REVIEW
Stillbirth e is it
a preventable public health
problem in the 21st century?
Alina Vais
Lucy Kean
Abstract
The grief of stillbirth continues to affect a large number of parents in the
21st century. The causes vary throughout the world, with the most prom-
inent being fetal growth restriction, fetal abnormalities, pre-existing
maternal medical conditions and infections. Worldwide, as some causes
are becoming less prevalent, new causes are emerging, for example
maternal obesity. This article reviews the aetiology of stillbirth and
attempts to explain the apparent plateauing of stillbirth numbers.
Suggestions are made for ways of reducing these rates in various settings
throughout the world. Addressing lifestyle factors and the obesity
epidemic as well as more effective screening for growth restriction are
two interventions most likely to achieve further reductions in stillbirth
rates in high-income countries.
Keywords antenatal care; fetal growth restriction; gestational diabetes;
infection; intrapartum care; maternal obesity; stillbirth
Introduction
Almost 3 million stillbirths happen worldwide every year. The
grief of a stillbirth brings the months of excitement and antici-
pation of pregnancy to a tragic end. In low-income countries,
where 98% of all stillbirths occur, at least half occur during
labour or birth. It therefore follows that the number of stillbirths
would be greatly reduced by aiming for availability of skilled
delivery assistants and caesarean section capability in these
settings.
In high-income countries like the UK, intrapartum stillbirths
are relatively rare (around 16% of the total number of stillbirths)
but still 17 sets of parents each day take home a dead baby; in
most cases these are victims of ante-partum stillbirth.
In the UK, mortality in singleton pregnancies declined from
36.9 per 1000 births in 1953 to 8.9 per 1000 in 1993 and has
subsequently plateaued. The latest figure available from CESDI is
7.6 per 1000 in 2008. Around 40% of ante-partum deaths are
unexplained; this rate has barely changed over the years. It also
Alina Vais MRCOG is a Maternal Medicine Clinical Fellow at St. Thomas’
Hospital, Guy’s & St. Thomas’ NHS Foundation Trust, London, UK.
Conflicts of interest: none declared.
Lucy Kean MRCOG is a Consultant Obstetrician and Fetal Medicine
Specialist at Nottingham University Hospitals NHS Trust, City Hospital
Campus, Nottingham, UK. Conflicts of interest: none declared.
OBSTETRICS, GYNAECOLOGY AND REPRODUCTIVE MEDICINE 22:5
represents a higher rate than in many other high-income coun-
tries in Europe, as well as Canada and the USA.
This article aims to discuss the aetiology of stillbirths and
possible interventions to reduce rates.
Aetiology
There are several broad causes for stillbirth, and these will be
discussed in detail below. Fetal causes include chromosomal
problems and fetal structural abnormalities. Maternal associa-
tions include obesity, smoking and diseases of the endocrine,
renal cardiac and haematological systems. Infection accounts for
some fetal losses. Morphological placental complications account
for 12% of stillbirths. These involve marginal insertions (present
in 5e7% of pregnancies) and velamentous insertions (where the
cord inserts into the external membranes of the placenta);
placental vessels are more vulnerable to injury and can result in
fetal death. A large number of fetal losses are due to problems of
placental vascularization/fetal growth restriction and there is
growing evidence that at least 50% of unexplained stillbirths
may also be due to fetal growth restriction.
Fetal causes
Chromosomal abnormalities: these account for 30e60% of
early fetal demise and 7% of fetuses with chromosomal abnor-
malities survive to term. The commonest chromosomal abnor-
mality is autosomal trisomy and the risk increases with maternal
age.
In high-income countries, techniques are available to deter-
mine the karyotype of the fetus either antenatally or after
delivery. Postnatally, the failure rate for karyotypic evaluation
can be high and if there is a high index of suspicion, amnio-
centesis before delivery might be recommended. However, most
women find it distressing to consider this when a diagnosis of
stillbirth is first made and are then left with the option of
obtaining fetal DNA post-delivery from fetal skin or a fetal
intracardiac blood sample. Fetal chondrocytes extracted from an
iliac crest bone sample may yield better results. It is unlikely that
any of these techniques are routinely available in low-income
countries and so parents in these settings will not receive an
adequate explanation for their loss unless the baby’s phenotype
is strongly suggestive of a recognized syndrome.
Fetal structural abnormalities: these account for 35% of fetal
deaths, and commonly include cardiac and renal abnormalities.
If severe these may be diagnosed antenatally on ultrasound. Data
from Scotland (1985e1999) suggest that amongst lethal anoma-
lies, 22% involve the cardiovascular system, 14% the central
nervous system, 9% the renal system and 18% are chromosomal
disorders.
Fetal growth restriction (FGR)
There is a strong association between gestational size less than
the 10th percentile and an increased risk of stillbirths, mediated
by placental dysfunction. 50% of unexplained stillbirths are
associated with FGR, accounting for around 1000 babies a year
in the UK. Growth restriction can be thought of as being of
maternal, fetal or placental origin. Fetal origin is mostly
accounted for by chromosomal, genetic or structural
129 Ó 2012 Elsevier Ltd. All rights reserved.
 REVIEW
abnormality (as above), although infections lead to FGR.
Maternal disease (e.g. cardiac, renal, autoimmune) generally
causes FGR through placental failure. There are also other
maternal factors, such as smoking, obesity or maternal age
which cause growth restriction, most likely through adverse
effects on placental function. Purely placental causes include
mosaicism, ante-partum haemorrhage, placental tumours or
vascular and cord abnormalities.
All known thrombophilias (factor V Leiden mutations,
prothrombin gene mutations, hyperhomocysteinaemia, activated
protein C resistance, antithrombin III deficiency and anti-
cardiolipin antibodies) are associated with increased risk of fetal
demise through an increased risk of placental abruption, FGR and
pre-eclampsia. Pregnancy outcome in women with anti-
phospholipid syndrome is improved by using low-dose aspirin and
low-molecular-weight heparin if the woman has had previous
thromboses or pregnancy losses. Extrapolating this management
to women without prior morbidity is controversial, but widely
practised and endorsed by recent ACOG guidelines. Screening for
thrombophilia is routine after a pregnancy loss, however, timing is
important to exclude confounders such as low protein S and
C levels which are commonly found in normal pregnancies
without a thrombophilia. A recent case-control study in Israel
(2004) has shown that, whilst thrombophilias do not directly cause
stillbirth, they can cause severe FGR and it is those babies that are
most vulnerable. Therefore, routine thrombophilia screening in
women who lose appropriately grown fetuses is not warranted.
A recent meta-analysis by Flenady et al in the five high-income
countries with the highest numbers of stillbirths (Australia,
Canada, Netherlands, UK and USA) showed that sub-optimal fetal
growth, as defined by a gestational size below the 10th centile, is
associated with a four-times higher risk of stillbirth.
Research in Ireland and New Zealand using customized
growth charts rather than population centiles has demonstrated
increased detection rates for growth restriction, in keeping with
the belief that most of unexplained stillbirths are also due to FGR.
Another population-based cohort study in West Midlands
examined 2625 stillbirths over a 7-year period, and showed that
a new classification system aimed at identifying the relevant
condition present at the time of fetal death can attribute a cause
in 85% of cases. This ReCoDe classification led to only 15% of
stillbirths being deemed unexplained and identified that the
single largest contributor to fetal death is growth restriction,
associated with 43% of all stillbirths and 63% of intrapartum
deaths.
Infection
This accounts for 3% of stillbirths in UK and is usually a non-
recurring but potentially preventable cause of fetal loss. Infec-
tions include ascending bacterial infections (E. Coli, Group B
streptococcus), viruses (parvovirus B19) or parasites (toxoplas-
mosis, malaria). Bacterial infections trigger a cytokine cascade
leading to fetal damage, preterm labour and intrauterine death.
Worldwide syphilis is a major health issue.
Syphilis: worldwide, this preventable infection causes a large
number of stillbirths. In Sub-Saharan Africa, where 20% of
women of reproductive age are infected with syphilis, the
infection is responsible for 25e50% of all stillbirths. Within
OBSTETRICS, GYNAECOLOGY AND REPRODUCTIVE MEDICINE 22:5
functioning health systems, prevalence of the disease is less than
1%. Programmes for the elimination of syphilis as a cause of
stillbirth involve screening all pregnant women and offering the
appropriate treatment. The treatment is easy and inexpensive
and more cost-effective than screening and treatment of HIV,
however, lack of resources and poor access to antenatal services
in low-income countries have prevented this problem from being
addressed.
Malaria: 40% of births worldwide occur in areas where malaria
is endemic. Primiparous women infected with Plasmodium fal-
ciparum, especially if this is their first infection, have the worst
outcomes in terms of maternal and fetal death, preterm birth and
FGR. Placental malaria occurs in 13e63% of affected women;
placental insufficiency is caused by lymphocyte and macrophage
accumulation, leading to thickening of the basement membrane
impeding blood flow through the placenta, and restriction of
transfer of oxygen and nutrients to the fetus. This problem is
further compounded by the severe maternal anaemia which often
co-exists. Studies in various African countries report a 2e7 fold
increased risk of stillbirth in infected women compared to
healthy women. In Tanzania malaria was responsible for 32% of
all stillbirths. There is evidence that intermittent antimalarial
prophylaxis and use of insecticide-treated bed nets could reduce
the adverse outcomes associated with malaria infection,
including stillbirth rates.
Listeria: Listeria monocytogenes is a Gram positive bacillus which
the mother acquires from contaminated food (unpasteurized soft
cheese, undercooked meat, smoked salmon or pre-washed salads).
During bacteraemia, the organisms are transmitted to the placenta
and can cause villous necrosis and microabscesses. Stillbirth is the
result of placental dysfunction and fetal infection; the mortality rate
is 50%.
Chorioamnionitis/ascending infection: organisms that ascend
from the vagina into the uterus enter the amniotic fluid either
through intact membranes or after membrane rupture. The fetus
breathes in contaminated amniotic fluid and so the fetal lung
becomes infected e pneumonitis is a common autopsy finding in
stillbirth. E. Coli and organisms which cause bacterial vaginosis
are frequently implicated. Ascending infection appears to cause
proportionally more stillbirths in resource-poor African countries
compared to the USA; this may be attributable to reduced
immunity of malnourished women in Africa.
There is some evidence that in women with preterm prema-
ture rupture of membranes, prophylactic antibiotics reduce
histological chorioamnionitis, however, this is not mirrored in
a reduction of stillbirths. Stillbirths may also be associated with
intrauterine infections preceding membrane rupture, however,
effective strategies to detect such infections are yet to be
identified.
Viruses: the relationship between viral infection and stillbirth is
difficult to study, as many infections are difficult to diagnose and
involve expensive molecular techniques (e.g. PCR of viral DNA
or RNA) and a specific requirement to look for the virus at
autopsy. These tests are not routinely available in high-income
countries and virtually inaccessible in lower-income countries.
130 Ó 2012 Elsevier Ltd. All rights reserved.
 REVIEW
Common childhood diseases (measles, rubella, chickenpox,
parvovirus) are rare causes of stillbirth in high-income countries
with well-established vaccination programmes but are a problem
in low and middle-income countries. The burden of HIV in Sub-
Saharan Africa, where a fifth of the pregnant population is
infected, contributes a significant proportion of stillbirths. In
high-income countries, the emergence of influenza H1N1 over
the last 2 years had led to significant maternal and fetal mortality
and morbidity, such that vaccination is recommended in preg-
nancy. The enterovirus family (enterovirus, echovirus, coxsackie
and polio) can all cross the placenta and cause fetal death.
Parvovirus causes a mild disease in children but is an
important cause of stillbirth through development of severe
anaemia and hydrops, as well as through direct viral attack of the
fetal myocardium.
Cytomegalovirus (CMV) prevalence varies throughout the
world and appears to be more common in low socio-economic
areas and lower-income countries. In healthy adults, infection
is usually asymptomatic, although 10% can develop fever,
malaise, lymphocytosis and mild lymphadenopathy. More
serious complications occur in immunosuppressed individuals.
The virus can be transmitted through sexual contact, and is
intermittently shed in genital secretions. Fetuses and neonates
can be infected despite maternal antibodies due to this inter-
mittent shedding of virus, and shedding is more likely at
advanced gestations. Vertical transmission to fetuses is as high as
20e50% in primary infection; mortality amongst affected fetuses
is 20e30% and 90% of survivors suffer late complications (the
most common being deafness).
Where possible, vaccination offers the best approach to
reducing infections in pregnancy. However, vaccines are not
currently available for all infections (e.g. CMV, parvovirus).
Toxoplasmosis: this is caused by the parasite Toxoplasma gondii
which can be transmitted to humans from under or uncooked meat
(cured pork, salami, pork, mutton, wild game) or through inad-
vertent ingestion of oocytes present in cat faeces (cat litter, soil,
unwashed fruit and vegetables). Adults are mostly asymptomatic
or have a glandular-fever like illness. Transplacental transmission
occurs in primary infection and this is highest in the third trimester
(65%). However, fetal disease is more severe if transmission is
during the first trimester (17% transmission) leading to fetal loss in
17%. 70% of babies affected late in pregnancy are born with no
problems but 10% can have chorioretinitis. Other congenital
problems are microcephaly, hydrocephalus, intracerebral calcifi-
cation and mental retardation and there is a small risk of fetal loss
(1e2%) with disseminated disease, partly mediated by FGR. Once
diagnosed, treating the mother with spiramycin can reduce the risk
of transmission to the fetus. Reactivation of toxoplasmosis can
occur in immune compromised individuals and poses the highest
risk in women with untreated HIV.
Maternal causes
Diabetes: prior to the introduction of insulin, diabetic women had
a short life expectancy. With regards to reproductive risk they had
high rates of infertility, miscarriage and an almost 100% stillbirth
rate. Even nowadays, despite insulin treatment and apparent
good glycaemic control, a diabetic pregnancy is associated with a
five times greater stillbirth and perinatal mortality rate compared
OBSTETRICS, GYNAECOLOGY AND REPRODUCTIVE MEDICINE 22:5
to non-diabetic pregnancies. A recent study calculated that 3e5%
of all stillbirths in high-income countries are attributable to dia-
betes; this approximates to 2000 babies a year.
Gestational diabetes is becoming more prevalent worldwide,
especially in high-income countries. This condition is also asso-
ciated with an increased risk of fetal death. The increase in
prevalence is associated with increased rates of obesity and
higher maternal age. Lifestyle modification presents the greatest
opportunity to reduce the risks, but evidence based strategies for
achieving this are few.
Maternal age: the effect of maternal age on perinatal deaths is
illustrated by a U-shaped curve with the highest death rates in
very young (<20) and older mothers (>35). Mothers older than
40 have the highest rates of stillbirth. Throughout high-income
countries, more and more women are delaying motherhood
beyond the age of 35, thus increasing their risk, not only of
stillbirth, but also of miscarriage, impaired fetal growth and
maternal complications. A recent meta-analysis by Flenady et al
concluded that age >35 increases the odds of stillbirth by 65%,
and the risk doubles if maternal age is over 40. Overall, 7e11%
of stillborn babies (or 4200 babies a year) are born to mothers
aged >35 in high-income countries.
The same authors found two studies in women younger than 15;
they reported a 57% increased risk or an OR of 1.57, which is
similar to the risk of a 39 year old. The latest CMACE report in 2009
in the UK showed that mothers younger than 20 years had the
highest neonatal mortality rate (14.4 per 1000), which may reflect
the associated social deprivation and high rate of preterm delivery
in this age group. Teenage maternities contribute 9.6% to the
overall neonatal mortality in England, Wales and Northern Ireland.
Maternal BMI: the latest CEMACE report of 2009 has shown that
among women who suffered a stillbirth, 10% had a BMI >35. Other
studies have demonstrated that nulliparous women with a BMI
greater than 30 have a four-fold increase in the risk of intra-uterine
fetal death (IUFD) compared with women with a BMI between 20
and 25. The latest meta-analysis by Flenady et al in high-income
countries suggests that the risk of stillbirth is increased by 23% in
overweight women (BMI ¼ 25e30) and by 60% in obese women
(BMI >30). If BMI is >40, the risk of stillbirth is doubled. In the five
high-income countries included in the meta-analysis (USA, UK,
Canada, Australia, Netherlands), 28e58% of the population was
overweight or obese and 16,822 stillbirths a year were attributed to
this risk factor. There is increasing evidence, especially from
research using customized growth charts, that the mechanism
involved in this increased stillbirth rate is FGR which is more
difficult to pick up and act upon in obese mothers.
A large Swedish study also showed that the risk of stillbirth
increases linearly with weight gain during pregnancies. If BMI
increased by three points between first and second pregnancy,
irrespective of the initial starting weight, the risk of stillbirth
increased by 60%. As the effect was stronger for term than preterm
pregnancies, the effect is likely to be mediated by an effect on
placental function. Whether the same mechanism as impacts on
pregnancies of women with diabetes at term is unclear.
Maternal smoking: Flenady et al identified four studies which
investigated the relationship between smoking and the risk of
131 Ó 2012 Elsevier Ltd. All rights reserved.
 REVIEW
stillbirth. Any amount of smoking increased the odds of stillbirth
by 36%. Two studies looked at smoking over 10 cigarettes a day,
and showed the risk almost doubled in these circumstances
(OR ¼ 1.86, 95% CI 1.59e2.17). Actual numbers of stillbirths
attributable to smoking are almost 3000 a year in high-income
countries or 4e7% of stillbirths. Smoking could contribute as
many as 20% of stillbirths in low-income countries.
Other factors
A nuchal cord is found in 23% of all deliveries, both live and
stillborn infants and multiple nuchal loops are found in 3.7% of
stillborns. A post-mortem examination is required to determine if
this was the cause of death, as the fetus may become entangled in
the cord during delivery but after death. True umbilical knots
occur in 1% of pregnancies but are only associated with fetal
demise in 2.7% of cases, as loose knots will maintain adequate
fetal circulation. It is vital to have post-mortem confirmation
before attributing a fetal death to a cord complication to enable
correct counselling of the bereaved couple.
Obstetric cholestasis is a poorly understood condition which
has historically been associated with a high perinatal mortality
rate that may be improving with active management (13.4 in
1984 to 8.4 in 2002). The cause of the fetal death is thought to be
anoxia, possibly related to the placental passage of bile salts
causing fetal myocardial dissociation. Randomized control trial
evidence for active management is lacking. The Pregnancy
Intervention Trial in Cholestasis (PITCH) aims to answer the
questions regarding the effect that ursodeoxycholic acid and
early delivery have on pregnancy outcome in cholestasis.
Rhesus disease is worldwide an important cause of fetal loss.
In the UK, Rhesus negative women are administered anti-D
prophylactically during pregnancy, at times of presumed sensi-
tization (uterine evacuation for miscarriage, amniocentesis/CVS,
ante-partum haemorrhage) and after delivery of a rhesus-positive
infant to reduce the risk of future pregnancy loss.
Why are the rates not changing?
Worldwide, as some things improve (for example, availability of
skilled birth attendants to reduce intrapartum deaths), other risk
factors emerge (such as Diabetes and raised maternal BMI). Most
stillbirths in high-income countries are ante-partum events,
frequently associated with placental dysfunction and growth
restriction.
In high-income countries 30e40% of the pregnant population
are now obese at the start of pregnancy and frequently these
women are also in low socio-economic classes, which is in itself
an independent risk factor for stillbirth. Gestational diabetes and
hypertensive disease are also increasing in prevalence and these
are also independent risk factors for stillbirth. Also more women
with co-morbidities like heart disease (acquired and congenital)
or renal disease (e.g. transplants, diabetic nephropathy or auto-
immune disease) are becoming pregnant; these are high-risk
pregnancies with high rates of premature deliveries and associ-
ated poor perinatal outcomes.
The most contentious area is that of screening for FGR which
accounts for at least a quarter of all stillbirths in high-income
countries and potentially more in low-income countries where
maternal nutrition may be inadequate. In the UK, NICE
OBSTETRICS, GYNAECOLOGY AND REPRODUCTIVE MEDICINE 22:5
recommends measurement of the symphysial-fundal height with
a tape measure as a screening tool for fetal size. However,
a Cochrane review does not support this method as being suffi-
ciently good and many authorities argue that ultrasound
assessment is much more sensitive.
Customized growth charts show promise in increasing
sensitivity of community symphysial-fundal height measure-
ments. Rather than using an arbitrary cut-off for defining growth
restriction of the 5th or 3rd percentile for population growth,
customized charts plot fetal weight against percentiles calcu-
lated for that particular woman, taking into account maternal
height, weight, parity and ethnic origin. This is data routinely
collected by community midwives at booking. Producing the
customized chart requires access to complex computer software
(see www.gestation.net) but has the advantage of identifying
a third of the small-for-gestational age population which is not
recognized by conventional population-based centile charts. For
example, this includes babies of large mothers who are not
achieving their growth potential but are missed by conventional
clinical growth assessments. These babies picked up as growth
restricted by customized charts are at the highest risk of
stillbirth, around 10 times the risk of babies deemed small-
for-gestational age according to population centile charts.
Customized charts identify more accurately the babies truly at
risk of mortality and excludes the constitutionally small babies
(i.e. those of short and light mothers) who are traditionally in
the lowest 10% on population centile charts but not at increased
risk of adverse outcome because they are achieving their growth
potential. However, further research is required to establish if
the method maintains its high sensitivity in the obese antenatal
population.
Proponents of ultrasound screening for FGR argue for the
introduction of a routine third trimester ultrasound scan to
complement the dating and anomaly scans which are routinely
offered nationwide. Such a scan would also identify malpre-
sentations, however, there is reluctance for routine introduction
on the grounds of cost until the evidence exists that outcomes are
improved. A pilot of 2000 women in Northern Ireland (2003) has
shown that two ultrasound scans at 30e32 weeks and 36e37
weeks in a low-risk antenatal population improves the detection
of FGR babies. This strategy would enable timely delivery of
babies at risk of ante-partum stillbirth. The study demonstrated
that admissions were not increased. However, there are resource
implications in providing all women with two extra ultrasound
scans during pregnancy and potentially additional maternal
morbidity from increased intervention (rate of intervention was
31.3% in the study group of the pilot versus 16.9% in the control
group). The rate of instrumental delivery was the same in both
groups, however the intervention group had a 1.5% higher
chance of caesarean delivery. A routine third trimester scan may
be worthwhile, but larger studies are needed to identify the best
timing and ensure that the decreased perinatal mortality does not
translate into unacceptably high maternal morbidity.
What can be done to reduce stillbirth rates?
Bhutta et al (Lancet series) identified 10 interventions during
pregnancy and childbirth which could prevent 45% of stillbirths
in 68 countries. The 10 interventions are summarized in Box 1.
132 Ó 2012 Elsevier Ltd. All rights reserved.
 REVIEW

In high-income settings like the UK, most of the 10 points are

Interventions to prevent stillbirth
Pre-pregnancy and basic antenatal care
C periconceptual folic acid supplementation
C prevention of malaria (insecticide-treated bed nets or
intermittent prophylaxis with anti-malaria drugs)
C syphilis detection and treatment
Advanced antenatal care (likely to be unavailable in low-income
and some middle-income settings)
C detection and management of hypertensive disease in
pregnancy (includes hospital care, treatment with magne-
sium sulphate and caesarean delivery if indicated)
C detection and management of diabetes in pregnancy
C detection and management of FGR
C identification and induction of mothers >41/40 gestation
Labour and delivery care
C skilled care at birth and immediate care for neonates
C basic emergency obstetric care
C comprehensive emergency obstetric care
Box 1
already common practice. However, detection of gestational dia-
betes is targeted towards high-risk groups, and some women
deemed to be at low risk may not be discovered until investigations
following the loss of a baby. Effective screening of all women at
high risk of developing diabetes has increased workload dramati-
cally, as maternal BMI at the start of pregnancy is increasing. FGR
remains the highest contributor to antenatal fetal deaths, and at
present cost effective screening has not been identified.
Worldwide, adequate provision of skilled birth attendants and
safe intrapartum care can reduce intrapartum deaths, as illus-
trated in Table 1. Availability of skilled personnel in labour
mirrors lower intrapartum fetal losses and lower numbers of
stillbirths overall. Some interventions (e.g. routine induction of
labour at 41/40) are only practical in health systems with effec-
tive intrapartum fetal and maternal monitoring. In low-income
settings calculation of gestational age may not be accurate, and
induction with poor intrapartum monitoring stands to increase
maternal and fetal morbidity and mortality through uterine
hyperstimulation and even uterine rupture.
Even in high-income countries, women of low education and
those who book late have an increased risk of stillbirth, thus
emphasizing the relationship between lack of social opportuni-
ties and adequate antenatal care and a higher perinatal mortality
rate. Ensuring equity and combating poverty remain important
factors in the fight to reduce perinatal mortality worldwide.

Summary of interventions required to reduce SB rates in different settings throughout the world by 2015 (adapted from
Pattinson et al Lancet series 2011)
>25/1000 births 15e24.9/1000 births 5e14.9/1000 births <5/1000 births

Region/Country South Asia, (India, South-East and East Asia West Asia, Latin America Europe, USA, Canada,
Bangladesh, Pakistan), (Indonesia, Vietnam), (Brazil), Caribbean Singapore
Sub-Saharan Africa North Africa
Number SB 1,120,000 1,010,000 470,000 45,000
Intrapartum SB 563,000 (50%) 509,000 (50%) 110,000 (23%) 7000 (16%)
Skilled birth 50% 65% 98% 100%
attendance rate
Priorities to reduce Ensure availability and Focus on hypertensive IOL for post-term pregnancy Improve professional care
SB rates access to family planning disease Effective screening for fetal Undertake audits
Basic AN care growth restriction
Skilled birth attenders þ Increase detection and
emergency obstetric care þ management of diabetes
clean and safe delivery
environment
Specific interventions Prevent malaria (bednets As previous column þ folic Address lifestyle factors Address lifestyle factors
and intermittent acid supplementation (obesity, smoking cessation,
prophylaxis) reduce alcohol
Prevent mother to child consumption)
transmission of HIV
Healthcare policy Strengthen district health Increase coverage of skilled Improve quality of care & Improve quality of care &
principles facilities care and referral systems ensure equity ensure equity
Build on outreach services Target poorest individuals
Close equity gaps

Table 1

OBSTETRICS, GYNAECOLOGY AND REPRODUCTIVE MEDICINE 22:5 133 Ó 2012 Elsevier Ltd. All rights reserved.
 REVIEW
What do the strategies above mean for the quest to reduce
stillbirth rates in the UK?
 Improving professional care and audit
The National Maternity Service Framework (NMSF)
calls for audit of all stillbirth prevention strategies to
identify future research and action needs. They also call for
improved parent education, through production and
dissemination in the community of information cards
about the 10 most important things to know about still-
birth. Access to bereavement midwives and national
guidelines for optimal care after stillbirth are also likely to
help bereaved parents and ensure cohesive professional
counselling after a fetal loss.
 Improving information available from post-mortem
There is a need for more skilled perinatal pathologists
to ensure the appropriate cause of death is assigned to each
stillbirth and that experienced professionals look for all the
signs of growth restriction. Data from NMSF suggests that
a post-mortem will find useful information regarding the
cause of death in 50e60% of cases, changing the diagnosis
in 10%. As couples realize that a cause for their loss is
likely to be found, and that screening in a future pregnancy
is possible, they also become more likely to accept a post-
mortem investigation.
 Should we routinely introduce a third trimester ultrasound
scan to effectively screen for FGR?
Most stillbirths occur in women deemed to have low-
risk pregnancies at booking. Routinely offered growth
screening strategies identify only 16% of IUGR infants.
Larger multicentre trials are needed to work out the benefit
and optimum timing of a 3rd trimester scan in the quest of
increasing FGR detection without increasing unnecessary
intervention.
 Addressing lifestyle factors
Effective intervention regarding smoking cessation,
weight reduction and optimum age for childbearing are
required. The UK remains one of the high-income coun-
tries with high teenage pregnancy rates and these women
show high rates of stillbirths due to age, low BMI and
social deprivation. The quest for the optimum strategy to
combat this problem continues. Programmes offering
additional support to women deemed to be at high risk of
growth restriction due to social disadvantage have not
been shown to reduce the incidence of low birth weight.
However, smoking cessation programmes have been
shown to be of benefit. Strategies aimed at ensuring that
women enter pregnancy within the optimum weight range
and non-smoking is a priority for high-income countries,
and research should be targeted at identifying the most
useful approaches for this.
Conclusion
A reduction in the incidence of stillbirth remains an achievable goal
across the world and even in high-income countries. In the UK,
OBSTETRICS, GYNAECOLOGY AND REPRODUCTIVE MEDICINE 22:5
efforts to improve the health and wellbeing of women at the start of
pregnancy are likely to yield the best results, but these interven-
tions are difficult. Additional ultrasound examination may be cost
effective but as yet has not been shown to be so and until the
benefits can be shown to outweigh the risks in terms of unneces-
sary intervention this must remain a subject for research. Further
research into the mechanism of fetal death in obesity may also yield
results, as may focus on dietary intervention in pregnancy. A
FURTHER READING
Gardosi J, Kady SM, McGeown P, Francis A, Tonks A. Classification of
stillbirth by relevant condition at death (ReCoDe): population based
cohort study. BMJ 2005; 331: 1113e7.
Flenady V, Koopmans L, Middleton P, et al. Major risk factors for stillbirths
in high-income countries: a systematic review and meta-analysis.
Lancet 2011; 377: 1331e40.
Goldenberg RL, McClure EM, Saleem S, Reddy UM. Infection-related
stillbirths. Lancet 2011; 375: 1482e90.
Pattinson R, Kerber K, Buchmann E, et al. Stillbirths: how can health
systems deliver for mothers and babies? Lancet 2011; 377: 1610e23.
Siddiqui F, Kean L. Intrauterine fetal death. Obstet Gynaecol Reprod Med
2008; 19: 1e6.
Sarris I, Bewley S, Agnihotri S, eds. Training in obstetrics and gynae-
cology e the essential curriculum, 1st edn. Oxford University Press,
2009.
Weiner Z, Beck-Fruchter R, Weiss A, Hujirat Y, Shalev E, Shalev SA.
Thrombophilia and stillbirth: possible connection by intrauterine
growth restriction. BJOG 2004; 111: 780e3.
National Maternity Support Foundation Prevention Agenda 2011.
Cousens S, Blencowe H, Stanton C, et al. National, regional and world-
wide estimates of stillbirth rates in 2009 with trends since 1995:
a systematic analysis. Lancet 2011; 377: 1319e30.
Lawn JE, Blencowe H, Pattinson R, et al. Stillbirths: Where? When? Why?
How to make the data count? Lancet 2011; 377: 1448e63.
CMACE. Saving mothers’ lives: reviewing maternal deaths to make
motherhood safer 2006e2008. Available at: www.rcog.org.uk; 2011.
Practice points
C FGR is an important cause of stillbirth throughout the world
C Effective screening strategies for growth restriction in low-risk
pregnant women have not yet been identified; more stillbirths
occur in the low-risk pregnant population than the high-risk
population
C Infection causes few stillbirths in high-income countries but
a large number in low-income countries; syphilis and malaria
are big contributors
C Maternal obesity is an important association, with the risk of
stillbirth being double in women with BMI >40 compared to
women with BMI <25. The mechanism may involve poorer
detection of FGR in overweight women
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