Causes of Maternal Death

Haemorrhage remains the leading cause of maternal mortality, accounting for approximately one third of
deaths. Sepsis, prolonged or obstructed labour, hypertensive disorders of pregnancy, especially eclampsia,
and complications of unsafe abortion, claim further lives.
The complications leading to a maternal death can occur without warning at any time during pregnancy and
childbirth. And for every woman who dies, approximately 20 more suffer injuries, infection and disabilities.
Most maternal deaths can be prevented if births are attended by skilled health personnel doctors,
nurses and midwives who are regularly supervised, have the proper equipment and supplies, and can refer
women in a timely manner to emergency obstetric care services when complications are diagnosed.
Complications require prompt access to quality obstetric services equipped to provide lifesaving drugs,
antibiotics and transfusions and to perform Caesarean sections and other surgical interventions.

Haemorrhage is the leading cause of maternal death worldwide causes of maternal

death (19972007)

Source: WHO, Systematic Review of Causes of Maternal Death (preliminary data), 2010.

Lifetime risk of maternal death

Lifetime risk is the probability that a woman will die from complications of pregnancy and childbirth over her
lifetime; it takes into account both the maternal mortality ratio and the total fertility rate (probable number
of births per woman during her reproductive years). Thus in a high-fertility setting a woman faces the risk of
maternal death multiple times, and her lifetime risk of death will be higher than in a low-fertility setting. The
lifetime risk of maternal death in the developing world in 2008 as a whole was 1 in 120, compared with
industrialized regions with an estimated 1 in 4300. Among the regions, women in sub-Saharan Africa face
the highest lifetime risk 1 in 31 followed by , South Asia 1 in 110.

Lifetime risk of maternal death remains high in sub-Saharan

Africa

Adult lifetime risk of maternal death, 2008

Source: Trends in Maternal Mortality 1990-2008. WHO, UNICEF, UNFPA and The World Bank.

References
J. Wilmoth, C. Mathers, L. Say and S.Mills Maternal deaths drop by one-third from 1990 to 2008: a
United Nations analysis, Bulletin of the World Health Organization 2010; Article ID: BLT.10.082446
WHO, UNICEF, UNFPA and The World Bank, Trends in Maternal Mortality in 1990-2008, Geneva, 2010
UNICEF, Progress for Children: Achieving the MDGs with Equity, New York, 2010.
UNICEF, Progress for Children: A Report Card on Maternal Mortality, New York, 2008.
Khan, Khalid S. et al. WHO Analysis of Causes of Maternal Deaths: A Systematic Review, The Lancet,
2006 Vol. 367. Issue 9516, pp. 1066-1074.
C. AbouZahr and T. Wardlaw, Maternal mortality at the end of the decade: What signs of progress?
Bulletin of the World Health Organization, 2001 Vol. 79, No. 6, pp. 561-573.
UNICEF, WHO and UNFPA, Guidelines for Monitoring the Availability and Use of Obstetric Services,
New York, 1997.
WHO and UNICEF, The Sisterhood Method for Estimating Maternal Mortality, Guidance notes for
potential users, Geneva 1997.
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What is prolonged pregnancy?

After 41 weeks your pregnancy is considered prolonged (overdue). Approximately 10%

of
all pregnancies are prolonged.

Current evidence on management of prolonged pregnancy

The evidence available suggests that:
there are very small additional risks to the baby after 41 weeks of pregnancy (the
risk
of stillbirth is about 1 in 1,000)
beyond 42 weeks however, the risks are increased further (to about 3 in 1,000)
there is no perfect way to monitor the health of every baby that is overdue
an induction of labour when your pregnancy is prolonged (at 41 weeks gestation)
decreases the chance you will need a Caesarean section.
If your pregnancy is normal, but clearly prolonged, you will be offered an induction of
labour. If you choose not to be induced at this stage, you will be offered increased
fetal
monitoring.

Women wishing to await spontaneous labour

If yourhttp://www.kemh.health.wa.gov.au/brochures/consumers/wnhs0147.pdf

The major causes of maternal mortality are excessive bleeding during childbirth (generally
among home deliveries),(38%) obstructed and prolonged labour,(5%) infection/ sepsis (11%),
unsafe abortion,(8%) disorders related to high blood pressure(5%) and other condition including
anaemia.(34%).Forty seven per cent of maternal deaths in rural India are attributed to excessive
bleeding and anaemia resulting from poor nutritional practices. Intermediate causes, which are
the first and second delays in care-seeking, include the low social status of women, lack of
awareness and knowledge at the household level, inadequate resources to seek care, and poor
access to quality health care. Causes of third delay are untimely diagnosis and treatment, poor
skills and training of care providers, and prolonged waiting time at the facility due to lack of
trained personnel, equipment and blood. There are insufficient facilities for antenatal care and
more than half of all deliveries are still conducted at home, very often by untrained helpers. The
link between pregnancy-related care and maternal mortality is well established
Article Source: http://EzineArticles.com/2459716
Vib Ban Basic Author Joined: June 10, 2009 2 Articles
http://ezinearticles.com/?Maternal-Health-in-India&id=2459716

The leading causes of maternal deaths among the women were obstetric haemorrhage (19.1%), sepsis (18.0%),
prolonged obstructed labour/ruptured uterus (16.9%) and pre-eclampsia/eclampsia (16.9%). The in-depth interviews
corroboObstet Gynaecol. 2005 Aug;25(6):569-74.

Maternal mortality in health institutions with emergency obstetric care facilities

in Enugu State, Nigeria.
Onah HE, Okaro JM, Umeh U, Chigbu CO.

Source
Department of Obstetrics and Gynaecology, University of Nigeria Teaching Hospital, Enugu, Nigeria.
hyacinon@yahoo.com
rated the high maternal mortality ratio recorded and the type 3 delays in tackling obstetric
emergencies
http:/ http://www.ncbi.nlm.nih.gov/pubmed/16234142

Oxytocin-Induced Labor: Effects on Fetal Oxygen Saturation and Heart Rate Patterns

Improved vigilance is warranted during oxytocin-induced uterine hyperstimulation.

In the context of fetal well-being, less is known about assessment of uterine activity than about
fetal heart rate (FHR) monitoring. Researchers conducted a retrospective study in 56 healthy
nulliparous women admitted for elective labor induction to evaluate effects of oxytocin-induced
uterine hyperstimulation in labor on fetal oxygen saturation (FSpO2) and FHR patterns.
Electronic fetal monitoring and FSpO2 sensors were used.
All participants had singleton, vertex presentations with reassuring FHR patterns. Uterine
hyperstimulation was identified based on two definitions: five or more but fewer than six
contractions in 10 minutes (group 1) or six or more contractions in 10 minutes (group 2). The
preceding 30 minutes of normal uterine activity were used as a comparator (group 3).
Differences in FSpO2 and FHR during the 5 minutes before and the last 5 minutes of each 30minute evaluation period were analyzed. Interventions to treat hyperstimulation included
decreasing or discontinuing oxytocin, lateral repositioning, and intravenous bolus administration
of lactated Ringers solution. Hyperstimulation was considered to be resolved when fewer than
five contractions per 10 minutes occurred for at least 20 minutes.
Approximately one hundred 30-minute periods for group 1 and 56 for group 2 were evaluable,
which represented 15% of the total oxytocin-exposure time. Hyperstimulation was identified in
41 patients. FSpO2 was significantly lower at the end than at the beginning of the 30-minute
intervals for both group 1 and group 2, but the absolute decrease in FSpO2 was greater in group 2
than in group 1 (P<0.001). As contraction frequency increased, the effect on FSpO2 became more
pronounced, with progressive oxygen desaturation during the 30 minutes of hyperstimulation.
For groups 1 and 2, compared with group 3, no differences were observed in baseline FHR, but

more periods of absent and minimal FHR variability, fewer accelerations, and more late and
recurrent decelerations occurred. Changes in FHR variability first appeared after 24 and 22
minutes of excessive uterine activity for groups 1 and 2, respectively, but fetal O2 desaturation
occurred within the first 5 minutes and decreased during the entire 30-minute period. Use of all
three interventions resolved hyperstimulation episodes more quickly than did one or two
interventions.
Comment: Finally, uterine hyperstimulation in labor is getting our full attention. Despite this
studys small sample size, its numerous evaluable periods of hyperstimulation support the
conclusion that fetal O2 desaturation begins within the first 5 minutes of excessive uterine
activity and has already progressed before any nonreassuring changes in FHR occur. The authors
propose redefining uterine hyperstimulation as five or more contractions during a 10-minute
period and suggest that the three concurrent interventions are best for rectifying
hyperstimulation. Clearly, oxytocin use in the labor setting requires closer surveillance and more
attention from obstetricians, midwives, and nurses.
Diane J. Angelini, EdD, CNM, FACNM, FAAN, NEA-BC
Published in Journal Watch Women's Health June 19, 2008

Citation(s):
Simpson KR and James DC. Effects of oxytocin-induced uterine hyperstimulation during labor
on fetal oxygen status and fetal heart rate patterns. Am J Obstet Gynecol 2008 Mar 13; [e-pub
ahead of print]. (http://dx.doi.org/10.1016/j.ajog.2007.12.015)

http://womens-health.jwatch.org/cgi/content/full/2008/619/1