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<pre>
 
 
 
 
 
 
 

Maternal, Perinatal and Infant  
Mortality in South Australia 

2003 
Including the South Australian Protocol 

for Investigation of Stillbirths 
 
 
 
 
 
 
 
 
 
 
 

DEPARTMENT OF HEALTH 

June 2005 



ii 

 
 

Eighteenth Report of The Maternal, Perinatal and 
Infant Mortality Committee on maternal, perinatal 
and post-neonatal deaths in 2003 including the South 
Australian Protocol for investigation of Stillbirths 

 

 DEPARTMENT OF HEALTH 
June 2005 

 

 

 

Address 

Pregnancy Outcome Statistics Unit 

Department of Health 

PO Box 6, Rundle Mall, Adelaide 

South Australia  5000 

Australia 

www.dh.sa.gov.au/pehs/pregnancyoutcome.htm 

 

 

 

Telephone 

(08)  8226 6371 or (08)  8226 6357 

Fax  (08) 82266291 

 

 

 

ISSN 1032-4801 

 

 



iii 

 
 
 
 
 
 
 
 
 
 

EIGHTEENTH REPORT OF THE MATERNAL,  
PERINATAL AND INFANT MORTALITY COMMITTEE 

on maternal, perinatal and post-neonatal deaths in 2003  
including the South Australian Protocol for investigation of Stillbirths 

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

DEPARTMENT OF HEALTH 

Adelaide 

June 2005 
 



iv 

Contents 
 

Maternal Perinatal and Infant Mortality Committee vi 

Acknowledgments vii 

Summary viii 

I Introduction  1 

II Maternal, perinatal and infant mortality statistics 2003 3 
1 Maternal mortality 2003 3 
2 Perinatal mortality 2003 5 

(1) Perinatal mortality rates 5 
(2) Birthweight-specific perinatal mortality 9 
(3) Gestation-specific perinatal mortality 10 

3 Post-neonatal and infant mortality 2003 11 

III Causes of death 2003 13 
1 Causes of maternal deaths 2003 13 
2 Causes of perinatal deaths 2003 14 

(1) Classification of perinatal deaths 14 
(2) Aboriginal perinatal deaths 23 
(3) Autopsies in perinatal deaths 24 

3 Causes of post-neonatal deaths 2003 25 

IV Recommendations 30 
1 Maternal Subcommittee recommendations 30 
2 Perinatal Subcommittee recommendations 30 
3 Post-neonatal Subcommittee recommendations 32 

V Education Subcommittee Report 35 

Appendices 
1 Terms of reference, Subcommittees of the Maternal, Perinatal  
 and Infant Mortality Committee  36 
2A Medical certificate of cause of perinatal death  38 
2B Doctor s certificate of cause of death 39 
3 Definitions 41 
4 Perinatal Society of Australia and New Zealand-Perinatal Death  
 Classification (PSANZ-PDC), SA perinatal deaths, 2003 43 
5 Perinatal Society of Australia and New Zealand-Perinatal Death  
 Classification (PSANZ-PDC) by birthweight, SA, 2003  47 
6 Obstetric Cause - specific classification of perinatal deaths,  
 SA, 2003 (Amended Whitfield)  48 
7  Perinatal Society of Australia and New Zealand-Neonatal Death  
 Classification (PSANZ-NDC), SA neonatal deaths, 2003  51 
8 South Australian Protocol for investigation of stillbirths 53 
9 Placental histology guidelines  57 
10 Australian birthweight percentiles for singleton boys  58 
 Australian birthweight percentiles for singleton girls  59 



v 

 Birthweight percentile values (g) for live singleton males,  
 Australia, 1991-1994  60 
 Birthweight percentile values (g) for live singleton females, 
 Australia, 1991-1994  61 
11 Co-sleeping while breastfeeding: advice to health professionals 62 
 Advice to parents on sleeping in the same bed as your baby  62 

Tables 
1 Maternal mortality by category of death, SA, 1961-2003 4 
2 Perinatal mortality, SA, 2003  5 
3 Perinatal mortality rate, Australian states, 1990   2002 6 
4 Perinatal mortality by birthweight, SA, 2003 9 
5 Time of perinatal death by birthweight, SA, 2003 10 
6 Perinatal mortality by gestational age at birth, SA, 2003 10 
7 Post-neonatal death rate, SA, 1971 - 2003 11 
8 Infant mortality rates, Australian states, 1987 - 2002 12 
9 Classification of perinatal deaths, PSANZ-PDC, SA, 2003 15 
10 Amended Whifield Classification of perinatal deaths, SA, 2003 21 
11 Autopsy status of perinatal deaths by place of death, SA, 2003 24 
12 Causes of post-neonatal deaths, SA, 1986   2003 25 

Figures 
1 Maternal mortality ratio, South Australia 1961-2003  4 
2 Perinatal mortality rates, South Australia and Australia 1990-2002 7 
3 Perinatal mortality rate (&gt;= 400g / 20 weeks gestation),  
 South Australia 1983-2003 8 
4 Perinatal mortality rate (&gt;= 1,000g / 28 weeks gestation),  
 South Australia 1983-2003  8 
5 Trends in post-neonatal death rates, South Australia, 1971   2003 13 
6 Trends in infant mortality rates, South Australia and Australia,  
 1979   2002  13 
7 Perinatal deaths in South Australia, 2003, by PSANZ-PDC  16 
8 Causes of perinatal deaths, amended Whitfield Classification, 
 South Australia 2003  22 
9 Age distribution of post-neonatal deaths, South Australia, 2003 26 



vi 

Maternal, Perinatal and Infant Mortality Committee 
Professor Jeffrey Robinson Obstetrician, Chairperson 

Dr Aileen F. Connon Obstetrician, Deputy Chairperson 

Dr Brian Wheatley Obstetrician 

Dr Scott Simmons Obstetric anaesthetist 

Dr Nicola Spurrier Paediatrician 

Dr James Harvey Obstetrician 

Dr Julia Lilley Neonatal paediatrician 

Professor Marc JNC Keirse Obstetrician 

Assoc. Professor T. Yee Khong Pathologist 

Dr George Kokar General practitioner 

Mrs Elizabeth Wood Midwife 

Mrs Jane Warland Midwife 

Dr Annabelle Chan Public health physician, Medical Secretary 

Maternal subcommittee 
Professor Jeffrey Robinson  Obstetrician, Chairperson 

Dr Scott Simmons Obstetric anaesthetist 

Dr William Hague Obstetric physician 

Dr James Harvey Obstetrician 

Assoc. Professor T. Yee Khong Pathologist 

Mrs Elizabeth Wood Midwife 

Dr George Kokar General Practitioner 

Dr Annabelle Chan  Public health physician, Medical Secretary 

Perinatal subcommittee 
Professor Marc JNC Keirse  Obstetrician, Chairperson 

Professor Gustaaf Dekker Obstetrician, Deputy Chairperson 

Dr Elinor Atkinson Obstetrician 

Dr Diana Cox General practitioner 

Assoc. Professor T. Yee Khong Pathologist 

Ms Jackie Kitschke Midwife 

Dr Jill Lipsett 
Dr Brian Peat 

Pathologist 
Obstetrician 

Ms Margaret Hampton Manager, Aboriginal health service 

Mrs Jane Warland Midwife 

Dr Andrew Grieve Paediatrician 



vii 

Dr Scott Simmons  Obstetric anaesthetist 

Dr Scott Morris Neonatal paediatrician 

Dr Geoffrey Matthews Obstetrician 

Dr Annabelle Chan  Public health physician, Medical Secretary 

Post-neonatal subcommittee 
Dr Aileen F. Connon  Obstetrician, Chairperson 

Dr Susan M. Beal  Paediatrician 

Dr Harry Burnell Paediatrician 

Professor Roger Byard Pathologist 

Dr Julia Lilley Neonatal paediatrician 

Dr Nicola Spurrier Paediatrician 

Dr Lynette Moore Pathologist 

Assoc. Professor Victor Nossar Community paediatrician 

Dr Annabelle Chan  Public health physician, Medical Secretary 

Education subcommittee 
Dr Brian Wheatley Obstetrician, Chairperson 

Dr David Morris Obstetrician 

Dr Chris Barnett Neonatal paediatrician 

Mrs Julia Ats Midwife 

Dr Annabelle Chan  Public health physician, Medical Secretary 

 
Committee staff:  Ms Robyn Kennare  Senior midwife/Minute secretary  
 

Acknowledgements 

We gratefully acknowledge the valuable assistance of the following: 
  Medical practitioners who completed confidential reports on maternal, perinatal or 

post-neonatal deaths and submitted autopsy reports; 
  The pathology departments of teaching hospitals for providing autopsy reports; 
  Ms Val Edyvean, Registrar of Births, Deaths and Marriages and staff of the Births, 

Deaths and Marriages Registration Division. 
  Mr Wayne Chivell, State Coroner, and the staff of the Coroner's Office; 
  and Ms Robyn Kennare for preparing the graphs. 



viii 

Summary 

 This is the Eighteenth Annual Report of the Maternal, Perinatal and Infant Mortality 
Committee 
1. There were two maternal deaths in South Australia in 2003.  Both were direct 

maternal deaths resulting from obstetric complications. One was due to amniotic 
fluid embolism and the other was due to the complications of pre-eclampsia. The 
maternal mortality ratio for direct and indirect deaths in the last eight years remains 
low at 9.7 per 100,000 confinements. 

2. The Committee reviewed all 176 perinatal deaths, which included 134 stillbirths and 
42 neonatal deaths occurring among South Australian born babies in 2003.  The 
perinatal mortality rate for all births (of at least 400g or 20 weeks gestation) was 9.9 
per 1,000 births, and the neonatal mortality rate 2.4 per 1,000 live births. The early 
neonatal mortality rate used for international comparisons remained very low at 0.7 
per 1,000 live births.  

3. The leading causes of perinatal death were congenital abnormalities (22%), stillbirths 
of unknown cause (19%), spontaneous preterm labour or rupture of membranes 
(16%), fetal growth restriction (13%) and specific perinatal conditions (12%). Seventy-
eight percent of the perinatal deaths occurred in preterm babies (less than 37 weeks 
gestation). Eleven percent were multiple births.  There were 33 stillbirths of 
unknown cause, a rate of 1.8 per 1,000 births in 2003.  The Committee has prepared a 
protocol for the investigation of stillbirths which has been distributed to all obstetric 
units (Appendix 8). Twenty-two deaths were attributed to fetal growth restriction. 
This has been associated with smoking during pregnancy. Twenty percent of women 
who gave birth in South Australia in 2003 smoked during pregnancy.  

4. There were eight perinatal deaths of babies of Aboriginal mothers, consisting of five stillbirths 
and three neonatal deaths. The perinatal mortality rate of 16.9 per 1,000 births for births to 
Aboriginal mothers in 2003 was lower than in the previous two years but remained much 
higher than the rate of 9.7 per 1,000 for births to non-Aboriginal mothers.  Births to 
Aboriginal mothers continue to be associated with rates of preterm and small-for-gestational-
age births twice as high as among non-Aboriginal mothers. The proportion of low birthweight 
births was three times as high  in 2003. These births are associated with a higher rate of 
smoking during pregnancy of 59% among Aboriginal women compared with 20% among 
non-Aboriginal women.  

5. The Committee also reviewed all 24 post-neonatal deaths among South Australian 
born babies in 2003.  The post-neonatal mortality rate was 1.4 per 1,000 live births. 
The rate of 0.2 per 1,000 live births due to SIDS (Sudden Infant Death Syndrome), as 
in 2002, was the lowest ever recorded in the state. This rate declined dramatically 
following the introduction in 1990 of the educational campaign aimed at reducing 
the prevalence of risk factors for SIDS, including prone sleeping.  In 2003 there were 
only four post-neonatal deaths from SIDS compared with an annual average of 38 in 
1986-1990. The infant mortality rate in 2003 was 3.7 per 1,000 live births. There were 
three post-neonatal deaths of babies of Aboriginal mothers. The 2003 infant mortality rate for 
babies of Aboriginal mothers of 12.8 per 1,000 live births was still substantially higher than 
that for babies of non-Aboriginal mothers (3.5 per 1,000 live births).  



ix 

6. From reviewing maternal and perinatal deaths in 2003, the Committee recommends 

  the importance of caring for pregnant women in a setting which is appropriate 
for the level of risk the pregnancy presents for both mother and baby; 

  the need for review by a physician early in pregnancy of women with current or 
previous serious medical conditions; 

  vigilance to ensure that fetal growth restriction is not missed; 
  that health professionals encourage women not to smoke during pregnancy. 

7. From reviewing these deaths in recent years, the Committee also recommends 

  appropriate training and maintenance of competence in cardiotocograph (CTG) 
interpretation for all levels of medical and midwifery staff; 

  the institution of streamlined arrangements between rural/level I hospitals and 
their regional level II/III maternity service in situations where on-site CTG 
expertise in the rural/level I hospital is insufficient; 

  the development of statewide protocols for level I, II and III maternity services 
with an emphasis on timely recognition and proactive management of common 
obstetric problems such as fetal growth restriction, preterm rupture of 
membranes, meconium-stained liquor, antepartum haemorrhage and pre-
eclampsia. 

  greater use of the recently-revised guidelines for investigating stillbirths, which 
has been sent to all maternity units in South Australia (Appendix 8). 

  the importance of seeking parental permission for autopsy,  which may provide 
information  most valuable in the counselling of parents and in the management 
of future pregnancies; and of sending placentas for histological examination (see 
Appendix 9). The State Perinatal Autopsy Service is available at no cost to the 
parents and may be contacted by telephone on 08-8161-7333. Certain categories 
of death should be reported to the State Coroner (see page 40). 

8. From the review of the post-neonatal deaths in 2003, the Committee recommends the 
following; 

  health professionals providing care in the antenatal or postnatal period should 
ensure that women are provided with information about safe infant sleeping 
practices and prevention of SIDS. Falling asleep with the infant at the breast and 
other forms of co-sleeping or bed sharing may be hazardous.  

  a well-coordinated system of appropriate and ongoing support, supervision and 
referral should be offered to families with known risk factors for adverse child 
outcome, such as those involving substance abuse, psychiatric illness, extreme 
youth of the mother or violence in the household. This should be continued at 
least until the end of infancy,  if not for a longer period of time. 

  professional advice should be sought for infants who are excessively drowsy or 
irritable, who  should be considered seriously ill unless proved otherwise, and 
also for infants who are feeding poorly, as infants can become dehydrated very 
quickly. 



x 

9. In reviewing infant deaths in recent years, the Committee recommends  

  babies should never be left alone in a bath with water, with or without a device 
such as a ring bath seat, even for a minute.  

  ensure the safety of the infant s environment, including the sleeping 
environment.  The latter relates to cots meeting safety standards, co-sleeping 
especially when intoxicated (see Appendix 11), care with the use of blankets, 
pillows and other items in cots which may cause suffocation, and infants 
sleeping unattended in stroller-prams and bouncinettes.  

  vigilance to ensure safe feeding in children under four years of age. Foods that 
can break off into pieces should not be given, as accidental asphyxiation may 
occur. 

  the importance of monitoring growth in children, which can be undertaken using 
the weight percentiles in the child s Personal Health Record (Blue Book), and  of 
investigating why a child is not thriving. 

  the importance of immunisation of children in the prevention of infectious 
disease. 

 
 



1 

I  Introduction 

This is the Eighteenth Annual Report of the South Australian Maternal, Perinatal and 
Infant Mortality Committee. The Committee was established in 1985 under the South 
Australian Health Commission Act. Its terms of reference under Section 15 (formerly 
Section 16) of the Act are as follows: 
To advise the Chief Executive of the South Australian Department of Health on: 
1. The pattern and causation of maternal, perinatal and infant deaths in the state. 
2. The avoidability of any factors associated with such deaths and any measures 

which could be taken to assist with the prevention of such deaths, including 
improvements in health services in the state. 

3. Education and training for members of the medical, midwifery and nursing 
professions and for the community generally in order to assist in the reduction of 
maternal, perinatal and infant morbidity and mortality in the state. 

The terms of reference of the Subcommittees (Maternal, Perinatal, Post-neonatal and 
Education) are provided in Appendix 1.  Under the provisions of the Health 
Commission Act, members of the Committee and its Subcommittees are authorized, 
under strict confidentiality rules, to conduct research into the causes of mortality and 
morbidity in the state, and legal protection is given to notifiers who provide 
information. 
The Subcommittees receive notifications of deaths from the following sources: 
1. The Births, Deaths and Marriages Registration Division, from medical certificates of 

cause of perinatal death (Appendix 2A) and death certificates of children under 1 
year of age and pregnancy-related deaths (Appendix 2B); 

2. The Coroner's Office, from Burial Orders; 
3. Hospitals and medical practitioners, in cases of maternal death. 
New legislation governing the registration of births, deaths and marriages in South 
Australia came into operation on 3 June 1996, and with it a revised form of medical 
certificate of cause of death (Appendix 2B), which identifies pregnancy within three 
months before death and assists in identifying maternal deaths. The new form requires 
identification as to whether the deceased was of Aboriginal or Torres Strait Islander origin. 
Further information is obtained from medical practitioners identified as having been in 
charge of clinical care through the completion of confidential medical reports, and these 
are supplemented by autopsy information from the Coroner's Office and hospital 
pathology services.  Case summaries are prepared by the Committee's senior midwife 
and the medical secretary for discussion by the Subcommittees.  These do not contain 
any identifying information but the members are made aware of the type of health 
services available in each case, eg location (metropolitan or country) and hospital 
category.  Where certain aspects of a case require clarification, a member of the 
Subcommittee may discuss it further with the medical practitioner concerned.  In the 
Post-neonatal Subcommittee a paediatrician acts as the consultant for each case and 
obtains detailed clinical information where necessary.  The discussions aim to identify 
the factors associated with the death, and to assign a cause or causes of death in each 



2 

case.  Comments or recommendations made by the Subcommittees are included in the 
Committee Report. 
Definitions used by the Committee are provided in Appendix 3 of this Report.  The 
Committee receives notifications of maternal, perinatal and post-neonatal deaths 
occurring in South Australia.  However, statistics presented for perinatal and post-
neonatal deaths relate only to those occurring in babies born in South Australia.  Deaths 
of South Australian born babies occurring in other states are also included in the 
statistics where information is available for them.  This Eighteenth Report of the 
Committee incorporates information on maternal, perinatal and post-neonatal deaths in 
South Australia in the year 2003. 
Findings relating to Aboriginal mothers and babies have been italicised for easy identification in 
response to the request of the Aboriginal Health Council of South Australia.  The Aboriginal 
Services Division of the Department of Health has a nominee on the Committee to address areas 
of concern in relation to Aboriginal maternal, perinatal and infant health. 



3 

II Maternal, Perinatal and Infant Mortality Statistics 2003 

1. Maternal mortality 2003 
The World Health Organization (WHO) defines maternal death as the death of a 
woman while pregnant or within 42 days of termination of pregnancy, irrespective of 
the duration and the site of the pregnancy, from any cause related to or aggravated by 
the pregnancy or its management, but not from accidental or incidental causes.  This 
definition includes both direct and indirect maternal deaths (see Appendix 3)*.  In 
Australia, incidental deaths, where the pregnancy is unlikely to have contributed 
significantly to the death, have been included in the past, because of difficulty in 
classification between indirect and incidental deaths.  
The Australian Institute of Health and Welfare National Advisory Committee on 
Maternal Mortality  now complies with international reporting protocols** and reports 
a maternal mortality ratio (see Appendix 3) which only includes pregnancy-related 
deaths, ie direct and indirect maternal deaths per 100,000 confinements. The South 
Australian Maternal, Perinatal and Infant Mortality Committee will continue to review 
incidental deaths to ensure that indirect deaths are not missed. It will, however, report 
only maternal mortality ratios for pregnancy-related deaths to be consistent with 
national and international protocols. At the request of this national committee, 
pregnancy-related deaths of women occurring from 42 days to within a year of the end 
of pregnancy ( late maternal deaths ) are also reviewed, but these are not included in 
the South Australian statistics on maternal deaths or maternal mortality ratios. 
There were two direct maternal deaths in 2003. Maternal deaths in South Australia for 
the three categories of deaths from 1961 to 1995 are presented in Table 1 by 5-year 
periods, and for eight years for the most recent period 1996-2003. Maternal mortality 
ratios have been calculated for direct and indirect deaths  (Table 1 and Figure 1). The 
maternal mortality ratio  for the last 8-year period 1996-2003 remains low at 9.7 deaths 
per 100,000 confinements. While this is higher than the Australian ratio for 1997-1999, 
which was 8.2 deaths per 100,000 confinements, there may have been differences in the 
allocation of deaths between indirect and incidental deaths in the different states, eg in 
deaths attributed to asthma, epilepsy and depression.  
* World Health Organization. International Statistical Classification of Diseases and Related Health Problems.  
   Tenth Revision. Volume 2. Geneva: WHO, 1993. 
 
**Slaytor EK, Sullivan EA, King JF. Maternal Deaths in Australia 1997-1999. Canberra:AIHW,  2004. 
 
Of a total of 36 pregnancy-related maternal deaths in the period 1986-2003, 14 were direct 
deaths and 22 were indirect deaths. Three of the 14 direct deaths and four of the 22 indirect 
deaths were those of Aboriginal women. As Aboriginal women accounted for only 2% of 
confinements in South Australia during this period, this represents a high maternal mortality 
ratio for pregnancy-related deaths among Aboriginal women when compared with non-
Aboriginal. 



4 

 

Table 1: Maternal mortality by category of death, South Australia, 1961   2003 

Years Direct 
deaths

Indirect 
deaths 

Incidental 
deaths

Total 
maternal 

deaths

Direct and indirect 
deaths

 Number Number Number Number Number Maternal 
mortality 

ratio*

1961   1965 34 6 13 53 40 37.8
1966   1970 21 4 8 33 25 23.7
1971   1975 17 1 6 24 18 17.2
1976   1980 6 6 2 14 12 12.9
1981   1985  3 5 3 11 8 8.3
1986   1990 4 8 4 16 12 12.3
1991   1995 4 6 5 15 10 10.2
1996 - 2003 6 8 5 19 14 9.7

* Expressed as deaths per 100,000 confinements 

 

Figure 1: Maternal mortality ratio, South Australia, 
1961 - 2003 

0

10

20

30

40

1961-
65

1966-
70

1971-
75

1976-
80

1981-
85

1986-
90

1991-
95

1996-
03

Years

M
at

er
na

l m
or

ta
lit

y 
ra

tio

Direct and Indirect Deaths per 100,000 confinements

 
 



5 

2.  Perinatal mortality 2003 

(1) Perinatal mortality rates 
In 2003 there were 17,844 births of at least 400g birthweight or 20 weeks gestation 
notified to the South Australian perinatal data collection.  Of these, 134 were stillbirths. 
Of the 17,710 live births, 42 died within 28 days of birth (neonatal deaths).  Table 2 
shows the numbers of stillbirths and neonatal deaths for specified birthweights or 
gestations. 
The perinatal mortality rate for all births in 2003 was 9.9 deaths per 1,000 births. The 
stillbirth rate was 7.5 deaths per 1,000 births and the neonatal mortality rate 2.4 deaths 
per 1,000 live births. Thirty-three of the 176 perinatal deaths (18.8%) were terminations 
of pregnancy. The exclusion of terminations would have resulted in a perinatal 
mortality rate of 8.0 deaths per 1,000 births. Thirty-five perinatal deaths were less than 
400g birthweight. For international comparisons, only births of at least 1,000g 
birthweight are included, and only early neonatal deaths within the first seven days of 
life. This perinatal mortality rate for international comparisons was 3.9 deaths per 1,000 
births and the early neonatal mortality rate was 0.7 deaths per 1,000 live births. 

Table 2: Perinatal mortality, South Australia, 2003 

Specified 
birthweight/ 
gestation 

Total 
births 

Live 
births 

Stillbirths Neonatal deaths Perinatal deaths

   Number Deaths 
per 

1,000 
births

Number Deaths 
per 

1,000 
live 

births 

Number Deaths 
per 

1,000 
births

?400g/20 weeks 17,844 17,710 134 7.5 42 2.4 176 9.9

?500g/22 weeks* 17,786 1,7696 90 5.1 32 1.8 122 6.9

   **26 1.5 **116 6.5

?1,000g/28 
weeks* 

17,679 17,623 56 3.2 17 1.0 73 4.1

   **13 0.7 **69 3.9

  

* For national statistics as recommended by WHO, only fetuses and infants of at least 500g birthweight, or, when  
   birthweight is unavailable, the corresponding gestational age (22 weeks) or body length (25cm crown-heel), are  
   included.   

* For international comparisons, only fetuses and infants of at least 1,000g birthweight, or when birthweight is  
   unavailable, the corresponding gestational age (28 weeks) or body length (35cm crown-heel) are included. 

** This number includes only neonatal deaths occurring within the first 7 days of life, as recommended by WHO for  
    national and international comparisons.  All other numbers for neonatal deaths refer to deaths within the first 28 days  
    of life.  Rates for neonatal deaths are expressed as deaths per 1,000 live births. 

Table 3 shows that the perinatal mortality rate for South Australia over the years has 
generally tended to be lower than the national rate. The rates for South Australia and 
Australia for 1990-2002 from the Australian Bureau of Statistics (ABS) are presented 
graphically in Figure 2. The South Australian rates provided by the ABS may differ 
slightly from those provided by the Committee as the ABS rates are based on deaths 



6 

and births of at least 400g birthweight (or, if birthweight was unavailable, 20 weeks 
gestation) registered (not occurring) in the year and adjusted for state of usual residence 
of the mother.  Statistics provided by the Australian Bureau of Statistics on Aboriginal 
births and perinatal and infant deaths also include births where either parent is 
Aboriginal, whereas the Committee's reports are based on the perinatal data collection 
which categorises births only by mother's ethnicity.   
South Australian perinatal mortality rates, including stillbirth and neonatal mortality 
rates, for 1983-2003 from Committee data are presented in Figure 3 for all births. Rates 
for births of at least 1,000g birthweight (or when birthweight was unavailable, 28 weeks 
gestation,) are presented in Figure 4.  Figure 4 includes only neonatal deaths occurring 
within the first seven days of life (WHO recommendation for international statistics).  
The graphs demonstrate that the fall in the perinatal mortality rate has received a 
greater contribution from the fall in the neonatal mortality rate than from that in the 
stillbirth rate. The stillbirth rate for all births has not decreased over the last two 
decades, although a decrease is evident if only births of at least 1,000g birthweight are 
considered. 

Table 3: Perinatal mortality rate*, Australian states, 1990   2002 

Year NSW VIC Qld SA WA Tas NT ACT AUSTRALIA

1990 11.7 11.6 10.2 11.0 10.4 10.6     18.1 13.8 11.3
1991 11.0 9.8 11.1 9.0 10.3 11.9 18.2 12.5 10.6
1992 11.8 9.4 10.6 9.9 9.8 9.1 19.3 9.4 10.7
1993 9.5 8.5 9.4 8.8 8.3 10.0 21.1 7.7 9.2
1994 9.2 9.3 8.9 8.5 8.3 8.4 16.9 6.9 9.1
1995 8.9 9.2 9.8 9.9 9.3 9.7 16.3 9.2 9.4
1996 11.0 8.8 10.0 8.6 10.2 9.5 12.6 8.8 10.0
1997 9.8 8.5 9.1 8.2 8.1 11.6 15.5 6.6 9.2
1998 8.1 7.7 9.6 7.2 7.5 9.8 13.1 12.2 8.3
1999 8.1 9.2 8.2 6.6 8.3 10.7 16.1 11.7 8.5
2000 7.7 7.9 8.9 8.2 8.4 10.6 14.5 8.3 8.3
2001 7.8 8.7 9.7 8.5 7.9 5.6 12.2 8.3 8.4
2002 7.2 8.3 8.8 8.3 7.1 12.9 10.4 5.6 8.0

 

* Rates are expressed as deaths per 1,000 births for births of at least 400g birthweight (or if birthweight  
  unavailable, 20 weeks gestation), neonatal deaths within the first 28 days of life, based on registered  
  births according to usual residence of mother.  

Source: Australian Bureau of Statistics. 2002 Causes of Death Australia. Catalogue No 3303.0. Canberra: 
2003. 

 

 



7 

 

 

 

 

 

Figure 2: Perinatal mortality rates, South Australia and 
Australia 1990-2002

0

2

4

6

8

10

12

19
90

19
91

19
92

19
93

19
94

19
95

19
96

19
97

19
98

19
99

20
00

20
01

20
02

Year

 

Australia
South Australia

Deaths per 1,000 births (of at least 400g birthweight or 20 weeks 
gestation if birthweight unavailable)

Source: Australian Bureau of Statistics, 2002 Causes Of  Death Australia. 
Cat. No. 3303.0, 2003

 

 
 
 
 
 
 



8 

 

Figure 3: Perinatal mortality rate (&gt;=400g / 20 weeks 
gestation),  South Australia 1983-2003

0
2
4
6
8

10
12
14

19
83

19
85

19
87

19
89

19
91

19
93

19
95

19
97

19
99

20
01

20
03

Year

D
ea

th
s 

pe
r 1

,0
00

 b
irt

hs

Perinatal mortality rate, deaths per 1,000 births
Stillbirth rate, deaths per 1,000 births
Neonatal mortality rate, deaths per 1,000 live births

(Births of at least 400g birthweight or 20 weeks gestation)

 

Figure 4: Perinatal mortality rate (&gt;=1,000g / 28 weeks 
gestation), South Australia 1983-2003

0

1

2

3

4

5

6

7

19
83

19
85

19
87

19
89

19
91

19
93

19
95

19
97

19
99

20
01

20
03

Year

D
ea

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pe
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,0
00

 b
irt

hs

Perinatal mortality rate, deaths per 1,000 births
Stillbirth rate, deaths per 1,000 births
Neonatal mortality rate, deaths per 1,000 live births

(Births of at least 1,000g birthweight or 28 weeks gestation if birthweight is 
unknown, neonatal deaths within the first 7 days of life, as recommended by 
WHO for international comparisons)

 



9 

(2) Birthweight-specific perinatal mortality 
The distribution of stillbirths and neonatal deaths by birthweight, and birthweight-
specific perinatal mortality rates for 2003 are provided in Table 4.  One hundred and 
thirty-four (76.1%) of the 176 perinatal deaths occurred in babies of low birthweight 
(&lt;2,500g) and 138 (78.4%) of the deaths were preterm births. 
One hundred and thirty-four stillbirths accounted for 76.1% of the perinatal deaths in 
2003. There were 47 intrapartum stillbirths, 44 of which were under 750g birthweight 
(Table 5). Twenty-nine of these intrapartum stillbirths were terminations of pregnancy. 
Thirty-three of the 42 neonatal deaths (78.6%) were low birthweight babies and three 
resulted from terminations of pregnancy. 

Table 4: Perinatal mortality by birthweight, South Australia, 2003, (all births of at least 400g or 20 weeks 
gestation) 

Birthweight 
(grams) 

Total 
births 

Live 
births 

Stillbirths Neonatal deaths Perinatal deaths 

   Number Deaths 
per 

1,000 
births

Number Deaths 
per 

1,000 
live 

births

Number Deaths 
per 

1,000 
births

&lt;500* 58 14 44 758.6 10 714.3 54 931.0
500-749** 61** 33 28** 459.0 14 424.2 42** 688.5

750-999 46 40 6 130.4 1 25.0 7 152.2

1,000-1,499 118 108 10 84.7  3 27.8 13 110.2

1,500-1,999 235 230 5 21.3  0 0  5 21.3

2,000-2,499 732 724 8 10.9  5 6.9 13 17.8

2,500-2,999 2,707 2692 15 5.5  4 1.5 19 7.0

3,000-3,499 6,414 6400 14 2.2  1 0.2 15 2.3

3,500-3,999 5,398 5395 3 0.6  3 0.6  6 1.1

4,000-4,499 1,747 1746 1 0.6  0 0  1 0.6

4500+ 328 328 0 0 1 3.0  1 3.0

Total 17,844 17,710 134 7.5 42 2.4 176 9.9

 

* Includes  35 stillbirths or neonatal deaths of &lt;400g birthweight. None of the infants &lt;400g birthweight survived.  
** includes one stillbirth of unknown birthweight at 23 weeks gestation. 



10 

Table 5: Time of perinatal death by birthweight, South Australia, 2003 (births of at least 400g birthweight 
or 20 weeks gestation) 

Birthweight 
(grams) 

Stillbirths Neonatal deaths Total

 Antepartum Intrapartum   

&lt;500 16 28 10 54

500-749* 12 16* 14 42*

750-999 5 1 1 7

1,000-1,499 10 0 3 13

1,500-1,999 5 0 0 5

2,000-2,499 8 0 5 13

2,500-2,999 15 0 4 19

3,000-3,499 13 1 1 15

3,500-3,999 2 1 3 6

4,000-4,499 1 0 0 1

4,500+ 0 0 1 1

Total 87 47 42 176

* Includes one stillbirth of unknown birthweight at 23 weeks gestation. 

 

(3) Gestation-specific perinatal mortality 
The distribution of perinatal deaths by gestational age is provided in Table 6. 

Table 6: Perinatal mortality by gestational age at birth, South Australia, 2003 (births of at least 400g or 20 
weeks gestation) 

Gestational 
age at birth 
(weeks) 

Total 
births 

Live 
births 

Stillbirths Neonatal deaths Perinatal deaths 

   Number Deaths 
per 1,000 

births

Number Deaths per 
1,000 live 

births

Number Deaths 
per 1,000 

births

&lt;24 76 21 55 723.7 18 857.1 73 960.5

24-27 70 54 16 228.6 7 129.6 23 328.6

28-31 163 150 13 79.8  4 26.7 17 104.3

32-36 1,195 1,177 18 15.1  5 4.2 23 19.2

37-41 16,191 16,160 31 1.9 8 0.5 39 2.4

42+ 149 148 1 6.7  0 0 1 6.7

Total 17844 17,710 134 7.5 42 2.4 176 9.9

 



11 

3. Post-neonatal and infant mortality 2003 
There were 24 post-neonatal deaths in South Australian-born babies in 2003. 
The post-neonatal death rate for South Australia for 2003 was 1.4 deaths per 1,000 live 
births. The post-neonatal death rate due to Sudden Infant Death Syndrome (SIDS) 
remained at the lowest level of 0.2 deaths per 1,000 live births.  The post-neonatal death 
rates for South Australia for all years from 1971 to 2003 are presented in Table 7 and 
Figure 5, together with the relative contribution from SIDS. 

Table 7: Post-neonatal death rate, South Australia, 1971   2003 

Year Post-neonatal death rate per 1,000 
live births 

Year Post-neonatal death rate per 
1,000 live births 

 All causes SIDS  All causes SIDS 

1971 4.2 1.4 1988 2.7 1.6 
1972 5.0 1.9 1989 3.6 1.8 
1973 4.5 1.8 1990 3.1 1.6 
1974 4.2 2.1 1991 2.0 1.0 
1975 3.7 1.8 1992 2.1 1.2 
1976 4.4 1.8 1993 1.9 0.7 
1977 3.2 1.3 1994 1.5 0.6 
1978 5.1 2.4 1995 2.4 0.8 
1979 3.6 2.0 1996 1.4 0.6 
1980 3.6 1.6 1997 1.8 0.4 
1981 3.3 1.5 1998 1.5 0.4 
1982 4.3 2.2 1999 2.0 0.3 
1983 3.3 1.4 2000 1.2 0.3 
1984 3.6 2.0 2001 1.4 0.3 
1985 3.8 1.9 2002 1.5 0.2 
1986 3.3 2.1 2003 1.4 0.2 
1987 3.8 2.5    

 
The infant mortality rate for South Australia for 2003 was 3.7 deaths per 1,000 live 
births, the lowest recorded in the state. This includes all deaths of infants under 1 year 
of age ie both the 42 neonatal deaths and the 24 post-neonatal deaths  (Appendix 3).  
The infant mortality rate for babies of Aboriginal mothers (with three post-neonatal deaths and 
three neonatal deaths out of 468 live births) was 12.8 deaths per 1,000 live births, which is  
considerably higher than the infant mortality rate of 3.5 deaths per 1,000 live births for babies of 
non-Aboriginal mothers.  Infant mortality rates for all Australian states for 1987-2002 from 
the Australian Bureau of Statistics  are presented in Table 8: the rates for 2003 are not 
yet available.  Rates for South Australia compared with Australia for 1979-2002 (Figure 
6) demonstrate that the South Australian infant mortality rate has generally been lower 
than the national rate. The differences in our Committee s rate and that of the ABS lie in 
the ABS including only registered births and deaths in any year of at least 400g 



12 

birthweight ( or 20 weeks gestation if birthweight unavailable) and adjusting for state of 
usual residence. 

Table 8: Infant mortality rates (per 1,000 live births), Australian states, 1987   2002 

Year NSW Vic Qld SA WA Tas NT ACT Australia

1987 8.5 8.1 9.3 8.6 8.4 10.0 15.6 9.0 8.7
1988 9.2 7.8 8.4 7.9 8.5 9.6 19.2 8.1 8.7
1989 8.7 6.5 8.5 7.4 7.8 10.6 14.5 6.5 8.0
1990 8.1 7.8 7.7 8.5 8.6 8.9 15.2 9.4 8.2
1991 7.2 6.5 7.6 5.5 7.2 9.0 14.2 7.6 7.1
1992 7.4 5.6 7.9 6.1 7.0 6.6 15.5 6.3 7.0
1993 6.2 5.4 7.0 5.2 5.9 5.9 15.3 4.3 6.1
1994 6.3 5.1 6.2 4.7 5.6 7.5 11.3 4.7 5.9
1995 5.7 4.9 6.3 5.8 5.1 5.8 13.3 4.8 5.7
1996 5.8 5.0 6.4 4.9 6.5 4.5 11.5 5.7 5.8
1997 5.2 4.9 5.8 4.7 5.3 6.5 12.5 3.8 5.3
1998 4.3 4.7 6.4 4.0 5.0 5.7 12.4 6.0 5.0
1999 5.8 5.6 5.7 4.3 4.7 7.6 11.7 5.6 5.7
2000 5.2 4.5 6.2 4.6 4.3 5.8 11.7 4.2 5.2
2001 5.3 4.8 5.9 4.6 5.1 6.2 10.7 3.0 5.3
2002 4.6 5.0 5.8 5.1 4.3 6.2 11.3 3.4 5.0

 

Source:  Australian Bureau of Statistics. Deaths Australia 2002. Catalogue No 3302.0.Canberra: ABS 2003 



13 

 
 

Figure 5: Trends in post-neonatal death rates, South 
Australia, 1971-2003

0

1

2

3

4

5

6

19
71

19
74

19
77

19
80

19
83

19
86

19
89

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92

19
95

19
98

20
01

Year

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All causes
SIDS

 
 

 

Figure 6: Trends in infant mortality rates, South 
Australia and Australia, 1979 - 2002

0

2

4

6

8

10

12

19
79

19
81

19
83

19
85

19
87

19
89

19
91

19
93

19
95

19
97

19
99

20
01

Year

D
ea

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pe
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00

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hs

Australia
South Australia

Source: Australian Bureau of Statistics. Deaths Australia 2002. 
Catalogue No. 3302.0. 2003

 
 



14 

III Causes of death 2003 

1. Causes of maternal deaths 2003 
There were two maternal deaths in South Australia in 2003. The first mother was 
multiparous and in her thirties. She had labour induced a few days after term as she 
had musculoskeletal discomfort late in pregnancy. Induction was performed with 
prostaglandin gel followed by artificial rupture of membranes.  As labour was not 
established, a Syntocinon infusion was commenced. This was followed by the 
development of regular painful contractions and an epidural was inserted. Shortly after, 
the mother felt unwell and a cardiotocograph (CTG) showed decelerations. Syntocinon 
was ceased, but as fetal bradycardia persisted, a caesarean section was performed and a 
stillborn baby delivered. At surgery there was considerable uterine bleeding: the uterus 
was noted to be atonic and the blood did not clot. Amniotic fluid embolism was 
suspected. Attempts to stop the bleeding using a Syntocinon infusion, prostaglandin 
and Ergometrine injections and a Sengstaken-Blakemore tube were unsuccessful. Blood 
taken showed a profound coagulation disturbance. Several packed cell, fresh frozen 
plasma and platelet transfusions as well as volume expanders were given before and 
after transfer to intensive care at a Level III hospital, but all efforts at resuscitation were 
unsuccessful. Autopsy showed extensive haemorrhage at many sites and histological 
evidence of amniotic fluid embolism in the lungs and uterus. This was a direct maternal 
death from amniotic fluid embolism (ICD-10-AM code O88.1). 
The second woman, a primigravida in her twenties, developed a transient increase in 
her blood pressure at 30 weeks gestation. Her blood pressure was noted to be elevated 
again at 34 weeks and she was admitted into a private hospital and transferred to a 
Level III hospital the following day. Ultrasound showed fetal growth to be at the lower 
limits of normal. A few days later, she developed epigastric pain, increasing 
hypertension and evidence of haemolysis.  Severe pre-eclampsia was diagnosed. An 
emergency caesarean section was performed and a live infant delivered and later 
discharged home well. The mother developed severe thrombocytopenia and 
neurological symptoms within 24 hours of giving birth. A CT scan showed widespread 
mid-brain haemorrhage with raised intracranial pressure. She was transferred to an 
intensive care unit. She did not improve and died 17 days after giving birth. Autopsy 
showed large bilateral pulmonary thrombo-emboli and intracranial haemorrhages. This 
was a direct maternal death from intracranial haemorrhage and pulmonary thrombo-
embolism complicating pre-eclampsia (ICD-10-AM code O14.1). 
A maternal death in 2002 has also been reviewed by the Maternal Subcommittee. This 
mother, in her thirties, had a past history of caesarean sections and chemotherapy and 
radiotherapy for Hodgkin s lymphoma. She was receiving treatment with cholesterol 
lowering agents. When she was first seen early in pregnancy, she was well, with the 
lymphoma apparently in remission. She developed slight shortness of breath late in 
pregnancy and was found to be hypertensive when she attended her obstetrician two 
days later at 36 weeks gestation. She was admitted to hospital and as the blood pressure 
rose much higher the following day, a caesarean section was performed, with delivery 
of a healthy livebirth.  A Hydralazine infusion was used to control her blood pressure 
after delivery but she continued to have very mild shortness of breath on effort. Two 
days later, her blood pressure rose again and a Hydralazine infusion was 



15 

recommenced. However, her breathlessness became severe and she lost consciousness. 
All attempts at resuscitation were unsuccessful. Autopsy showed cardiac hypertrophy, 
coronary artery stenosis and calcification, acute myocardial infarction, pulmonary and 
cerebral oedema. The uterine vessels showed acute atherosis and thromboses. This 
maternal death was attributed to pre-eclampsia (ICD-10AM code O14.1), with 
myocardial infarction as the terminal event. Contributing factors were radiotherapy and 
chemotherapy for Hodgkin s lymphoma, coronary artery disease and hyperlipidaemia. 

2.  Causes of perinatal deaths 2003 

(1) Classification of perinatal deaths 
The Perinatal Subcommittee classified each of the 176 perinatal deaths which occurred 
in 2003 according to the Perinatal Society of Australia and New Zealand   Perinatal 
Death Classification (PSANZ-PDC). This classification, together with the Australian 
birthweight/gestation percentile charts (for singletons as well as twins), is available on 
the PSANZ website http://www.psanz.org.au (and access through the PSANZ Home 
Page) and will be regularly updated by the PSANZ Perinatal Mortality Special Interest 
Group.  
The classification of perinatal deaths in 2003 according to PSANZ-PDC is as follows 
(Table 9): 

Table 9: Classification of perinatal deaths, PSANZ-PDC, South Australia, 2003 

 PSANZ-PDC  Number Percent Deaths per 1,000 
births

1. Congenital abnormality 39 22.2 2.2
2. Perinatal infection 8 4.5 0.4
3. Hypertension 4 2.3 0.2
4. Antepartum haemorrhage (APH) 9 5.1 0.5
5. Maternal conditions 5 2.8 0.3
6. Specific perinatal conditions 21 11.9 1.2
7. Hypoxic peripartum death 7 4.0 0.4
8. Fetal growth restriction 22 12.5 1.2
9. Spontaneous preterm 28 15.9 1.6

10. Unexplained antepartum death 33 18.8 1.8
11. No obstetric antecedent 0 0 0

 Total 176 100.0 9.9
 

The PSANZ-PDC for perinatal deaths in 2003 is shown graphically in Figure 7 and its 
breakdown by subgroups and birthweight groups is provided in Appendix 4 and 
Appendix 5.  



16 

Figure 7: Perinatal deaths in South Australia, 2003, by 
PSANZ-PDC  (n = 176)

Congenital 
abnormality 

(22.2%)

Specific perinatal 
conditions 
(11.9%)Hypoxic 

peripartum death 
(4.0%)

Fetal growth 
restriction 
(12.5%)

Spontaneous 
preterm (15.9%)

Unexplained 
antepartum death 

(18.8%)

Perinatal 
infection (4.5%)

Hypertension 
(2.3%)

Maternal 
conditions (2.8%)

Antepartum 
haemorrhage 

(5.1%)

 
A brief description of each of the 11 groups follows. 

1. Congenital abnormality   39 deaths 
This group of 39 deaths includes terminations of pregnancy at 20 weeks gestation or 
greater for fetuses with congenital abnormalities. It accounted for the largest proportion 
(22.2%) of perinatal deaths. The types of abnormalities were as follows, with the 
numbers of terminations of pregnancy also shown in parentheses: 

  

Central nervous system 6 (6)

Cardiovascular 6 (3)

Urinary tract 5 (5)

Chromosomal 8 (7)

Multiple 7 (6)

Other 7 (3)

  
Of the six infants with central nervous system abnormalities, four had neural tube 
defects. The fifth fetus had abnormalities of the cerebrum and the sixth had 
hydrocephalus associated with serous effusions in the pericardial and pleural cavities 
and abdomen. 
The six infants with cardiovascular abnormalities had the following: 

  A mass almost completely filling the left ventricle, detected in one fetus of a twin 
pregnancy on prenatal ultrasound at 18 weeks gestation. Fetal death occurred in 
this twin at 25 weeks gestation. 



17 

  Aortic atresia, tricuspid and mitral incompetence and abnormal myocardium. 
This infant became breathless and cyanosed shortly after birth and died at one 
day of age. 

  Pulmonary valve atresia, dilated tricuspid valve and right atrium; 
  Pulmonary valve atresia, hypoplasia of tricuspid valve and right ventricle;  
  Hypoplastic left heart syndrome.  
  Congenital cardiomyopathy (non-compaction of the myocardium) with hydrops. 

Five babies had the following urinary tract abnormalities: 

  Bladder exstrophy with epispadias. 
  Bilateral renal agenesis (two babies). 
  Bladder outlet obstruction, with a  grossly dilated bladder and bilateral 

hydronephrosis (two babies). This was attributed to posterior urethral valves in 
one baby who had also developed cystic dysplastic kidneys and pulmonary 
hypoplasia, and to urethral atresia in the other. 

The eight babies with chromosomal abnormalities had the following: 

  Down s syndrome (three babies);  
  Trisomy 13.  
  Turner s syndrome with fetal hydrops. 
  A chromosomal deletion, associated with severe cleft lip and palate; 
  Mosaic trisomy 16 associated with multiple defects. 
  An additional marker chromosome. 

There were seven babies with multiple congenital abnormalities, as follows: 

  Vascular steal phenomenon, with exomphalos, persistent vitelline artery, anal 
atresia and genital abnormalities. 

  Amniotic band syndrome with cleft lip and palate, limb reduction defects and an 
abdominal wall defect. 

  VATER association with bilateral renal agenesis, genital abnormalities, 
malrotation of the intestines, rectal and anal atresia and vertebral abnormalities.  

  Hydrocephalus, cerebral anomalies, bilateral anophthalmia and cleft lip and 
palate. 

  Polydactyly, polycystic kidney disease and pulmonary hypoplasia. 
  Hydrocephalus, pulmonary lobation and vertebral anomalies. 
  Cystic hygroma, exomphalos, cleft soft palate, renal, cardiovascular and 

intestinal abnormalities. 
Of the seven deaths with  other  fetal abnormalities, three had musculoskeletal 
abnormalities: one baby had exomphalos and two had thanatophoric dysplasia (one 
Type I and one Type II). 



18 

One infant with respiratory abnormalities presented with cyanosis at birth and died at 
one day of age. Autopsy findings were consistent with a rare disorder, pulmonary 
alveolar capillary dysplasia. 
Three other infants had diaphragmatic hernia with severe pulmonary hypoplasia. One 
infant had a repair performed but died of chronic lung disease, pulmonary 
haemorrhage, pneumonia and septicaemia. 

2. Perinatal infection   eight deaths 
This group included one neonatal death due to infection with Group B Streptococcus. 
This mother was treated for signs of infection at 23 weeks gestation. Amniocentesis 
yielded turbid fluid, and labour was induced. The infant was in poor condition at birth 
and died shortly after. The placenta showed acute chorioamnionitis and funisitis and a 
heavy growth of Group B Streptococcus was obtained from the high vaginal swab. 
There were two deaths from E coli sepsis. One mother had recurrent bleeding from 14 
weeks and had an amniocentesis performed for increased risk of Down s syndrome. 
Two days later she presented with abdominal pain and signs of infection, for which she 
was treated. However, labour with spontaneous rupture of membranes followed two 
days later. The placenta showed acute severe chorioamnionitis and yielded a heavy 
growth of E coli. A second mother presented with a history of reduced fetal movements 
at 37 weeks and intrauterine fetal death was confirmed. The placenta showed 
chorioamnionitis and fetal vascular thrombosis and E coli was cultured from both fetal 
blood and the placenta. 
One death was attributed to perinatal infection with Enterococcus. Another mother 
from overseas had an ultrasound scan at 21 weeks which showed asymmetrical 
dilatation of the lateral cerebral ventricles. Serial serology showed toxoplasma IgM, 
consistent with current infection. Severe hydrocephalus, hepatosplenomegaly and 
general hydrops developed and labour occurred spontaneously at 29 weeks. The infant 
was stillborn and autopsy confirmed infection with Toxoplasma gondii. The bacteria 
were not identified in three other deaths from infection which occurred at 23-24 weeks 
gestation. One of these was associated with maternal smoking, marijuana use and a 
urinary tract infection.  

3. Hypertension   four deaths 
One death was associated with essential hypertension, with fetal death in utero 
occurring at 30 weeks. The placenta was very small and showed multiple infarcts and 
fetal stem vessel vasculopathy. Two deaths were associated with pre-eclampsia and 
APH, with placental abruption confirmed in one case. In the fourth case, fulminant pre-
eclampsia was superimposed on essential hypertension and complicated by abruption, 
disseminated intravascular coagulation and postpartum haemorrhage. 

4. Antepartum haemorrhage   nine deaths 
There were seven deaths from placental abruption, one from APH from placenta 
praevia  and one from APH of undetermined origin, in a pregnancy complicated by 
gestational diabetes.  



19 

5. Maternal conditions - five deaths 
Of the five deaths from maternal causes, three were attributed to diabetes mellitus. One 
mother had poorly controlled insulin-dependent diabetes and experienced an 
intrauterine fetal death at 36 weeks gestation. The second mother with insulin-
dependent diabetes experienced fetal death of a macrosomic baby at 37 weeks 
gestation. Both placentas were small. A third mother had non-insulin-dependent 
diabetes and suffered a fetal loss at 23 weeks. The placenta showed chronic decidualitis.  
Another mother sustained lap/sash seat belt  trauma across the lower abdomen and 
placental abruption following a high speed motor vehicle accident. Fetal death was 
confirmed by ultrasound. The mother developed disseminated intravascular 
coagulation.  
The mother of the fifth infant in this group died of amniotic fluid embolism. Labour 
was induced at term but decelerations occurred with poor recovery when Syntocinon 
was introduced and were followed by fetal bradycardia and maternal deterioration. A 
caesarean section was performed but the fetus was stillborn. The mother developed 
disseminated intravascular coagulation and severe postpartum haemorrhage.  

6.  Specific perinatal conditions   21 deaths 
These deaths consisted of the following: 

  Twin-twin transfusion   six deaths from four twin pregnancies. There were two 
pregnancies in which both twins died. Fetal deaths occurred spontaneously at 30 
weeks in one twin pregnancy and the other twin pregnancy was terminated after 
a poor response to amnioreductions. Twin-twin transfusion was detected at 19 
weeks gestation in a third twin pregnancy and multiple amnioreductions and 
Doppler studies were performed. At 26 weeks, caesarean section was performed 
as one twin had died in utero and the other twin showed signs of fetal distress 
(this baby later died in the post-neonatal period). The stillborn twin was growth 
restricted and showed cerebral vascular occlusion resulting in cerebral atrophy. 
In the fourth twin pregnancy, twin-twin transfusion was treated by 
amnioreductions, but one twin died spontaneously at 24 weeks gestation. 

  Fetomaternal haemorrhage   three deaths.  In maternal blood, at least 1.5% of red 
blood cells were of fetal origin on Kleihauer testing. All three intrauterine fetal 
deaths occurred at 37-39 weeks gestation.  

  Antepartum cord complications   three deaths. One death occurred in a twin at 
22 weeks. Autopsy showed a velamentous insertion of the cord into the dividing 
membrane, which may be associated with unequal placental parenchymal 
sharing, uncompensated anastomoses and prenatal demise. A second fetus died 
spontaneously at about 37 weeks gestation. Autopsy showed a tight true knot in 
the cord, marked congestion between the knot and the fetus and relative pallor 
of the cord distal to the knot, suggesting a significant obstruction of blood flow. 
In the third spontaneous fetal death, which occurred at 31 weeks gestation, the 
cord was found to be excessively coiled and thrombi were found within the 
umbilical vein, chorionic plate vessels and fetal vessels of stem villi. The fetus 
also had a congenital dyshormogenetic goitre.  



20 

  Uterine abnormalities   four deaths, all of which were associated with cervical 
incompetence. One mother also had a bicornuate uterus. Three of these mothers 
had previous histories of miscarriage or preterm births and went into labour at 
20-23 weeks gestation. Acute chorioamnionitis was associated with two of these 
deaths. 

  Idiopathic hydrops   four deaths. One death was associated with congenital 
hydrothorax and bilateral pulmonary hypoplasia, and another with 
polyhydramnios, pre-eclampsia and placental abruption. 

  Other specific perinatal conditions   one death. This mother presented with an 
intrauterine fetal death at 37 weeks gestation. Autopsy showed bilateral renal 
vein thrombosis with calcification and ischaemic necrosis of sphlanchnic bed 
organs. The mother was heterozygous for the factor V Leiden mutation. 

7. Hypoxic peripartum death   seven deaths 

  One death was associated with uterine rupture during labour in a woman with a 
previous caesarean section. 

  Another was associated with macrosomia and shoulder dystocia. The glucose 
tolerance test yielded a normal result. There was some difficulty in delivery of 
the shoulders and the liquor was meconium-stained. The infant was in poor 
condition at birth and could not be resuscitated. 

  There were no apparent complications in four other deaths.  Two intrapartum 
deaths occurred among 88 planned home births, 28 of which were born in 
hospitals. The Committee is concerned about this and will keep reviewing the 
perinatal mortality rates in different settings. In one of these babies, the placenta 
showed extensive chronic villitis and acute chorioamnionitis and there was a 
possibility of postmaturity. The third pregnancy in this group was complicated 
by essential hypertension and gestational diabetes. Fetal growth restriction was 
suspected at one stage but growth measurements improved. Fetal bradycardia 
was detected at a routine visit at 36 weeks gestation. The baby was in poor 
condition when delivered by emergency caesarean section. There was fetal 
thrombotic vasculopathy on placental histology. In the fourth death in this 
group, CTG showed variable decelerations during labour. The infant was 
severely acidotic and developed multi-organ failure. Autopsy showed evidence 
of disseminated intravascular coagulation. 

  In one death, spontaneous preterm labour commenced at 25 weeks gestation but 
there was no descent of the presenting part after full dilatation while there was 
evidence of non-reassuring fetal status. Despite an emergency caesarean section, 
the infant showed signs of hypoxic ischaemic encephalopathy and suffered a 
severe cerebral haemorrhage. 

8. Fetal growth restriction   22 deaths 
In 13 deaths in this group, there was evidence of uteroplacental insufficiency; in six 
there was no evidence of this or of chronic villitis and in the remaining three there was 
no placental examination. 



21 

9. Spontaneous preterm (&lt;37 weeks gestation)   28 deaths 
In 17 deaths the membranes were ruptured for less than 24 hours: in seven of these 
there was histological evidence of chorioamnionitis; in five there was no 
chorioamnionitis and in the remaining five the placenta was not examined. 
In ten deaths, the membranes had been ruptured for at least 24 hours and six showed 
evidence of chorioamnionitis; there was no chorioamnionitis in three placentas and one 
placenta was not examined. In one of these deaths, spontaneous preterm prelabour 
rupture of membranes occurred at 16 weeks resulting in severe oligohydramnios, for 
which labour was induced at 20 weeks. 
In one death, in which the duration of membrane rupture was unknown, there was 
evidence of chorioamnionitis.  

10. Unexplained antepartum death   33 deaths 
In 10 deaths there was evidence of uteroplacental insufficiency; in one there was 
chronic villitis; in 19 there was no evidence of uteroplacental insufficiency or chronic 
villitis, and the placenta was not examined in three cases. 

11. No obstetric antecedent 
There were no deaths in this group. 

Whitfield Classification of perinatal deaths 
The classification of the 176 perinatal deaths into the 12 groups of the amended 
Whitfield Classification is presented in Table 10 and Figure 8.  Subgroups of the 
classification are also included in Appendix 6. 

Table 10: Amended Whitfield Classification of perinatal deaths, South Australia, 2003 

 Amended Whitfield Classification Number of 
deaths

% Deaths per 1,000 
births

1. Spontaneous preterm 32 18.2 1.8
2. Intrauterine growth restriction (IUGR) 22 12.5 1.2
3. Unexplained intrauterine death 33 18.8 1.8
4. Birth trauma 0 0 0
5. Intrapartum asphyxia 7 4.0 0.4
6. Hypertension 4 2.3 0.2
7. Maternal disease 5 2.8 0.3
8. Antepartum haemorrhage (APH) 9 5.1 0.5
9. Fetal abnormality 39 22.2 2.2

10. Haemolytic disease 0 0 0
11. Infection 8 4.5 0.4
12. Other 17 9.7 1.0
 Total 176 100.0 9.9

 



22 

Figure 8: Causes of perinatal deaths, amended Whitfield 
Classification, South Australia 2003

Spontaneous pre-term 
18%

IUGR 
12%

Intrapartum asphyxia 
4%

Hypertension 
2%

Maternal disease 
3%

Fetal abnormality 
22%

Infection 
5%

Other 
10%

APH 
5%

Unexplained 
intrauterine death 

19%

 

Perinatal Society of Australia and New Zealand   Neonatal Death Classification 
The classification of the 42 neonatal deaths according to the Perinatal Society of 
Australia and New Zealand   Neonatal Death Classification (PSANZ-NDC), formerly 
called the Australia and New Zealand Neonatal Death Classification (ANZNDC) is 
provided in Appendix 7. This classification is also available, together with PSANZ-
PDC, on the PSANZ website.  

Perinatal deaths of babies born interstate in 2003 
There was one neonatal death in South Australia of a baby born at an interstate hospital 
in 2003. This mother was an itinerant worker and was first seen at an interstate hospital 
at 32 weeks gestation. There was a reported episode of hypertension. She presented 
again at 39 weeks in early labour. Apparently there was  evidence of non-reassuring 
fetal status during augmentation of labour with Syntocinon. The infant was in very 
poor condition at birth and after initial resuscitation was transferred to an Adelaide 
level III hospital but died at one day of age. 



23 

(2) Aboriginal perinatal deaths 
There were eight perinatal deaths (five stillbirths and three neonatal deaths) among the 473 
notified births to Aboriginal mothers.  Five of the babies who died were born in teaching 
hospitals and the remainder in country hospitals. Five were preterm and six were low 
birthweight. The causes of the eight deaths were as follows: 
(1) Congenital abnormality   one neonatal death. The mother of this baby lived in an 

interstate country town and was referred to Adelaide when an ultrasound morphology 
scan at 18 weeks suggested the presence of multiple congenital abnormalities. These 
abnormalities were confirmed. The family wished to continue the pregnancy. The mother 
was admitted at 34 weeks. Spontaneous rupture of membranes occurred with labour 
following and the baby died shortly after birth. 

(2) Antepartum haemorrhage   one term stillbirth. This mother smoked and suffered from 
depression and anaemia. She presented at 37 weeks gestation with loss of fetal movements. 
Multiple clots were passed vaginally. Ultrasound confirmed fetal death in utero, which 
was attributed to placental abruption. 

(3) Hypoxic peripartum death   one term neonatal death. This mother had a previous 
caesarean section. She attended antenatal care regularly but was a very heavy smoker. She 
was admitted at 38 weeks in labour. There were no apparent complications but when the 
membranes ruptured, the liquor was meconium-stained and severe decelerations developed. 
At emergency caesarean section a large uterine rupture was noted and abdominal  
hysterectomy was performed. The infant had severe metabolic acidosis and was retrieved to 
a level III hospital from the country. It had signs of hypoxic ischaemic encephalopathy 
including seizures and died of aspiration pneumonia.  

(4) Fetal growth restriction   one term stillbirth. This mother smoked, used substances during 
pregnancy and was anaemic. She attended only two antenatal visits and presented at 37 
weeks with no fetal movements. Fetal death in utero was confirmed. Autopsy showed fetal 
growth restriction and chorioamnionitis. 

(5) Spontaneous preterm   two stillbirths and one neonatal death. In one pregnancy, which 
resulted in a stillbirth, preterm prelabour rupture of membranes occurred at 16 weeks 
gestation. An ultrasound scan at 20 weeks showed severe oligohydramnios and labour was 
induced.  No significant placental pathology was found. In the second pregnancy resulting 
in stillbirth there were many adverse social factors including domestic violence and alcohol 
abuse. The mother was itinerant and had a urinary tract infection early in the pregnancy. 
She developed lower abdominal pain at 20 weeks and fetal death was found to have 
occurred. The membranes ruptured spontaneously shortly after admission. This mother 
also had a postpartum haemorrhage. The third mother was a teenager and a smoker with a 
history of self-harming behaviours and many adverse social factors. She presented at 24 
weeks with ruptured membranes, in the second stage of labour. An emergency caesarean 
section was performed, presumably for breech presentation. The infant was resuscitated 
with difficulty and died at nine days of age of the complications of prematurity.   

(6) Unexplained stillbirth   one stillbirth. This mother made only two antenatal visits during 
pregnancy and had some vaginal bleeding during early pregnancy. The pregnancy was 
also complicated by gestational diabetes. She presented at 28 weeks with reduced fetal 
movements and intrauterine fetal death was confirmed. Autopsy did not reveal a cause of 
death. 

In 2003, the perinatal mortality rate for births to Aboriginal mothers was 16.9 per 1,000 births 
compared with 9.7 per 1,000 births for non-Aboriginal mothers. The perinatal mortality rate for 



24 

births to Aboriginal mothers was higher in the country compared to the metropolitan area  (20.7 
v 9.3 per 1,000 births). 
The Subcommittee notes, with concern, the high proportion of Aboriginal women who smoke 
during pregnancy. In 2003, this proportion (59.1%) was higher than in the previous year. This 
increase contrasts with the decreasing rate (19.8% in 2003) among non-Aboriginal women.  
The proportions of preterm births and small-for-gestational-age births remain considerably 
higher than for non-Aboriginal births in 2003 - 17.8% v 8.0% and 19.6% v 8.7%, respectively. 
As a result, the proportion of low birthweight births remains considerably higher than among 
non-Aboriginal births - 18.0% v 6.5%.   
The Committee acknowledges that community development projects are being undertaken in the 
State to improve the health, education and wellbeing of Aboriginal communities with a focus on 
improving nutrition and reducing tobacco use. Other initiatives are aimed at reducing alcohol 
intake and improving attendance for antenatal care, breastfeeding and health education in 
relation to maternal and child health. 

 (3) Autopsies in perinatal deaths 
Autopsies were performed in 60.2% of perinatal deaths, and the distribution by place of 
death is presented in Table 11. 

Table 11: Autopsy status of perinatal deaths by place of death, South Australia, 2003 

Place of death Deaths Autopsies performed 

                                                         Number Number Percent of deaths

Metropolitan Level III* hospitals (teaching) 121 75 62.0

Other metropolitan teaching hospitals 22 12 54.5

Metropolitan private hospitals with 500+ births 
per annum 

11 4 36.4

Metropolitan private hospitals with &lt;500 births 
per annum 

1 1 100.0

Country hospitals with 400+ births per annum 3 2 66.7

Country hospitals with &lt;400 births per annum 15 10 66.7

Home 3 2 66.7

Total 176 106 60.2

*  Levels as defined in  Operational Policy, Guidelines and Standards for Maternal and Neonatal  
    Services in South Australia. Adelaide: Department of Human Services, January 2000 . 

A good quality autopsy is invaluable in confirming antenatal diagnoses, eliciting other 
findings of clinical significance, particularly significant negative ones, and determining 
the time course of events leading to death.  It may thus be invaluable in alleviating 
parental guilt, helping with the grieving process and parental counselling, and gaining 
understanding of the patterns and evaluation of fetal and neonatal disease.  Parental 
permission should therefore be sought as often as possible.   
Medical practitioners are advised that the State Perinatal Autopsy Service is available 
at no cost to the parents and this includes transportation and return of the body from 
the place of death.  This Service may be contacted by telephone.  The number is (08) 
8161-7333.   



25 

All hospitals with maternity services will have received a folder with information on 
the Service. The Department of Health has produced an Autopsy Request and 
Authority form for use for all non-coronial autopsy examinations together with a 
booklet entitled  The Hospital Autopsy Process. When a person dies --- information for 
family and friends.  These forms should be used and are available from the Perinatal 
Autopsy Service (Phone (08) 8161-7333). 

  

3. Causes of post-neonatal deaths 2003 
In 2003 there were 24 post-neonatal deaths notified of infants born in South Australia.  
Autopsies (including two limited autopsies) were performed in 14 out of the 24 cases 
(58.3%), which included 12 coronial cases. The autopsy rate was only 16.7% among the 
non-coronial cases (two limited autopsies in 12 deaths).  The causes of death are 
presented in Table 12, together with comparative statistics for 1986 - 2002. 

Table 12: Causes of post-neonatal deaths, South Australia, 1986   2003 

Causes of death 1986   2002 2003 

                                                         Number Percent Number Percent

SIDS 313 44.0 4 16.7

Congenital abnormalities 146 20.5 10 41.7

Conditions originating in the perinatal 
period 

88 12.4 3 12.5

Accidents, poisoning and violence 60 8.4 0 0

Infections 56 7.9 2 8.3

Other 48 6.8 5 20.8

Total 711 100.0 24 100.0
 
Among the 24 post-neonatal deaths in 2003, there were 14 males and 10 females.  Nine 
infants (37.5%) were born preterm.  The distribution by age at death of the 24 infants 
(Figure 9)  shows that 11 deaths (45.8%) occurred in the first three months of the post-
neonatal period.  Three of the 24 post-neonatal deaths (12.5%) were the children of Aboriginal 
mothers. 



26 

Figure 9: Age distribution of post-neonatal 
deaths, South Australia, 2003

0

1

2

3

4

5

6

7

1 2 3 4 5 6 7 8 9 10 11
Age in months

N
o 

of
 d

ea
th

s

Other deaths
SIDS deaths

 
 

(1) Sudden Infant Death Syndrome (SIDS) 
Only four deaths in the post-neonatal period in 2003 were attributed to SIDS. All four 
infants were placed to sleep on their backs, but subsequently two were found in the 
prone position. One infant had a viral infection two weeks before its* death and was 
found in the prone position with its head under bedding at the foot of the cot. A second 
infant had a small vomit the day before its death, but was just a little unsettled next 
day. It was found blue in its bed in the afternoon and could not be resuscitated. A third 
infant was treated for  fever following immunisation six days before its death. It was 
found pale and cold in its bassinette and did not respond to resuscitation. The fourth 
infant, who died at five months of age, had been quite well and was found in the prone 
position in its cot.  
In 2003, SIDS again accounted for a much smaller proportion of post-neonatal deaths 
(16.7%) than before 1990, when the public educational campaign to reduce risk factors 
for SIDS was commenced.  There were 159 post-neonatal deaths from SIDS, accounting 
for 60.5% of post-neonatal deaths in the four-year period 1986-1989, and resulting in a 
SIDS post-neonatal death rate of 2.0 per 1,000 livebirths. In comparison, in the four-year 
period 2000-2003, there were only 18 deaths from SIDS, accounting for 19.1% of post-
neonatal deaths and resulting in a SIDS post-neonatal death rate of 0.3 per 1,000 
livebirths.  In 2003 the post-neonatal death rate due to SIDS (0.2 per 1,000 live births) 
remains the lowest recorded in South Australia.  
In many of the deaths attributed to SIDS there are often other circumstances such as co-
sleeping, which raise the possibility that some of these deaths may be due to accidental 
asphyxia.  As the autopsy findings in cases of infantile asphyxia seem often identical to 
those found in SIDS, differentiation of these entities may be extremely difficult. For this 
reason comprehensive death scene examination and parental interview by trained 
personnel have become essential features in the assessment of unexpected infant 
death. Cases have occurred in South Australia where both induced and accidental 
asphyxia have been initially incorrectly diagnosed as SIDS due to the non-specificity 



27 

of autopsy pathology.  Pertinent information often assists in formulating an initial 
correct diagnosis. 
*  The neuter gender is used here and elsewhere in this report for reasons of confidentiality 

(2) Congenital abnormalities 
Congenital abnormalities were the leading cause of post-neonatal death in 2003, 
accounting for 10 deaths (41.7%). One of these infants had an Aboriginal mother. The types 
of abnormalities were as follows: 

  D-2 hydroxy glutaric aciduria, an autosomal recessively inherited disorder 
which is currently not diagnosable before birth unless there is a known family 
history. It cannot be treated. It is associated with neurological symptoms and 
cardiomyopathy which is often fatal. 

  Pyruvate carboxylase deficiency. The diagnosis was made shortly after birth and 
the infant treated with Biotin. This condition has a poor prognosis. The infant fed 
poorly, had anaemia, oedema, seizures and episodes of apnoea and died at five 
months of age. 

  Goldenhar syndrome, with defects of the ear, hemifacial microsomia, cleft palate, 
scoliosis and multiple ventricular septal defects. This infant was treated for 
congestive cardiac failure. It suffered a cardiac arrest after cardiac surgery, and 
subsequently had seizures and episodes of aspiration pneumonia leading to 
death. 

  IPEX syndrome (Immune-dysregulation, Polyendocrinopathy, Enteropathy, X-
linked), diagnosed on gene analysis at two months of age. This condition has a 
poor prognosis and the infant failed to thrive, had congenital diabetes, multiple 
infections and required continuous total parenteral nutrition.  

  Diamond-Blackfan syndrome (congenital red cell aplasia), associated with other 
defects, including renal and cardiovascular defects. This infant, a twin, was born 
preterm and had many of the problems of prematurity. It was treated with blood 
transfusions and prednisolone and a bone marrow transplant was planned. 
Nasogastric feeding was required but the infant did not thrive and succumbed to 
pneumococcal septicaemia at five months of age. A small spleen was found at 
autopsy.  Although a review of the bone marrow suggested that the condition 
might be Fanconi s anaemia, this was not supported by chromosome fragility 
studies in the identical twin. 

  Congenital diaphragmatic hernia, with pulmonary hypoplasia and dysplasia, 
persistent pulmonary hypertension, patent ductus arteriosus (PDA) and 
dyskinesia of the oesophagus. This infant had surgery to close the diaphragmatic 
hernia and later a ligation of the PDA but could not be weaned from the 
ventilator. A tracheostomy was performed but did not result in marked 
improvement. The infant s condition deteriorated with the development of 
Parainfluenza pneumonia, which caused its death. 

  Multiple cardiac abnormalities and microcephaly. This infant died following 
aspiration of gastric contents. 

  Ebstein s anomaly of the tricuspid valve, associated with a large atrial septal 
defect (ASD), absence of flow across the pulmonary valve and a PDA. This infant 
was considered a high risk surgical candidate but unlikely to survive without 



28 

surgery. The infant had cardiac surgery, continued to have problems with 
feeding, present since birth, and succumbed to Rotavirus gastroenterits. 

  Two infants with velo-cardio-facial syndrome, associated with a microdeletion 
on chromosome 22. One infant had multiple cardiovascular abnormalities 
including double outlet right ventricle, pulmonary atresia and multiple 
aortopulmonary collateral arteries (MAPCAs). It had cardiac surgery and 
treatment for the MAPCAs. There were many problems postoperatively, 
including sepsis. In the terminal episode the infant developed endocarditis and 
Rotavirus gastroenterits. The second infant with pulmonary atresia, a ventricular 
septal defect (VSD) and MAPCAs also had cardiac surgery. It developed a 
respiratory illness with respiratory distress leading to multiorgan failure. 

(3) Conditions originating in the perinatal period 
There were three deaths in this group, one of which was the infant of an Aboriginal mother. All 
were extremely preterm births, and all died of the complications of prematurity. One 
baby was the first of twins in a pregnancy complicated by twin-twin transfusion 
detected at 19 weeks gestation and treated with many ultrasound guided 
amnioreductions. The twins were delivered by emergency caesarean section at 26 
weeks as the second twin had died in utero and this twin showed signs of fetal distress. 
This first twin was in poor condition at birth and suffered many complications 
including hyaline membrane disease, electrolyte disturbances, hypovolemia, 
pneumoperitoneum and an acute abdomen requiring surgery, anaemia and 
thrombocytopenia requiring blood transfusions, and seizures. Head scans 
demonstrated widespread cerebral atrophy which may have resulted from 
embolisation. Death occurred at one month of age.  
The second infant was born after the onset of preterm labour at 22 weeks, and was 
treated for mild hyaline membrane disease, hypotension, intraventricular haemorrhage, 
metabolic acidosis, anaemia and thrombocytopenia requiring many blood transfusions, 
and septicaemia. The infant deteriorated in the second week of life with an acute 
abdomen and bloody stools and required exploratory abdominal surgery. It 
deteriorated and died at one month of age: the cause of death was presumed to be 
necrotising enterocolitis. The third infant was born at 24 weeks gestation following an 
antepartum haemorrhage and preterm labour. It was also treated for many 
complications of prematurity including chronic lung disease and a PDA which required 
ligation. Necrotising enterocolitis developed at five weeks and required  bowel 
resection surgery. The course was then complicated by E coli and Enterococcus sepsis, 
breakdown of abdominal wounds and multiorgan failure, resulting in death at two 
months of age. 

(4) Infections 
Two infants died of infections. One infant was the child of an Aboriginal mother. This 
pregnancy was complicated by chronic hypertension, and the baby was born small-for-
gestational-age at 34 weeks. It was found at birth to have Down s syndrome, a large 
perimembranous VSD and a secundum atrial septal defect. Cardiac surgery was 
undertaken at two months of age. The infant was discharged home apparently well 
after resolution of feeding difficulties, although it was still fed via a nasogastric tube. It 
was found dead in bed next morning. Autopsy found evidence of dehydration and 
widespread sepsis. Death was attributed to overwhelming Klebsiella pneumoniae 



29 

septicaemia and dehydration in a child with Down s syndrome and congenital heart 
disease.  
The second infant was the second of twins in a pregnancy complicated by spontaneous 
preterm prelabour rupture of membranes at 18 weeks gestation. The mother s vaginal 
swab yielded a heavy growth of Group B Streptococcus and she was treated for this. 
Labour commenced spontaneously at 24 weeks, and the first twin died during labour. 
The second twin s cord prolapsed during labour. It was treated in the neonatal 
intensive care unit for many prematurity complications, including severe lung disease 
which led to chronic lung disease. At two months of age the infant developed and died 
of late-onset Group B Streptococcal meningitis. 
It is pleasing to note that there were no deaths from infection in otherwise healthy 
infants in 2003. The Committee would like to stress that infection is still an important 
cause of infant death.  Any infant who is excessively drowsy should be considered 
seriously ill until proved otherwise. The seeking of advice and, if necessary, retrieval 
are of utmost importance.  

(5) Other causes 
There were five deaths of undetermined cause in this group. The first infant, who died 
at one month of age, developed an upper respiratory tract infection (URTI) a few days 
before its death. The infant was sleeping between its parents with a queen size quilt 
pulled up to the chest. It was found dead in bed later in the morning. There were 
findings of minor facial trauma and possible cerebral trauma and asphyxia at autopsy. 
The second infant was born at term small-for-gestational-age. It had a cold for two 
weeks and was treated for fever two days before its death at five months of age. The 
infant was sleeping between its parents and was found dead the next morning.  
Findings at autopsy suggested an asphyxial mode of death. The third infant was born at 
term and was well after treatment for respiratory distress and sepsis after birth. Two 
weeks before its death at two months of age, it had an upper respiratory tract infection, 
slight wheezing and vomiting. It was crying and vomiting in the afternoon before its 
death and would not settle late that evening after being put in its cot. The mother found 
that it had vomited in its cot; it stopped breathing when she picked it up and could not 
be resuscitated. Autopsy found old and recent subdural haemorrhage and minor 
bruising on the upper limbs. The fourth infant was born a few weeks before term and 
spent some time in special nursery care.  It was unsettled the evening after receiving its 
first immunisation at two months of age. The mother settled the infant to sleep on her 
chest, where it was found not breathing when she awoke. It died of hypoxic ischaemic 
encephalopathy after resuscitation. The fifth infant died at five months of age after 
being unwell for two days. Although there was evidence of infection it was not 
considered adequate to explain its death. 

Deaths of babies born interstate 
There was one post-neonatal death in 2003 of an infant born interstate. This three month 
old infant had a history of a fall and was transferred unconscious to a South Australian 
hospital from an interstate hospital. The infant s condition deteriorated and it died the 
next day. 



30 

IV Recommendations 

1. Maternal Subcommittee recommendations 
(1) The care of women with current or previous serious conditions during pregnancy 

should only be undertaken in settings which are equipped to deal appropriately 
with such situations. 

(2) Strong consideration should be given for review by a physician early in pregnancy 
of women with current or previous serious medical conditions. 

2. Perinatal Subcommittee recommendations 
(1) The Subcommittee would like to advise practitioners of the importance of caring for 

pregnant women in a setting appropriate for the level of risk the pregnancy presents 
for both mother and baby. For example, women with severe hypertension or 
insulin-dependent diabetes should be managed in at least a level II hospital with 24 
hour on-site medical cover. 

(2) The need for development of evidenced-based statewide protocols for level I, II and 
III maternity services with an emphasis on timely recognition and appropriate 
management of common obstetric problems such as fetal growth restriction, 
preterm rupture of membranes, meconium-stained liquor, antepartum 
haemorrhage and pre-eclampsia. Practitioners must ensure that pregnant women 
with a higher level of risk than defined for their hospital level of care are referred 
promptly and appropriately. 

(3) Vigilance in the recognition of fetal growth restriction. Fetal growth restriction was 
the cause of death for 12.5% of perinatal deaths in 2003.  Practitioners are asked to 
be vigilant so that fetal growth restriction is not missed. 

(4) Health professionals should encourage women not to smoke during pregnancy. 
Smoking in pregnancy has been associated with fetal growth restriction. Smoking 
cessation programmes implemented during pregnancy have been demonstrated to 
reduce smoking significantly, with reductions in low birthweight and preterm birth 
and an increase in mean birthweight.*  

* Lumley J, Oliver S, Waters E. Interventions for promoting smoking cessation during pregnancy.  
  Cochrane Pregnancy and Childbirth Group. The Cochrane Database of systematic Reviews Vol 3 2003. 

The rate of smoking in pregnancy has decreased, but not among Aboriginal women, whose 
rate in 2003 was 59% compared with 20% among non-Aboriginal women. Births to 
Aboriginal women continue to be associated with rates of preterm and small-for gestational-
age birth more than twice those of births to non-Aboriginal women. The proportion of low 
birthweight births is three times higher. 

(5) Appropriate training and maintenance of competence in cardiotocograph (CTG) 
interpretation for all levels of medical and midwifery staff.  

(6) The institution of streamlined arrangements between rural/level I hospitals and 
their regional level II/III maternity service in situations where there is a lack of on-
site CTG expertise. 

(7) The greater use of the recently revised guidelines for investigating stillbirths 
including a more systematic approach to investigate the potential involvement of 



31 

thrombophilias (Appendix 8). This statewide protocol for the investigation of all 
stillbirths has been sent to all maternity units in South Australia. The rate of 
unexplained stillbirths of 1.8 deaths per 1,000 births is still of concern, although 
slightly lower than that of 2.0 deaths per 1,000 births in the years 1995-1998.  

(8) Autopsy often provides considerable information that is not available otherwise and 
should be strongly recommended. The decrease in the autopsy rate in perinatal 
death over the past few years is of grave concern. When parents decline autopsy, 
we recommend that photographic and X-ray documentation be obtained. The State 
Perinatal Autopsy Service is available at no cost to the parents and may be 
contacted on (08) 8161-7333. 

(9) Placentas should be sent for examination in all cases of perinatal death (See 
Appendix 9). Histopathological examination of the placenta provides considerable 
additional information and should be attainable for 100% of perinatal deaths.  

As a guide, all placentas should be sent to Pathology, at least for: 
1. All stillborn infants, early neonatal deaths and mid-trimester miscarriages. 
2. All multiple pregnancies with same sex infants. 
3. All triplet and higher order multiple pregnancies. 
4. All cases of discordant twin growth with greater than 20% weight difference. 
5. All cases of prolonged rupture of membranes or suspected chorioamnionitis or 

maternal fever (any cause). 
6. All preterm deliveries. 
7. All cases where birthweight is less than the 10th percentile or greater than the 95th 

percentile for gestational age. 
8. All cases of fetal malformation. 
9. All cases of pregnancy complicated by oligohydramnios, polyhydramnios or 

placental abnormalities detected prenatally (vascular channels, chorioangioma, 
etc). 

10. All cases with a physical abnormality in the placenta (eg. a mass, abnormal 
colour, malodour). 

11. All cases subjected to chorion villus sampling or amniocentesis, if complications 
occur. 

12. All cases of pre-existing diabetes, pre-eclampsia, systemic lupus erythematosus 
and documented thrombophilias known to be associated with fetal hazard. 

13. All cases of placental abruption. 
14. All retrievals. 
15. All cases where the infant is transferred to a Level III nursery or the infant is 

severely depressed at birth (Apgar score &lt;5 at five minutes). 
16. All cases of maternal death. 

(10) The  Subcommittee also recommends the use of the birthweight/gestation   
percentile charts for singletons and twins prepared using national perinatal data ( 
Roberts CL, Lancaster PAL. Australian national birthweight percentiles by 



32 

gestational age.  Med J Aust 1999; 170: 114-118; Roberts C, Lancaster P. National 
birthweight percentiles by gestational age for twins born in Australia. J Paediatr 
Child Health 1999;35:278-82). The singleton charts have been reproduced in 
Appendix 10 with the permission of the Medical Journal of Australia. The twin 
charts are available on the PSANZ website with the PSANZ perinatal death 
classifications. 

3. Post-neonatal Subcommittee recommendations 
The following recommendations are pertinent to the deaths in 2003: 
(1)  Health professionals providing care both in the antenatal and postnatal period 

should ensure that women are provided with information about safe infant 
sleeping practices and prevention of SIDS.   
Falling asleep with the infant at the breast and other forms of co-sleeping or bed 
sharing may be hazardous, particularly if the adults are intoxicated (see Appendix 
11). 
All mothers should be advised that babies must not be placed in cots with any 
pillows, U-pillows, cot bumpers, large soft toys, thick blankets or quilts or other 
items which may overheat or suffocate the infant. 

(2)  A well-coordinated system of appropriate and ongoing support, supervision and 
referral should be offered to families with known risk factors for adverse child 
outcome eg, parental substance abuse, parental psychiatric illness, household 
violence, extreme youth of the mother and poor social circumstances. This should 
be continued at least until the end of infancy, if not for a longer period of time. 
In reviewing the causes of death in 2003 and other recent years, the Committee has 
been concerned about the number of deaths in which adverse factors such as 
smoking, alcohol and substance abuse, bed sharing when intoxicated, physical 
abuse and poor social circumstances are present.  

(3)  Urgent medical advice should be sought for all infants who are excessively drowsy, 
irritable  and/or are feeding poorly. These infants, who may not be showing the 
classical signs of infection, should be considered seriously ill until proven 
otherwise. Small infants also become dehydrated very rapidly. Infants with 
cyanotic heart disease are more prone to the complications of dehydration and 
specialist advice should be sought. Urgent retrieval may be necessary for any infant 
who is thought to be suffering from a significant bacterial infection. The 
Subcommittee notes that infection remains an important cause of infant death.    

The following recommendations made in previous reports are still relevant: 
(1) Provision of a safe infant sleeping environment: 

  Babies should be placed on their backs to sleep, unless there is a contra-
indication.  Sleeping supine is not contraindicated in babies with gastro-
oesophageal reflux.   

  Vigilance is necessary to ensure that potential hazards are removed from the 
infant s sleeping environment.  

  Mattresses which do not fit cots properly should not be used, especially in cots 
that have expansible sides. 



33 

  Ensure that all new cots meet Australian Standards and only use old ones that 
do. 

  Infants should not be left to sleep unattended in stroller-prams or bouncinettes. 
(2) Vigilance is needed to ensure that potential hazards in the home are removed from 

the infant s environment.  These include long hanging curtain cords, which may 
catch around the neck, and water in containers or baths in which an infant may 
drown. Infants should never be left unattended in a bath or near water, even for a 
minute. This warning also applies to infants using devices such as ring bath seats. 
These devices have been  banned in some Australian states due to deaths from 
drowning associated with their use. 

(3) Vigilance is always needed to ensure safe feeding for children under four years of 
age. Foods which can break off into pieces and cause choking should not be given 
eg raw carrot, celery sticks, grapes, pieces of apple, cherry tomatoes, sausages, 
frankfurts, popcorn, nuts, hard lollies and corn chips. Food for toddlers should be 
finely chopped. Children should be supervised while eating. If they run, play, 
laugh or cry while eating, they are more likely to choke on their food. The 
Committee was pleased to note that there were no deaths in 2003 from feeding 
accidents. 

(4) Recording and charting of child s weight 
The Subcommittee would also like to stress to both parents and health professionals 
the importance of recording the child s weight in the Personal Health Record (Blue 
Book) and charting the weight on the percentile growth charts to identify children 
who are not thriving. It is important to investigate why a child is not thriving. Any 
child who is not thriving should be referred to a medical practitioner. 

(5) The Subcommittee would also like to stress the importance of immunisation in the  
prevention of infectious disease in children. There is some evidence that there is a 
reduced rate of SIDS in immunised compared with non-immunised children.* 

* Mitchell EA, Stewart AW, Clements M, Ford RPK, on behalf the New Zealand Cot Death Study Group.  
  Immunisation and the sudden infant death syndrome. Arch Dis Child 1995;73:498-501. 

 

(6) Reporting of deaths to the State Coroner 
A death must be reported to the State Coroner where the death has occurred from a 
violent or unusual cause or the cause of death is unknown, or a person has died 
during an anaesthetic procedure or within 24 hours of the administration of an 
anaesthetic. Other categories of death which must be reported to the Coroner 
include all deaths in an institution, a prison or in police custody.  

(7) The Subcommittee would like to draw attention once again to the importance of 
autopsy in eliciting the cause of death, which should always be carefully recorded 
in the clinical history.  The autopsy rate (including two limited autopsies) among all 
post-neonatal deaths in 2003 was 58.3% (14 out of 24), but only 16.7% (two limited 
autopsies) among the 12 non-coronial cases.   
There have been several cases in which autopsy has identified a previously 
unsuspected cause of death.  This is most valuable in the management of future 
pregnancies and counselling of parents, including grief counselling.  A detailed 



34 

examination of the death scene by appropriately trained personnel in cases of 
unexpected death is also essential in eliciting causative or potentially contributory 
factors.  Standard protocols such as those developed by SAPOL (South Australian 
Police) and SIDS and Kids South Australia should be used in those circumstances.  

(8) The Committee would also like to draw attention to three websites that offer 
important information: 
The SIDS website is www.sidsandkids.org from which hospital staff may print 
information in different languages. 
The South Australian Pregnancy Information website of the Department of Health: 
www.health.sa.gov.au/pregnancy  
The South Australian Parenting and Child Health website www.cyh.com.au of 
Child and Youth Health. 
This Committee report is also available on the Department of Health s Pregnancy 
Outcome Unit s website: www.dh.sa.gov.au/pehs/pregnancyoutcome.htm.  



35 

V  Education Subcommittee Report 

The eighth annual educational meeting was organized on the evening of August 10th 
2004 by what is now known as the Education Subcommittee of the Maternal, Perinatal 
and Infant Mortality Committee. 
These meetings commenced in 1997 to facilitate a recommendation that private 
perinatal units in the metropolitan area be involved in some form of regular peer 
review and continuing professional education for midwifery and medical staff 
providing care within those units.  Initially these meetings were annual events 
organized by an ad hoc group chaired by the late Dr. Brian Pridmore, then Chair of the 
Perinatal Subcommittee. The enthusiastic response to the meetings from midwives and 
medical practitioners led to their expansion to include personnel from all the perinatal 
services within the state. There have been endeavours to include a wider audience in 
rural centres by the use of teleconferencing but there was varied success when many 
country units (up to 17) participated, due to difficulties in transmission. 
The desire to ensure that these meetings become formalized as part of the South 
Australian perinatal  scene  led to the formation of the Education Subcommittee. The 
intention was also to allow a forum for dissemination of findings and recommendations 
from the Maternal, Perinatal and Infant Mortality Committee to those at the  coal face . 
The eighth meeting, held at the Women s and Children s Hospital, was titled  Issues 
Surrounding Caesarean Section  and included a panel consisting of Professor Jeffrey 
Robinson, Associate Professor Deborah Turnbull, Dr Chris Wilkinson and Dr Chris 
Barnett. A wide ranging discussion took place between the panel members and the 
audience of 100 including qualified and student midwives and medical practitioners, 
representatives of community interest groups and allied health professionals. 
Dr Brian Wheatley, Chair of the Education Subcommittee also communicated the main 
recommendations of the Committee made in this report for 2003. The general feedback 
was very positive.  
The Subcommittee thanks the panel and participants for their continued support of 
what will continue to be an important part of perinatal services within South Australia. 
  



36 

APPENDIX 1 

Terms of reference, Subcommittees of the Maternal, Perinatal and Infant 
Mortality Committee: 

Maternal Subcommittee 
1. To review the causes of death associated with pregnancy and childbirth; to 

determine whether these may have been preventable, and to establish what were 
the avoidable factors, if any, presented in the case history. 

2. To report to the Maternal, Perinatal and Infant Mortality Committee. 
3. To undertake review, educational and advisory roles as appropriate from time to 

time, by initiation or by invitation. 

Perinatal Subcommittee 
1. To review each perinatal death from an obstetric, paediatric and pathological 

perspective and to collate this information. 
2. To determine and monitor the epidemiology of perinatal deaths in South 

Australia. 
3. To identify avoidable factors and confidentially provide feedback information to 

clinicians. 
4. To identify areas which need special study and/or action. 
5. To liaise with other national and international perinatal mortality study groups. 
6. To report to the Maternal, Perinatal and Infant Mortality Committee. 

Post-neonatal Subcommittee 
1. To review the causation of post-neonatal deaths in South Australia. 
2. To prepare education commentaries for inclusion in the Annual Report of the 

Maternal, Perinatal &amp; Infant Mortality Committee. 
3. To report to the Maternal, Perinatal and Infant Mortality Committee. 
4. To liaise with other national and international mortality study groups. 
5. To set priorities for special studies into causes of death in this age group. 

Education Subcommittee 
1. To provide an annual interactive forum for the continuing education of midwives 

and medical practitioners involved in the provision of perinatal services within the 
metropolitan and regional South Australia. 

2. To act as an additional means of communication to the above providers, other health 
professionals and the community generally from the other subcommittees of the 
Maternal, Perinatal and Infant Mortality Committee. 

3. The membership and chairperson will be nominated by the chairperson of the 
Maternal, Perinatal and Infant Mortality Committee. 
 



37 

 
 

4. The membership shall consist of: 

  An obstetrician in metropolitan private practice. 
  A neonatal paediatrician in metropolitan private practice. 
  A midwife from the metropolitan private hospital services. 
  An epidemiologist / medical secretary from the Pregnancy Outcome Unit. 

5. The Subcommittee may co-opt members as required. 
 
 



 
38 

APPENDIX 2A 

 
 



 
39 

APPENDIX 2B 

 
 
 



 
40 

 

 
 

 

 



 
41 

APPENDIX 3  

Definitions 
Maternal death is defined as the death of a woman while pregnant or within 42 days of 
termination of pregnancy, irrespective of the duration and the site of the pregnancy, 
from any cause related to or aggravated by the pregnancy or its management, but not 
from accidental or incidental causes.* 
Maternal deaths in South Australia are classified as follows: 

1. Direct obstetric deaths: those resulting from obstetric complications of the 
pregnant state (pregnancy, labour and puerperium), from interventions, 
omissions, incorrect treatment, or from a chain of events resulting from any of 
the above.* 

2. Indirect  obstetric deaths:  those resulting from previous existing disease or 
disease that developed during pregnancy and which was not due to direct 
obstetric causes, but which was aggravated by physiologic effects of pregnancy.* 

3. Incidental deaths in pregnancy: examples of incidental deaths are deaths from 
drowning and road accidents, where the pregnancy is unlikely to have 
contributed significantly to the death, although it may be possible to postulate a 
remote association. 

In order to avoid missing indirect deaths which may be difficult to distinguish from 
incidental deaths occurring in pregnant women, the Maternal, Perinatal and Infant 
Mortality Committee reviews all deaths in pregnancy and within 42 days of the end of 
pregnancy. However, only direct and indirect deaths (pregnancy-related deaths) are 
included in the calculation of the maternal mortality ratio. 
Maternal mortality ratio: 

000,100 =
 yearsame the in tsconfinemen of Number

 yeara in deaths indirect and direct of Number  

*World Health Organization. International Statistical Classification of Diseases and Related 
Health Problems. Tenth Revision. Volume 2. Geneva: WHO, 1993. 

Perinatal death: includes stillbirth (late fetal death) and neonatal death. 
Stillbirth: birth of a fetus at or after 20 weeks gestation and/or with a birthweight of 
400g or more, with no signs of life at birth. 
Confinement: a pregnancy ending with the birth of one or more fetuses (dead or alive) 
at or after 20 weeks of gestation and/or with a birthweight of 400g or more. 
Stillbirth rate: 

000,1 =
 yearthat in sstillbirth and livebirths of Number

 yeara in sstillbirth of Number  

 
Neonatal death: death of a liveborn infant within 28 days of birth 



 
42 

Neonatal death rate: 

= 000,1 
 yearthat in livebirths of Number

 yeara in deaths neonatal of Number  

Perinatal mortality rate: 

= 000,1 
 yearthe in livebirths + sstillbirth of Number

  yeara in deaths neonatal + sstillbirth of Number  

 
 Infant death: death of a liveborn infant within the first year of life 
 Infant mortality rate: 

= 000,1 
 yearsame the in livebirths of Number

 yeara in deaths infant of Number  

Infant deaths include neonatal and post-neonatal deaths.  
Post-neonatal death: death of a liveborn infant occurring between 28 days and the first 
birthday 
Post-neonatal death rate 

= 000,1 
 yearsame the in livebirths of Number

 yeara in deaths neonatal-post of Number  



 
43 

APPENDIX 4 

Perinatal Society of Australia and New Zealand-Perinatal Death Classification 
(PSANZ-PDC), SA perinatal deaths, 2003 

 
  No. %

1. CONGENITAL ABNORMALITY  
(including terminations for congenital abnormalities) 

39  22.2

 1.1   Central nervous system 6    3.4
 1.2   Cardiovascular system 6    3.4
 1.3   Urinary tract 5    2.8
 1.4   Gastrointestinal tract 0       0
 1.5   Chromosomal 8    4.5
 1.6   Metabolic 0       0
 1.7   Multiple 7    4.0
 1.8   Other 7    4.0
        1.81   Musculoskeletal 3  
        1.82   Respiratory 1  
        1.83   Diaphragmatic hernia 3   
 1.9   Unspecified 0       0

2. PERINATAL INFECTION 8   4.5
 2.1   Bacterial    4   2.3
         2.11    Group B Streptococcus 1 
         2.12    E coli 2 
         2.13    Listeria monocytogenes 0  
         2.18    Other bacterial 

       2.19    Unspecified bacterial 

1 

0 

 

 2.2   Viral          0      0
         2.21     Cytomegalovirus 0  
         2.22     Parvo virus 0 
         2.23    Herpes simplex virus 0 
         2.24    Rubella virus 0 
         2.28    Other viral 

        2.29    Unspecified viral 

0 

0 
 2.3   Protozoal eg toxoplasmosis 

2.4   Spirochaetal eg syphilis 

2.5   Fungal 

1 

0 

0 

   0.6

      0

      0
 2.8   Other 0       0
 2.9   Unspecified organism 3    1.7

 



 
44 

 

  No. %

3. HYPERTENSION 4    2.3

 3.1   Chronic hypertension: essential 

3.2   Chronic hypertension: secondary, eg renal disease 

3.3   Chronic hypertension: unspecified 

3.4   Gestational hypertension 

3.5   Pre-eclampsia 

3.6   Pre-eclampsia superimposed on chronic hypertension 

3.9   Unspecified hypertension 

1 

0 

0 

0 

2 

1 

0 

  0.6  

      0

      0

      0

   1.1

   0.6

      0

4. ANTEPARTUM HAEMORRHAGE (APH) 9    5.1

 4.1   Placental abruption 

4.2   Placenta praevia 

4.3   Vasa praevia 

4.8   Other APH 

4.9   APH of undetermined origin 

7 

1 

0 

0 

1 

   4.0

   0.6

      0

      0

   0.6

5. MATERNAL CONDITIONS 5    2.8
 5.1   Termination of pregnancy (other than for congenital (fetal) 

abnormality) 

5.2   Diabetes / Gestational diabetes 

5.3   Maternal injury    

        5.31 Accidental 

        5.32 Non-Accidental 

5.4   Maternal sepsis 

5.8   Other maternal conditions, eg Lupus obstetric syndrome 

0 

3 

1  

1 

0 

0 

1 

      0

 

   1.7

0.6

  0

0.6

6. SPECIFIC PERINATAL CONDITIONS 21 11.9

 6.1   Twin-twin transfusion 6   3.4

 6.2   Fetomaternal haemorrhage 3   1.7

 6.3   Antepartum cord complications (eg cord haemorrhage; true 
knot with evidence of occlusion) 

3   1.7

 6.4   Uterine abnormalities, eg bicornuate uterus, cervical 
incompetence 

4   2.3

 6.5   Birth trauma (typically infants of &gt;24 weeks gestation or 
&gt;600g birthweight) 

0      0

 6.6   Alloimmune disease 0      0

 6.7   Idiopathic hydrops 

6.8   Other specific perinatal conditions (includes iatrogenic 
conditions such as rupture of membranes  after 
amniocentesis, termination of pregnancy for suspected but 
unconfirmed congenital abnormality) 

4 

1 

  2.3

  0.6

 



 
45 

 

  No %

7. HYPOXIC PERIPARTUM DEATH  
(typically infants of &gt;24 weeks gestation or &gt; 600g 
birthweight) 

7   4.0

 7.1   With intrapartum complications 

        7.11 Uterine rupture 

        7.12 Cord prolapse 

        7.13 Shoulder dystocia 

        7.18 Other 

2 

1 

0 

1 

0  

   1.1

 7.2   No apparent complications 4    2.3
 7.9   Unspecified hypoxic peripartum death 1    0.6

8. FETAL GROWTH RESTRICTION (FGR) 22 12.5
 8.1   With evidence of uteroplacental insufficiency eg significant 

infarction, acute atherosis, maternal vascular thrombosis or 
maternal floor infarction 

13   7.4

 8.2   With chronic villitis 

8.3   Without the above placental pathology 

0 

6 

    0

 3.4
 8.4   No examination of placenta 

8.9   Unspecified FGR or not known whether placenta examined 

3 

0 

  1.7

     0

9. SPONTANEOUS PRETERM (&lt;37 weeks gestation) 28  15.9
 9.1   Spontaneous preterm with intact membranes, or membrane 

rupture &lt;24 hours before delivery 
17 9.6

 9.11 with chorioamnionitis 7 
 9.12 without chorioamnionitis 5 
 9.13 no examination of placenta 5 
 9.19 unspecified or not known whether placenta examined 0 
 9.2   Spontaneous preterm with membrane rupture ?24 hours 

before delivery 
10 5.7

 9.21 with chorioamnionitis 6 
 9.22 without chorioamnionitis 3 
 9.23 no examination of placenta 1 
 9.29 unspecified or not known whether placenta examined 0 
 9.3   Spontaneous preterm with membrane rupture of unknown 

duration before delivery 
1 0.6

 9.31 with chorioamnionitis 1 
 9.32 without chorioamnionitis 0 
 9.33 no examination of placenta 0 
 9.39 unspecified or not known whether placenta examined 0 
 



 
46 

 

    No. %

10. UNEXPLAINED ANTEPARTUM DEATH     33  18.8
 10.1   With evidence of uteroplacental insufficiency, eg significant    

infarction, acute atherosis, maternal vascular thrombosis or 
maternal floor infarction 

  10    5.7

 10.2   With chronic villitis 

10.3   Without the above placental pathology 

  1 

19 

 0.6

 10.8
 10.4   No examination of placenta   3  1.7
 10.9   Unspecified unexplained antepartum death or not known 

          whether placenta examined 
  0 0

11. NO OBSTETRIC ANTECEDENT   0 0
 11.1   SIDS    

          11.11 Consistent with SIDS 

          11.12 Possible SIDS 

 

 

 0 

0 

0 

0

 11.2   Postnatally acquired infection   0 0
 11.3   Accidental asphyxiation   0 0
 11.4   Other accident, poisoning or violence (postnatal)   0 0
 11.8   Other   0 0
 11.9   Unknown / Unexplained   0 0
 TOTAL   176 100.0
 



 
47 

APPENDIX 5 

Perinatal Society of Australia and New Zealand Perinatal Death Classification 
(PSANZ-PDC) by birthweight, SA, 2003 

 

PSANZ-PDC Birthweight (g) Total 

  &lt;500 
500 

-749 
750

-999
1,000

-1,499
1,500

-1,999
2,000

-2,499
2,500+ No. %

1 Congenital abnormality 21 9 2 0 0 4 3 39 22.2

2 Perinatal infection 1 4 0 0 0 1 2 8 4.5

3 Hypertension 0 1 1 1 0 1 0 4 2.3

4 Antepartum haemorrhage 2 1 0 2 0 0 4 9 5.1

5 Maternal conditions 2 0 0 0 0 0 3 5 2.8

6 
Specific 
perinatal 
conditions 

7 4 0 3 1 0 6 21 11.9

7 
Hypoxic 
peripartum 
death 

0 0 1 0 0 0 6 7 4.0

8 Fetal growth restriction 3 3 1 5 2 4 4 22 12.5

9 Spontaneous preterm 11 16* 0 1 0 0 0 28 15.9

10 
Unexplained 
antepartum 
death 

7 4 2 1 2 3 14 33 18.8

11 No obstetric antecedent 0 0 0 0 0 0 0 0 0.0

 Total 54 42* 7 13 5 13 42 176 100
 % 30.7 23.9 4.0 7.4 2.8 7.4 23.9 100 %

 
*includes one stillbirth of unknown birthweight born at 23 weeks gestation 



 
48 

APPENDIX 6 

Obstetric cause-specific classification of perinatal deaths, SA, 2003 
(Amended Whitfield) 

 

  No %

1. SPONTANEOUS PRETERM  
&lt;37 weeks, normally formed, appropriately grown.  32 18.2

 1.1   Multiple pregnancy 7 

 1.2   Previous bleeding 5 

 1.3   Previous spontaneous rupture of membranes 
        &gt;12 hours before labour 9 

 1.4   Cervical incompetence 4 

 1.5   Other, eg uterine malformation 0 

 1.6   Idiopathic 7 

2. INTRAUTERINE GROWTH RESTRICTION (IUGR) 
&lt;10th percentile for gestational age 22 12.5

   

3. UNEXPLAINED INTRAUTERINE DEATH 
Normally formed fetuses without IUGR where fetal death is 
known to have preceded labour in the absence of any other 
primary complication 

33 18.8

   

4. BIRTH TRAUMA 
?1.5kg, with evidence of lethal trauma at autopsy even when 
labour and delivery were not complicated by mechanical 
difficulty 

0 0

 4.1   Cord complication 0 

 4.2   Breech delivery 0 

 4.3   Caesarean section 0 

 4.4   Forceps delivery 0 

 4.5   Ventouse delivery 0 

 4.6   Other delivery 0 

5. INTRAPARTUM ASPHYXIA  
?1.5kg with evidence of intrapartum hypoxia and confirmed 
by hypoxic changes at autopsy 

7 4.0

 5.0   Vaginal 4 

 5.1   Cord complication 0 

 5.2   Breech delivery 0 

 5.3   Caesarean section 2 

 5.4   Forceps delivery 0 

 5.5   Ventouse delivery 0 

 5.6   Other delivery &amp; unspecified 1 



 
49 

 

  No. %

6. HYPERTENSION 4 2.3

 6.0   Unspecified 0 

 6.1   Pre-existing hypertension 1 

 6.2   Pre-eclampsia 2 

 6.3   Pre-existing hypertension and pre-eclampsia 1 

7. MATERNAL DISEASE 5 2.8

 7.0   Unspecified 0 

 7.1   Maternal injury 1 

 7.2   Abdominal operation 0 

 7.3   Diabetes/Gestational diabetes 3 

 7.4   Malignancy 0 

 7.5   Infection 0 

 7.8   Maternal death 0 

 7.9   Other 1 

8. ANTEPARTUM HAEMORRHAGE  (APH)   9 5.1

 8.1   Placental abruption 7 

 8.2   Placenta praevia 1 

 8.3   APH undetermined origin 1 

 8.4   Vasa praevia 0 

9. FETAL ABNORMALITY 39 22.2

 9.1   Central nervous system 6 

 9.2   Cardiovascular system 6 

 9.3   Urinary tract 5 

 9.4   Gastrointestinal tract 0 

 9.5   Chromosomal 8 

 9.6   Metabolic 0 

 9.7   Multiple 7 

 9.9   Other 7 

10. HAEMOLYTIC DISEASE 0 0

 10.1   Rhesus incompatibility 0 

 10.2   Other feto-maternal blood group incompatibility  
          (eg Kell) 

0 

 10.3   Haemoglobinopathy 0 

 



 
50 

 

  No. %

11. INFECTION   
Pathological evidence of infection required.  Infections 
occurring as primary factors including deaths with 
chorioamnionitis or congenital pneumonia preceding 
membrane rupture.  

8 4.5

 11.0   Unspecified 3 

 11.1   Streptococcus, Group B 1 

 11.2   Escherichia coli 2 

 11.3   Other bacterial 1 

 11.4   Toxoplasma 1 

 11.5   Syphilis 0 

 11.6   Cytomegalovirus 0 

 11.7   Other viral 0 

 11.8   Fungal 0 

 11.9   Other 0 

12. OTHER 17 9.7

 12.1   Non-immune hydrops 4 

 12.2   Feto-maternal haemorrhage 3 

 12.3   Twin-twin transfusion 6 

 12.4   Accident, poisoning or violence (Postnatal) 0 

 12.5   SIDS 0 

 12.8   Unknown/unexplained 0 

 12.9   Other 4 

 TOTAL 176 100
 



 
51 

APPENDIX 7 

Perinatal Society of Australia and New Zealand-Neonatal Death Classification 
(PSANZ-NDC), SA neonatal deaths, 2003 

 

 No %
1.    CONGENITAL ABNORMALITY 10 23.8

 1.1   Central nervous system 1   2.4

 1.2   Cardiovascular system 2   4.8

 1.3   Urinary tract 0     0

 1.4   Gastrointestinal tract 0      0

     1.5   Chromosomal 2    4.8

 1.6   Metabolic 0      0

 1.7   Multiple 1  2.4

 1.8   Other congenital abnormality 4   9.5

 1.9   Unspecified congenital abnormality 0      0

2 EXTREME PREMATURITY 
 (typically infants of &lt;=24 weeks gestation or &lt;=600g birthweight) 

15 35.7

Includes infants deemed too immature for resuscitation or continued life support 
beyond the delivery room 

 3       CARDIO-RESPIRATORY DISORDERS 2 4.8
3.1   Hyaline membrane disease / Respiratory distress syndrome (RDS) 0    0

 3.2   Meconium aspiration syndrome 0    0

 3.3   Primary persistent pulmonary hypertension 0    0

 3.4   Pulmonary hypoplasia 0    0

 3.5   Chronic neonatal lung disease (typically, bronchopulmonary dysplasia) 0     0

3.8   Other 2  4.8

4. INFECTION 3  7.1
4.1   Bacterial    

        4.11 Congenital bacterial 

2

2

 4.8

                     4.12 Acquired bacterial 0  

4.2   Viral          

        4.21 Congenital viral 

0

0

 

                     4.22 Acquired viral 0  

4.3   Protozoal eg Toxoplasma 0     0

4.4   Spirochaetal eg Syphilis 0     0

4.5   Fungal 0     0

4.8   Other 0     0

4.9   Unspecified organism 1  2.4
   

 



 
52 

 

 No. %
5.    NEUROLOGICAL 11  26.2

5.1   Hypoxic ischaemic encephalopathy / Perinatal asphyxia (typically infants of 
        &gt;24 weeks gestation or &gt;600g birthweight) 

8 19.0

5.2   Intracranial haemorrhage 3  7.1

5.8   Other 0      0

6.    GASTROINTESTINAL 1   2.4
6.1   Necrotising enterocolitis 1   2.4

6.8   Other 0      0

7.    OTHER 0      0
7.1   SIDS     

        7.11 Consistent with SIDS 

0

0

     0

                     7.12  Possible SIDS 0  

7.2   Multi-system failure - only if unknown primary cause or trigger event  0      0

7.3   Trauma 0      0

7.8   Other 0     0

7.9   Undetermined / Unknown 0      0

TOTAL 42 100.0
 
  



 
53 

APPENDIX 8  

South Australian Protocol for investigation of stillbirths 

Working party members: 
Dr R Watson (Chair) 
Professor  MJNC Keirse 
Professor G Dekker 
Dr TY Khong 
Dr W Hague 

Introduction 
The perinatal mortality rate for South Australia in 2003 of 3.9 deaths per 1,000 births for 
infants of at least 1,000g birthweight or 28 weeks gestation is low by international 
standards. The rate for infants of at least 400g birthweight or 20 weeks gestation was 9.9 
deaths per 1,000 births that year. Seventy-six percent of these perinatal deaths were 
stillbirths.  The Perinatal Subcommittee of the South Australian Maternal, Perinatal and 
Infant Mortality Committee seeks, amongst other roles, to identify patterns and 
avoidable factors in perinatal deaths within the state. In 2003, 25% of stillbirths had no 
cause identified, possibly, in part due to the lack of a systematic and up-to-date 
approach to the investigation of stillbirths for which there is no immediate obvious 
cause. Currently protocols for investigating such cases vary markedly between 
hospitals and generally have not kept pace with advances in obstetric knowledge, 
particularly in the area of vasculopathies. 
A working party was set up in 1997 by the Perinatal Subcommittee to address this issue. 
It is hoped that the result will facilitate a more systematic and uniform approach to the 
investigation of stillbirths, resulting not only in a greater understanding of the 
demographics and underlying pathology, but the possibility of more accurate diagnosis 
and counselling, and potentially a reduction in recurrences. 
In order to adequately assess causative and contributing factors in cases of stillbirth, 
certain investigations will be required in all cases, while others can be directed to 
discovering underlying factors for an obvious cause of death. Lastly, some 
investigations are best suited to those cases in which no cause of death is apparent.  The 
following protocol attempts to provide a logical approach to each of these areas. 

Core investigations  
(to be performed in all cases of stillbirth) 

  A detailed history and examination of the mother along with a careful review 
of the antenatal record can often provide clues to intercurrent infection, 
previously undiagnosed pre-eclampsia, drug use or intra-hepatic cholestasis of 
pregnancy. 

  Autopsy of the stillbirth. With parental consent, autopsy should be conducted 
by the State Perinatal Autopsy Service. 



 
54 

  Guthrie card. Where permission for an autopsy has been declined, parents 
should be asked if blood can be taken for the Newborn Screening Guthrie Card 
that is requested for all babies in Australia. This blood could be drawn from a 
heel prick or from the cut end of the umbilical cord of the placenta. 

  Histopathology of placenta.  Whether or not an autopsy is performed the 
placenta should be placed in a dry sterile container (no formalin or saline), the 
container surrounded in ice and forwarded to the State Perinatal Autopsy 
Service. Histopathological examination combined with other investigations can 
provide a diagnosis for a current pregnancy and information that can be helpful 
in planning another pregnancy.  

  Maternal blood should be drawn for a Kleihauer test and sent along with a 
sample of maternal serum with the placenta with or without the baby. A slide for 
Kleihauer will be prepared but only examined if required. 

  External examination of the baby.   In cases where parental consent for autopsy 
cannot be obtained, external examination of the baby by a pathologist 
experienced in this area, where possible, should be sought. If this is not possible 
an X-ray of the baby and/or a clinical photograph should be taken and sent to a 
major centre for review. 

Genetic termination of pregnancy 
In cases where a termination of pregnancy has been carried out for fetal malformation, 
an autopsy may still be desirable to confirm the diagnosis or discover unexpected 
associated malformations. 

Congenital anomaly 
Investigations to be performed when an intrauterine fetal death occurs in conjunction 
with a known fetal abnormality. 

  Karyotype - preferably on amniotic fluid obtained by amniocentesis since this 
provides the least contaminated sample, but if maternal consent for this cannot 
be obtained then on cord blood (if obtainable) or fetal skin. The sample should be 
obtained, but karyotyping should only proceed if an anomaly which is indicative 
of a chromosomal abnormality is found at birth or autopsy.  

  Maternal serology for syphilis, CMV, Toxoplasma, Herpes and Parvovirus.  
Serum should be taken and forwarded with the baby. Investigation for 
congenital infection should be pursued if anomalies indicative of infection are 
found (eg. hydrocephalus, hepatomegaly, cataracts, calcification of brain or 
placenta). 

  Maternal antibody screen - serum forwarded with baby for later investigation if 
hydrops is evident at autopsy. 



 
55 

Vasculopathies  
Pre-eclampsia/hypertension, placental abruption and intrauterine growth restriction. 
All should have a thrombophilia screen comprising   
1. At time of delivery   

  Anti-cardiolipin antibody. 
  Lupus anticoagulant. 
  Activated Protein C Resistance. 

2. At three months post-partum   

  Activated Protein C Resistance if previous result low or borderline (&lt;2.5). 
  Homocysteine - may be done earlier if follow-up uncertain. 
  Protein S. 

Pre-eclampsia or non-proteinuric hypertension  
Attention is drawn to those investigations for monitoring maternal welfare published 
by the Australasian Society for the Study of Hypertension in Pregnancy *   
*Brown MA, Hague WM, Higgins J, Lowe S, McGowan L, Oats J, Peek MJ, Rowan JA, Walters BNJ. Consensus 
Statement. The detection, investigation and management of hypertension in pregnancy. Aust NZ J Obstet Gynaecol 
2000;40:133-138.  
Those with early onset pre-eclampsia (&lt;28 weeks) should also have 

  Anti-nuclear antibody 
  Fetal karyotype (see "Congenital anomaly") 

In cases of placental abruption a history of trauma, including domestic or other 
violence, should be sought. The Kleihauer slide (see "Core investigations") should be 
examined if the diagnosis is in doubt and in all Rhesus negative women to determine 
the required dose of anti-D. 
Where intrauterine growth restriction is evident without further evidence of a 
vasculopathy (hypertension, abruption), the following should be performed in addition 
to the thrombophilia screen:   

  Maternal serology for CMV, Toxoplasma and Rubella (if not immune) on held 
maternal serum (see "Core investigations ") 

  Fetal karyotype (see "Congenital anomaly ) 
  Maternal urinary drug screen as well as a drug related history 

Intrapartum deaths which are associated with hypertension, abruption or 
intrauterine growth restriction should be investigated as such, but in the absence of 
these and when the fetus is over 1,000g: - 

  Kleihauer slide examined (See "Core investigations") 
  Cord (or heart) blood (haemoglobin, platelets, nucleated red blood cells) 



 
56 

Unexplained stillbirths 
In the absence of discernible factors pertaining to fetal demise, or any obvious 
congenital anomaly, in addition to the  Core investigations : -  

  Maternal serum bile acids - cord blood bile acids if possible. 
  Maternal serum glucose. 
  Thrombophilia screen (see "Vasculopathies"). 
  Maternal serology - syphilis, CMV, Toxoplasma, Herpes, Parvovirus. 
  Microbiology - fetal throat swab, placental intermembranous swab. 
  Drug history and urine drug screen. 
  Cord or heart blood - haemoglobin, platelets, nucleated red blood cells, blood 

group (for anti-D if mother Rhesus negative). 

  Maternal antibody screen. 
  Kleihauer slide examined. 



 
57 

APPENDIX 9 

Placental histology guidelines 
Histological examination of the placenta provides additional information about 
perinatal deaths and placentas should be sent for examination where possible. 
As a guide, placentas should be sent to Pathology at least from: 
1. All stillborn infants, early neonatal deaths and mid-trimester miscarriages. 
2. All multiple pregnancies with same sex infants. 
3. All triplet and higher order multiple pregnancies. 
4. All cases of discordant twin growth with greater than 20% weight difference. 
5. All cases of prolonged rupture of membranes or suspected chorioamnionitis or 

maternal fever (any cause). 
6. All preterm deliveries. 
7. All cases where birthweight is less than the 10th percentile or greater than the 95th 

percentile for gestational age. 
8. All cases of fetal malformation. 
9. All cases of pregnancy complicated by oligohydramnios, polyhydramnios or 

placental abnormalities detected prenatally (vascular channels, chorioangioma, 
etc). 

10. All cases with a physical abnormality in the placenta (eg. a mass, abnormal colour, 
malodour). 

11. All cases subjected to chorion villus sampling or amniocentesis, if complications 
occur. 

12. ll cases of pre-existing diabetes, pre-eclampsia, systemic lupus erythematosus and 
documented thrombophilias known to be associated with fetal hazard.  

13. All cases of placental abruption. 
14. All retrievals. 
15. All cases where the infant is transferred to a Level III nursery or where the infant 

is severely depressed at birth (Apgar score &lt;5 at five minutes). 
16. All cases of maternal death. 



 
58 



 
59 

Australian birthweight percentiles for 
singleton girls

0

1000

2000

3000

4000

5000

22 24 26 28 30 32 34 36 38 40 42 44

Gestational age (weeks)

Weight (grams) Percentile

3

97

75

50

25

10

90

From: Roberts CL &amp; Lancaster PAL. Australian national birthweight percentiles by gestational age.
MJA 1999;170: 114-118.  Copyright 1999. The Medical Journal of Australia - reproduced with permission.  



 
60 

Birthweight percentile values (g) for live singleton males, Australia, 1991-1994 

Gestation No. births Mean Standard Percentile (gm) 

(weeks) (gm) Deviation 1st 3rd 5th 10th 25th 50th 75th 90th 95th 97th 99th

20 27 385 76 330 380 430

21 43 447 66 410 440 490

22 74 495 80 400 440 490 540 600

23 95 607 92 470 500 550 610 660 710 780

24 135 690 129 470 480 520 610 680 780 860 930 990

25 180 791 132 560 580 620 700 785 870 980 1000 1030

26 235 921 158 610 620 720 840 920 1020 1130 1160 1170

 27 284 1017 209 610 650 740 900 1000 1140 1280 1350 1440

28 361 1157 240 570 670 720 850 1000 1170 1300 1440 1550 1600 1790

29 397 1316 261 670 760 840 950 1170 1340 1480 1640 1740 1810 1900

30 571 1477 313 730 860 960 1080 1270 1490 1680 1860 1950 2050 2270

31 743 1682 311 910 1070 1130 1310 1490 1670 1870 2070 2170 2280 2450

32 1117 1875 378 1020 1150 1230 1400 1640 1890 2100 2320 2470 2690 2980

33 1471 2142 415 1210 1360 1450 1640 1900 2120 2370 2650 2920 3060 3300

34 2657 2358 418 1310 1560 1670 1840 2100 2350 2600 2870 3080 3250 3530

35 4092 2610 413 1600 1830 1960 2110 2360 2590 2850 3140 3330 3490 3770

36 8788 2835 432 1780 2020 2150 2320 2560 2820 3100 3380 3570 3730 3960

37 18660 3089 442 2030 2270 2380 2550 2800 3080 3370 3660 3840 3960 4200

38 51404 3317 431 2310 2520 2620 2780 3030 3310 3600 3870 4050 4160 4390

39 72871 3471 426 2500 2690 2790 2940 3180 3460 3750 4020 4200 4310 4520

40 141553 3610 432 2630 2830 2920 3070 3320 3600 3890 4170 4340 4460 4680

41 55946 3739 443 2730 2930 3030 3180 3440 3730 4030 4310 4490 4600 4820

42 14781 3787 463 2730 2950 3040 3210 3470 3780 4090 4390 4570 4680 4910

43 1267 3698 501 2510 2770 2910 3080 3360 3680 4000 4360 4580 4670 4970

44 409 3612 474 2620 2720 2850 3050 3290 3590 3900 4270 4440 4530 4790

From:  Roberts CL &amp; Lancaster PAL.  Australian national birthweight percentiles by gestational age. MJA 1999; 170:  114-118.                                                                         
 Copyright 1999. The Medical Journal of Australia-reproduced with permission 



 
61 

Birthweight percentile values (g) for live singleton  females, Australia, 1991-1994.  

Gestation No. births Mean Standard Percentile (gm) 

(weeks) (gm) Deviation 1st 3rd 5th 10th 25th 50th 75th 90th 95th 97th 99th

20 12 418 184 345

21 25 414 55 400 420 440

22 71 485 85 400 430 480 540 600

23 79 591 103 470 520 580 640 740

24 115 661 95 490 500 540 600 660 720 780 830 850

25 136 760 116 510 560 620 700 750 840 900 960 980

26 188 865 158 540 550 680 780 865 960 1040 1130 1180

27 231 944 183 600 620 730 830 950 1070 1180 1250 1280

28 287 1060 228 610 700 760 900 1070 1200 1340 1400 1440

29 325 1233 247 630 720 810 890 1070 1250 1400 1510 1580 1660 1820

30 440 1403 275 740 860 945 1045 1220 1420 1560 1730 1885 1950 2100

31 548 1581 336 800 990 1050 1140 1360 1590 1765 2000 2130 2330 2560

32 877 1797 383 920 1070 1170 1340 1560 1780 2000 2230 2470 2640 2970

33 1200 2038 403 1135 1280 1385 1520 1790 2040 2265 2515 2755 2955 3150

34 2086 2282 439 1260 1440 1570 1760 2010 2260 2530 2810 3090 3290 3510

35 3418 2523 433 1520 1740 1840 2030 2260 2490 2760 3100 3340 3500 3710

36 7320 2738 433 1740 1950 2060 2220 2450 2720 3000 3300 3505 3650 3860

37 16105 2967 432 1940 2170 2280 2430 2680 2960 3240 3520 3700 3830 4050

38 47809 3187 419 2220 2420 2520 2660 2900 3170 3460 3730 3900 4020 4220

39 68846 3329 412 2390 2580 2670 2820 3050 3320 3600 3860 4030 4140 4340

40 137570 3463 414 2530 2720 2810 2950 3180 3450 3730 4000 4170 4280 4490

41 53260 3577 421 2630 2820 2910 3050 3290 3560 3850 4130 4300 4410 4620

42 13318 3627 442 2630 2830 2930 3080 3320 3610 3920 4210 4370 4500 4700

43 1285 3539 463 2460 2710 2770 2950 3240 3540 3840 4120 4320 4430 4620

44 433 3490 448 2420 2590 2720 2930 3180 3490 3800 4070 4230 4320 4470

From:  Roberts CL &amp; Lancaster PAL.  Australian national birthweight percentiles by gestational age. MJA 1999: 170:  114-118.                                                                             
 Copyright 1999.  The Medical Journal of Australia-reproduced with permission 



 
62 

APPENDIX 11 

Co-sleeping while breastfeeding: advice to health professionals*  
Bed sharing while breastfeeding has been associated in some studies with unexpected 
infant death.  This was usually when the mother was very fatigued or under the 
influence of alcohol or drugs and therefore difficult to arouse once asleep.  The 
mechanism is not thought to be the mother physically compressing the infant but rather 
the breast interfering with the infant s airflow.  Some infants are particularly susceptible 
to respiratory arrest from minor airway occlusion.  Bed sharing with a parent who 
smokes (even if not smoking in bed and not breastfeeding) increases the risk of Sudden 
Infant Death Syndrome (SIDS). 

Recommendations 
1. Mothers are encouraged to sit up, in or out of bed, with a light on while 

breastfeeding at night.  When a mother is unable to sit up unassisted, breastfeeding 
should be supervised. 

2. Mothers who are taking medication which is sedating or who are excessively 
fatigued are to be supervised while breastfeeding. 

3. A pre-requisite to unattended breastfeeding is a verbal assurance from the mother 
that clarifies to the staff that the mother is in no significant discomfort, is lucid and 
feels competent to breastfeed. 

4. Infants should sleep in a cot next to their mother s bed when she is sleeping. 
5. Pregnant women should receive written information antenatally about the risks 

when breastfeeding and sedated or fatigued, and about co-sleeping especially if a 
parent is a smoker.  This information should be included in any breastfeeding 
information, which is distributed in antenatal clinics or antenatal classes. 

* Adapted from Flinders Women and Children Department of Flinders Medical Centre, Adelaide, 2002,  
   with permission. 

Advice to parents on sleeping in the same bed as your baby* 
Bed-sharing while breastfeeding has been associated in some studies with unexpected 
infant death.  This has usually been when the mother was very fatigued or under the 
influence of alcohol or drugs and therefore difficult to arouse once asleep.  The 
mechanism is not thought to be the mother physically compressing the infant but rather 
the breast interfering with the infant s airflow.  Some infants are particularly susceptible 
to respiratory arrest from minor airway occlusion.  Bed sharing with a parent who 
smokes (even if not smoking in bed and not breastfeeding) increases the risk of Sudden 
Infant Death Syndrome (SIDS). 

Recommendations 
1. If you plan to bring your baby to bed, sit up with a light on while breastfeeding. 
2. If you are unable to sit up, are taking medication that sedates you, or are 

excessively tired, it would be a good idea to have someone else in the room while 
you are breastfeeding. 



 
63 

3. When you plan to go to sleep, it may be better to put your baby in a cot next to your 
bed. 

4. If you decide to keep your baby in your bed, the mattress should be firm, soft quilts 
or pillows should not be placed under your baby, he/she should be placed on 
his/her back and waterbeds should not be used. 

5. If you smoke or have smoked during pregnancy, it would be better if you didn t 
bed-share with your baby, as this has been associated with an increased risk of 
SIDS. 

 
* Adapted from Flinders Women and Children Department of Flinders Medical Centre, Adelaide, 2002,  
   with permission. 

 


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