40) (6).While obesity is a well-known risk factor for fetal

overgrowth (7), a dual risk for intrauterine growthrestriction (IUGR) remains controversial. In a studyof the Danish National Birth Cohort including 54,505patients, the birthweights of fetal deaths were lower

Correspondence: Mark Christopher Alanis, Department of Obstetrics andGynecology,Medical University of South Carolina, 96 Jonathan Lucas Street, CSB 634,Charleston, South Carolina 29425, USA. E-mail: alanis@musc.edu

(Received 13 May 2009; accepted 25 January 2010)

ISSN 0001-6349 print/ISSN 1600-0412 online � 2010 Informa UK Ltd. (Informa Healthcare, Taylor & Francis AS)DOI: 10.3109/00016341003657884

among women with obesity compared to the entiremedian cohort (8). These cases of fetal deaths werealso five times as likely to be related to placentaldysfunction compared to normal weight individuals.Observational and cross-sectional studies reportmixed findings, with some studies reporting increasedodds of IUGR among obese mothers and othersreporting no relation between obesity and IUGR.Most studies examining the relation between obe-

sity and adverse pregnancy outcomes, including fetalgrowth disturbances, have treated obesity as a dichot-omous outcomes (BMI ‡ 30 or not), despite it beingwell established that obesity, as measured by the BMI,is related to worse pregnancy outcomes in a dose-dependentfashion.Itremainsunclear,however, if thereis a thresholdof severeobesitybeyondwhichpregnancycomplications do not increase. The maximum obesityseverity in current classification schema is 40 or more.While the prevalence of obesity has stabilized since2004, the severity of obesity among those who arealready obese continues to climb. Between 1986 and2000, therateof individualswithaBMI‡50quintupled(9). The term ‘super-obese’was first coined byMasonet al. in 1987 to classify patients with a BMI ‡ 50 tohighlight their increased risk for poor outcomes follow-ing vertical banded gastroplasty (10). Given theincreased risk these individuals have for co-morbiditiessuch as chronic hypertension, diabetes, diabetes melli-tus, asthma, and obstructive sleep apnea compared toother obese individuals (11), it is plausible that super-obesity may have special implications in pregnantwomen. A search of the medical literature revealednopublished studies regarding the risk of super-obesityin relation to pregnancy (MEDLINE Database1950–2009 search on October 18, 2009). This study’sprimaryobjectivewastodetermine ifdeliveryofasmall-for-gestational age (SGA) or large-for-gestational age(LGA) infant is increased in women with a BMI ‡ 50compared to all other women or to other, less obesewomen. Secondary objectives included comparingthe rates of adverse pregnancy outcomes, includingpreeclampsia, gestational diabetes, cesarean delivery,and low Apgar scores, in super-obese women to other,less obese women.

Material and methods

This cross-sectional study included maternal-neonatalpairs delivered between January 1, 1996 andDecember31, 2007 at the Medical University of South Carolina,the region’s tertiary referral center (approved by theInstitutional Review Board). The women and babieswere identified by the center’s validated perinatalresearch database (12). Inclusion criteria included

women with recorded height and weight at the timeof admission for delivery, singleton gestation, andrecorded birthweight (g). Height was determined bymeasurements taken earlier during the woman’s pre-natal care, and maternal weight was determined by thelast weight recorded during outpatient prenatal care orby patient recall. Gestational age was determined bythe last menstrual period or by ultrasound dating,according to the American College of Obstetrics andGynecology (13). Subjects with missing maternalheight and weight, birthweight, and births < 20 or‡ 44 weeks of gestation were excluded.BMI (kg/m2)was calculated frommaternal height and

weight and characterized into one of seven classes accor-ding to modified guidelines reported jointly by theNational Heart, Lung, and Blood Institute and theNational Institute ofDiabetes andDigestive andKidneyDiseases: underweight (< 18.5), normal (‡ 18.5 and< 25), overweight (‡ 25 and < 30), obese class I(‡ 30and< 35), obese class II (‡ 35 and< 40), andobeseclass III (‡40 and < 50) (14). In addition, ‘super-obese’was defined as a BMI‡ 50. SGA and LGA werecalculated by a birthweight < 10th or > 90th percen-tile for gestational age, respectively, according to thesmoothed population birthweight percentiles byAlexander et al. (15).All covariates were dichotomous (yes or no) except

maternal age at delivery (years) and gestational age(weeks). Pregestational diabetes was determined bythe patient’s medical history of type 1 or type 2diabetes. Gestational diabetes was determined byabnormal diagnostic testing during pregnancyaccording to guidelines published by the AmericanDiabetes Association (16). Chronic hypertension wasdefined by the personal medical history, or by ‡ 2elevated blood pressures (systolic ‡ 140 mmHg ordiastolic ‡ 90 mmHg) on at least two separate occa-sions before 20 weeks. Preeclampsia was defined bynew-onset hypertension (systolic blood pressure ‡ 140mmHg or diastolic blood pressure ‡ 90 mmHg onat least two separate occasions) and proteinuria(‡ 300 mg in a 24-hour collection or ‡ 1+ on acatheterized urine specimen in the acute setting) after20 weeks according to published guidelines from theAmerican College of Obstetricians and Gynecologists(17) and determined by an attending physician.Congenital anomaly included any birth defect andwas determined during the neonatal period by thepediatrician or pediatric subspecialist.

Statistical Analysis

Measures of center and spread for continuous vari-ables were reported using median and interquartile

Maternal super-obesity 925

range. Univariate summaries for categorical variableswere reported as frequencies and percents. The pri-mary exposure was super-obesity (yes or no), and thetwo primary outcomes were SGA (yes or no) and LGA(yes or no). Bivariable analyses were performed toassess associations between covariates and the twoprimary outcomes among all women in the studyand also among obese women only. Wilcoxon ranksum tests and chi-squared tests were used to assessassociations between continuous variables and dichot-omous categorical variables with both SGA and LGA,respectively. Pregestational and gestational diabeteswere analyzed as a single, combined variable for bivar-iate analyses. Multivariable logistic regression analyseswere performed in order to assess the effect of super-obesity on delivery of an SGA or LGA infant, whilecontrolling for black race, any smoking duringpregnancy, and congenital anomaly. These covariateswere chosen based on their well-known associationwith birthweight. Adjusted odds ratios (ORs) and95% confidence intervals (CIs) were reported for theassociation between super-obesity and SGA andbetween super-obesity and LGA compared to allwomen. In addition, associations between super-obesity and SGA and LGA were determined afterrestricting the analyses to only obese women. Becausediabetes, preeclampsia, and chronic hypertension arepart of the causal pathway from maternal obesity toeffects on birth weight, these covariates were notincluded in these regression analyses. The Breslow-Day test was performed for all possible two-way inter-actions between dichotomous covariates used inmultivariable analyses. The fit of each multivariable

model was assessed by the Hosmer-Lemeshowgoodness-of-fit test.To address the secondary objectives of the study,

associations between all BMI classes and adversepregnancy outcomes were evaluated using theCochran Armitage test for trend. These adverseoutcomes included preeclampsia, gestational diabe-tes, cesarean delivery, and low 5-minutes Apgarscores. Multivariable regression analyses were alsoused to assess the relation between super-obesityand these adverse pregnancy outcomes relative toother, less obese women. Given the wide range ofpregnancy complications studied, each regressionmodel included an individualized set of covariatesselected based on their well-known association withthe dependent variable. Tests for interaction andgoodness-of-fit were equivalent to the primary mul-tivariable analyses previously mentioned. Two-tailedp-values < 0.05 were considered significant for alltests. Statistical analyses were performed with SASV9.1 (SAS Institute, Inc. Cary, North Carolina,USA).

Results

There were 19,700 eligible maternal-neonatal pairsduring the study period. During this period, theincidences of obesity and super-obesity were 49.5%(n = 9,749) and 2.2% (n = 425), respectively. Thelowest median birthweight occurred in underweightwomen, and the median birthweight steadilyincreased with increasing BMI class (Figure 1).

<18.5

010

0020

0030

00

Bir

th w

eig

ht

(g)

4000

5000

6000

18.5 - 24.9 25 - 29.9 30 - 34.9

BMI (kg/m2)

35 - 39.9 40 - 49.9 50+

Figure 1. Box-and-Whiskers plots of birth weight by BMI class. The median birthweight clearly increases with increasing BMI class.Note: BMI, body mass index.

926 M.C. Alanis et al.

Overall, the rates of SGA and LGA during thestudy period were 15.1 and 6.3%, respectively.Tables 1 and 2 demonstrate the rates of covariateswith and without SGA and with and without LGAamong all included women and obese womenonly, respectively. There was significant interactionbetween black race and smoking and black raceand congenital anomaly on SGA (Breslow-Day testp < 0.001 and p = 0.01, respectively). There were nointeraction terms for LGA. After controlling for

confounding and interaction terms, super-obesityresulted in a 44% reduction in the odds of deliver-ing an SGA infant (adjusted OR = 0.55, 95%CI 0.40–0.76; p < 0.001) compared to all otherwomen and a non-significant 25% reduction com-pared to other, less obese (BMI 30.0–49.9) women(adjusted OR = 0.75, 95% CI 0.54–1.03; p = 0.07).Super-obesity increased the odds of delivering anLGA infant 3.5-fold (adjusted OR 3.49, 95% CI9.1–22.0; p < 0.001) compared to all other women

Table 1. Summary of associations between patient factors and SGA and LGA in all included women (n = 19,700).

Variable

SGA LGA

Yes(n = 2,967)a

No(n = 16,733)a p-Valueb

OR(95% CI)

Yes(n = 1,246)a

No(n = 18,454)a p-Valueb

OR(95% CI)

Maternal age atdelivery (years)

23 (20–29) 24 (20–30) < 0.001c NA 27 (22–32) 24 (20–30) < 0.001c NA

Gestational age (weeks) 38 (37–39) 39 (37–40) < 0.001c NA 39 (38–40) 39 (37–40) < 0.001c NAParity 1.0 (0–2) 1.0 (0–2) 0.02 NA 1.0 (1–2) 1.0 (0–2) 0.005 NASuper-obesity 1.5 (44) 2.3 (381) 0.006 0.65 (0.47–0.88) 5.1 (64) 2.0 (361) < 0.001 2.7 (2.07–3.56)Black race 66.1 (1,960) 51.1 (8,552) < 0.001 1.86 (1.72–2.02) 33.3 (415) 54.7 (10,097) < 0.001 0.41 (0.37–0.47)Smoking 16.7 (496) 10.2 (1,713) < 0.001 1.76 (1.58–1.96) 6.3 (79) 11.5 (2,130) < 0.001 0.52 (0.41–0.65)Chronic hypertension 6.5 (194) 4.2 (701) < 0.001 1.60 (1.36–1.89) 5.6 (70) 4.5 (825) 0.06 1.27 (0.98–1.63)Diabetes mellitus 4.6 (135) 6.8 (1,137) < 0.001 0.65 (0.54–0.79) 18.9 (236) 5.6 (1,036) < 0.001 3.93 (3.36–4.59)Preeclampsia 11.8 (349) 5.4 (909) < 0.001 2.32 (2.04–2.64) 5.6 (70) 6.4 (1,188) 0.25 0.87 (0.68–1.11)Preterm birth 23.2 (689) 16.4 (2,748) < 0.001 1.54 (1.40–1.69) 4.3 (53) 18.3 (3,384) < 0.001 0.20 (0.15–0.26)Congenital anomaly 8.5 (253) 4.2 (695) < 0.001 2.15 (1.85–250) 3.5 (44) 4.9 (904) 0.03 0.71 (0.52–0.97)

aContinuous variables are described by medians (IQR), and categorical variables are described in terms of column percents (number ofobservations).bp-Values for categorical variables calculated with the use of the chi-square test unless stated otherwise.cWilcoxon rank sum test.Note: SGA, small-for-gestational age; LGA, large-for-gestational age; OR, odds ratio; CI, confidence interval.

Table 2. Summary of associations between patient factors and SGA and LGA in obese women only (n = 9,749).

Variable

SGA LGA

Yes(n = 1,159)a

No(n = 8590)a p-Valueb

OR(95% CI)

Yes(n = 914)a

No(n = 8835)a p-Valueb

OR(95% CI)

Maternal age atdelivery (years)

25 (21–30) 25 (21–30) 0.38 NA 27 (23–32) 25 (21–30) < 0.001c NA

Gestational age (weeks) 38 (37–39) 39 (38–40) < 0.001c NA 39 (38–40) 39 (37–40) < 0.001c NAParity 1.0 (0–2) 1.0 (0–2) < 0.001 NA 1.0 (0–2) 1.0 (0–2) < 0.001 NASuper-obesity 3.8 (44) 4.44 (381) 0.32 0.85 (0.61–1.17) 7.0 (64) 4.1 (361) < 0.001 1.8 (1.34–2.32)Black race 70.8 (821) 56.3 (4,839) < 0.001 1.88 (1.65–2.15) 37.8 (345) 60.2 (5,315) < 0.001 0.40 (0.35–0.46)Smoking 15.6 (181) 9.7 (834) < 0.001 1.72 (1.45–2.05) 6.4 (58) 10.8 (957) < 0.001 0.56 (0.42–0.73)Chronic hypertension 11.9 (138) 7.1 (613) < 0.001 1.76 (1.45–2.14) 7.4 (68) 7.7 (683) 0.75 0.96 (0.74–1.24)Diabetes mellitus 8.2 (95) 10.5 (905) 0.01 0.76 (0.61–0.95) 22.7 (207) 9.0 (793) < 0.001 2.97 (2.50–3.52)Preeclampsia 16.8 (195) 7.8 (669) < 0.001 2.40 (2.01–2.85) 7.1 (65) 9.0 (799) 0.05 0.77 (0.59–1.00)Preterm Birth 24.4 (283) 14.2 (1218) < 0.001 1.95 (1.69–2.27) 4.1 (37) 16.6 (1,464) < 0.001 0.21 (0.15–0.30)Congenital anomaly 9.2 (106) 4.1 (353) < 0.001 2.35 (1.87–2.95) 3.5 (32) 4.8 (427) 0.07 0.71 (0.50–1.03)

aContinuous variables are described by medians (IQR), and categorical variables are described in terms of column percents (number ofobservations).bp-Values for categorical variables calculated with the use of the chi-square test unless stated otherwise.cWilcoxon rank sum test.Note: SGA, small-for-gestational age; LGA, large-for-gestational age; OR, odds ratio; CI, confidence interval.

Maternal super-obesity 927

and 2-fold when compared to other, less obesewomen (adjusted OR = 2.18, 95% CI 1.65–2.89;p < 0.001). Results from the Hosmer-Lemeshow testindicated adequate goodness of fit for the multivari-able models, except for LA among only obese women(p = 0.02).The highest rates of black race, chronic hyperten-

sion, pregestational and gestational diabetes mellitus,preeclampsia, LGA, and cesarean delivery weredemonstrated in the super-obese group of women(Table 3). Apgar scores < 7 at 1-minute were highestin this group of women as well, but there was nosignificant trend at 5 minutes (Table 2). The greatestincidence of smoking, nulliparity, preterm birth,placental abruption, and SGA occurred in under-weight women (Table 3). There was significantdeclining risk of stillbirth with increasing BMI class,but this observation was limited by very small num-bers among underweight and super-obese women(Table 3). Results of multivariable logistic regression

analyses exploring the effect of super-obesity onthese adverse pregnancy outcomes relative to otherobese (BMI 30.0–49.9) women are presentedin Table 4. Super-obesity increased the risk signif-icantly for preeclampsia, gestational diabetes, con-genital anomalies, cesarean delivery and low Apgarscores.

Discussion

This study shows that super-obesity is associated withadverse pregnancy outcomes and fetal overgrowth,which may explain the increased rate of cesareandelivery in these women compared to other obeseand non-obese women. Clearly, the risk of preeclamp-sia, gestational diabetes, delivering an LGA infant andcesarean delivery does not peak at levels of severeobesity traditionally described. Therefore, super-obesity has immediate clinical implications for

Table 3. Selected dichotomous background and outcome variables by BMI class with trend analyses (n = 19,700).

VariableaUnderweight

(n = 63)Normal

(n = 3235)Overweight(n = 6,653)

Obese I(n = 4,977)

Obese II(n = 2,644)

Obese III(n = 1,703)

Super-obese(n = 425)

Missingdata(n) p-Valueb

Maternal age ‡ 35 y/o(n = 2,020)

0 (0) 7.8 (252) 10.3 (687) 10.3 (514) 10.7 (284) 12.4 (211) 16.9 (72) 0 <0.001

Nulliparous (n = 7,971) 47.6 (30) 46.6(1,508)

43.4 (2,887) 38.0(1,889)

35.6 (942) 34.7 (591) 29.2 (124) 2 <0.001

Black race (n = 10,512) 58.7 (37) 52.7(1,705)

46.8 (3,110) 52.2(2,598)

60.8(1,608)

66.8(1,137)

74.6 (317) 0 <0.001

Hispanic ethnicity (n = 2,793) 15.9 (10) 12.2(393)

17.0 (1,128) 16.8 (836) 11.0 (292) 6.9 (117) 4.0 (17) 0 <0.001

Smoking (n = 2,209) 15.9 (10) 13.1(424)

11.4 (760) 11.1 (551) 10.1 (268) 9.3 (158) 8.9 (38) 0 <0.001

Chronic hypertension(n = 895)

1.6 (1) 1.1 (34) 1.6 (109) 3.5 (175) 8.1 (213) 14.3 (244) 28.0 (119) 0 <0.001

Pregestational diabetes(n = 455)

0 (0) 0.3 (10) 1.2 (81) 2.3 (113) 3.6 (95) 6.3 (107) 11.5 (49) 0 <0.001

Stillbirth (n = 287) 3.2 (2) 2.4 (77) 1.4 (91) 1.0 (51) 1.2 (32) 1.8 (30) 0.9 (4) 0 0.005Neonatal death (n = 285) 4.8 (3) 1.9 (61) 1.3 (88) 1.2 (61) 1.6 (43) 1.2 (20) 2.1 (9) 0 0.292Preterm birth (n = 3,437) 38.1 (24) 25.0 (809) 16.6

(1,103)711 (14.3) 16.4 (434) 16.2 (276) 18.8 (80) 0 <0.001

SGA (n = 2,967) 28.6 (18) 22.6 (730) 15.9(1,060)

11.9 (593) 12.1 (320) 11.9 (202) 10.4 (44) 0 <0.001

LGA (n = 1,246) 0 (0) 1.5 (47) 4.3 (285) 7.6 (379) 10.2 (269) 11.9 (202) 15.1 (64) 0 <0.001Gestational diabetes (n = 819) 1.6 (1) 1.1 (34) 2.2 (146) 4.5 (224) 6.8 (180) 10.5 (179) 12.9 (55) 0 <0.001Preeclampsia (n = 1,258) 4.8 (3) 3.0 (97) 4.42 (294) 6.5 (324) 9.4 (249) 12.7 (217) 17.4 (74) 0 <0.001Placental abruption (n = 153) 3.2 (2) 1.3 (41) 0.8 (56) 0.5 (26) 0.6 (16) 0.53 (9) 0.7 (3) 0 <0.001Cesarean delivery (n = 5,070) 20.3 (13) 15.8 (511) 21.5

(1,428)27.2(1,353)

32.9 (869) 38.64 (658) 56.0 (238) 0 <0.001

Congenital anomaly (n = 948) 7.9 (5) 5.0 (162) 4.8 (322) 4.4 (217) 4.7 (125) 5.1 (87) 7.1 (30) 0 0.6721-Minute Apgar <7 (n = 3,438) 23.8 (15) 17.0 (548) 15.7 (1,043) 16.9 (839) 19.2 (507) 22.0 (373) 26.6 (113) 37 <0.0015-Minute Apgar <7 (n = 1,164) 11.1 (7) 7.0 (226) 5.3 (353) 5.1 (253) 6.3 (166) 7.0 (119) 9.4 (40) 27 0.222

aDichotomous variables represented by column percents (frequencies).bCochrane Armitage test for trend unless otherwise noted (two-tailed values).Note: BMI, body mass index.

928 M.C. Alanis et al.

obstetricians with regards to minimizing and evalu-ating risks during the antepartum and intrapartumperiods.In addition, it does not appear that super-obesity

has a dual-fold impact on increased rates of both SGAand LGA compared to normal-BMI women. Con-trary to previous publications (18,19), obesity was notpositively associated with SGA. While super-obesitywas protective against delivering an SGA infant com-pared to all other women, rates of SGA were notdifferent between super-obese and other, less obesewomen. Therefore, increasing BMI beyond mild obe-sity results in increasing delivery rates of LGA infantswhile not further affecting rates of SGA. It had beenhypothesized that the delivery rate of SGA infantswould be increased in super-obese women comparedto women with a normal BMI, presumably related tohigh rates of placental dysfunction. Other studiesagree with our observations of the effect of BMI onrates of LGA and SGA (20,21). Potential explana-tions for differences in findings between studiesinclude variations in the clinical setting from whichstudy patients were derived, differences in data anal-ysis and definitions of SGA. For example, the study byRode et al. included women from a racially andethnically homogenous population (Denmark) whodelivered after 37 weeks gestation, and known con-founders for fetal growth restriction, including smok-ing, race, and congenital anomaly were not controlledfor in the analysis (18). In addition, the rate of lowbirthweight infants (defined as < 2500 g) was muchlower (1.0–2.8%) than the rate reported in the presentinvestigation (15.1%), reflectingdifferences inpatientsand settings.Likewise, the studybyRosenberget al. didnot have the maternal height available (19) and theiranalyses did not control for gestational age.

Therefore, obesity appears to be associated withexcessive fetal growth and not undergrowth. Theremay be subpopulations of obese women who are atincreased risk for fetal growth restriction that have yetto be identified. While Nøhr et al. demonstrated asignificantly lower birthweight among stillbirths fromobese mothers compared to the cohort median (8),there were too few stillbirths among super-obesewomen to make these comparisons in our study.The strengths of the present study include a singleinstitution analysis and a relatively large number ofstudy patients. In addition, these findings are consis-tent with the known risks of obesity and adversepregnancy complications. Study limitations includethe cross-sectional design and the unavailability inthe perinatal database of certain variables, includingmaternal gestational weight gain, pre-pregnancyweight, and postpartum maternal and neonatal com-plications. While gestational weight gain is likely toresult in an increase in BMI classification duringpregnancy for women with low pre-pregnancy BMI,obese women are unlikely to demonstrate similar shifts(22).We feel, therefore, that the use of BMI at delivery,which takes into account insufficient or excessive ges-tational weight gain, is appropriate for the outcomeswhich we described. However, our results may not bereadily comparable to other studies that use the pre-pregnancy BMI as the primary exposure variable.Future studies to examine the effect of super-obesityand other degrees of obesity on fetal growth patternsshould include prospective ultrasound measurementsbefore fetal death may occur, as well as birthweight andfollow-up studies of growth during childhood. In addi-tion investigations into the impacts of modifiable beha-viors (e.g. maternal weight gain during pregnancy) onobesity-related pregnancy outcomes should focus on

Table 4. Association between adverse pregnancy outcomes and super-obesity versus women with BMI 30.0–49.9 (n = 9,749).

Outcome variableSuper-obese(n = 425)

BMI 30.0–49.9(n = 19,275) Unadjusted ORa

Unadjusted95% CIa Adjusted OR

Adjusted95% CI

Stillbirth 0.9 (4) 1.2 (113) 0.77 0.28–2.11 0.68 0.25–1.86Preterm birth 18.8 (80) 15.2 (1,421) 1.29 1.00–1.66 1.21 0.94–1.56Preeclampsia 17.4 (74) 8.5 (790) 2.28 1.75–2.96 2.14 1.64–2.80Gestational diabetes 12.9 (55) 6.3 (583) 2.23 1.66–2.99 1.90 1.40–5.57Congenital anomaly 7.1 (30) 4.6 (429) 1.57 1.07–2.31 1.47 1.00–2.16Placental abruption 0.7 (3) 0.8 (150) 0.91 0.29–2.85 N/A N/ACesarean delivery 56.0 (238) 30.9 (2,880) 2.85 2.34–3.47 2.86 2.35–3.49Apgar 1-minute <7 26.6 (113) 18.5 (1,719) 1.60 1.28–2.00 1.59 1.26–2.01Apgar 5-minute <7 9.4 (40) 5.8 (538) 1.70 1.21–2.37 1.74 1.19–2.55

Categorical variables described by column percents (frequencies).ap-Values and unadjusted ORs (95% CIs) calculated by Wald chi-squareModels controlling for: stillbirth- maternal age, black race, smoking; preterm birth- black race, smoking, parity; preeclampsia- maternal age,black race, smoking, parity; gestational diabetes-maternal age, black race or Hispanic ethnicity; congenital anomaly-maternal age; cesareandelivery- nulliparity, congenital anomaly, gestational age; 5-minute Apgar < 7-gestational age.Note: BMI, body mass index; SGA, small for gestational age; LGA, large for gestational age; OR, odds ratio; CI, confidence interval.

Maternal super-obesity 929

super-obesity, as these women appear to have thehighest rates of pregnancy complications.

Declaration of interest: The authors report noconflicts of interest. The authors alone are responsiblefor the content and writing of the paper.

References

1. American College of Obstetricians and Gynecologists. ACOGCommittee Opinion Number 319: the role of the obstetrician-gynecologist in the assessment and management of obesity.Obstet Gynecol. 2005;106:895–9.

2. Ogden CL, Carroll MD, Curtin LR, McDowell MA,Tabak CJ, Flegal KM. Prevalence of overweight and obesityin the United States, 1999–2004. JAMA. 2006;295:1549–55.

3. Reece EA. Perspectives on obesity, pregnancy and birth out-comes in the United States: the scope of the problem. Am JObstet Gynecol. 2008;198:23–7.

4. Goffman D, Madden RC, Harrison EA, Merkatz IR,Chazotte C. Predictors of maternal mortality and near-missmaternal morbidity. J Perinatol. 2007;27:597–601.

5. Lashen H, Fear K, Sturdee DW. Obesity is associated withincreased risk of first trimester and recurrent miscarriage:matched case-control study. Hum Reprod 2004;19:1644–6.

6. Salihu HM, Dunlop AL, Hedayatzadeh M, Alio AP,Kirby RS, Alexander GR. Extreme obesity and risk ofstillbirth among black and white gravidas. Obstet Gynecol.2007;110:552–7.

7. Weiss JL, Malone FD, Emig D, Ball RH, Nyberg DA,Comstock CH, et al. Obesity, obstetric complications andcesarean delivery rate: a population-based screening study.Am J Obstet Gynecol. 2004;190:1091–7.

8. Nøhr EA, Bech BH, Davies MJ, Frydenberg M,Henriksen TB, Olsen J. Prepregnancy obesity and fetal death:a study within the Danish National Birth Cohort. ObstetGynecol. 2005;106:250–9.

9. Sturn R. Increases in clinically severe obesity in the UnitedStates, 1986–2000. Arch Intern Med. 2003;163:2146–8.

10. Mason EE, Doherty C, Maher JW, Scott DH, Rodriguez EM,Blommers TJ. Super obesity and gastric reduction procedures.Gastroenterol Clin North Am. 1987;16:495–502.

11. Kral JG. Morbidity of severe obesity. Surg Clin North Am.2001;81:1039–61.

12. Hulsey TC, Levkoff AH, Alexander GR. Birth weights oninfants of black and white mothers without pregnancycomplications. Am J Obstet Gynecol. 1991;164:1299–302.

13. American College of Obstetricians and Gynecologists. ACOGPractice Bulletin Number 55: management of posttermpregnancy. Obstet Gynecol. 2004;104:639–46.

14. National Heart, Lung, and Blood Institute andNational Institute of Diabetes and Digestive and KidneyDisease. NIH Publication 98-4083. Clinical guidelines onthe identification, evaluation, and treatment of overweightand obesity in adults. The evidence report. Obes Res. 1998;6:S51–210.

15. Alexander GR, Himes JH, Kaufman RB, Mor J, Kogan M. AUnited States national reference for fetal growth. ObstetGynecol. 1996;87:163–8.

16. American Diabetes Association. Diagnosis and classificationof diabetes mellitus. Diabetes Care. 2008;31:S55–60.

17. American College of Obstetricians and Gynecologists. ACOGPractice Bulletin Number 33: diagnosis and management ofpreeclampsia and eclampsia. Obstet Gynecol. 2002;99:159–67.

18. Rode L, Nilas L, Wøjdemann K, Tabor A. Obesity-relatedcomplications in Danish single cephalic term pregnancies.Obstet Gynecol. 2005;105:537–42.

19. Rosenberg TJ, Garbers S, Chavkin W, Chiasson MA.Pregnancy weight and adverse perinatal outcomes in anethnically diverse population. Obstet Gynecol. 2003;102:1022–7.

20. Sukalich S, Mingione MJ, Glantz C. Obstetric outcomes inoverweight and obese adolescents. Am J Obstet Gynecol.2006;195:851-5.

21. Cnattingius S, Bergström R, Lipworth L, Kramer MS. Pre-pregnancy weight and the risk of adverse pregnancy outcomes.N Engl J Med. 1998:338:147–52.

22. Rode L, Hegaard HK, Kjægaard HK, Møller LF, Tabor A,Ottesen B. Association between maternal weight gain andbirth weight. Obstet Gynecol. 2007;109;1309–15.

930 M.C. Alanis et al.