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10.1576/toag.11.1.25.27465 www.rcog.org.uk/togonline

2009;11:2531

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Review Obesity: impact on

obstetric practice and outcome
Authors Frances M Stewart / Jane E Ramsay / Ian A Greer

Key content:
Prepregnancy obesity is increasingly common.
More than half of all women who died from direct or indirect causes in the
200305 report, Saving Mothers Lives, were overweight or obese.
Obese mothers have an increased risk of complications.

Learning objectives:
To learn about the increased incidence of miscarriage, congenital malformation
and metabolic complications.
To learn about the increased risks of intrapartum complications.

Ethical issues:
Should medical assistance to conceive be withheld until BMI!35?
More of the healthcare budget should be spent on prevention rather than
treatment of obesity.
Keywords congenital abnormality / deep vein thrombosis / gestational diabetes
mellitus / hypertension / perinatal mortality
Please cite this article as: Stewart FM, Ramsay JE, Greer IA. Obesity: impact on obstetric practice and outcome . The Obstetrician & Gynaecologist 2009;11:2531.

Author details
Frances M Stewart MD MRCOG
Consultant, Obstetrics and Gynaecology
Antrim Area Hospital, Bush Road, Antrim,
County Antrim BT41 2RL, UK
Email: francesstewart1@hotmail.com
(corresponding author)

Jane E Ramsay MD MRCOG

Consultant in Obstetrics and Gynaecology
Ayrshire Maternity Unit, Crosshouse Hospital,
Kilmarnock KA2 OBE, UK

2009 Royal College of Obstetricians and Gynaecologists

Ian A Greer MD MRCP(UK) FRCP FRCPI FFFP

FMedSci FRCOG

Consultant in Obstetrics and Gynaecology

Hull York Medical School, University of York,
Heslington,
York YO10 5DD, UK

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Introduction
The 200305 report of the Confidential Enquiries
into Maternal Deaths in the United Kingdom1
highlighted obesity as a significant risk for
maternal death. More than half of all women who
died from direct or indirect causes were either
overweight or obese.
For the mother, obesity increases the risk of
obstetric complications during the antenatal,
intrapartum and postnatal period, as well as
contributing to technical difficulties with fetal
assessment (Box 1). The offspring of obese mothers
also have a higher rate of perinatal morbidity and
an increased risk of long-term health problems.

The epidemiology of obesity

The prevalence of obesity, defined as a body mass
index (BMI) "30 kg/m2, has significantly increased
during the last three decades, both in the USA and
other countries in the developed world.American
trends are now seen among the European population.
In a health survey of England,2 the Department of
Health reported that 32% of women aged 3564 years
are overweight (BMI 2530) and 21% are obese
(BMI #30). In a British Womens Heart and Health
Study,3 one-quarter of the 4000 participants in
England, Scotland and Wales were found to be
clinically obese. One-fifth of the women were inactive
and two-fifths did not eat one portion of fresh fruit a
day. The Department of Health has predicted that, if
current trends continue, by 2010, 6 million women in
England will be obese.2 In line with this, a large
Scottish maternity hospital has observed a two-fold
increase in the proportion of women with a booking
BMI #30 over the last decade.4 Obesity amongst
women is of worldwide concern, as shown in
Australia by Callaway et al.5 in 2006. They noted that
35% of Australian women aged 2535 years were
overweight or obese. Obesity accounts for #280 000
deaths annually in the USA and will, if current trends
continue, soon overtake smoking as the primary
preventable cause of death.6

Antenatal health issues

Obesity is associated with an increased risk of first
trimester and recurrent miscarriage and fetal
Box 1

Complications that are more

prevalent among obese women
before and during pregnancy

26

Prepregnancy

Menstrual disorders, infertility

Early pregnancy

Miscarriage, fetal anomalies, difficult and

less accurate ultrasound examination

Antenatal

Pregnancy-induced hypertension,
pre-eclampsia, gestational diabetes,
venous thromboembolism

Intrapartum

Induction of labour, shoulder dystocia,

caesarean section, operative
anaesthetic difficulties

Postpartum

Haemorrhage, infection, venous

thromboembolism

Fetal

Macrosomia, fetal distress, perinatal

morbidity and mortality, birth injury

anomaly, in both women with polycystic ovary

syndrome and those with normal ovarian
morphology. A meta-analysis7 of 13 studies looking
at gonadotrophin-induced ovulation in women
with normogonadotrophic anovulatory infertility
found obesity and insulin resistance to be the most
clinically useful predicting factors for poor clinical
outcome. The incidence of spontaneous miscarriage
has been reported to rise as insulin resistance
increases.8 It has been suggested that insulinsensitising agents, such as metformin, also reduce
miscarriage rates.9 One potential mechanism for
this observation is an increased production of
inflammatory and prothrombotic agents produced
by adipose tissue or released from endothelium
secondary to stimulation by adipocyte-derived
factors. It has been suggested that plasminogen
activator inhibitor-type 1 (PAI-1) is associated with
increased rates of miscarriage in association with
maternal obesity. Treatment with metformin
appears to reduce PAI-1 and miscarriage rates.10,11
Several studies have shown up to a two-fold
increase in risk for neural tube defects where there
is prepregnancy maternal obesity. The greater the
maternal BMI, the higher the risk of congenital
malformation.12 It is well recognised that maternal
diabetes is a risk factor for the development of
congenital abnormality, including central nervous
system defects. A cumulative effect on the risk of
central nervous system birth defects when maternal
obesity and gestational diabetes coexist has also
been highlighted. Anderson et al.13 evaluated an
American population in a case control study
(n$477). After adjusting for maternal ethnicity,
age, education, smoking, alcohol use and
periconceptional vitamin use, obese women still
had substantially increased risks of delivering
offspring with anencephaly (odds ratio [OR] 2.3,
95% CI 1.24.3), spina bifida (OR 2.8, 95% CI
1.74.5) and isolated hydrocephaly (OR 2.7, 95%
CI 1.55.0). When gestational diabetes was
examined in isolation, the only anomaly seen more
frequently was holoprosencephaly.
The mechanisms that link obesity and congenital
anomaly are not fully understood. Several possible
hypotheses have been suggested, one being the
prevalence of undiagnosed type II diabetes or
significant insulin resistance without frank glucose
dysregulation. Epidemiological data from both the
USA and Europe have suggested that 3050% of
adults with type II diabetes are undiagnosed. Some
studies suggest that prepregnancy diagnosis of
diabetes may permit appropriate intervention prior
to conception and that obese women planning a
pregnancy should be screened and offered a highdose folic acid supplement. One could postulate
that weight reduction and tight glycaemic control
could help reduce the rates of congenital
abnormality in this high-risk group.
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Ultrasound and obesity

Obstetric ultrasound is widely practised
throughout the developed world. Initially, its major
indications were pregnancy dating and detection of
multiple pregnancy and fetal growth restriction.
With improved resolution the detection of fetal
anomaly has become possible. The limitations of
obstetric ultrasound as a screening test are dictated
by the expertise of the clinician, the quality of the
equipment and the habitus of the woman. By
absorbing the associated energy, adipose tissue can
significantly attenuate the ultrasound signal.
Therefore, a high-frequency, higher-resolution
signal would be more significantly absorbed at a
lesser depth, sacrificing image quality and depth of
field. A worrying consequence of maternal obesity,
consequently, is the reduced sensitivity of
ultrasound as a screening test for fetal anomaly. In
1990, Wolfe et al.14 examined the efficacy of
scanning the obese pregnant population. They
showed that scans performed on women with a
BMI greater than the 90th centile during the second
and third trimester had a 14.5% reduction in
visualisation of organs compared with lean women.
This reduction was most marked when visualising
the fetal heart, umbilical cord and spine.
Hypertension
Independent of pregnancy, hypertensive disorders
are more prevalent in obese women than in their
lean counterparts. Elevated prepregnancy BMI is an
independent risk factor for the development of
pregnancy-induced hypertension.15 Even when the
degree of excess body fat is moderate, the incidence
of hypertension and pre-eclampsia is significantly
higher in comparison with control patients.16 Most
published work suggests a two- to three-fold
increase in the risk of pre-eclampsia with a
BMI #30. Waist circumference has also been
reported to be a sensitive predictive marker of
possible pregnancy hypertensive complications.
Sattar et al.17 examined early pregnancy body
composition data from 1142 pregnant women.
Odds ratios were calculated for risk of hypertensive
complications of pregnancy in association with a
waist circumference #80 cm at %16 weeks of
gestation. The risk of pregnancy-induced
hypertension was approximately doubled (OR 1.8,
95% CI 1.12.9) and of pre-eclampsia tripled
(OR 2.7, 95% CI 1.16.8) in association with
central obesity.
OBrien et al.16 identified 13 cohort studies,
comprising nearly 1.4 million women. The risk of
pre-eclampsia typically doubled with each
57 kg/m2 increase in prepregnancy BMI. This
relationship persisted in studies that excluded
women with chronic hypertension, diabetes
mellitus and multiple gestation, or after
adjustment for other confounding factors. A recent
systematic review by Cnossen et al.18 aimed to
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determine the accuracy of maternal BMI in

predicting pre-eclampsia and to explore the
clinical potential for selecting women for
treatment with low-dose aspirin. A total of 36
studies, testing 1 699 073 pregnant women (60 584
with pre-eclampsia) were included. They found
that among women with a BMI #35 as the only
risk, the incidence of pre-eclampsia was only 3%,
resulting in 714 women needing treatment to
prevent one case of pre-eclampsia. When a woman
with a BMI #35 also had other risk factors,
however, such as primigravidity or diabetes, the
risk was greatly elevated and the number needed to
treat in order to prevent one case of pre-eclampsia
was only 37.18 This is a very useful paper for clinical
practice and it highlights the importance of
holistic evaluation of risk at booking for antenatal
care. Most studies within the literature conclude
that pregnancies amongst the obese population
should be considered high risk and appropriate
antenatal care provided. The need for
prepregnancy counselling and advice for this
group of women is highlighted repeatedly.
The mechanism of effect
As stated, obesity is a risk factor for many maternal
obstetric complications, including pre-eclampsia
and gestational diabetes. The mechanisms involved
are complex but one possible unifying hypothesis is
that there may be a syndrome of insulin resistance,
low-grade inflammation, dyslipidaemia and an
alteration in systemic microvascular function. This
metabolic and vascular derangement mirrors that
of the metabolic syndrome observed among those
with coronary heart disease and/or diabetes,
particularly in later life. In a prospective study,
Stewart et al.19 demonstrated that obese women
have a pro-inflammatory phenotype, with
impaired microvascular function, from early in
pregnancy. In lean women, inflammatory features
were acquired in later pregnancy. The excessive
inflammatory burden seen in the obese pregnant
woman may fuel this process, explaining some of
the increased association of obesity with preeclampsia and gestational diabetes.
Gestational diabetes mellitus and obesity
Gestational diabetes mellitus affects about 5% of all
pregnancies.20 In the NICE consultation
document21 on diabetes and pregnancy, a BMI #30
is considered a risk factor for the development of
gestational diabetes. The policy has changed from
offering no screening for gestational diabetes
mellitus to targeted screening in the healthy
maternal population, using clinical risk factors
(Box 2).
Striking data from a large prospective populationbased Swedish study,22 which included 151 025
women, warns of the implications of
interpregnancy weight gain. This study shows that
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Box 2

Criteria meriting antenatal

screening for gestational diabetes21

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BMI # 30
Previous gestational diabetes
Previous macrosomic baby "4.5 kg
Family history of diabetes (first-degree relative with type 1
diabetes)
Belonging to a high-risk ethnic group, including:
South Asian (Indian, Pakistani, Bangladeshi)
Black Caribbean
Chinese

if an increase in maternal BMI of 12 units occurs

between pregnancies, the risk of gestational
diabetes rises by 2040%. If a woman weighs 63 kg
and is 1.65 m tall (BMI 23) and gains 3 kg before
her second pregnancy, her BMI rises by 1 unit and
her risk of gestational diabetes rises by #30%. If she
gains 6 kg and, therefore, becomes overweight
(gaining 2 BMI units), her risk of gestational
diabetes rises by 100%. If she becomes obese, her
risk of gestational diabetes rises by 200%.22
Effective treatment of gestational diabetes does
reduce the risk of macrosomia. Instrumental and
operative delivery rates, however, are increased even
in the absence of fetal macrosomia.23 Crowther
et al.24 conducted a randomised clinical trial to
determine whether treatment of women with
gestational diabetes mellitus reduced the risk of
perinatal complications. The rate of serious
perinatal complications was significantly lower
among the infants of subjects in the intervention
group than among the infants of the women in the
routine care group (1% versus 4%, P$0.01).24
If gestational diabetes mellitus is diagnosed, tight
metabolic control should be achieved through diet
and, when indicated, insulin therapy. Insulin
therapy is required more often in obese women
with gestational diabetes mellitus than in lean
women.25 Treatment using insulin reduces maternal
and fetal morbidity.26 Mothers who develop
gestational diabetes have a 50% higher risk of
developing diabetes during their lifetime27 and this
risk may be greatest in obese woman.28 For the
obese individual with gestational diabetes,
pregnancy offers an ideal opportunity to give them
future lifestyle advice in terms of exercise and
weight loss and, therefore, to reduce the potential
for vascular disease in the long term.

Intrapartum issues
Obesity and diabetes are independently associated
with adverse pregnancy outcomes. Rosenberg
et al.29 undertook a large population-based study.
Data were collected from the 1999, 2000 and 2001
New York City birth files for 329 988 singleton
births, containing information on prepregnancy
weight and antenatal weight gain. During
pregnancy, obese women are at increased risk of
several adverse perinatal outcomes, including
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anaesthetic, perioperative and other maternal and

fetal complications.30 Obese women have higher
rates of induction of labour31 and failed induction
(7.9% versus 10.3% versus 14.6% with increasing
BMI).32 Caesarean section rates in nulliparous obese
women are higher than in lean women (20.7% in
the control group versus 33.8% in the obese group
and 47.4% in the morbidly obese group; P # 0.01).33
A higher rate of obstetric complications among
obese women has been reported, including
operative vaginal delivery (8.4% versus 11.4% and
17.3% with increasing BMI; P % 0.001), shoulder
dystocia (1% versus 1.8% and 1.9% with increasing
BMI; P % 0.021) and third/fourth-degree
lacerations (26.3% versus 27.5% and 30.8% with
increasing BMI; P % 0.001) compared with the
normal BMI group.32 The frequency of both elective
(8.5% versus 4%) and emergency caesarean section
(13.4% versus 7.8%) is almost doubled for very
obese women compared with the normal BMI
group.34 When other factors such as macrosomia,
nulliparity, induction or diabetes were accounted
for, maternal obesity was still found to influence the
mode of delivery independently.35 In another study
of 126 080 deliveries,36 after excluding women with
diabetes and hypertensive disease, there was a threefold increased risk of failure to progress in the first
stage and almost a trebling of caesarean section rate
from 10.8% to 27.8% (OR 3.2) among obese
women when compared with lean.
From the anaesthetic perspective, the risks of failed
epidurals, increased aspiration during general
anaesthesia and difficulty with intubation are the
most commonly cited compucations. Increased
rates of caesarean delivery, macrosomia, shoulder
dystocia, difficulty obtaining peripheral
intravenous access and inaccurate or difficult blood
pressure monitoring are also reported.37 Common
operative complications include loss of landmarks,
making vascular access difficult, and increased risk
of respiratory complications, such as aspiration and
pneumonitis. Increased retention of lipid-soluble
agents, increased drug distribution and more rapid
desaturation have also been reported.
The anaesthetist plays an important role in
preventing serious complications and must be
aware of the many potential hazards. Extra
vigilance is required to guide these women safely
through the perioperative period. There are very
few trials in the literature on the use of epidural and
spinal anaesthesia in the obese woman. Many case
reports exist on the difficulty of technique and
reductions in drug dosage requirements.

Postpartum issues
It is now recognised that adipose tissue produces a
variety of bioactive peptides, collectively termed
adipokines. Alteration of adipose tissue mass in

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obesity affects the production of most adiposesecreted factors: there is an increase in several
adipokines. Increased levels of angiotensinogen
have been implicated in hypertension; PAI-1 in
impaired fibrinolysis; and acylation-stimulating
protein, tumour necrosis factor-alpha, interleukin-6
and resistin in insulin resistance.38 Pregnancy is a
prothrombotic state, secondary to an increase in
activity of coagulation factors XII, X and VIII, as
well as fibrinogen.39 In the puerperium, deep
venous thrombosis, endometritis, postpartum
haemorrhage, prolonged hospitalisation and
wound infection and dehiscence are also seen with
increased frequency in obese women.37
The leading cause of maternal mortality remains
venous thromboembolism and the postpartum
period is the time of greatest risk, secondary to
vascular damage at childbirth. The coagulation
cascade is activated by inflammatory cytokines
causing endothelial activation and this is further
increased with obesity. Several studies have shown
that obese patients have higher plasma
concentrations of all prothrombotic factors
(fibrinogen, von Willebrand factor [VWF] and
factor VII), compared with non-obese controls,
with a positive association with central fat.40 It has
been proposed that the secretion of interleukin-6
by adipose tissue, combined with the actions of
adipose tissue-expressed tumour necrosis factoralpha in obesity, could underlie the association of
insulin resistance with endothelial dysfunction,
coagulopathy and coronary heart disease.40

Implications for the fetus of

the obese mother
Short-term
Lower Apgar scores have been reported in the
neonates of obese mothers compared with those of
lean mothers.41 Prepregnancy BMI is a strong
positive predictor of birthweight. In fact, the odds
ratio for an obese mother delivering a large-fordates infant is 1.418.41 Macrosomia increases the
risk of shoulder dystocia, birth injury and the
incidence of low Apgar scores and perinatal death.
A recent 3-year retrospective analysis42 examined
the mode of delivery of infants weighing #4000 g.
The incidence of caesarean section among the
macrosomic group was 25.8%, compared with
13.1% (P%0.0001) for the general population
during the study period.
Infants born to obese mothers are more likely to
require admission to a neonatal intensive care unit
(NICU). In a retrospective study carried out in
France,43 the percentage of infants requiring
admission to a NICU was 3.5 times higher when
maternal obesity was present. The higher incidence
of diabetes mellitus and gestational diabetes in the
obese population may contribute to this effect, with

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an increased risk of neonatal admission to the NICU

for glycaemic control. The increased incidence of
macrosomia and consequent birth trauma may also
contribute to increased rates of perinatal morbidity
in the offspring of obese mothers.
One cohort study carried out in Denmark42
examined the relationship between maternal
prepregnancy BMI and the risk of stillbirth and
neonatal death. Maternal obesity was associated
with almost a three-fold increased risk of stillbirth
(OR 2.8, 95% CI 1.55.3) and neonatal death (OR
2.6, 95% CI 1.25.8) compared with women of
normal weight. Adjustment for maternal cigarette
smoking, alcohol and caffeine intake, maternal age,
height, parity, gender of the child, years of
schooling, working status and cohabitation with
the partner did not change the conclusions, nor did
exclusion of women with hypertensive disorders or
diabetes mellitus. No single cause of death
explained the higher mortality in children of obese
women but more stillbirths were either
unexplained intrauterine deaths or associated with
fetoplacental dysfunction among obese compared
with normal weight women.42
Long-term
Barkers hypothesis44 describes a theory of
intrauterine programming, which suggests that
babies who are small at birth or during infancy,
secondary to maternal starvation during
pregnancy, have increased rates of cardiovascular
disease and type 2 diabetes in adult life. Forsn
et al.45 examined the association between maternal
BMI and the risk of coronary heart disease in the
next generation. Men whose mothers had a high
BMI in pregnancy had an increased risk of
coronary heart disease. The highest death rates
were, therefore, in men who had a low birthweight
and a low placental weight but whose mothers had
a high BMI during pregnancy. The effects were
large and highly significant. While undernutrition
is uncommon in the developed world, obesity and
cardiovascular disease are common. The direct
effects of maternal obesity on fetal programming
are under-researched. The concept of fetal
programming being related to the quality of
nutrition, rather than the quantity, needs to be
addressed. One may hypothesise that, in addition to
maternal malnutrition secondary to famine,
malnutrition secondary to an inappropriate diet of
highly processed, high-fat food lacking in essential
vitamins and nutrients, i.e. the modern Western
diet, may contribute to long-term adult ill health of
offspring through fetal programming.

Cost implications
In 2000, a prospective study46 examined the cost of
care of 435 women seen consecutively within their
obstetric service. The average cost in terms of
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antenatal care and duration of hospital stay was five

times higher for women who had a higher
prepregnancy BMI compared with normal weight
controls and duration of hospital stay was 3.9 to
6.2fold higher among the overweight mothers.
The overall financial burden of obesity on the
National Health Service is difficult to determine. The
implications of rising rates of maternal obesity for
maternity services include increased medicalisation
of labour and delivery and greater pressure on
neonatal services and antenatal and postnatal beds.

Conclusion and
recommendations
It is essential that obstetricians have guidelines for
management of the obese woman. Obesity is a risk
factor for both gynaecological and obstetric
complications. A multidisciplinary approach to
management is necessary to decrease the risks of
morbidity and mortality. There are a number of
recommendations for clinical management prior to
and during pregnancy:
Provide prepregnancy counselling for morbidly
obese women (in primary care/subfertility/
recurrent miscarriage/diabetic clinics).
Consider high doses of folic acid (5 mg).
A healthy diet and exercise are important in
pregnancy: refer to a dietician, advise to avoid
excessive weight gain, consider screening for
diabetes.
Provide an early booking visit to plan pregnancy
management.
Prescribe low-dose aspirin in the presence of
additional clinical risk factors for pre-eclampsia.
Consider antenatal thromboprophylaxis if there
are additional clinical risk factors for venous
thromboembolic disease.
Recommend a detailed anomaly scan and serum
screening for congenital abnormality.
Consider glucose tolerance testing at 28 weeks,
with the potential for repeating it in later pregnancy.
This group of women requires both primary and
secondary care intervention if we are to limit or
even reverse the epidemic of obesity within Western
society.
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