20050926evidence Base

Evidence base to a preventive
health assessment in Aboriginal

and Torres Strait Islander peoples
Prepared by the National Aboriginal
Community Controlled Health
Organisation as lead agency of the
Chronic Disease Alliance of Non-
Government Organisations, and
endorsed by The Royal Australian
College of General Practitioners
Introduction
Evidence base to a preventive health assessment in Aboriginal and Torres Strait Islander peoples
1
Evidence base to a preventive health assessment
in Aboriginal and Torres Strait Islander peoples
Prepared by the National Aboriginal Community Controlled Health Organisation, lead agency of the
Chronic Disease Alliance of Non-Government Organisations (Aboriginal and Torres Strait Islander
Health).
Members of the Chronic Disease Alliance
National Aboriginal Community Controlled Health Organisation
National Heart Foundation of Australia
National Stroke Foundation
Kidney Health Australia
The Cancer Council Australia
Diabetes Australia
National Rural Health Alliance
Heart Support Australia
The Fred Hollows Foundation
Asthma Foundation
Mental Health Foundation
Australian Tuberculosis and Chest Association
Prepared for The Royal Australian College of General Practitioners
Funded by the Australian Government Department of Health and Ageing
Disclaimer
The Evidence to a preventive health assessment in Aboriginal and Torres Strait Islander peoples is for
information purposes only, and is designed as a general reference and catalyst to seeking further
information about some aspects of preventive care provision to Aboriginal and Torres Strait Islander
peoples.
The RACGP is not engaged in providing medical or other advice or services, and is not responsible for
the results of any actions taken by any person on the basis of any information in this publication, or for
any error in, or omission from, this publication.
While this publication was made possible with funding support from the Australian Government
Department of Health and Ageing, it is a publication of The Royal Australian College of General
Practitioners. The Australian Government Department of Health and Ageing does not warrant or
represent that the information contained in this publication is accurate, current or complete. People
should exercise their own independent skill or judgment or seek professional advice before relying on
the information contained in this publication. The Commonwealth of Australia does not accept any legal
liability or responsibility for any injury, loss or damage incurred by the use of, or reliance on, or
interpretation of, the information contained in this publication.
Published by:
The Royal Australian College of General Practitioners
College House
1 Palmerston Crescent
South Melbourne, Victoria 3205
Australia
Tel 03 8699 0414
Fax 03 8699 0400
Web http://www.racgp.org.au
ISBN 0 86906 264 6
Published August 2005
National Aboriginal Community Controlled Health Organisation. All rights reserved.
Introduction 2
CONTENTS
ACKNOWLEDGMENTS 3
ACRONYMS 5
PREAMBLE 7
METHODOLOGY 10
ADULT HEALTH 16
ALCOHOL PREVENTION OF PROBLEM DRINKING 16
CANCER 27
Early detection of breast cancer 27
Prevention of cervical cancer 36
DENTAL HEALTH 43
DIABETES PREVENTION AND EARLY DETECTION 51
EYE HEALTH 66
Visual acuity 66
Active trachoma 68
Trichiasis 70
KIDNEY DISEASE PREVENTION 73
RESPIRATORY DISEASE COMMUNICABLE 84
Influenza 84
Pneumococcal pneumonia 88
RESPIRATORY DISEASE NON-COMMUNICABLE 100
Smoking 100
Chronic obstructive pulmonary disease 105
SEXUAL HEALTH 116
SUICIDE PREVENTION 127
VASCULAR HEALTH 134
Blood pressure 134
Physical activity 138
Cholesterol and lipids 142
Overweight and obesity 147
Ischaemic heart disease 153
Stroke prevention 161
CHILD HEALTH 176
Anaemia 176
Growth failure 180
Hearing loss 185
Kidney disease 191
Vaccine preventable diseases 194
APPENDIX: CARDIOVASCULAR RISK TABLES 209
Introduction 3
ACKNOWLEDGMENTS
This project acknowledges the direction and guidance in the development of this project provided by the
late Dr Puggy Hunter, National Aboriginal Community Controlled Health Organisation chair until
September 2001.
This project also acknowledges the Kimberley Aboriginal Medical Services Council (Broome, Western
Australia) in the use of the periodic health examination chapter of Aboriginal primary health care: an
evidence-based approach (1999).
Organisational liaison representatives
Dr Sophie Couzos, National Aboriginal Community Controlled Health Organisation
Dr Andrew Boyden, National Heart Foundation of Australia
Dominique Cadilhac, National Stroke Foundation
Tim Mathew, Kidney Health Australia
Dorothy Reading, The Cancer Council Australia
John Lawrence, National Rural Health Alliance
Tanya Cramp, Diabetes Australia
Deborah Schalor, Heart Support Australia
Olga Havnen, The Fred Hollows Foundation
Anne Wilson, Asthma Foundation
Megan McQueenie, Mental Health Foundation
Peter Bradfield, Australian Tuberculosis and Chest Association
Chronic Disease Alliance consultants (Aboriginal and Torres Strait Islander Health)
The following people contributed to the National guide to a preventive health assessment in Aboriginal
and Torres Strait Islander peoples as authors:
Dr Sophie Couzos (editor) Alison Amos
Susan Anderson Dr Andrew Boyden
Professor David Brewster Kate Broun
Domenique Cadilhac Associate Professor Stephen Colagiuri
Dr Ruth Colagiuri Associate Professor Dennis Gray
Professor Graeme Hankey Julie Hassard
Professor Ernest Hunter Tracey Johnston
Dr Rowena Ivers Dr Erin Lalor
Traven Lea Dr Graeme Maguire
Associate Professor Tim Mathew Dr Sandra Meihubers
Dr Richard Murray Dorothy Reading
Dr Steven Skov Professor Hugh Taylor
Melanie Thomas Professor Mark Thomas
Introduction 4
Reviewers
The following people contributed information that was used in the National guide or provided comments
on various drafts of this publication or the review of the Evidence base used to form the National guide.
Acting as a reviewer does not necessarily reflect endorsement of the recommendations in the National
guide.
Susan Anderson
Dr Maggie Brady
Dr Jonathan C Craig
Tania Cramp
Dr Dan Ewald, Central Australian Rural
Practitioners Association
Kathy Hamaguchi
Anthea Hepburn
Professor Joe Hung
Professor Ernest Hunter
Dr Rowena G Ivers
Geoff Miller and Dr Paul Sandery, Northern
Zone Management Unit, Clearing House
for Indigenous Rural and Remote Projects,
Queensland Health
Associate Professor Tim Mathew
Dr Peter Morris
Dr Richard Murray
Professor Frank Oberklaid
Naomi Ralph
Dr Jenny Reath
Mark Shepherd
Dr Michael Stowasser
Associate Professor David Sullivan
Professor Andrew Tonkin
Associate Professor Paul Torzillo
Professor Lindon Wing
Victorian Aboriginal Community Controlled
Health Organisation
National Indigenous Australians Sexual
Health Committee (with particular
acknowledgment to Dr Jan Savage,
Dr David Bradford and Professor
John Kaldor)
Centre for Disease Control (Territory Health
Services), Communicable Disease Control
(SA), Communicable Disease Unit (Qld)
Australian Government Department of Health
and Ageing
Australian Lung Foundation
The Royal Australian College of General Practitioners Technical Reference Group
Dr Jenny Reath, Liaison Officer, The Royal Australian College of General Practitioners
Dr Paul Mercer, The Royal Australian College of General Practitioners National Standing Committee
Quality Care
Dr Nelle van Buuren, Australian Centre for Rural and Remote Medicine
Dr Louis Peachey, Australian Indigenous Doctors Association
Dr Bronwen Harvey, Primary Care Division, Australian Government Department of Health and Ageing
Dr Moira McKinnon, Population Health Division, Australian Government Department of Health and
Ageing
Dr Patricia Fagan, Office for Aboriginal and Torres Strait Islander Health, Australian Government
Department of Health and Ageing
Logistical support
The Board and Secretariat of the National Aboriginal Community Controlled Health Organisation
Sharon Dowsett, Administrative Assistant, and Robyn Milthorpe, Rural, Remote, Aboriginal and Torres
Strait Islander Program of the National Heart Foundation
Dr Jenny Reath and Pauline Curtis, Aboriginal and Torres Strait Islander Health Projects, RACGP
National Rural Faculty
Teri Snowdon, Linda Bailey, Sharon Benson, Jane London, Dr Vivienne Miller, Linda McLaughlan and
Sally Kincaid, RACGP national office
Introduction 5
ACRONYMS
7vPCV 7-valent pneumococcal conjugate vaccine
23vPPV 23-valent pneumococcal polysaccharide vaccine
ABS Australian Bureau of Statistics
ACCHS Aboriginal Community Controlled Health Services
ACEI angiotensin converting enzyme inhibitors
ACIP Advisory Committee on Immunisation Practices
ACIR Australian Childhood Immunisation Register
ACR albumin-creatinine ratio
ACT Australian Capital Territory
AHW Aboriginal Health Worker
AIDS acquired immunodeficiency syndrome
AIHW Australian Institute of Health and Welfare
ALPA Arnhem Land Progress Association
AMI anterior myocardial infarction
AOM acute otitis media
APSGN acute poststreptococcal glomerulonephritis
ARA angiotensin receptor antagonist
ASPRN Australian Sentinel Practice Research Network
AST aspartate aminotransferase
ATSIC Aboriginal and Torres Strait Islander Commission
AUDIT Alcohol Use Disorders Identification Test
BHPS British Heart Protection Study
BMI body mass index
BP blood pressure
BSE breast self examination
CAAAPU Central Australian Aboriginal Alcohol Programs Unit
CARPA Central Australian Rural Practitioners Association
CBE Clinical breast examination
CCCH Centre for Community Child Health
CDC Centers for Disease Control
CER control event rate
CERA Centre for Eye Research in Australia
CHD coronary heart disease
CI confidence interval
COPD chronic obstructive pulmonary disease
CSOM chronic suppurative otitis media
CV cardiovascular
CVD cardiovascular disease
DASH Dietary Approaches to Stop Hypertension
DBP diastolic blood pressure
DCCT Diabetes Control and Complications Trial
DTP diphtheria, tetanus, pertussis
ECG electrocardiography
ESRD end stage renal disease
ESRF end stage renal failure
FBC full blood count
FBG fasting blood glucose
FPG fasting plasma glucose
FTT failure to thrive
GDM gestational diabetes mellitus
GET global elimination of blinding trachoma
GFR glomerular filtration rate
GGT gamma glutamyl transferase
GP general practitioner
GSAT Guidelines, Standards and Audit Team
GTT glucose tolerance test
HBV hepatitis B virus
HDL high density lipoprotein
HDL-C high density lipoprotein cholesterol
HIV human immunodeficiency virus
HPV human papilloma virus
HSV herpes simplex virus
Introduction 6
IARC International Agency for Research on Cancer
IFG impaired fasting glycaemia
IGT impaired glucose tolerance
IM intra muscular
IPD invasive pneumococcal disease
ISP Indigenous Sport Program
MCV mean cell volume
MI myocardial infarction
MV microvascular
NAA nucleic acid amplification
NACCHO National Aboriginal Controlled Community Health Organisation
NAHS National Aboriginal Health Strategy
NATSIS National Aboriginal and Torres Strait Islander Survey
NHFA National Heart Foundation of Australia
NHMRC National Health and Medical Research Council
NIDDM non-insulin dependent diabetes mellitus
NIPII National Indigenous Pneumococcal and Influenza Immunisation Program
NNT number needed to treat
NSW New South Wales
NT Northern Territory
NZ New Zealand
NZMU Northern Zone Management Unit
OATSIH Office of Aboriginal and Torres Strait Islander Health
OM otitis media
OME otitis media with effusion
PCV pneumococcal conjugate vaccine
PEER patient expected event rate
PID pelvic inflammatory disease
PPM part per million
PPV pneumococcal polysaccharide vaccine
RACGP The Royal Australian College of General Practitioners
RRR relative risk reduction
SA South Australia
SANDS Servier Australia National Diabetes Study
SBP systolic blood pressure
SES socioeconomic status
SIDS sudden infant death syndrome
STI sexually transmitted infection
STOP NIDDM Prevent Non-Insulin Dependent Diabetes Mellitus
TIA transient ischaemic attack
TRIPOD Troglitazone in Prevention of Diabetes
UK United Kingdom
UKPDS UK Prospective Diabetes Study
UKWPCHS UK Working Party on Child Health Surveillance
UNICEF United Nations Childrens Fund
URTI upper respiratory tract infection
USA United States of America
USPSTF United States Preventive Services Task Force
VACCHO Victorian Aboriginal Community Controlled Health Organisation
WA Western Australia
WC waist circumference
WHO World Health Organisation
WHR waist-hip ratio
WIC Women, Infants and Children
WPHC well persons health check
Introduction 7
PREAMBLE
The National guide to a preventive health assessment in Aboriginal and Torres Strait Islander peoples
(National guide) is an initiative of the National Aboriginal Community Controlled Health Organisation,
lead agency of the Chronic Disease Alliance of Non-Government Organisations. The Royal Australian
College of General Practitioners (RACGP) supported the development of this guide.
The National guide is intended for all health professionals delivering primary health care to the
Aboriginal and Torres Strait Islander population. This includes general practitioners (GPs), Aboriginal
health workers, nurses and those specialists with a role in delivering primary health care.
The National guide package consists of the following:
The National guide
Recommendations compiled from the review of the Evidence base
Child and adult preventive health life cycle summaries.
Review of the Evidence base
This review of the Evidence base documents the research literature used to form the National guide.
The Chronic Disease Alliance determined that recommendations in the National guide should be based
on a review of the evidence, seeking where possible, existing systematic reviews addressing questions
related to preventive health care, expert opinion and consensus statements of relevance to the
Aboriginal and Torres Strait Islander population. Users of the National guide are encouraged to access
this Evidence base for more information.
Health care providers (particularly in regional and remote areas) are also encouraged to refer to local
guidelines (where they are appropriate and available) in order to optimise preventive health
assessments. Many of the recommendations in the National guide describe health problems that may
be of concern only in certain regional areas. For example, trichiasis screening is not appropriate in
Victoria except when an elderly Aboriginal client from northern Australia is assessed. Consequently,
many recommendations highlight the importance of clinical discretion in decision making.
The National guide makes specific recommendations regarding the elements of a preventive health
assessment in the non-pregnant adult Aboriginal and Torres Strait Islander population as well as
children. The aim is to provide a national evidence based resource that can inform health providers and
policy makers on a defined set of activities that are of particular relevance to this population, or that are
different from those for the non-Indigenous population.
These activities may prevent disease, detect early and unrecognised disease, and promote health in the
Aboriginal and Torres Strait Islander population while allowing for variations based on regional and local
circumstances.
General practitioners should use the recommendations to enhance the clinical care they provide to their
Aboriginal and Torres Strait Islander clients. The National guide aims to complement the RACGP
Guidelines for preventive activities in general practice (known as the red book) by dealing with health
issues that are specific to the Aboriginal and Torres Strait Islander population. The chosen subject areas
represent the key health issues that are amenable to primary health care intervention and contribute to
morbidity and mortality in the Aboriginal and Torres Strait Islander population. Where issues common in
the general Australian population have not been dealt with in this guide (eg. osteoporosis), GPs are
encouraged to cross reference with the red book which is available on the RACGP website at:
http://www.racgp.org.au.
To assist health care providers, the Evidence base used to form the National guide provides a summary
of recommendations from the red book as well as other groups, such as the Central Australian Rural
Practitioners Association and the Northern Zone Management Unit of Queensland Health in north
Queensland.
The authors have presented the information in this guide so that it can apply to both Aboriginal and
Torres Strait Islander peoples. It is recognised that while the health of Torres Strait Islanders is very
similar to the Aboriginal population, they represent a distinct Indigenous Australian population.
Health care providers should use the National guide to systematically appraise current preventive
practice, especially where recommendations for the general population have previously been applied to
Aboriginal and Torres Strait Islander clients. Providers may also benefit by appraising certain screening
Introduction 8
activities for which there is little evidence. These activities may draw resources away from other
activities to improve the health of the Aboriginal and Torres Strait Islander population, eg. risk factor
modification and immunisation programs.
General practitioners may undertake preventive health assessment activities as part of their normal
consultations. Medicare benefits are payable for a medical examination or test on a symptomless patient
by that patients own medical practitioner in the course of normal medical practice, to ensure the patient
receives any medical advice or treatment necessary to maintain his/her state of health.
Specific Medicare rebates for preventive health assessments are also available for Aboriginal and
Torres Strait Islander peoples in two different age groups:
the Enhanced Primary Care (EPC) health assessment for older Australians items (704 and 706)
provide for annual voluntary health assessments for Aboriginal and Torres Strait Islander people
aged 55 years and over, and
the Aboriginal and Torres Strait Islander adult health check item (710) provides for 2-yearly health
checks for Aboriginal and Torres Strait Islander people aged 1554 years inclusive.
The Medicare requirements for the EPC 55+ health assessment and adult health check items vary in
some respects from the recommendations contained in the National guide. The National guide covers all
age groups, whereas the Medicare items are designed for specific age groups. In some areas, the
National guide recommends checking/testing more frequently than 2-yearly. The National guide does
not cover some elements of the 55+ EPC health assessment (eg. activities of daily living) and some of
the optional elements of the adult health check (eg. reproductive health, skin conditions and hearing loss
in adults). Refer to the RACGP Standards and guidelines for the Enhanced Primary Care Medical
Benefits Schedule items (2000) for more information on older age health assessments.
While the National guide is a valuable and important reference document for GPs providing health
assessments for Aboriginal and Torres Strait Islander people, GPs need to be aware of, and comply
with, the specific MBS requirements when providing these services. General practitioners are advised
to check the requirements in the current edition of the Medicare Benefits Schedule before claiming these
items.
Why preventive health assessments are necessary
There is strong evidence that the delivery of clinical preventive health services improves health
outcomes in the general population.
1
These services include five types of interventions: immunisation,
screening for asymptomatic disease, chemoprophylaxis (using medication to prevent the onset of
disease), counselling and other ways to encourage client behavioural change, as well as primary health
care influences over environmental factors.
Primary care providers often miss opportunities for the prevention of chronic disease and associated
complications, especially if clients are Aboriginal or Torres Strait Islanders. Health service utilisation
data indicates that this population has reduced access to mainstream health services and most hospital
admissions are attributable to potentially preventive health conditions.
2
Aboriginal people and Torres
Strait Islanders used the MBS at only one-quarter of the rate of other Australians in 19951996, and at
just over one-third in 19981999, yet their overall health needs are approximately three times higher.
3,4
When preventive opportunities are missed, this leads to a higher dependency on hospital care which
increases health costs. The Aboriginal and Torres Strait Islander population has much higher rates of
hospital admission for almost every health problem than other Australians. In 19981999, Indigenous
Australians were admitted to hospitals across Australia nearly two times more than other Australians.
Consequent life expectancy is much lower Aboriginal or Torres Strait Islander males born in
19982000 expected to live to 56.0 years, almost 21 years less than the 76.6 years expected for all
males.
5
Many chronic diseases within the Aboriginal population are unrecognised by clients. This has been well
documented for diseases known for their insidious onset such as diabetes, hypertension, cardiovascular
disease and chronic renal failure. The preventive approach requires the service to seek the client while
the client is asymptomatic. It involves activity for primary prevention (to prevent the onset of disease),
secondary prevention (to detect preclinical disease for cure or prevention of disease progression) and to
a less extent, tertiary prevention (to minimise the consequences for those who already have disease).
Preventive health assessments also involve the assessment of comorbidity in clients who already have
chronic disease.
Introduction 9
The preventive approach to health has shown returns on investment in mainstream Australia, especially
federal expenditure on immunisation, public health campaigns and the incorporation of preventive
measures into primary care.
6
Aboriginal and Torres Strait Islander people have a significant capacity to
benefit from preventive health care.
Given the reduced access to preventive health care of this population and the huge burden of
undiagnosed disease, effort needs to focus on measures to ensure Aboriginal and Torres Strait Islander
clients who are symptomatic of disease, as well as those who do not yet know they have disease
(subclinical), have access to help.
Implementation of preventive interventions
Implementation of preventive health assessments requires health care providers to identify the target
population. General practitioners report problems with identifying Aboriginal or Torres Strait Islander
clients within their practice, eg. targeting for pneumococcal vaccination.
7,8
Indigenous Australians are
also significantly under-represented in encounters within private general practice.
Most private GPs see few Indigenous Australians as clients and are often unable to develop specific
expertise in delivering primary health care to this population. They are uncertain about identifying
Indigenous clients and find it difficult to develop links with the Aboriginal and Torres Strait Islander
communities or workforce. General practitioners have an important role in facilitating the self
identification of Aboriginal and Torres Strait Islander clients.
In order for a person to self identify as being Aboriginal or Torres Strait Islander and accept this being
recorded on their medical records, a culturally supportive and culturally safe environment needs to be
established and continuously demonstrated. Guidelines have been developed to assist GPs with this
issue.
9
Most preventive interventions are efficiently delivered opportunistically in the clinical encounter where
primary health care services are available. Others are delivered through integrated approaches between
primary health care providers and other services such as in the planning and delivery of breast cancer
screening. Community based screening using Aboriginal community visits (especially for sexual health
screening) has been widely implemented in north Queensland
10,11
and also in Victoria.
12
Implementation of a preventive health assessment and preventive interventions ideally involves
strategies for both clients and health care providers. Usually multiple strategies are most effective as
exemplified by those used to increase adult vaccination (see Respiratory disease Communicable
section). These strategies may include opportunistic screening (case finding) and reminder systems
within clinic settings, as well as outreach programs such as vaccination in non-traditional settings.
A preventive assessment may be undertaken in a single session between client and health provider,
which may or may not simultaneously address other concerns the patient may have, or be delivered
incrementally over a number of sessions. Whether clinic based or community based, systems used to
deliver a preventive assessment need to support a holistic assessment of the client in recognition of the
interdependence of many risk factors and determinants of disease.
Implementation of a preventive health assessment should be undertaken by health care providers who
have the capacity to undertake, or to arrange for, appropriate management of any abnormalities found
during the assessment. Providers should be aware of the potential psychosocial impact of preventive
care, particularly when screening results in the diagnosis of a new condition. Informed consent should
be obtained for the screening and adequate counselling provided when the patient is advised of the
result.
A supportive health policy is also critical to the implementation of a preventive health assessment such
as through the provision of financial incentives and workforce support. Those who have been screened
also need to be treated, and consequently, an effective screening program will increase the demand for
care when many primary health care services whose clientele are primarily Aboriginal or Torres Strait
Islander are already under-resourced. Any plans to reduce premature and excess Aboriginal morbidity
and mortality will need to include investment in the management of previously unrecognised disease.
Introduction 10
METHODOLOGY
The National guide was developed under the leadership of the National Aboriginal Community
Controlled Health Organisation (NACCHO) by a consortium of non-government organisations. This
alliance, known as the Chronic Disease Alliance (CDA) for Aboriginal and Torres Strait Islander health
was established in September 2000. The project for developing the National guide was instigated by the
former Chair of NACCHO in July 2001.
Organisational liaison representatives from the alliance membership formed the project management
team whose role was to coordinate the drafting teams within their respective institutions in the
development of the National guide. The Royal Australian College of General Practitioners (RACGP)
assisted in the development of the guide by convening the Technical Review Group (TRG) which
included representation from the following organisations:
The RACGP National Standing Committee Quality Care
Australian Indigenous Doctors Association
Australian College of Rural and Remote Medicine
Australian Department of Health and Ageing (Office of Aboriginal and Torres Strait Islander Health,
Primary Care Division and Population Health Division).
The purpose of the TRG was to appraise the content of the National guide and provide advice regarding
its development. This guide formed one of the projects supported by the RACGP National Rural Faculty
as part of the Aboriginal and Torres Strait Islander Health projects funded by the Australian Department
of Health and Ageing.
Organisational liaison representatives from the alliance membership met on several occasions to
develop the National guide, however, most of the work was conducted within their own organisations
and communicated electronically to the coordinating institution (NACCHO).
It was agreed at the commencement of the project that the methodology used to develop Aboriginal
primary health care: an evidence-based approach,
13
which had summarised evidence pertaining to a
preventive health assessment in the Aboriginal and Torres Strait Islander population, would be used in
this project. This earlier product was in need of revision and was used for the development of the
National guide with the authors permission.
14
Using predefined methodology ensured early and immediate commencement of this work and the pre-
existing product had a reputation and credibility among Aboriginal Community Controlled Health
Services and other health care providers to Aboriginal populations.
The selection of elements comprising a preventive health assessment
The broad scope of the National guide required the identification of key subject areas early in its
development. The organisational liaison representatives from the alliance membership selected these
subject areas as representation of the key health issues that were potentially amenable to primary
health care intervention and contributable to morbidity and mortality in the Aboriginal and Torres Strait
Islander population. Consequently, many elements of the preventive health assessment were uniquely
applicable to the Aboriginal and Torres Strait Islander population.
Despite its breadth, it was not possible to include all health issues considered important by the project
management team and the TRG. Limitations resulted from time and resource constraints, as well as a
lack of availability of experts in certain subject areas. Some preventive activities were omitted because
they were considered to be undertaken outside the primary care clinical consultation (eg. screening for
tuberculosis). A future edition may examine the research evidence for a number of additional elements
of preventive health assessment in the Aboriginal and Torres Strait Islander population. These might
include: prepregnancy screening and counselling, preventive interventions for a range of mental and
social health issues including illicit substance use, and other health problems such as incontinence and
skin infections (see Review date).
Preventive interventions were based on five categories; immunisation, screening, behavioural factors,
chemoprophylaxis and environmental influences. The research evidence relevant to each form of
preventive intervention was then investigated, provided the intervention was applicable within primary
health care service delivery models (including many population based interventions).
Other factors that influenced the selection of interventions for evaluation included:
Introduction 11
knowledge of interventions that had the potential to free up resources within primary health care by
documenting where effort may be better invested
issues which had a high level of interest among providers and decision makers.
Development teams
In view of the broad and multidisciplinary nature of the preventive interventions considered in the
National guide, organisational liaison representatives from the alliance membership agreed that each
organisation would appoint development teams to research and draft subject areas in the guide. The
structure of the development team was different in each non-government organisation. Usually one
person was nominated to conduct the review of the literature in consultation with other organisational
experts. In some, multidisciplinary teams were formed to review the evidence (eg. the National Stroke
Foundation team included public health, epidemiology, nursing, medical and allied health expertise).
Others used existing clinical committees and relevant members of these committees to review the
literature (eg. National Heart Foundation and Cancer Council Australia). As drafts of sections were
produced, they were appraised by the organisational representatives before submission to NACCHO for
further research and editing as required.
Additional consultants were invited to draft sections that were unable to be completed by alliance
members. These included experts in areas such as dental health, problem drinking, suicide prevention
and sexually transmitted infections. Independent expert committees were also consulted to review
drafts, eg. the National Indigenous Sexual Health Committee appraised the section on Sexually
transmitted infections.
Review of the evidence
The primary form of evidence collated by authors comprised systematic reviews and meta-analyses of
the primary research literature. These were found through MEDLINE searches,
15
use of the Cochrane
Database of Systematic Reviews
16
, use of Clinical Evidence (BMJ),
17
and search of databases such as
the Agency for Healthcare Research and Quality (USA),
18
Centers for Disease Control (USA),
19
Canadian Task Force for Preventive Health Care,
20
Health Technology Assessments from the UK,
21,22,23
USA
24
and New Zealand.
25
This methodology was adopted to avoid duplicating existing syntheses of the
research literature.
In the absence of systematic reviews, the primary research literature (randomised controlled trials and
others studies) were found using MEDLINE. Other evidence based clinical practice guidelines were also
sought.
26,27,28
A search for grey literature was rarely necessary, but when used, the source was the
Aboriginal and Torres Strait Islander HealthInfonet.
29
Government and non-government reports and
research publications from the Australian Institute of Health and Welfare and the Australian Bureau of
Statistics were also sourced.
Contact was also made with a number of professional and government institutions for the provision of
additional and unpublished information.
Where recent and relevant clinical practice guidelines had already been developed, these were sourced
without going back to the primary research literature (eg. current National Heart Foundation Clinical
Guidelines and the National Cancer Prevention Policy).
The Central Australian Remote Practitioners Association (CARPA) provided drafts of revised
recommendations from the Northern Territory CARPA Standard treatment manual for cross referencing
within the National guide. The Northern Zone Management Unit also provided drafts from the Adult
Health Check Program in north Queensland for use in the review of the Evidence base underpinning the
National guide. Providers of the Well Persons Health Check Programs such as the Victorian Aboriginal
Community Controlled Health Organisation also provided information useful to the review.
Summarising the evidence
Each team was provided with a framework to assist in summarising the body of evidence that
considered each of the five types of preventive interventions (immunisation, screening, behavioural
factors, chemoprophylaxis and environmental influences) and identified gaps in the evidence.
Introduction 12
In gathering the evidence, we asked two main questions:
Are mainstream resources already available to assist providers in managing these problems?
How could differences in the epidemiology and determinants of these health problems (as
documented for the Aboriginal and Torres Strait Islander population) alter their management? Eg.
when considering immunisation, the recommendations of existing expert bodies was collated, in
addition to research evidence for strategies which would enhance vaccine coverage in the
Indigenous Australian population.
When assessing screening activities for inclusion in the guide, we considered the World Health
Organisation screening criteria where possible.
30
The criteria helped to make decisions for or against
screening for diseases or risk factors.* Screening recommendations are subject to modification
according to different prevalence of disease. The higher the prevalence of disease, the better the
predictive value of the screening test. This was applied to diabetes screening in the Evidence base.
As the bulk of the research evidence comprised secondary research (meta-analyses, systematic
reviews and existing evidence based guidelines), no explicit inclusion or exclusion criteria for synthesis
of the evidence were used. The context in which the studies were done (eg. characteristics of the
population) was reported where possible in the narrative summary of the evidence, however, the quality
of the studies was not assessed. This was because often the evidence used was already assessed for
quality, eg. Cochrane reviews. Moreover, we found few Australian clinical trials on prevention and
treatment relevant to the Aboriginal and Torres Strait Islander population which supported the finding
reported elsewhere.
31
Consequently, expert opinion was very important in interpreting the evidence and making judgments
about its relevance to Aboriginal and Torres Strait Islander health. Expert opinion was occasionally used
to form judgments regarding whether or not a preventive intervention should be recommended,
however, more often it was necessary to reach agreement regarding the frequency of intervention or the
age to commence an intervention. On the basis of disease prevalence data, almost all preventive
interventions are recommended to commence at an earlier age in Aboriginal and Torres Strait Islander
people than the general population. For example, disease prevalence data was used to justify earlier
screening for diabetes in the Aboriginal and Torres Strait Islander population.
Recommendations pertaining to normal thresholds for measurements such as body mass index or waist
circumference were based on data from the general population in the absence of data specific to the
Aboriginal and Torres Strait Islander population.
The absence of data led to questions regarding the requirement for specific data pertaining to Aboriginal
people and Torres Strait Islanders before clinical recommendations can be evidence based. The
National guide was developed with the view that there had to be evidence against the ability to
generalise before interventions were deemed not to apply to the Aboriginal and Torres Strait Islander
population.
Given the heterogeneity within this population with regions facing different health problems, or the same
health problems but to different degrees, the need for regional or community specific (perceived to be
potentially duplicative) research is controversial. The effectiveness of preventive interventions involving
medications may be less dependant on differences in pharmacodynamics between Aboriginal and non-
Aboriginal recipients of therapy than on Aboriginal community values, culture, social expectations,
expertise in program delivery and resources. The key message regarding generalisability is that too
much emphasis is placed on whether research findings apply to a certain patient population. When in
fact, energy currently devoted to agonising over the minutiae of the inclusion and exclusion criteria
used to generate the research evidence is better spent considering how it can be applied to the special
situations and values of our patients.
32
The recommendations that make up the National guide were drafted from the narrative summary of the
evidence in the review. When there were disagreements regarding the interpretation of the evidence,
development teams used an informal consensus process, including discussion with independent
reviewers to reconcile these differences.

* Screening involves the systematic detection and management of disease before symptoms develop (preclinical
phase). Screening is warranted when management of the disease in the preclinical phase confers benefits
additional to those obtained if the disease is diagnosed and treated when the patient becomes symptomatic and
seeks clinical help
Introduction 13
Review of drafts
The National guide process used numerous independent expert reviewers to appraise the drafts of each
subject area (see Acknowledgments). In addition, members of the TRG as well as external committees
such as the National Indigenous Australians Sexual Health Committee reviewed drafts of the National
guide.
Role of the funding source
The National guide was initiated by NACCHO and the Chronic Disease Alliance of NGOs before the
receipt of funding. Two grants from the Australian Government Department of Health and Ageing were
subsequently provided through the RACGP the first to assist in the development of the content of the
National guide and the second to assist with the editing and endorsement process. The sponsor of this
project had no involvement in the conception and design of the guide, collection, analysis, and
interpretation of data. Departmental representatives appraised drafts and made recommendations to
NACCHO and the RACGP for improvements in some areas of content and the format of the guide.
The grants were used to support NACCHO and the RACGP in coordinating, drafting and editing the
guide. Alliance members were not funded from this grant except in the provision of a small subsidy for
the cost of consumables. The generosity of each alliance member is acknowledged in covering the cost
of his/her transport, time and expenses incurred in the drafting process.
Review date
Organisational liaison representatives of the CDA and members of the TRG recommend that this guide
be reviewed and revised no later than 3 years after its publication.
Levels of evidence
The definitions of the type of evidence used in the National guide are those used by the RACGP in the
Guidelines for preventative activities in general practice (Updated 5th edn, July 2002). These were
adapted from those published by the National Health and Medical Research Councils (NHMRC) How to
use the evidence: assessment and application of scientific evidence (2000) which is available on the
NHMRCs website at: http://www.nhmrc.gov.au/publications/pdf/cp69.pdf.
The RACGP evidence grading scheme was used because the NHMRC levels of evidence exclude
expert opinion and consensus from an expert committee in the grading (shown as level V below). A vast
number of grading schemes have been developed from around the world in the past few decades.
Readers are advised that selection from these evidence grading systems is dependant on the reason for
measuring evidence strength, the type of studies that are being summarised, staff, time, and financial
resources.
33
The RACGP grading scheme describes research related to therapy, prevention, or
aetiology/harm. It does not describe research related to diagnostic (such as laboratory testing), or
prognostic studies or economic analyses.
The definitions of the levels of evidence used in the National guide are set out as follows:
Level Type of evidence
I
Evidence obtained from a systematic review (SR) of all relevant randomised controlled trials
II
Evidence obtained from at least one properly designed randomised controlled trial
III Evidence from any of the following:
well designed pseudo-randomised controlled trials
comparative studies (including SR of such studies) with concurrent controls and allocation
not randomised
cohort studies
case control studies
interrupted time series with a control group
comparative studies with historical control or interrupted time series without a control group
IV
Evidence obtained from case series, either post- or pre-test and post-test
V Opinions of respected authorities based on clinical experience, descriptive studies or reports
of expert committees
Introduction 14

References
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and Torres Strait Islander and other Australian populations. Aust N Z J Public Health
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3 Expenditures on health services for Aboriginal and Torres Strait Islander people, op. cit.
4 Australian Institute of Health and Welfare. Expenditures on health services for Aboriginal and
Torres Strait Islander people 19989. AIHW Cat. no. IHW 7. Canberra: Australian Institute of
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[Accessed 22 June 2004].
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8 Population Health Education for Clinicians (PHEC) Consortium. Population health module in
Aboriginal health. Canberra: Commonwealth of Australia, 2001.
9 NACCHO. The conjugate pneumococcal vaccine and the issue of Aboriginal identification.
Canberra: NACCHO, January 2001. [Unpublished].
10 OATSIH. Better health care: studies in the successful delivery of primary health care services for
Aboriginal and Torres Strait Islander Australians, 2001. Available at:
http://www.health.gov.au/oatsih/pubs/bhcs.htm. [Accessed 22 June 2004].
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May 2001, Sydney.
12 Briggs L. Well person's health check. [Abstract] 12th National Health Promotion Conference:
Inequalities in health reflecting back, stepping forward. 29 October 1 November 2000, Hotel
Sofitel, Melbourne.
13 Couzos S, Murray RB. Aboriginal primary health care: an evidence-based approach. 2nd edn.
Melbourne: Oxford University Press, 2003.
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health care: an evidence-based approach. Melbourne: Oxford University Press, 1999.
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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi. [Accessed 29 June 2004].
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17 BMJ Publishing Group. Clinical Evidence, 2004. Available at: http://www.clinicalevidence.com.
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at: http://www.ahrq.gov. [Accessed 29 June 2004].
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http://www.cdc.gov. [Accessed 29 June 2004].
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Available at: http://www.ctfphc.org. [Accessed 29 June 2004].
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http://www.ncchta.org/htapubs.htm#314. [Accessed 29 June 2004].
22 National Institute for Clinical Excellence. Published appraisals, 2004. Available at:
http://www.nice.org.uk/catrows.asp?c=153. [Accessed 29 June 2004].
23 Centre for Reviews and Dissemination. CRD systematic reviews and other projects, 2004.
Available at: http://www.york.ac.uk/inst/crd/listcomp.htm. [Accessed 29 June 2004].
24 National Library of Medicine. Health services/technology assessment text, 2004. Available at:
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat. [Accessed 29 June 2004].
Introduction 15

25 Christchurch School of Medicine. New Zealand health technology assessment clearing house for
health outcomes and health technology assessment, 2004. Available at: nzhta.chmeds.ac.nz/.
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28 Diabetes Australia. Minimising the impact of diabetes, 2004. Available at:
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31 Morris PS. Randomised controlled trials addressing Australian aboriginal health needs: a
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systematic reviews to individual patients. Evidence-Based Medicine 1998;3(6):1656.
33 West S, et al. Systems to rate the strength of scientific evidence: evidence report/technology
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Evidence-based Practice Center under contract no. 290-97-0011). AHRQ Publication No. 02-E016.
Rockville, MD: Agency for Healthcare Research and Quality, April 2002.
Alcohol Prevention of problem drinking
16
ADULT HEALTH
ALCOHOL PREVENTION OF
PROBLEM DRINKING
Authors
Dr Sophie Couzos, Public Health Officer, National Aboriginal Community Controlled Health Organisation
Professor Ernest Hunter, University of Queensland
Associate Professor Dennis Gray, National Drug Research Institute, Curtin University of Technology
Dorothy Reading, Cancer Council Australia
Acknowledgment
Dr Maggie Brady, Centre for Aboriginal Economic Policy Research, Australian National University
PROBLEM DRINKING
Burden of disease
Excessive alcohol consumption can lead to significant multi-system disease and death. It can also have
many social consequences, such as family disruption, child abuse, unemployment, depression, suicide,
violence, homicide and incarceration in prison.
In 1998, the National Drug Strategy Household Survey indicated that 8% of Australian male drinkers and
4% of females usually drink alcohol at levels considered hazardous to health. The overall proportion of
Aboriginal and Torres Strait Islander people who drink alcohol (62%) is smaller than that of the non-
Indigenous population (72%), however, those who do drink do so in more harmful quantities. This risky
drinking occurs most commonly in the 2534 year age group.
1
In the 2001 National Health Survey, 45%
of Indigenous adults reported consuming no alcohol over the preceding week or never having consumed
alcohol, compared with only 34% non-Indigenous Australians. Approximately 11% of both Indigenous
and non-Indigenous Australians drank alcohol at levels considered risky for health. In the 1824 year
age group, Indigenous males were less likely than non-Indigenous males to consume alcohol at risky
levels (6% compared with 14% respectively).
High rates of problem drinking have been correlated with indicators of socioeconomic disadvantage
such as leaving school early (before 15 years), unemployment, welfare dependency and poverty
(earning capacity <$10 000 per annum) in the 1995 National Health Survey of Indigenous Australians.
2
A study in Albany, Western Australia (WA) reported that Indigenous Australians aged 1517 years who
were unemployed were 13.5 times more likely to be frequent poly-drug users (frequent users of some
combination of tobacco, alcohol and cannabis and occasional users of volatile substances or other
drugs) than those who were employed, in training, or still at school (p = 0.007).
3
Problem drinking
contributes substantially to Aboriginal ill health.
4
In WA in the period 19831991, Aboriginal males were
five times more likely to die from alcohol related causes than non-Indigenous males.
5
Aboriginal and Torres Strait Islander people experience higher rates of alcohol related deaths and
greater hospitalisation rates than the non-Indigenous population. Excessive alcohol consumption
contributes to Aboriginal and Torres Strait Islander deaths due to homicide, suicide, injuries, untreated
pneumonia, alcohol related liver disease and road accidents and compounds comorbid physical and
mental health conditions.
6
Problem drinking increases the risk of sexually transmitted infections.
7
Death
rates for injuries are much higher (more than four times) in Aboriginal people and Torres Strait Islanders
than in the non-Indigenous population.
8,9
At least 50% of all injuries and 88% of assault injuries in
Aboriginal communities in Cape York, Queensland over 19961997 were alcohol related.
10
The National
17
Mental Health Strategy notes that there are alarming rates of comorbidity of alcohol abuse with mental
health problems.
11
Excessive alcohol is also a risk factor for certain cancers. For cancers of the larynx, oropharynx and
oesophagus, there is evidence that alcohol and tobacco smoking have a synergistic effect (ie. act in
combination to increase the risk more than the effect of each risk factor on its own).
12
Very high levels of
alcohol consumption (>2000 g/month) significantly increase the risk of lung cancer by 1.5 times
compared with non-drinkers in meta-analysis of cohort and case control studies.
13
There are also
indications that alcohol and hepatitis B virus infection may exert a joint effect in cancer of the liver.
14
An
important difference was noted in liver cancer between Australian Aboriginal and non-Indigenous
Australians, where the incidence rate and the rate of deaths from liver cancer were 3.5 and 3.6 times
higher for Aboriginal males in a WA study.
15
Exposure to alcohol in-utero can also damage infants.
16
While data are limited, data for the period
19801993 from the Birth Defects Registry of Western Australia reveals that almost three-quarters of
the identified cases of foetal alcohol syndrome occurred in Aboriginal infants, with a birth prevalence
rate of 1.1 per 1000. This compares with the rate of 0.02 per 1000 for non-infants. These figures
suggest levels of increased risk similar to that among Native Americans in North America, where alcohol
and pregnancy is now considered a major public health issue.
17
Studies of alcohol consumption among Aboriginal and Torres Strait Islander people highlight several
important points:
18,19,20
The frequency of alcohol consumption among Aboriginal and Torres Strait Islander people is related
to where they live and to the availability of alcohol and financial resources
Living in a town and being in paid employment is associated with more moderate use of alcohol
About one-sixth of Aboriginal and Torres Strait Islander drinkers give up alcohol, generally in their
40s
The most common reasons given for giving up alcohol are health and family concerns.
Types of preventive intervention
Immunisation Screening Counselling Chemoprophylaxis Environmental
modification
Nil Yes
assessment
tools to
measure
intake
(AUDIT)
Yes
brief
intervention
Yes
acamprosate
naltrexone
disulfiram
(Antabuse)
Yes
community based
programs
liquor licensing
regulations
marketing and
industry
regulation
strategies to
prevent alcohol
impaired driving
Evidence of the effectiveness of preventive interventions
Methods for the control of alcohol abuse are varied and include an individual approach or a community
approach.
Screening and counselling
In 1998, only 56% of Australians surveyed could correctly identify the number of standard drinks
required for safe drinking.
21
The National Health and Medical Research Council (NHMRC)
22
has
identified risk levels for various patterns of drinking on the basis that one standard drink contains 10 g of
alcohol (Table 1).
18
Table 1. Risk levels for various patterns of drinking
23
Risk of harm in the short term
Low risk
standard drinks
Risky
standard drinks
High risk
standard drinks
Males on any one day Up to 6 on any one
day, no more than 3
days per week
710 on any one day 11 or more on any one day
Females on any one day Up to 4 on any one
day, no more than 3
days per week
56 on any one day 7 or more on any one day
Risk of harm in the long term
Low risk
standard drinks
Risky
standard drinks
High risk
standard drinks
Males on an average day Up to 4 per day 56 per day 7 or more per day
Men overall weekly level Up to 28 per week 2942 per week 43 or more per week
Females on an average day Up to 2 per day 34 per day 5 or more per day
Females overall weekly level Up to 14 per week 1528 per week 29 or more per week
Adapted from NHMRC. Australian alcohol guidelines: health risks and benefits, 2001
Numerous systematic reviews have reported that screening for problem drinking followed by brief
intervention (provision of information and advice) is effective in reducing consumption of alcohol.
24
A
meta-analysis of studies with a 612 month follow up showed that brief (520 minutes) and extended
(several visits) interventions by general practitioners (GPs) providing information on alcohol
consumption and risks aimed at reducing alcohol intake within primary health care were effective for
women and decreased alcohol intake by an average of half a drink per day.
25
In addition, interventions delivered by a range of health care professionals (generalist and specialist
physicians, psychiatrists, nurses and social workers) to reduce alcohol consumption among problem
drinkers in various health care settings (primary care, specialist clinic, hospital but excluding clients
attending alcohol treatment clinics) appear effective in general populations.
26
Brief interventions in this
systematic review comprised patient assessment, patient education, counselling, goal setting and
monitoring of serum gamma glutamyl transferase (GGT) levels. None of the studies demonstrated any
statistically significant differences in alcohol related morbidity in response to the intervention. The
optimal intensity of treatment and the most effective components of brief interventions were unclear.
A further meta-analysis reported that brief interventions of less than 1 hour incorporating simple
motivational counselling techniques, education in the harm of heavy drinking and advice to moderate
drinking with follow up sessions after the initial intervention (up to three sessions) were effective in
moderating drinking patterns in heavy drinkers. Heavy drinkers who received a brief intervention were
twice as likely to moderate their drinking 612 months after an intervention when compared with heavy
drinkers who received no intervention.
27
A systematic review of studies involving use of screening questionnaires such as the 10 question
Alcohol Use Disorders Identification Test (AUDIT) showed that this was most effective in identifying
subjects with at-risk, hazardous or harmful drinking (sensitivity 5197%; specificity 7896%). The use of
formal screening instruments over other clinical measures to increase the recognition of alcohol
problems in primary care was supported.
28
The AUDIT is widely used by Aboriginal and Torres Strait Islander health care providers and can be
accessed via the internet.
29
However, some difficulties with using this test have been reported in the
Aboriginal health setting. One study reported that use of the AUDIT was intrusive and some questions
were poorly understood. Screening for alcohol intake using two questions examining the average days
per week the client drank and the amount and type of drinks per day were preferred, although any
questioning regarding alcohol intake was thought to be intrusive for some health workers.
30
In the Aboriginal and Torres Strait Islander population, detection of hazardous drinking from a young
age is important as few persons take up drinking after 30 years. Early detection and brief intervention
may alleviate ongoing medical or social problems and reduce future risks from excessive alcohol intake,
although few studies have evaluated brief interventions in the Aboriginal and Torres Strait Islander
context.
31
19
The elements of brief intervention recommended by the Office of Aboriginal and Torres Strait Islander
Health (OATSIH) are shown in Box 1. The manner in which counselling is delivered is important, as
responses to stereotypes can have a significant impact on the delivery of appropriate public health
services when socioeconomic dilemmas are considered moral disabilities.
32
Biased attitudes from health
providers may perpetuate poor health status, reinforce negative stereotypes and reduce the
effectiveness of their health care provision.
33
Some outcomes expected from early detection and reduced problem drinking in the Aboriginal and
Torres Strait Islander population are shown in Table 2, based on the reported effectiveness of
interventions in the general population.
Box 1. Elements of brief intervention for problem drinkers
34
Simple advice about safe drinking
Personalised advice based on a presenting problem or test result
Referral to specialist service or therapist
Brief motivational interview
Discussion of practical ways to reduce or avoid alcohol consumption, relevant to the experience
and home environment of the client.
Extracted from: OATSIH. National recommendations for the clinical management of alcohol related problems in
Indigenous primary care settings, 2000
Screening for problem drinking using biological markers such as GGT has been shown to offer good
specificity (7889%) but poor sensitivity (4052%) and therefore is only advocated for monitoring
alcohol consumption in those attempting reduction and not for routine population screening.
35
There is
anecdotal evidence that it is useful as a trigger for motivating behavioural change.
36
The mean corpuscular volume of erythrocytes has also been used as an indicator of alcohol abuse and
in combination with GGT is useful for diagnosis with acceptable sensitivity but poor specificity.
37
Others
have reported that a combination of common laboratory tests (to create an alcohol consumption score)
including bilirubin ratio, monocyte count, high density lipoprotein (HDL) cholesterol, GGT and aspartate
aminotransferase (AST) predict heavy drinking.
38
Chemoprophylaxis
The role of chemoprophylaxis in preventing problem drinking is changing. While there was enthusiasm
by some practitioners in the 1970s and 1980s for the use of aversive conditioning using disulfiram in
Indigenous populations, current international evidence does not support its widespread use. There is,
however, some anecdotal evidence of its adjunctive use with carefully selected clients.
39
The
effectiveness of more recent approaches (acamprosate and naltrexone) shown to be effective in other
populations, has not as yet been studied for the Aboriginal and Torres Strait Islander population.
Three Cochrane reviews have examined pharmacotherapy for the control of problem drinking. While the
impact of these treatments in the prevention of alcohol related morbidity and mortality was not
examined, control of problem drinking can prevent alcohol related injuries (27% reduction in drinking
related injuries and accidents and 65% reduction in accidental and violent deaths) as shown in a
systematic review of trials. Whether this is mediated by reductions in alcohol consumption, which is the
most plausible explanation, or by other aspects of treatment for problem drinking (such as social
support) is unclear
40,41
(see also Table 1).
There is good evidence that acamprosate enhances abstinence, reduces drinking days and is well
tolerated. Studies involving disulfiram have been methodologically weak and have mixed results.
42,43
Natrexone at a dose of 50 mg/day is effective in reducing alcohol consumption in the short term. There
appears to be insufficient evidence that naltrexone is superior to acamprosate and it may be less
effective than disulfiram. Combined naltrexone and acamprosate treatment is currently being trialled.
44
There is little clinical experience with the use of acamprosate in the Aboriginal and Torres Strait Islander
population.
45
Environmental factors
Community based preventive and treatment programs for problem drinking need to be planned,
implemented and evaluated at the community level by people trusted and respected by the community
to ensure a culturally appropriate program. They also need to be integrated within a wider strategic
approach to alcohol misuse and its consequences, which by necessity should involve initiatives in four
key areas: prevention, harm reduction, clinical care, and alcohol specific services.
46
20
Bennelongs Haven, the first Aboriginal community controlled rehabilitation centre, was established in
New South Wales in 1974.
47
Since then, a number of Aboriginal community controlled rehabilitation
programs have been established in both residential and community settings. In the 19992000 financial
year, there were 38 residential treatment projects (several of which also provided outreach services) and
67 non-residential treatment programs.
48
While there are numerous general articles describing Aboriginal treatment projects, there have been few
formal evaluations of such projects.
An evaluation of treatment/rehabilitation services provided by 14 Aboriginal organisations for the
Western Australian Alcohol and Drug Authority in 1988 was based on semi-structured interviews with
program staff and collection of statistical data on workloads and client characteristics. While few clients
achieved the goal of continuing abstinence, programs that included residential facilities or dry camps
gave clients time out from drinking, enabling them to improve their health status.
49
An evaluation of three programs run by the Council for Aboriginal Alcohol Program Services in the
Northern Territory (two residential and one non-residential) and a community based field worker
program was based upon a review of documentary data, program records and comparisons of the
drinking status of ex-clients and samples of community members. It found that a suggestion that
attendance at (one family oriented program) has modest but real effects on drinking behaviour.
However, outcomes at other locations were equivocal. It was concluded that community based field
workers constitute an essential complement to residential programs.
50
The results of an evaluation of the Central Australian Aboriginal Alcohol Programs Units (CAAAPU)
residential program were similarly equivocal. The evaluation involved a review of client registration and
discharge forms, interviews with staff and residents, and follow up with 25 ex-clients. It found that there
were no agreed criteria against which success could be measured and that even if there had been such
criteria, CAAAPU was inadequately funded to obtain necessary follow up data on ex-clients.
51
The
evaluation identified problems in the administration of CAAAPU, which in part, led to its subsequent
closure. However, it has since re-opened.
52
An evaluation of Jungarni-Jutiya Alcohol Action Council Aboriginal Corporations treatment program in
Halls Creek, WA, reported that 55% of clients had reduced the risk of harm to themselves or others. The
benefits extended to the community in that a proportion of these clients had become valuable
community members. The reviewers noted that the outcomes of the Alcohol Centres treatment program
were equal to those reported for various residential treatment programs. However, what is particularly
impressive about them is that unlike many residential programs, which have high rates of relapse when
clients return to their communities, these outcomes have been achieved and maintained within a
community setting.
53
An effective community based approach is to enable Aboriginal people through their own communities
to gain control of their lives and, where possible, to influence or control alcohol availability (eg. dry
communities, restricted takeaway alcohol, changes to liquor licensing hours or the development of social
clubs).

Legislative approaches involving the declaration of dry areas in Aboriginal communities have
been shown to be effective in some cases where there is both community and statutory support.
54
Restrictions in the supply of alcohol appear to be effective in reducing alcohol consumption and its
consequences in several Australian reports involving Aboriginal communities.
55,56
While there are several reports that describe recreational elements as interventions or components of
alcohol misuse interventions, there are few evaluation reports on the outcomes of such interventions. A
cross sectional study that included interviews with 105 out of 110 young Aboriginal people residing in
Albany, Western Australia in early 1996 found no association between levels of alcohol and other drug
use and participation (or lack thereof) in a range of recreational activities, the number of recreational
activities in which the young people participated, or the amount of time spent in such activities. It was
concluded that for some young people alcohol and other drug use was simply another form of
recreational activity.
57
A systematic review of evidence found that laws that limit blood alcohol
concentration when driving, laws for minimum legal drinking age, sobriety checkpoints and training
programs for servers of alcoholic beverages were effective in preventing alcohol impaired driving in the
general population.
58
Frequency of intervention
In Australia, the Royal Australian College of General Practitioners recommends that all clients from 14
years should be asked about the quantity and frequency of alcohol intake, reaffirming that men should
limit consumption to no more than four standard drinks per day and women to two per day.
59
21
A number of international guidelines recommend that all adult and adolescent clients (from 18 years) be
screened to detect problem drinking. Alcohol dependent clients are encouraged to accept referral to
appropriate specialists or community alcohol treatment programs.
60,61
Older drinkers entering that period of their lives when they are most likely to heed medical advice may
benefit from regular counselling at the primary health care level. Younger drinkers, for whom
behavioural consequences are greatest and access hardest, may benefit from opportunistic counselling
interventions.
Recommendations of other groups
The Central Australian Rural Practitioners Association and the Northern Zone Management Unit in
northern Queensland recommend that the assessment of problem drinking be commenced from 15
years as part of an annual Aboriginal and Torres Strait Islander adult health check.
62
Guidelines from
OATSIH recommend screening for alcohol problems in the Aboriginal and Torres Strait Islander
population be administered as part of well persons health checks and routine examinations followed by
brief intervention. Biological markers should only be used in combination with other means of
assessment, such as clinical judgment.
63
Summary of recommendations
Hazardous ingestion of alcohol is more prevalent among Indigenous Australian males
and females aged 3544 years than among the general population.
EVIDENCE
Level of
evidence
Hazardous ingestion of alcohol contributes substantially toward poor health in Aboriginal
and Torres Strait Islander peoples through chronic disease, acute infection, injury, mental
health issues, cancer, and foetal alcohol syndrome.
IV
Control of problem drinking can prevent alcohol related injuries. I
Opportunistic assessment reduces problem drinking and may reduce alcohol related
consequences in the general population, especially when followed by brief intervention
by general practitioners or other health care providers.
I
Few studies have evaluated the effectiveness of brief intervention for problem drinking in
the Aboriginal and Torres Strait Islander population. Given the burden of disease
associated with alcohol, even a small reduction in alcohol consumption may have
significant public health benefits.
V
The use of screening questionnaires such as the Alcohol Use Disorders Identification
Test (AUDIT) is effective in identifying clients with, or at risk of, hazardous drinking in the
general population.
III
The AUDIT questionnaire is widely used as a tool by Aboriginal and Torres Strait Islander
health care providers to identify problem drinking and may be accessed via the internet
at: http://www.health.gov.au/oatsih/pubs/alco.htm. However, some difficulties in using this
test have been reported in the Aboriginal health setting.
IV
Aboriginal and Torres Strait Islander community based programs for problem alcohol
drinking are effective at reducing alcohol consumption and its consequences when there
is both community and statutory support.
IV
There is no optimal laboratory test for population based screening and detection of
problem drinking. A gamma glutamyl transferase (GGT) test is insensitive as a screening
test, but may be used for monitoring progress of those known to be problem drinkers,
especially if dishonesty about intake is suspected.
V
RECOMMENDATIONS
Base assessment of problem drinking on the National Health and Medical Research
Council guidelines (see Table 1). Follow by brief interventional counselling commencing
at a young age (1415 years) (see Box 1). Repeat opportunistically at least annually, but
care is needed to avoid jeopardising the clients ongoing relationship with the health care
provider.
V
Refer those who continue to have high levels of alcohol consumption for treatment.
Assess and manage comorbidities, including relevant preventive interventions (such as
vaccination for those at risk of pneumonia).
V
Strongly advise pregnant women and those likely to conceive to abstain from alcohol. V
Routine measurement of biochemical markers, such as GGT testing, is not
recommended as a screening tool for problem drinking.
V
22
Table 2. Health outcomes expected from reduced problem drinking
At-risk
Aboriginal and
Torres Strait
Islander
population
2065 years
N = 185 000
Intervention Event to be
prevented
Prevalence
of the
problem
Relative risk
reduction
(RRR) from
the
intervention
Follow
up time
Number
needed
to treat
(NNT) to
prevent
one
event
Control
event rate
(non-
Indigenous
data)
Patient expected
event rate (PEER)
(What would happen
to the patient if they
were not treated?)
Adjusted
NNT to
prevent
one event
(Aboriginal
risk)
Comments
Alcohol
consumption
Mainly 2034
years
100 000*
Detection of
problem drinking
and brief
intervention
Reduction
in problem
drinking
62% of the
total
Aboriginal
population
drink.
Among
those who
drink, 68%
consume
alcohol at
harmful
levels (ie.
42% of
total)
64
60% RRR of
problem
drinking to
target levels,
following
interventions
by GP
65
1 year NA NA 42% of population
aged 2034 years
would continue to be
problem drinkers
4 To reduce problem drinking
in one Aboriginal person
over 12 months, four need
to receive a brief clinic
intervention.
Brief intervention would be
expected to have some
effect in reducing problem
drinking in 25 000 young
Aboriginal people over 12
months.
The assumption is that
brief intervention would be
effective in young
Aboriginal people, given
the good evidence of
effectiveness in
international studies. The
public benefit is still
significant, even if brief
intervention is half as
effective.
Alcohol
consumption
Mainly 2034
years
Variety of
interventions
reported in
studies:
motivational
interventions
Alcohol
related
injury
49% of the
population
had 2.1
injuries per
year.
27% reduction
in drinking
related injuries
and accidents.
65% reduction
in accidental
and violent
deaths.
67
Variable
(3 mths
to 2 yrs)
NA NA Half of 49% of the
target population
would have alcohol
related injuries per
year (24.5%).
15 Reducing problem drinking
will reduce drinking related
injury.
If 15 people received
interventions to reduce
alcohol consumption, this
will prevent one alcohol
related injury.
23
100 000 interventions
family support
education
group therapy
rehabilitation
day centre
bi-weekly
contacts
brief advice
compulsory
in-patient
treatment.
At least 50%
of all injuries
and 88% of
assault
injuries are
alcohol
related.
66
Expect
24.5% of the
target
population to
have an
alcohol
related injury
per year.
42% of the
target
population
consumes
alcohol to
harmful
levels.
in accidental
and violent
deaths.
67
interventions to reduce
alcohol consumption, this
will prevent one alcohol
related injury.
If all those with problem
drinking received an
intensive intervention,
around 2800 young
Aboriginal people would be
prevented from developing
an alcohol related injury.
It is possible that the RRR
from interventions is
mediated by other aspects
of treatment for problem
drinking (eg. receipt of
medical attention and
social support).
* 1996 ABS census
Source: National Aboriginal Community Controlled Health Organisation. Medicare rebate for the health assessment of Aboriginal and Torres Strait Islander persons. Proposal to benefit Aboriginal health.
Submission to Commonwealth Department of Health and Aged Care, Medicare Benefits Branch, May 2001
24
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Cancer Early detection of breast cancer
27
ADULT HEALTH
CANCER EARLY DETECTION
OF BREAST CANCER
Authors
Tracey Johnston, Policy Officer, BreastScreen Victoria Inc
Dorothy Reading, Director, Cancer Education Unit, The Cancer Council Victoria
Alison Amos, Manager, Policy and Evaluation, BreastScreen Victoria
Acknowledgments
Dr Dan Ewald, Central Australian Rural Practitioners Association
Geoff Miller, Northern Zone Management Unit, Queensland Health
BreastScreen Victoria
BREAST CANCER
Burden of disease
An accurate assessment of the incidence and mortality associated with breast cancer in Aboriginal and
Torres Strait Islander women is difficult to obtain. Such data is scarce, possibly incomplete, subject to
bias and inaccuracies, and provides mostly state based indications rather than a national picture.
1
A
contributor to the quality of available data may lie in factors affecting the nomination and recording of
Aboriginal and Torres Strait Islander status. However, the available data has identified a number of
salient issues and potential areas of focus for future data collection and research strategies.
It has been stated that Aboriginal and Torres Strait Islander communities consider breast cancer a white
womans disease.
2
To some extent this is true, as the incidence rate of breast cancer has been reported
as lower among Indigenous Australian women than non-Indigenous women.
3
However, breast cancer is
one of the most common forms of cancer affecting Aboriginal and Torres Strait Islander women. In
addition, breast cancer incidence may be increasing for Aboriginal women. In the Northern Territory
(NT), there was a rapid increase in breast cancer incidence in Aboriginal women after 1995,
approximating that of non-Indigenous women by 1999.
4
Breast cancer mortality appears to be about the
same or greater for Indigenous Australian women as it is for non-Indigenous women.
5
For example, in a
review of cancer information specific to Aboriginal people in Western Australia (WA), it was reported that
for the period 19931997, the age standardised breast cancer incidence rate for Aboriginal women was
five-sixths that of non-Indigenous women.
6
The same review reported that breast cancer was the cause
of the most cancer deaths among Aboriginal women in WA and that the death rate was slightly lower
than that in non-Indigenous women. In the NT, the 5-year survival rate for breast cancer in Aboriginal
women after 1995 was less than 50% compared with 82% for non-Indigenous women.
7
The poor mortality profile for Aboriginal and Torres Strait Islander women may be due to these women
experiencing difficulties in accessing diagnostic and treatment services for breast cancer, resulting in
delayed presentation to health services and therefore poorer prognosis at diagnosis. This interpretation
is supported by data that indicates that Indigenous Australian women are less likely to participate in
screening programs and less likely than non-Indigenous women to be hospitalised for breast cancer.
8
28
Risk factors
Very little is known in relation to risk factors for breast cancer specific to Aboriginal and Torres Strait
Islander women.
9
Age, childbearing and breastfeeding
Generally, increasing age and being female have been identified as the major risk factors in the
development of breast cancer, with incidence rates rising significantly among women from 50 years or
more.
10
Childbearing reduces the risk of breast cancer, with greater protection for early first birth and a
larger number of births.
11
Two systematic reviews concluded that breastfeeding appeared to be a
protective factor but was of small magnitude compared with other known risk factors for breast
cancer.
12,13
This suggests that Aboriginal women may have a reduced risk of breast cancer due to
higher fertility rates.
14
The relationship between age, incidence of breast cancer and Indigenous Australian women is
potentially significant given that the average life expectancy is markedly lower in comparison with a non-
Indigenous women (63 years vs 82 years respectively).

Age at death profiles indicate that the majority of
deaths in Indigenous Australian women occur before 65 years, whereas this trend is reversed in non-
Indigenous women, with more deaths occurring after 65 years.
15
It has been suggested that the lower
incidence of breast cancer in Aboriginal and Torres Strait Islander women may be associated with life
expectancy profiles, indicating that many women may not reach an age where the incidence of breast
cancer is more prevalent.
16
However, this perception is not supported by age standardised data, which
adjusts for the differing age profiles between Indigenous and non-Indigenous women.
Family history
There are no known studies that have examined if family history influences risk in the development of
breast cancer in Aboriginal and Torres Strait Islander women.
17
As breast cancer is a common disease
that occurs in one in 11 women, the possibility of having a relative who has experienced the disease is
quite likely, with no associated increase in personal risk of the disease.
18,19
For women who have been
diagnosed with breast cancer, fewer than 20% have a family history of the disease.
20,21
In addition,
identified genes (eg. BRCA1 and BRCA2) which when inherited, incur a potentially high risk of breast
cancer, are present in fewer than 5% of cases of breast cancer.
22
Types of early detection/screening for breast cancer
modification
Nil Yes
mammography
breast self
examination/clinical
breast examination
(insufficient evidence)
Nil Nil Nil
Evidence of the effectiveness of early detection/screening
Early detection of breast cancer through a health assessment is presently limited to screening.
Although it is likely that mammary carcinogens from tobacco can reach breast tissue, there appears to
be no confirmed link between smoking and breast cancer.
23
The International Agency for Research on
Cancer (IARC), which is part of the World Health Organisation (WHO), has reported that there is now
clear evidence that smoking causes little or no increase in the risk of breast cancer.
24
29
Screening
Mammography is the most widely recognised and effective screening method for breast cancer and is
used as the primary early breast cancer detection method in organised screening programs for
asymptomatic women. Within BreastScreen Australia, screening employs film screen mammography
alone as the principle screening method.
25,26
Examination of the breasts by health professionals and the
examination of the breasts by women themselves are the methods most often used to complement
rather than replace mammography for breast cancer screening.
Mammography
Mammography (X-ray of the breast tissue) is the screening tool used around the world for the early
detection and potential prevention of deaths due to breast cancer in women. Based on randomised
trials, and following recommendations made by the Australian Health Ministers Advisory Council in
1991,
27
the National Program for the Early Detection of Breast Cancer (now known as BreastScreen
Australia) was established. In this program, mammography is funded by the Australian, state and
territory governments and implemented by jurisdictions in every state and territory.
The most widely quoted statistic on the effectiveness of mammography is that it can contribute to the
early detection of breast cancer and reduce mortality by up to 30% in women aged 5069 years through
screening with or without clinical breast examination.
28
This statistic emerged from the combined
analysis of several randomised trials of screening mammography conducted in the UK, Europe, the USA
and Canada between the 1960s and 1980s.
In a recent controversy, a Cochrane systematic review of the trials concluded that mass screening with
mammography did not lead to survival benefits. The review found that the best trials failed to show a
reduction in breast cancer mortality (pooling only showed a 3% reduction and this was not statistically
significant). The effect of mammography screening on all-cause mortality could not be ascertained. The
review criticised what it considered to be the flawed nature of many of the trials used to reach
conclusions.
29
Subsequently, a working group convened by IARC evaluated the trial evidence and found that there was
sufficient evidence for the efficacy of mammography screening in women aged 5069 years. The
effectiveness of screening programs is dependent on coverage, quality of mammography, treatment and
other factors, which confirmed the need for organised programs rather than sporadic screening of
selected groups of women.
30
The mortality benefit of mammography screening was also recently reaffirmed in a review of Swedish
randomised controlled trials (which showed a 21% reduction in risk of death due to breast cancer over
16 years).
31
The BreastScreen Australia Program provides a free population based mammography screening service
for asymptomatic women aged 40 years or more. Seventy percent of cancers occur in women aged 50
years or more. The program targets women aged 5069 years, where the mortality benefit is considered
greatest. Following their initial mammography screening, women aged 5069 are invited for re-
screening at 2-yearly intervals.
The benefit of mammography screening in women aged 4049 years is less clear as women in this age
group are often premenopausal and exhibit greater breast density which limits the radiological
visualisation of breast cancer lesions. Any benefit derived from mammography screening for women in
this age group must be weighed up against the potential harms (eg. false positive diagnosis, missed
cancers).
A recent study conducted for the Canadian Task Force on Preventive Health Care examined evidence
for the effectiveness of screening mammography among women aged 4049 years at average risk of
breast cancer. It concluded that there was insufficient evidence to include or exclude women in this age
group from screening programs. Once women reach 40 years, they should be provided with information
concerning the benefits and risks in order to assist with decisions concerning participation in
mammography screening.
32,33
In 1992 the National Health and Medical Research Council (NHMRC) undertook a review of
mammography screening for women less than 50 years. This review found that there was insufficient
evidence from which to conclude a mortality benefit for women less than 50 years. A subsequent review
of the evidence in 1997 supported this finding and concluded that in women aged 4049 years the costs
of routine screening outweighed the benefits in terms of deaths prevented. Based on this finding,
30
BreastScreen Australia provides screening to women aged 4049 years who choose to participate but
does not actively encourage them into the program.
34
For women aged 70 years or more, the breast cancer mortality risk is greater but the benefits of
screening are debatable. A recent study examining the balance between the benefits, harms and costs
of screening women 70 years or more, noted that women in this age group have a higher risk of death
from causes other than breast cancer, and while the possible negative effects of screening (eg. anxiety,
discomfort) may be sustained immediately, these women may not live long enough to experience the
benefits.
35
Within BreastScreen Australia, access is provided to the program for women aged 7079
years.
36
Barriers to mammography screening
The 2002 National Accreditation Standards for BreastScreen Australia require jurisdictional programs to
aim to achieve the same participation rates for Aboriginal and Torres Strait Islander women as for the
general population. The BreastScreen Australia Program aims to achieve a national participation rate
(the proportion of the population attending the program within the recommended screening interval) of
70% by all women in the 5069 target age range. The data for 20002001 shows the national
participation rate was 56.9%.
37
One of the programs objectives is to maximise the participation of
Aboriginal and Torres Strait Islander women in recognition that lower participation rates require targeted
strategies.
38
Despite the development of tailored strategies aimed at increasing the attendance of Indigenous
Australian women at mammography screening programs, existing state based data indicates that
participation rates are lower than those for all women.
39
These have ranged from as low as 14% in some
jurisdictions to 85% in some regions.
40
The participation rate in South Australia (SA) for Aboriginal
women aged 5069 years (calculated over a 24-month period until 30 June 2000) was 44.2%.
41
BreastScreen in WA (19971998) reported participation rates for Aboriginal women aged 5069 years
of 21% (metropolitan) and 41% (country) for the 24 months to June 1998. In comparison, rates of 50.2%
and 61.9% were reported for all women.
42
In Queensland during 1998, Indigenous womens
BreastScreen participation rates were 45.5% (5069 years) compared with 52.4% overall.
43
Considerable effort is required to boost Aboriginal and Torres Strait Islander womens mammography
screening participation rates. Recent studies have identified issues surrounding equity and access to
breast cancer screening for Aboriginal and Torres Strait Islander women.
44,45,46,47,48
These issues
include differing perceptions of health and wellbeing affecting what constitutes a health care priority, the
practicalities and cost of access to services (particularly for rural and remote communities), the cultural
appropriateness of those services, integration of breast screening with other well womens checks
coordinated within primary health care, an Indigenous workforce, improved general practitioner
responsiveness and reduction of disincentives, and the provision of appropriate information to Aboriginal
and Torres Strait Islander women.
A number of systematic reviews have investigated the effectiveness of strategies to increase womens
participation rates in mammography. A Cochrane review concluded that sending letters, making phone
calls, mailing educational materials and organising training activities with reminders for the women were
more effective than no intervention.
49
Other systematic reviews confirmed the effectiveness of mailed
invitations,
50,51
reminder

or office system prompts to both providers and clients, audits with feedback and
educational sessions

for providers (to enhance ordering of tests).
52
All these strategies constitute organised client and provider reminder and recall, which can take many
forms. These need to be modified in the context of the Aboriginal and Torres Strait Islander population
and integrated with primary health care provision. Strategies to assist primary health care providers to
deliver breast cancer screening as part of a continuum with diagnostic and treatment services have
been compiled. They stress the need for coordinated linkages with Aboriginal Community Controlled
Health Services (ACCHSs) and other providers, as well as program reform such as Medicare incentives
for holistic preventive health care delivered to Aboriginal and Torres Strait Islander women.
53
As part of BreastScreen Australias accreditation requirements, it is recommended that its services gain
an understanding of the demographic features and barriers to participation of the eligible population in
their area and develop recruitment strategies accordingly. Strategies may include the development of
and participation in culturally appropriate health education workshops or the facilitation of visits by
mobile screening services to remote communities or both. Consultation with Aboriginal medical services
is encouraged to contribute to appropriate service delivery.
54
It is clear, however, that strategies must take into account a variety of factors and should not simply
focus on single issues such as access. For example, there is evidence from extensive consultation in
31
the NT that mammography screening via mobile units is unlikely to be successful in remote regions
where a sense of ownership of the programs is lacking. Existing womens health programs in these
regions, which already embrace integrated and culturally appropriate systems and are run by Aboriginal
women trained as health workers, need to be involved in the preparation and conduct of this screening
in order to maximise the recruitment of Aboriginal women.
55
Clinical breast examination
Clinical breast examination (CBE) is a long established breast cancer detection method used in the
investigation of breast symptoms. Before the advent of mammography screening, it was also used as a
primary screening method. However, CBE has limitations and is restricted to the detection of palpable
breast cancer only (>1.0 cm lumps), whereas mammography can detect impalpable cancers. It has
been suggested that CBE may be a useful breast cancer detection method for younger women who are
not eligible for mammography screening programs and for whom the effectiveness of mammography as
a cancer detection tool is limited due to increased breast density.
56
Within screening programs, CBE is
used as a clinical assessment tool following an abnormal screen.
Debates are present within the literature about the sensitivity and specificity of CBE and its effectiveness
and applicability as a screening tool. To date there have been no randomised controlled trials
investigating its role alone and clarifying its benefit.
57
One meta-analysis concluded that CBE is valuable
as an adjunct to mammography because it helped to find cases that mammography missed.
58
However,
sensitivity was reported as poor (54%), which will result in large numbers of false negatives if used
alone.
A UK overview of Canadian studies suggested that CBE is as effective as mammography in reducing
breast cancer mortality, but should be directly compared in a new trial.
59
The US Preventive Services
Taskforce (1996) reported there was insufficient evidence to recommend annual CBE alone for women
aged 4069 years.
60
IARC reported that there is insufficient evidence that CBE or breast self
examination (BSE) reduce mortality from breast cancer.
61
The Royal Australian College of General
Practitioners (RACGP) does not recommend CBE as a routine screening test.
62
As CBE offers little in
addition to mammography, it is not employed as a principle screening method in the BreastScreen
Australia Program.
63
It may be impossible to standardise the technique of CBE. Palpable breast lumps can be detected by
CBE through the proper positioning of the client, thoroughness of search, use of a vertical strip search
pattern, proper position and movement of the fingers, and duration of at least 3 minutes per breast. The
value of inspection is unproved.
64
When practised proficiently, CBE is safe, non-invasive, does not
require specialised equipment and can be carried out in a primary health care setting. However,
evidence for its effectiveness as a stand alone screening tool is inconclusive at this time.
Breast self examination
Breast self examination has been widely promoted for many years as an empowering, safe and
inexpensive breast cancer screening tool. However, recently the balance between the potential benefits
and harms of this practice has been called into question and underlined by a lack of evidence to support
either a morbidity or mortality benefit.
In a recent systematic review of current evidence surrounding BSE, the Canadian Task Force on
Preventive Health Care recommended that BSE not be routinely taught to women 4069 years and that
it should be excluded from the periodic health examination of women.
65
In its assessment of the balance
between benefit, harm and costs, the review found that there was fair evidence of no benefit and good
evidence that women may experience harm as a result of practising BSE. The potential down sides of
teaching and encouraging women to practise BSE include increased visits to health care professionals
for the assessment of benign lesions and unnecessary biopsies.
The potential increase in morbidity associated with the routine practise of BSE was also supported in the
recently released results of a randomised controlled trial conducted in Shanghai, China.
66
The main aim
of this study, however, was to assess whether intensive instruction in BSE versus no instruction would
have an effect in reducing deaths from breast cancer. The results of the study showed little difference in
the number of breast cancer deaths between the instruction group and the control group and concluded
that the mortality benefit of BSE is unproven.
A report looking at the experiences of Indigenous women in Queensland in relation to breast cancer
identified a number of barriers to BSE. These included fear of diagnosis, limited opportunities for
education, instruction and reinforcement about BSE techniques and cultural beliefs that it is not
appropriate for women to feel their own bodies.
67
32
Within publicly available information about BSE, there currently exists a move away from the BSE model
toward a model of breast awareness that encourages women to become familiar with the normal look
and feel of their own breasts, and consult their doctor should any unusual changes be detected.
68
Aboriginal and Torres Strait Islander women should be offered the currently recommended schedule of
mammography screening offered to all other women. This is for 2-yearly mammography in women
5069 years (Box 2).
The Central Australian Rural Practitioners Association and the Northern Zone Management Unit
recommendations for breast cancer screening of Aboriginal and Torres Strait Islander women are based
upon those from BreastScreen Australia
69
are shown in Box 2 along with recommendations from the
RACGP
70
and other organisations.
A summary of breast cancer screening recommendations of other groups is shown in Box 2.
Box 2. Australian recommendations for breast cancer screening
71,72,73,74
Australian Health Ministers Advisory Council, 1990
Mammography screening should be made available to and publicised for women aged 40 years or
more, but recruitment strategies should be targeted at women 5069 years with the intent of re-
screening them every 2 years.
BreastScreen Australia National Accreditation Standards, 2002
The program seeks to provide equitable access to all eligible women in Australia. Services should aim to
achieve the same participation rates for special groups as for the general population. Special groups
include women from culturally and linguistically diverse, Indigenous rural and remote areas and low
socioeconomic backgrounds. Relevant special groups will differ between services. It is recognised that
not all services will meet this standard for special groups. If a service is not achieving a 70%
participation rate among all the special groups identified, the reasons for lower participation should be
analysed and targeted strategies for increasing participation implemented.
The Cancer Council Australia, 2001
Women aged 5069 years should undergo mammography screening every 2 years through the
BreastScreen Australia Program. Breast self examination is not recommended at the population level
due to insufficient evidence of a mortality benefit. However, it can be encouraged as part of public health
programs to enable women to become more breast-aware and urge them to consult their health
professional should changes be detected.
The Royal Australian College of General Practitioners, 2002
Mammography screening is recommended every 2 years for women aged 5069 years. There is no
evidence to recommend for or against mammography screening in women aged 70 years or more.
Mammography screening is not recommended in women less than 40 years unless they have a
significantly high risk factor.
In women aged 4049 years, evidence shows a small benefit in mammography screening.
Clinical breast examination is not recommended as a routine screening test.
Breast self examination has little impact on mortality. There is evidence that women are capable of
detecting tumours without practising BSE monthly. Women should be encouraged to know what is
normal for their breasts and have any changes investigated. Breast self examination should not be
promoted as a replacement for regular mammography.
33
Aboriginal and Torres Strait Islander women may be less likely than other women to be
diagnosed with breast cancer. However, the incidence of breast cancer may be increasing
(as reported in the Northern Territory). The risk of death due to breast cancer, the case
fatality, is greater for Aboriginal and Torres Strait Islander women than for the general
population.
EVIDENCE
Level of
evidence
Mammography may reduce breast cancer mortality in women aged 5069 years. I
Within the general population, organised client reminder and recall systems reduce
barriers to participation in screening for breast cancer.
I
Aboriginal and Torres Strait Islander women have lower participation rates than the non-
Indigenous in BreastScreen Australia programs.
III
There is evidence that breast self examination (BSE) offers no benefit in reducing
morbidity or mortality due to breast cancer. There is evidence that women may
experience harm as a result of practising it. (Aboriginal women also report difficulties
implementing BSE.)
III
RECOMMENDATIONS
Screen women aged 5069 years using mammography every 2 years. I
Advise women aged 4049 years that there may be a small benefit in mammography
screening when weighed against factors such as their age (the benefits of screening may
increase through the decade), family history, possible risk factors, personal concerns,
levels of anxiety, inconvenience, cost, and discomfort.
I
Clinical breast examination is not recommended for breast cancer screening alone or in
place of mammography.
III
Coordinate screening and recruitment strategies between local primary care service
providers, such as Aboriginal Community Controlled Health Services and mobile
BreastScreen Australia units in order to utilise client reminder and recall systems set up
for preventive health assessments.
V

References
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Islander women, 1996. Available at:
http://www.nbcc.org.au/resources/documents/BCA_Breast_cancer_and_aboriginal.pdf. [Accessed
28 June 1004].
2 ibid.
3 Edwards RW, Madden R. The health and welfare of Australias Aboriginal and Torres Strait
Islander peoples 2001, 2001. Available at: http://www.aihw.gov.au/publications/ihw/hwaatsip01/.
4 Zhao Y, et al. An investigation of the sudden increase in breast cancer deaths in the Northern
Territory (NT) in 1999. The NT Disease Control Bulletin 2002;9(3):239.
5 Carrick S, Clapham K, Paul C, Plant A, Redman S, op. cit.
6 Thomson N, Irvine J. A review of cancer among Aboriginal people in Western Australia. Perth:
Cancer Foundation of Western Australia, 2001.
7 Zhao Y, et al, op. cit.
9 ibid.
10 Fletcher SW, Black W, Harris R, Rimer BK, Shapiro S. Report of the International Workshop on
Screening Breast Cancer. J Natl Cancer Inst 1993;85(20):164456.
11 Key TJ, Verkasalo PK, Banks E. Epidemiology of breast cancer. Lancet Oncol 2001;2(3):13340.
12 Bernier MO, Plu-Bureau G, Bossard N, Ayzac L, Thalabard JC. Breastfeeding and risk of breast
cancer: a meta-analysis of published studies. Hum Reprod Update 2000;6(4):37486.
13 Lipworth L, Bailey LR, Trichopoulos D. History of breastfeeding in relation to breast cancer risk: a
review of the epidemiologic literature. J Natl Cancer Inst 2000 Feb;92(4):30212.
15 Edwards RW, Madden R, op. cit.
34

17 ibid.
18 Australian Institute of Health and Welfare. BreastScreen Australia monitoring report 2000.2001.
AIHW cat. no. CAN 20. Canberra: Australian Institute of Health and Welfare (Cancer Series no.
25).2003. Available at: http://www.aihw.gov.au/publications/index.cfm/title/9731. [Accessed 10 April
2005].
19 Australian Institute of Health and Welfare & Australasian Association of Cancer Registries. Cancer
in Australia 2001. AIHW cat. no. CAN 23. Canberra: AIHW (Cancer Series no. 28), 2004.
20 Pharoah PDP, Stratton JF and Mackay J. Screening for breast and ovarian cancer: the relevance
of family history. Br Med Bull 1998;54(4):82338.
21 Federico M, et al. Identification of families with hereditary breast and ovarian cancer for clinical and
mammographic surveillance: the Modena Study Group proposal. Breast Cancer Res Treat
1999;55:21321.
22 National Breast Cancer Centre. Advice about familial aspects of breast cancer and ovarian cancer:
a guide for health professionals. Woolloomooloo: iSource National Breast Cancer Centre, 2000.
23 Hecht SS. Tobacco smoke carcinogens and breast cancer. Environ Mol Mutagen
2002:39(23):11926.
24 International Agency for Research on Cancer (IARC). Press release no. 141, 2002. Available at:
http://www.iarc.fr/pageroot/PRELEASES/pr141a.html. [Accessed 28 June 2004].
25 Australian Health Ministers Advisory Council Breast Cancer Screening Evaluation Steering
Committee. Breast cancer screening in Australia: future directions: Australian Institute of Health:
prevention program evaluation series no 1. Canberra: AGPS, 1990.
26 National Quality Management Committee of BreastScreen Australia. National Accreditation
Standards: BreastScreen Australia quality improvement program. Canberra: BreastScreen
Australia, 2002.
27 ibid.
28 ibid.
29 Olsen O, Gotzsche PC. Screening for breast cancer with mammography (Cochrane Review). In:
The Cochrane Library, Issue 2, 2002. Chichester: Wiley.
30 IARC. Handbook of cancer prevention: vol. 7: breast cancer screening. Lyon: IARC Press, 2002.
31 Nystrm L, et al. Mammography screening: updated overview of the Swedish randomised trials.
Lancet North Am Ed 2002;359:90919.
32 Ringash J, Canadian Task Force on Preventive Health Care. Preventive health care 2001 update:
screening mammography among women aged 40-49 years at average risk of breast cancer. Can
Med Assoc J 2001;164(4):46976.
33 Miller AB, To T, Barnes CJ, Wall C. The Canadian national breast screening study 1: breast
cancer mortality after 1116 years of follow up: a randomised screening trial of mammography in
women age 40 to 49 years. Ann Intern Med 2002;137:30514.
34 National Breast Cancer Centre. Policy on screening women aged 4049 years: a summary of the
evidence for health professionals, 1998. Available at:
http://www.nbcc.org.au/bestpractice/resources/HPI_40-49screening.pdf. [Accessed 28 June 2004].
35 Barratt AL, Irwig LM, Glasziou PP, Salkeld GP, Houssami N. Benefits, harms and costs of
screening mammography in women 70 years and over: a systematic review. Med J Aust
2002;176:26671.
36 National Quality Management Committee of BreastScreen Australia, op. cit.
37 AIHW (2003), op. cit.
39 BreastScreen Australia. Indigenous indicator: Public Health Outcome Funding Agreements
(PHOFA) report 19992000. Canberra: Commonwealth of Australia.
41 BreastScreen Australia, op. cit.
42 BreastScreen Western Australian (WA). 19971998 statistical report, 1998. Available at:
http://www.breastscreen.health.wa.gov.au/content/health/health.asp. [Accessed 29 June 2004].
43 BreastScreen Queensland (QLD). BreastScreen Queensland: annual statistical report for 1998.
Brisbane: Queensland Health, BreastScreen QLD, Breastscreen Australia, 1999.
44 BreastScreen Australia. Barriers to breast cancer screening for Indigenous women. Canberra:
Australian Institute of Health and Welfare, 2002.
35

45 McLean MJ, Condon JR. A single issue program in an isolated area: mammography screening in
Darwin, NT. Aust N Z J Public Health 1999;23(4):35761.
46 Kirk M, et al. Breast cancer: screening diagnosis, treatment and care for Aboriginal women and
Torres Strait Islander women in Queensland. Brisbane: Queensland Health, 2000.
47 McMichael C, Kirk M, Manderson L, Hoban E, Potts H. Indigenous womens perceptions of breast
cancer diagnosis and treatment in Queensland. Aust N Z J Public Health 2000;24(5):5159.
48 School of Public Health and Tropical Medicine, James Cook University. Early detection and
management of breast and cervical cancer in Aboriginal and Torres Strait Islander women:
supporting the role of the general practitioner, 2002. Available at:
http://www.racgp.org.au/document.asp?id=7054. [Accessed 29 June 2004].
49 Bonfill X, Marzo M, Pladevall M, Mart J, Emparanza JI. Strategies for increasing the participation of
women in community breast cancer screening (Cochrane Review). In: The Cochrane Library, Issue
2, 2002. Chichester: Wiley.
50 Wagner TH. The effectiveness of mailed patient reminders on mammography screening: a meta-
analysis. Am J Prev Med 1998;14(1):6470.
51 Yabroff KR, Mandelblatt JS. Interventions targeted toward patients to increase mammography use.
Cancer Epidemiol Biomarkers Prev 1999;8(9):74957.
52 Mandelblatt JS, Yabroff KR. Effectiveness of interventions designed to increase mammography
use: a meta-analysis of provider-targeted strategies, Cancer Epidemiol Biomarkers Prev
1999;8(9):75967.
53 School of Public Health and Tropical Medicine, James Cook University, op. cit.
55 Rod OConnor and Associates. Implementation issues associated with the delivery of the National
Program for the Early Detection of Breast Cancer across the remote north of Australia. Canberra:
Commonwealth of Australia, 1993.
56 Flegg KM, Rowling Y. Clinical breast examination: a contentious issue in screening for breast
cancer. Aust Fam Physician 2000;29(4):3436.
57 McMurchie M. Clinical breast examination. Aust Fam Physician 2000;29(4):348.
58 Barton MB, Harris R, Fletcher SW. Does this patient have breast cancer? The screening clinical
breast examination: should it be done and how. JAMA 1999;282(13):127080.
59 Mittra I, Baum M, Thornton H, Houghton J. Is clinical breast examination an acceptable alternative
to mammographic screening? BMJ 2000;321(7268):10713.
60 United States Preventive Services Task Force. Screening for breast cancer. In: Guide to clinical
preventive services. 2nd edn. Baltimore: Williams and Wilkins, 1996.
61 IARC. Press release no.139: mammography screening can reduce deaths from breast cancer, 2002.
Available at: http://www.iarc.fr/pageroot/PRELEASES/pr139a.html .[Accessed 28 June 2004].
62 Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in
general practice. Updated 5th edn. Melbourne: RACGP, 2002.
Committee, op. cit.
64 Barton MB, Harris R, Fletcher SW, op. cit.
65 Baxter N, Canadian Task Force on Preventive Health Care. Preventive health care 2001 update:
should women be routinely taught breast self-examination to screen for breast cancer? CMAJ
2001;164(13):183746.
66 Thomas DB, et al. Randomised trial of breast self-examination in Shanghai: final results. JNatl
Cancer Inst 2002;94(19):144557.
67 Kirk M, et al, op. cit.
68 The Cancer Council Australia. National cancer prevention policy 20012003, 2001. Available at:
http://www.cancer.org.au/documents/National Cancer Prevention Policy.PDF. [Accessed 29 June 2004].
69 National Quality Management Committee of BreastScreen Australia. National Accreditation
Standards: BreastScreen Australia quality improvement program. Canberra: BreastScreen
Australia, 2002.
70 RACGP, op. cit.
Committee, op. cit.
72 The Cancer Council Australia, op. cit.
73 RACGP, op. cit.
Cancer Prevention of cervical cancer
Evidence base to a preventive health assessment in the Aboriginal and Torres Strait Islander peoples
36
ADULT HEALTH
CANCER PREVENTION OF
CERVICAL CANCER
Authors
Kate Broun, Community Programs Coordinator, PapScreen Victoria, The Cancer Council Victoria
Julie Hassard, Manager, PapScreen Victoria, The Cancer Council Victoria
Dorothy Reading, Director, Cancer Education Unit, The Cancer Council Victoria
Acknowledgment
CERVICAL CANCER
Burden of disease
Cervical cancer is the most common cause of cancer death among Aboriginal women,
1
with an overall
mortality rate that is over nine times greater than non-Indigenous women.
2
In contrast, for all Australian
women, cervical cancer is the fourteenth most common cause of cancer death.
3
Concerns about the completeness of data on cervical cancer incidence and mortality among Aboriginal
women are based on the fact that data has only been available from South Australia (SA), Western
Australia (WA) and the Northern Territory (NT). In WA over the period 19931997, the mortality rate
from cervical cancer among Aboriginal women was five times higher than non-Indigenous women.
4
While the death rate for cervical cancer among Aboriginal women fluctuated over the period 19821997,
the rate decreased significantly for non-Indigenous women.
5
Aboriginal women in the NT are 410 times
more likely to die from cervical cancer than non-Indigenous women.
6
In 2001, Queensland released its first analysis of cervical cancer incidence and mortality for the state.
7
Incidence rates among Aboriginal and Torres Strait Islander women in this state were five times the
state average and the mortality rate was 13 times greater than non-Indigenous women.
8
However, due
to the incomplete identification of Aboriginal and Torres Strait Islander people in cancer registrations,
some authorities consider that there is likely to be an underestimation of cervical cancer incidence and
mortality,
9,10,11
and that the above rates are likely to be minimum estimates of the differences between
the two populations.
12
Data from SA, WA and the NT death registers indicated that the risk of death from cervical cancer for
Aboriginal women increased according to geographical location.
13
The study found that Aboriginal
women in rural and remote areas of Australia are at significantly higher risk of death from cervical
cancer than either Aboriginal women in metropolitan areas or non-Indigenous women in any area. The
risk increased approximately 4-fold for women in metropolitan areas, to 10-fold for rural women, and 18-
fold for women in remote areas. While possible explanations for the increase could include
misclassification of data used or a change in residence after diagnosis with terminal cancer, the
relatively poor access to and utilisation of cervical cancer screening services for Aboriginal women in
rural and remote areas may offer the best explanation.
Deaths due to cervical cancer in Aboriginal women occur at a younger age than in non-Indigenous
women. Data taken from the three registers and examined over the period 19861997 indicated that the
mean age at death from cervical cancer for Aboriginal women was 52.8 years significantly lower than
the 61.7 years for non-Indigenous women.
14
37
The causal role of human papilloma virus (HPV) in cervical cancer is now well established.
15
Most
women are infected with HPV at some time in their life, so it could be deemed a normal part of being
sexually active. HPV is necessary but not sufficient for the development of cervical cancer,
16
but very
few women with HPV will ever develop cervical cancer. Most women who acquire the HPV infection in
their early years of sexual activity, clear the infection and develop a degree of immunity.
17
Women with
persistent HPV infection appear to be at greatest risk of developing a high grade abnormality.
18
Australia introduced a nationally coordinated response to cervical cancer prevention in 1991 (National
Cervical Screening Program). All jurisdictions are required to operate cervical cytology registries,
monitor screening policy, and work in partnership to promote biennial Pap test screening.
The program aims to achieve an 80% participation rate among women aged 2069 years with an intact
cervix.
19
For the period 20012002, the national participation rate in cervical screening for women in the
target group was 61%.
20
Rates ranged from 57% in Queensland to 65% in Victoria, SA and Tasmania.
The program is currently unable to report on national participation rates in cervical screening by
Aboriginal and Torres Strait Islander women. However, a recent study conducted in 13 rural and remote
Indigenous communities in Queensland indicated the overall biennial participation rate for women living
in these communities was 41.1%. This was 30% lower than the rest of Queensland.
21
In 1999, the program introduced a new target to reduce the annual cervical cancer mortality among
women aged 2069 years from the national average of 3.01.8 per 100 000 women by 2003.
22
In
comparison, the annual rate of cervical cancer mortality in Aboriginal women (NT, WA, SA) reported in
2000 from 19861997 data was 12.3 per 100 000.
23
Types of preventive intervention for cervical cancer
modification
Nil Yes
Pap test
Nil Nil Nil
Prevention of cervical cancer through a preventive health assessment is presently limited to screening.
Screening
There is international agreement that despite the absence of randomised controlled trials to demonstrate
that Pap test screening prevents cervical cancer, there is sufficient indirect support from cohort studies
to warrant continued cervical screening strategies.
24,25
Since the introduction of the Australian National
Cervical Screening Program in 1991, incidence and mortality rates from cervical cancer have reduced
significantly across the whole population. Cervical cancer mortality decreased by 40% in the period
19861998.
26
Data on cervical screening rates for Aboriginal and Torres Strait Islander women at a regional, state or
national level is limited. With the exception of the NT, cervical cytology registers across Australia do not
record identification of Indigenous clients and there is currently no system to monitor screening activity
through pathology laboratories.
27
Therefore, Aboriginal and Torres Strait Islander women's participation in cervical screening is
ascertained through descriptive studies, including those with historical controls which confirm lower
participation in urban, rural and remote locations. The proportion of Aboriginal and Torres Strait Islander
women who have never been screened ranged 3264%.
28
A recent descriptive analysis of data from the
Queensland Health Pap Smear Registry showed that the proportion of women living in the Indigenous
communities undergoing screening in the period March 1999 February 2001 was 41.1%. This was
30% lower than the rest of Queensland (59.1%). However, there was considerable variation among
Indigenous communities (19.963.5%).
29
Strategies to increase Pap test recruitment rates have included the use of financial incentives and these
have been shown to be effective in the United Kingdom.
30
In Australia, in 2001, the Australian
government announced financial incentives to general practitioners (GPs) for Pap test screening of
38
priority groups of women. These incentives are not accessible to the majority of Aboriginal Community
Controlled Health Services (ACCHSs),
31
Womens health nurses and Aboriginal Health Workers (AHWs)
who provide many of the Pap tests to Aboriginal women.
It is important that attempts to attain high recruitment rates do not lead to overscreening. The cost
effectiveness of screening is jeopardised if the strategy only results in the additional screening of
existing participants who may not be at high risk.
32
Women who have never been screened or are
significantly underscreened are considered to be at higher risk of cervical cancer. The priority targets for
the National Cervical Screening Program includes Aboriginal and Torres Strait Islander women among
others with low screening rates.
Strategies for recruiting high risk women to participate in cervical screening differ from the general
population and include mechanisms to overcome barriers in accessing screening services.
33,34,35,36,37
The Aboriginal and Torres Strait Islander Womens Forum of the National Cervical Screening Program
has developed cervical screening practice standards to assist primary care providers to enhance the
participation rates of Aboriginal and Torres Strait Islander women.
38
Research conducted in Queensland
found that barriers to service use related to mainstream health services being inaccessible, and
inappropriate in terms of culture and gender.
39
An assessment of the readability and accessibility of
resource material for Aboriginal women in New South Wales (NSW) on cervical cancer confirmed their
unsuitability.
40
Role of female health staff
An important recruitment strategy is for female health professionals including GPs, AHWs or nurses to
conduct Pap test screening and health promotion activities.
41,42
A systematic approach, combining
opportunistic screening with formal recall systems is also required.
43,44,45
A combined opportunistic and
vertical recruitment program involving AHWs was successful in a primary health care setting in the
Kimberley, WA. It targeted high risk Aboriginal women, without overscreening those who were not at
high risk.
46
Aboriginal and Torres Strait Islander womens health is seen as part of overall wellbeing and is linked to
the health of their families and communities. This means that health issues affecting the whole
community are also womens issues. For many Aboriginal and Torres Strait Islander women, female
health workers are the key to the implementation and acceptability of health care, for personal and
cultural reasons.
47,48
It follows that health promotion messages delivered by female AHWs are also an
important mechanism for achieving health gains. However, there are few AHWs who deliver cervical
screening in their own communities. Time constraints, lack of clinical support, and the social and kinship
relationship between the health worker and community women are some of the barriers to AHWs
performing Pap tests.
49
Mainstream strategies
A range of strategies leading to increased uptake of cervical screening in the general population have
been reported including invitation, computerised and paper recall reminder systems, educational
outreach, clinical audits, counselling, information resources and use of financial and other
incentives.
50,51
The Cochrane review concluded that invitation letters including telephone invitations
were effective at encouraging women to attend for Pap tests, but may not be applicable to less literate
or socioeconomically disadvantaged women and is very dependant on the accuracy of population
registers. Educational strategies including culturally tailored information, and using lay members of the
community to promote screening appeared to be effective amongst ethnic minority groups. Only one
USA study examined the provision of transport incentives to encourage follow up of abnormal Pap tests
and found them to be effective, particularly for socioeconomically disadvantaged women, although there
were some doubts about the quality of the study.
Australian governments are now required to report on steps to improve cervical screening among
Aboriginal and Torres Strait Islander women, including collaborations and partnerships with Indigenous
Australian communities. Targets for Aboriginal and Torres Strait Islander womens participation rates in
screening are no different from the general population.
52
39
The National Cervical Screening Program Guidelines recommend that Pap tests should be offered at
1820 years, or 12 years after sexual activity commences, whichever is later (see Box 3). Data is
lacking on the risk of delaying Pap tests until 18 years in those who have commenced sexual activity at
a younger age. There is some evidence that a higher proportion of Aboriginal girls may engage in sexual
activity at a young age (A Van de Sterren, October 1997).
53,54,55
While the current national guidelines do
not advocate cervical screening to commence earlier than 18 years, they state that in 'some cases', it
may be appropriate to do so. However, the guidelines offer no recommendations on determining which
cases should commence screening earlier.
In comparison with other nations, Australian recommendations on frequency of Pap tests for the general
population appear more conservative. For example, Canada and New Zealand recommend Pap tests
once every 3 years, and Ireland once every 5 years. A review in 1995 recommended that any changes
to the Australian policy would cause confusion and be unacceptable.
56
recommendations for the Pap test screening of Aboriginal and Torres Strait Islander women are based
upon those from the National Cervical Screening Program (Box 3).
57
A summary of cervical cancer screening recommendations for Australian women is shown in Box 3.
Box 3. Cervical screening recommendations for women
58,59,60
National Cervical Screening Program
Routine screening with Pap tests should be carried out every 2 years for women who have no
symptoms or history suggestive of cervical pathology. All women who have ever been sexually active
should commence Pap tests at 1820 years, or 12 years after first sexual intercourse, whichever is
later. In some cases, it may be appropriate to commence screening before 18 years. Pap tests may
cease at 70 years for women who have had two normal Pap tests within the past 5 years. Women more
than 70 years who have never had a Pap testshould be screened.
Interim Evaluation of the Organised Approach to Preventing Cancer of the Cervix, 1995 [Note 201]
Re-affirmed that older unscreened and Aboriginal women were a key national target group for
screening.
Pap tests should be performed every 23 years. Screening may cease at 70 years for women who have
had two normal tests in the preceding 5 years...There is no evidence to suggest that high risk groups of
women should be screened more often, with the exception of recent diagnosis and treatment of
abnormalities.
40
Cervical cancer is the most common cause of death due to cancer among Aboriginal
women. There is an overall mortality rate that is over nine times greater than non-
Aboriginal women. Aboriginal women in remote areas appear to be at higher risk than
those in urban areas.
EVIDENCE
Level of
evidence
With regular biennial Pap tests, up to 90% of the most common form of cervical cancer
can be prevented.
III
Aboriginal and Torres Strait Islander women have a lower participation rate than non-
Indigenous women in Pap test screening.
III
Evidence is lacking regarding the risk to the client of delaying Pap tests until age 18
years when sexual activity has commenced at a much younger age.
N/A
RECOMMENDATIONS
Screen women who have no symptoms or history suggestive of cervical pathology with
Pap tests every 2 years.
V
Commence Pap tests for all women who have ever been sexually active at 1820 years
or 2 years after their first sexual intercourse, whichever is later.
V
Use strategies to reduce barriers to uptake of Pap tests by Aboriginal and Torres Strait
Islander women. Examples of these strategies include the involvement of female health
workers, culturally appropriate educational materials, transport subsidies, and locally
appropriate recall and reminder systems.
IIIV

References
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Aboriginality, age and rurality. Int J Epi 2000;29:8136.
2 Australian Institute of Health and Welfare (AIHW) and the Commonwealth Department of Health
and Aged Care. National Cervical Screening Program, Cervical screening in Australia 19971998.
3 AIHW and the Commonwealth Department of Health and Aged Care, op. cit.
4 Thomson N., Irvine J. A review of cancer among Aboriginal people in Western Australia. Perth:
Cancer Foundation of Western Australia, April 2001.
5 ibid.
6 Plant AJ, Condon JR, Durling G. Northern Territory health outcomes: morbidity and mortality
197991. Darwin: Northern Territory Department of Health and Community Services, 1995.
7 Coory M, Ganguly I, Thompson A. Cancer among people living in rural and remote Indigenous
communities in Queensland. Queensland Health Information Circular 54 February 2001;18.
8 ibid.
9 ibid.
10 Thomson N, Irvine J, op. cit.
11 Bailie R, Sibthorpe B, Anderson I, Smith. Data for diagnosis, monitoring and treatment in
Indigenous health: the case of cervical cancer. Aust N Z J Public Health 1998;22(3):3036.
12 ibid.
13 OBrien E, Bailie RS, Jelfs PL, op. cit.
14 ibid.
15 Cuzick J, Sasieni P, Davies P, Adams J, Normand C, Frater A, van Ballegooijen M, van den Akker
E. A systematic review of the role of human papillomavirus testing within a cervical screening
programme. Br J Cancer 2000 Sep;83(5):5615.
16 Walboomers JM, et al. Human papillomavirus is a necessary cause of invasive cervical cancer
worldwide. Journal of Pathology, 1999;189 (1):129.
17 Saville M. Current status of HPV and cervical cancer [unpublished]. 2000.
18 Nobbenhuis MA, et al. Relation of human papillomavirus status to cervical lesions and
consequences for cervical cancer screening: a prospective study. Lancet 1999;354(9172):205.
19 National Public Health Partnership. Cervical cancer screening program: state plan 20012004.
Available at: hna.ffh.vic.gov.au/phd/cervicalcancer/index.htm. [Accessed 28 June 2004].
41

20 Australian Institute of Health and Welfare (AIHW) 2004. Cervical screening in Australia 20012002.
AIHW Cat no. 22. Canberra: Australian Institute of Health and Welfare (Cancer Series number 27).
Available at: http://www.aihw.gov.au/publications/index.cfm/title/10069. [Accessed 13 May 2005].
21 Coory MD, Fagan PS, Muller JM, Dunn NAM. Participation in cervical cancer screening by women
in rural and remote Aboriginal and Torres Strait Islander communities in Queensland. MJA,
2002;177:5447.
22 The Cancer Council Australia. National Cancer Prevention Policy 20012003, 2001;72. Available
at: http://www.cancer.org.au/content.cfm?randid=988667. [Accessed 28 June 2004].
23 OBrien E, Bailie RS, Jelfs PL, op. cit.
24 Report of the US Preventive Services Task Force. Chapter 9. Screening for cervical cancer. In:
Guide to clinical preventive services. Washington DC: Williams and Wilkins, 1996;108.
25 Quinn M, Babb P, Jones J, Allen E. Effect of screening on incidence of and mortality from cancer of
cervix in England: evaluation based on routinely collected statistics. BMJ 1999 Apr
3;318(7188):9048.
26 Commonwealth Department of Health and Aged Care. A decade of change: A Report on Australias
National Cervical Screening Program 19891999. Canberra: Commonwealth of Australia, 2000.
27 Bailie R, Sibthorpe B, Anderson I, Smith, op. cit.
28 James Cook University School of Public Health and Tropical Medicine. Early detection and
management of breast and cervical cancer in Aboriginal and Torres Strait Islander women:
supporting the role of the general practitioner: report commissioned by the RACGP Aboriginal and
Torres Strait Islander women's health project, 2002. Available at:
http://www.racgp.org.au/document.asp?id=9619. [Accessed 28 June 2004].
29 Coory MD, Fagan PS, Muller JM, Dunn NA. Participation in cervical cancer screening by women in
rural and remote Aboriginal and Torres Strait Islander communities in Queensland. Med J Aust.
2002 Nov 18;177(10):5447.
30 Quinn M, Babb P, Jones J, Allen E, op. cit.
31 National Aboriginal Controlled Community Health Organisation (NACCHO). NACCHO issues
paper: how can cervical cancer incentives benefit Aboriginal women? Federal Budget 20012002.
Canberra: NACCHO, 2001.
32 Straton JAY. Recruitment for cervical screening: a review of the literature. Commonwealth
Department of Human Services and Health. Canberra: AGPS, 1994;2,14,60.
33 Coory M, Ganguly I, Thompson A. Cancer among people living in rural and remote Indigenous
communities in Queensland. Queensland Health Information Circular 54 February 2001;18.
34 Bailie R, Sibthorpe B, Anderson I, Smith, op. cit.
35 Kirk M, Hoban E, Dunne A, Manderson L. Barriers to and appropriate delivery systems for cervical
cancer screening in Indigenous communities in Queensland (final report). Herston: Australian
Centre for International and Tropical Health & Nutrition, 1999.
36 James Cook University School of Public Health and Tropical Medicine, op. cit.
37 National Cervical Screening Program Aboriginal and TSI Womens Forum. Principles of practice,
standards and guidelines for providers of cervical screening services for Indigneous women.
38 ibid.
39 Kirk M, Hoban E, Dunne A, Manderson L, op. cit.
40 Jackson LR, Ward JE. An analysis of resources for indigenous women in NSW about cervical
screening. Aust N Z J Public Health 2000;24(3):32730.
41 Gilles M, Crewe S, Granites N, Coppola A. A community based cervical screening program in a
remote Aboriginal community in the Northern Territory. Aust J Public Health 1995;19:47781.
42 Couzos S, Wronski I, Murray R, Cox H. Augmentation of pap smear screening of high risk
Aboriginal women. Aust Fam Physician 1998;27(4):26974.
43 Straton JAY, op. cit.
44 Mak DB, Straton JA. The Fitzroy Valley Pap smear register. Med J Aust 1993;158:1636.
45 Hunt JM, Gless GL, Straton JA. Pap smear screening at an urban aboriginal health service: report
of a practice audit and an evaluation of recruitment strategies. Aust N Z J Public Health 1998
Oct;22(6):7205.
46 Couzos S, Wronski I, Murray R, Cox H, op. cit.
47 National Aboriginal Health Strategy Working Party. National Aboriginal Health strategy: report.
Canberra: Commonwealth of Australia, March 1989.
42

49 Kirk M, Hoban E, Dunne A, Manderson L, op. cit.
50 Forbes C, Jepson R, Martin-Hirsch P. Interventions targeted at women to encourage the uptake of
cervical screening (Cochrane Review). In: The Cochrane Library, Issue 3, 2002. Chichester: Wiley.
52 Commonwealth of Australia. Public Health Outcome Funding Agreement: 1999/002003/4 between
the Commonwealth of Australia and [State Governments], 1999. Available at:
http://www.health.gov.au/pubhlth/about/phofa/wa.htm. [Accessed 28 June 2004].
53 Stanley FJ, Mauger S. Birth-weight patterns in Aboriginal and non-Aboriginal singleton adolescent
births in Western Australia, 197983. Aust N Z J Obstet Gynaecol 1986;26(1):4954.
54 Hart G, MacHarper T, Moore D, Roder D. Aboriginal pregnancies and births in South Australia,
19811982. Med J Aust 1985;143(9 Suppl):S546.
55 Westenberg L, van der Klis KA, Chan A, Dekker G, Keane RJ. Aboriginal teenage pregnancies
compared with non-Aboriginal in South Australia 19951999. Aust N Z J Obstet Gynaecol
2002;42(2):18792.
56 Commonwealth Department of Human Services and Health. The interim evaluation of the
organised approach to preventing cancer of the cervix, 19911995. Report of the Evaluation
Steering Committee. Canberra: AGPS, 1995;12.
57 Australian Government Department of Health and Aging. National Cervical Screening Program.
Available at: http://www.health.gov.au/pcd/campaigns/cervical/index.htm. [Accessed 28 June
2004].
58 ibid.
59 Commonwealth Department of Human Services and Health, op. cit.
60 Royal Australian College of General Practitioners. Guidelines for preventive activities in general
practice. Updated 5th edn. Melbourne: RACGP, 2002.
Dental health
43
ADULT HEALTH
DENTAL HEATH
Author
Dr Sandra Meihubers
DENTAL DISEASE
Burden of disease
Many factors affect oral health, including age, exposure to fluoride, diet and nutrition, oral hygiene habits
such as tooth brushing and flossing, tobacco smoking, alcohol consumption, stress and general health.
The incidence of dental caries (tooth decay) is greater in younger populations, and again in older
groups, mainly due to people now keeping their teeth longer and the saliva inhibiting effects of many
common medications. Access to dental care, knowledge about the importance of dental health and
attitudes towards dental health are also important. Poor dental health can affect quality of life by causing
pain, infection, difficulties with speech and eating and embarrassment about appearance. There can
also be financial difficulties when facing the cost of some dental care.
1
The two main dental diseases are dental caries and periodontal (gum) disease. Other major conditions
of concern are oral cancer, tooth erosion (wearing away of the hard tissues of the teeth by acids such as
acidic foods and drinks) and oral trauma (eg. through sports injuries).
Dental caries and periodontal disease are more common in some Aboriginal and Torres Strait Islander
communities than in non-Indigenous communities and are entirely preventable. A national telephone
survey that included a small sample of Aboriginal and Torres Strait Islander people found that
Indigenous Australians had more dental problems, tooth extraction and edentulism (loss of teeth) than
the non-Indigenous population.
2
Access to dental care is difficult for many Indigenous Australians, with
one study revealing that 105 of the 254 discrete Aboriginal or Torres Strait Islander communities
surveyed had no dentist in the community, nor was there a regular visiting dental service. Each
community had a population of 50 or more, and was located 10 km or more from the nearest hospital.
The total population represented was 13 600.
3
Dental caries result from a combination of many factors: bacteria in dental plaque, diet, plaque deposits,
saliva quantity and quality, enamel quality, and tooth morphology. Other modifying factors can include
age, socioeconomic status and access to oral health services. Dental caries destroy the hard tissues of
the tooth, and are mainly caused by high sugar/carbohydrate diets coupled with poor oral hygiene.
Aboriginal people living a traditional lifestyle experienced very little oral disease.
4,5,6,7,8
Later studies in
Aboriginal communities documented deterioration in oral health as a consequence of a shift away from
traditional practices and diets towards a more westernised form of existence.
9,10,11,12,13,14,15
However,
the rate of dental caries was generally lower than that of the non-Indigenous population and in one
region in the Northern Territory (NT), this was attributed to the naturally high fluoride levels in the water
supply (bore water).
16
Since the late 1970s the dental caries rate of the overall Australian population has declined
considerably.
17
This has been attributed to several factors including water fluoridation, fluoride
toothpaste and increased availability of dental services.
18
In contrast, it appears that the rates of dental caries in Aboriginal communities are increasing in many
areas, particularly in children.
19,20,21,22
An increase in child caries rates in remote communities with
naturally fluoridated bore water supplies could reflect an increasing consumption of foods containing
sugar, and sweetened carbonated drinks. Tooth brushing is also irregular and not widely practised.
23
In
one remote region the caries rate for Aboriginal children was more than twice that for the NT and
Australian populations, in both deciduous (baby) and permanent (adult) teeth.
24
However, the same
report found that the adults had lower levels of caries when compared to Australian adults.
Dental health
44
Early childhood caries, or nursing bottle caries, is a condition affecting infants and young children
caused by sucking on sweetened drinks in bottles, particularly when going to sleep. Even milk can have
this effect, due to the lactose content. The result is gross caries in the deciduous teeth, particularly
affecting the upper anterior teeth and molars. One study of Aboriginal children in an urban environment
found that the number of decayed and filled deciduous teeth was more than twice the rate for children
aged 3 years in Australia. This increased caries experience was associated with high dental plaque
scores, high levels of streptococcus mutans (a bacterium producing decay), and consumption of milk
with added sugar when the children went to sleep.
25
Periodontal disease can range from a reversible gingivitis (gum inflammation) to more advanced
disease with gingival recession, loss of bone that supports the teeth, infection and abscesses. Dentists
working in Aboriginal communities have observed a high rate of periodontal disease in adults,
particularly in diabetics. Diabetes is a known risk factor for periodontal disease, which is more severe
and destructive in poorly controlled diabetics.
26,27,28
Uncontrolled diabetes combined with poor or no
plaque control and an unhealthy diet leads to a rapidly progressing periodontal problem, resulting in
bone destruction, periodontal abscesses, loss of tooth mobility, early tooth loss and diminished oral
function. This type of rapidly destructive periodontal disease is associated to a lesser extent with
smoking.
29
In remote Aboriginal communities, adults with diagnosed type 2 diabetes had significantly more teeth
missing than non-diabetics.
30,31
In one region, dentate adults (people with teeth still present) with
diabetes had a mean 5.51 missing teeth, compared with a mean 1.72 missing teeth for non-diabetic
adults. Edentulous adults (people with no teeth) accounted for 2.9% of the adults attending for dental
care, and all the edentulous adults had diabetes. This was a noticeable change from data recorded 13
years earlier, when there were no recorded cases of edentulism. Severe gingivitis was also observed in
children.
Aboriginal people are at greater risk of bacterial endocarditis from dental treatment due to the high rates
of rheumatic fever in Aboriginal and Torres Strait Islander population.
32
Dental procedures that cause
bleeding from the gingiva or bone or both, such as tooth extraction and scaling and cleaning of teeth,
usually cause a transient bacteraemia. There is also an increased risk of bacteraemia in an individual
with periodontal disease or with inflamed gingivae that bleed easily.
33
These blood borne bacteria may
infect damaged or abnormal heart valves or endocardium or endothelium close to congenital heart
defects.
Other dental conditions of concern are oral cancer, dental erosion, and oral trauma. There is no
published documentation on the levels of these conditions in the Aboriginal and Torres Strait Islander
population.
modification
Nil Yes
dental
examination
Yes
oral
hygiene
instruction
dietary
advice
smoking
cessation
advice
Yes
fluoride tablets,
rinses, drops
professionally
applied fluoride
Yes
food supply
fluoridation of
water
use of toothpaste
containing
fluoride
application of
dental sealants
access to regular
dental care
use of
mouthguards
There is much evidence for the effectiveness of clinical interventions and the development of
appropriate individual oral health behaviours, including good oral hygiene and attention to diet. There is
a lack, however, of studies that evaluate the effectiveness of preventive interventions in Aboriginal and
Dental health
45
Torres Strait Islander communities, particularly for the treatment of periodontal diseases in diabetics and
for people who have little or irregular access to dental care and advice.
Fluoridation of community water supplies is acknowledged to be the most effective method of dental
caries prevention.
34,35
It involves the controlled addition of fluoride to reticulated water supplies in levels
proven to be safe and effective. In temperate climates the amount of fluoride in the water is generally
one part per million (PPM); in hotter climates it may be adjusted to 0.6 or 0.7 PPM, allowing for a greater
consumption of water.
Water fluoridation is socially equitable in that it benefits all individuals, regardless of age and
socioeconomic status. It is also the most cost effective of all community based caries prevention
interventions. Its preventive action occurs through the following main mechanisms: inhibiting
demineralisation of enamel, promoting remineralisation of early carious lesions, inhibiting metabolic
processes of cariogenic bacteria (bacteria causing decay found in dental plaque), and reducing enamel
solubility in acid by integrating the fluoride ion into developing enamel.
In some Aboriginal communities in remote regions, there is a risk of fluorosis of tooth enamel due to the
high naturally occurring levels of fluoride in the water supply, generally from an underground (or bore)
source.
36
A high level of consumption of tea, which is also known to contain fluoride, can compound this
risk.
Access to regular dental care provides opportunities for assessment of disease risk status and adoption
of appropriate prevention strategies and interventions where necessary. The timing of recall
examinations should be assessed on an individual basis, mainly according to disease risk status
37
(see
Frequency of intervention).
The use of mouth guards has proven to be effective in the prevention of oral trauma, and their use is to
be encouraged by all who participate in contact or high risk sports.
38
There is no public health equivalent such as water fluoridation, or the use of preparations containing
fluoride for the prevention of periodontal disease.
39
Counselling and chemoprophylaxis
Offering dietary advice per se will not necessarily lead to the desired behavioural change (such as
avoiding over-consumption of sugar and carbohydrate containing food). Counselling needs to
incorporate individual motivation and learning styles.
40
Critical enabling factors include the availability
and affordability of nutritious foods in local stores.
The regular daily use (twice per day) of a toothpaste containing fluoride has been shown to achieve
1530% reduction in dental caries rates.
41,42
Greater caries reduction occurs with higher levels of
fluoride. Most toothpastes contain a range, from low, <500 PPM fluoride to an optimal level of 1000
PPM fluoride. Most toothpastes available in Australia contain fluoride in a range of types and
concentrations. The most common is monofluorophosphate at 1000 PPM. Because of the effect of
toothpaste containing fluoride on dental plaque reduction, regular use would also have a beneficial
effect on the prevention of periodontal disease.
The home use of mouth rinses containing fluoride (for those assessed to be at high risk of developing
dental caries) and fluoride supplements such as drops and tablets (sometimes prescribed in areas with
no or low fluoride levels in water supplies) have been effective in clinical trials. However, their overall
effectiveness is dependent on individual and family motivation, and often relies on continuing
professional support and advice.
43
Due consideration must be given to total fluoride intake before
prescribing these supplements.
Mouth rinses containing fluoride are generally used daily or weekly, often in school based programs.
However, their use is more appropriate as a targeted program for high risk groups, rather than a
population based strategy.
44
Much cooperation is needed from individuals to comply with the regimen,
and from schools to supervise activities. Any school based programs in Aboriginal and Torres Strait
Islander communities tend to be based on encouragement for daily tooth brushing. While there is no
evidence to demonstrate that this reduces dental disease, particularly in Aboriginal and Torres Strait
Islander people, it can encourage children to form a habit of daily brushing.
45
Dental health
46
While topical application of preparations containing fluoride is recommended for individuals with high
caries risk, there have been no published studies examining the effectiveness or otherwise of such
interventions on caries rates. Particularly in remote communities, where there could be naturally high
fluoride levels in drinking water, the use of high concentration fluoride products needs to be considered
carefully to avoid toxicity. Indiscriminate use of fluorides in very young children may increase the risk of
unsightly fluorosis.
46
In regions with low or no fluoride in the drinking water, it can be a challenge to
apply high fluoride preparations as regular attendance at a dental service (24 times per year) is
required. This can be difficult in areas that have little or no access to dental programs.
Professionally applied topical fluoride preparations have been successful in the reduction of dental
caries.
47
They are cost effective when targeting those people at higher risk of caries, and the agents
most commonly used are sodium fluoride (NaF), stannous fluoride (SnF2) and acidulated phosphate
fluoride. The successful outcome depends very much on regular attendance at a dental clinic, combined
with the use at home of a toothpaste containing fluoride.
A dental sealant (sometimes referred to as a pit and fissure sealant or fissure sealant) is a resin that is
professionally applied to the grooves, pits and fissures of teeth. Sealants are particularly used in molar
teeth. They are effective in the reduction of pit and fissure caries, especially so when placed soon after
eruption of the tooth into the mouth, and with regular checking of sealant retention and integrity.
48
Dental
sealants should be applied to a tooth once it is erupted enough to allow effective isolation and moisture
control. If moisture control and access are difficult, fluoride varnish can be applied to newly erupted
teeth as short term protection until the teeth can be sealed.
49
The prevention and control of periodontal disease requires regular removal of dental plaque and
deposits by the individual or a dental clinician. Removal of dental plaque by the individual requires
regular tooth brushing and use of dental floss or similar products to remove plaque from in between
teeth.
50
Oral hygiene instruction and dental health education, either on an individual or group basis, offer mixed
results. They have greatest effect when people are motivated and are able to manage change in their
behaviours and habits. Repeated messages over time have more effect than one-off instruction
sessions.
51
As smoking is a risk behaviour for periodontal disease, smoking cessation programs have been
conducted through dental practices. There is evidence that these programs have been effective, though
there are relatively few published studies.
52
As smoking is also a causal factor in oral cancer, along with
alcohol use, stopping the habit would also minimise the risk of developing oral cancer (see also
Smoking in the Respiratory disease Non-communicable section.
Recent work regarding the effectiveness of oral health education, including dietary and smoking
cessation advice, favours the adoption of a common risk factor approach. Since oral diseases are
largely caused by several factors including diet, hygiene, smoking, alcohol use, stress and trauma, there
are opportunities to incorporate oral health into other chronic disease and health promotion programs.
That is, a collaborative approach would have greater impact on health improvement.
53
Screening
Screening programs, or regular dental checks, can detect dental diseases in the early clinical or
preclinical stages. This provides an opportunity to deliver prompt and appropriate treatment and to
assess any risk factors for further development of disease. There is good evidence that professional
scaling and plaque removal in people with periodontitis prevents progression to more severe forms of
the disease.
54
However, there is no evidence that indicates suggested time intervals for whole
population groups.
55
Incorporating dental checks into chronic disease prevention programs for rheumatic heart disease, other
cardiovascular disease and diabetes is often overlooked. Since people with a previous history of
rheumatic fever or valvular heart disease are at greater risk of infective endocarditis, the prevention of
dental disease will minimise this risk. Health checks for such individuals should incorporate a dental
examination to detect early disease and offer appropriate treatment. Others at risk requiring antibiotic
prophylaxis before invasive dental treatment are those with prosthetic heart valve or surgically
constructed systemic-pulmonary shunts.
Diabetes screening and regular checks should also include dental examinations, in particular to check
periodontal health and oral hygiene.
Dental health
47
Dental checks of school children
School children are recognised as a priority group for dental care, and all states and territories in
Australia provide access to free or subsidised school dental programs for school aged children, where
dental therapists provide the bulk of care. Childrens services are a priority because children depend on
others. These services are relatively inexpensive and represent an investment in the future. Such
programs aim to prevent or control dental diseases in children and provide oral health promotion for
children and their families.
56
Access to these services varies, with many remote communities having little or no access to regular
school dental programs. Some dental services visit remote communities but there can be variations in
timing and frequency, often depending on seasonal conditions (eg. dry season visits only in tropical
zones) and available workforce. Attempts have been made to overcome this by developing oral health
training for Aboriginal Health Workers.
57
There is no established benchmark for timing of dental examinations for children. One suggested
minimum standard is that all eligible children receive a dental examination on average every 15 months,
with access to at least one course of general dental care every 2 years, including appropriate oral health
promotion. Those at higher risk of dental disease should be examined more frequently.
58
A proposed
benchmark for Aboriginal and Torres Strait Islander children could be that they have access to a dental
examination at least once every 12 months.
One dental program in Aboriginal communities in remote Australia recommended annual screening for
all school children and adults with chronic disease, especially diabetes. Achievement of this is facilitated
by good cooperation with other health and community programs, such as the school dental health
services, and access to population and chronic disease registers where they exist.
59
The timing, conduct and effectiveness of dental screening programs in Aboriginal and Torres Strait
Islander communities have not been studied.
While tooth brushing twice per day with a toothpaste containing fluoride has been proven to be effective
for the prevention of dental caries and periodontal disease, the achievement of this requires access to
affordable and appropriately designed good quality toothbrushes and affordable toothpaste. In remote
communities, there are also issues associated with poor water quality, which is sometimes unfit for
human consumption (water is generally used to rinse after brushing).
The optimal time for clients to return for dental examinations depends on the individuals level of caries
risk, from 24 months for low risk to 36 months for high risk. Again, this assumes that adults can access
an existing dental program and understand the need for such appointments. In many Aboriginal and
Torres Strait Islander communities, with competing health and social priorities, priority for preventive
dental health can be low, and many people often wait until they experience severe pain before seeking
dental care.
Those at high risk for periodontal disease (people with deep gum pockets or diabetes, particularly if they
are aged 1435 years) should ideally attend for recall and treatment visits at 13 month intervals.
People at moderate risk for periodontal disease (presence of gum pockets, and people aged 3659
years) require 3-monthly reviews for a thorough professional scaling and cleaning of teeth. Others at low
risk should be reviewed every 12 months. Public dental programs generally accord priority to those at
high risk.
60
These protocols rely heavily on assumptions that people are able to attend at such time
intervals, understand the reasons for doing so, and are motivated to carry out recommended home oral
hygiene care. Even when a dental service is available in a community for more than 15 years, there has
been evidence of deteriorating periodontal health, with many adults losing some or all of their teeth due
to periodontal disease.
61
The Central Australian Rural Practioners Association recommends that dental hygeine advice be
provided opportunistically to the Aboriginal and Torres Strait Islander population.
62
The Northern Zone
Managament Unit recommends that high risk clients should be encouraged to attend for annual dental
care, depending on availability of dental services (G Miller, 28 November 2002). The Royal Australian
College of General Practitioners recommends regular visits to a dentist, with the frequency determined
on an individual basis.
63
Dental health
48
The Aboriginal and Torres Strait Islander population has a higher risk of developing
dental caries and periodontal disease than the general Australian population.
EVIDENCE
Level of
evidence
There is good evidence for the effectiveness of the following clinical interventions in the
prevention of dental disease: access to timely clinical examination, brushing and
flossing, topical application of fluorides, application of dental sealants, scaling, and
other prophylactic measures.
IIV
Dental outcomes depend on access to dental services, an individuals ability and
motivation to look after their oral health, as well as affordable food and oral hygiene
items in stores. There is evidence that Aboriginal people have poor access to dental
services.
III
Aboriginal and Torres Strait Islander clients at high risk of dental caries and periodontal
disease include those:
with co-existing disease (eg. diabetes, valvular heart disease, past rheumatic fever)
who are aged 1435 years
who smoke
who have non-fluorinated water supplies
who are school children.
V
RECOMMENDATIONS
Consider dental health needs as part of the comprehensive health assessment of
clients. Identify those who are at high risk of dental caries and periodontal disease.
V
Encourage high risk clients to attend dental care at least annually, depending on the
availability of dental services. This should be coordinated with other relevant health
programs (such as diabetes, nutrition and oral health) in order to reinforce the advice
offered by dentists.
V
Encourage all clients to use fluorinated toothpaste twice per day, especially in regions
with little or no fluoride in the water supply.
I
Advocate fluorination of water in areas of need where communities have a well
monitored reticulated water supply.
V
Ensure annual dental assessments are undertaken by all school age children as part of
the school dental programs funded by state and territory governments. The promotion of
effective brushing of teeth and the use of fluorinated toothpaste may be enhanced by
cooperation with local schools.
IV
Involve Aboriginal Health Workers and community representatives in the planning and
delivery of dental services. Integrate these with other primary health care programs to
improve results.
V

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49

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24 Simmons B, Roberts-Thomson K, op. cit.
25 Seow W, Amaratunge A, Sim R, Wan A, op. cit.,916.
26 Teng Y-TA, et al. Periodontal health and systemic disorders. J Can Dent Assoc 2002;68:3:18892.
27 Committee on Research, Science and Therapy. Diabetes and periodontal diseases: position paper.
J Periodontol 2000;71:4:66478.
28 Schlossman M, Knowler WC, Pettitt DJ, Genco RJ. Type 2 diabetes and periodontal disease. J Am
Dental Assoc 1990;121:5326.
29 Committee on Research, Science and Therapy. Tobacco use and the periodontal patient: position
paper. J Periodontol 1999;70:4:141927.
30 Simmons B, Roberts-Thomson K, op. cit.
31 Endean C, Wooley S, Roberts-Thomson K, op. cit.
32 Torzillo PJ et al. Invasive pneumococcal disease in central Australia. Med J Aust 1995;162:1826.
33 Woods R. A guide to the use of drugs in dentistry. 12th edn. St Leonards: Australian Dental
Association Inc., 1996.
34 Green JC, Wycoff SJ, United States Preventive Services Task Force (USPSTF). Preventive
dentistry1 Dental caries. J Am Med Assoc 1989;262:345963.
35 National Health and Medical Research Council. The effectiveness of water fluoridation. Canberra:
AGPS, 1991.
36 Fitzgerald J, et al. Groundwater quality and environmental health implications, Anangu Pitjantjatjara
lands, South Australia. Canberra: Bureau of Rural Sciences, 2000.
37 Public Health Division, Department of Human Services, Victoria. Evidence-based health promotion.
resources for planning. no.1 oral health, 2000. Available at:
http://www.health.vic.gov.au/healthpromotion/quality/oral_health.htm - pdf. [Accessed 28 June
2004].
38 Jolly KA, Brearley-Messer L, Manton D. Promotion of mouthguards among amateur football players
in Victoria. Am J Public Health 1996;20:6309.
39 Burt BA, Eklund SA. Dentistry, dental practice and the community. 5th edn. Chapter 25.
Philadelphia: WB Saunders, 1999.
Dental health
50

40 Public Health Division, Department of Human Services, Victoria, op. cit.
41 Green JC, Wycoff SJ, USPSTF. Preventive dentistry 1 Dental caries. J Am Med Assoc
1989;262:345963.
42 National Health and Medical Research Council, op. cit.
43 Murray JJ, ed. The prevention of oral disease. 3rd edn. Oxford: Oxford University Press, 1996.
44 Burt BA, Eklund SA. Dentistry, dental practice and the community. 5th edn. Chapter 25.
Philadelphia: WB Saunders, 1999.
45 US Public Health Service, Department of Health and Human Services. Oral health program guide
for the Indian Health Service, 1997.
46 Nganampa Health Council. Dentistry in remote Aboriginal communities. Alice Springs: Nganampa
Health Council, 2001.
47 Burt BA, Eklund SA, op cit.
48 US Public Health Service, Department of Health and Human Services, op. cit.
49 Nganampa Health Council, op. cit.
50 Brothwell DJ, Jutai DKG, Hawkins RJ. An update of mechanical oral hygiene practices: evidence-
based recommendations for disease prevention. J Can Dent Assoc 1998;64:295304.
51 Public Health Division, Department of Human Services, op. cit.
52 Watt RG, Johnson NW, Warnakulasuriya KAAS. Action on smoking opportunities for the dental
team. Br Dent J 2000;189:7:35760.
53 Sheiham A, Watt, RG. The common risk factor approach: a rational basis for promoting oral health.
Community Dent Oral Epidemiol 2000;28:399406.
54 Brothwell DJ, Jutai DKG, Hawkins RJ. An update of mechanical oral hygiene practices: evidence-
based recommendations for disease prevention. J Can Dent Assoc 1998;64:295304.
55 Jendresen MD et al. Annual review of selected dental literature: report of the committee on
scientific investigation of the American Academy of Restorative Dentistry. J Pros Dent
1994;72:3977.
56 Australian Health Ministers Advisory Council, Steering Committee for National Planning for Oral
Health. Oral health of Australians: national planning for oral health improvement (final report).
Adelaide: South Australian Government Department of Human Services, 2001.
57 Pacza T, Steele L, Tennant M. Development of oral health training for rural and remote Aboriginal
health workers. Aust J Rural Health 2001;9:3:10510.
58 Australian Health Ministers Advisory Council, Steering Committee for National Planning for Oral
Health, op. cit.
59 Nganampa Health Council, op. cit.
60 US Public Health Service, Department of Health and Human Services, op. cit.
61 Endean C, Wooley S, Roberts-Thomson K, op. cit.
62 Central Australian Rural Practitioners Association. A clinical manual for primary health care
practitioners in remote and rural communities in central and northern Australia. 4th edn. Alice
Springs: Central Australian Rural Practitioners Association, 2003.
63 RACGP. Guidelines for preventive activities in general practice. Updated 5th edn. Melbourne:
RACGP, 2002.
Diabetes prevention and early detection
51
ADULT HEALTH
DIABETES PREVENTION AND
EARLY DETECTION
Authors
Thomas Melanie, Australian Centre for Diabetes Strategies
Dr Stephen Colagiuri, Department of Endocrinology, Prince of Wales Hospital
Dr Ruth Colagiuri, Australian Centre for Diabetes Strategies
Acknowledgments
Tania Cramp, Diabetes Australia
Anthea Hepburn, Australian Centre for Diabetes Strategies
DIABETES
Burden of disease
The overall prevalence of type 2 diabetes in the Aboriginal and Torres Strait Islander population lies at
1030% and is generally 34 times higher at any age than the general population, with an earlier age of
onset.
1
In northern Australia, the overall prevalence of type 2 diabetes is 4.519% in Aboriginal people,
rising to 40% in people older than 35 years.
2
While diabetes prevalence increases markedly with age, a
number of surveys have reported that the prevalence of type 2 diabetes in the Aboriginal population
aged less than 35 years may exceed 5% in some regions. Type 2 diabetes was reported in nearly 3% of
Aboriginal adolescents (mean age 18.5 years) in remote Western Australia (WA) in 1994.
3
This is much
higher than in the general population, where the prevalence of diabetes was only 0.3% (of which 0.1%
were undiagnosed) in those aged 2534 years in 2000.
4
The prevalence of undiagnosed type 2 diabetes is consistently above 5% in the Aboriginal and Torres
Strait Islander population aged more than 35 years in a number of prevalence studies.
5
Moreover, in
north Queensland, the prevalence of diabetes (based on fasting blood glucose testing of approximately
2862 Aboriginal and Torres Strait Islanders over 15 years) in 19982000, was 45% in those aged
1534 years.
6
The Aboriginal and Torres Strait Islander population experience 1217 times more deaths due to
diabetes than non-Indigenous Australians.
7
Figure 1 demonstrates this by comparing the number of
deaths per 100 000 population over a 16-year period between the Northern Territory (NT) Aboriginal and
non-Indigenous population, and the Australian population as a whole.
8
The prevalence of impaired glucose tolerance (IGT) in the Aboriginal and Torres Strait Islander
population has not been well documented, though a 319% range of the population less than 35 years
has been reported,
9
compared with 4.9% in the general population aged 2534 years in 2000.
10
The incidence of diabetes has been reported to be 10 times higher in the Aboriginal population than that
reported for the European and USA population. An 8-year follow up study of a population in remote
central Australia (19871995) indicated that 2% of the population developed diabetes every year. This
contrasts with rates of 0.25% per year reported by the authors for the European and USA population.
Obesity (body mass index [BMI] >33) increased the rate of diabetes so that every year, nearly five new
cases of diabetes occurred for every 100 people at this weight.
11
The AusDiab study on the general Australian population
12
confirmed that for every known case of
diabetes, there is an undiagnosed case. Among the Aboriginal and Torres Strait Islander population,
most studies support that the true prevalence of diabetes is twice that determined from known cases.
13
The Servier Australia National Diabetes Study (SANDS), which used a screening threshold for diabetes
52
lower than that recommended by the World Health Organisation (WHO) (an abbreviated glucose
tolerance test [GTT] in those with random glucose >5.5 mmol/L) and screened 52 000 patients across
Australia, revealed an undiagnosed diabetes prevalence of 2%.
14
The AusDiab study confirmed that
7.5% of the general Australian population aged 25 years and over had type 2 diabetes in 2000, and half
of them were previously undiagnosed.
Reprinted from: Condon J, Dempsey K. NT mortality in the Northern Territory 1979-1997. Darwin:
Territory Health Services Epidemiology Branch, 1999.
Figure 1. Diabetes: age adjusted death rates, Northern Territory Australia
15
modification
Nil Yes
fasting blood
glucose
random blood
glucose
finger prick blood
glucose
glucose tolerance
test
Yes
diet, weight
control and
physical
activity
Yes
oral hypoglycaemic
medication
Yes
food supply
recreational
facilities
community
support
Screening
Risk factors for, or associated with, diabetes include obesity, hypertension, hyperlipidaemia, family
history of type 2 diabetes, and, in women, a history of gestational diabetes mellitus.
16,17
In addition,
Indigenous populations who have been significantly influenced by western culture tend to develop
diabetes, obesity and hypertension,
18
and this has been reported to have occurred in the Australian
Aboriginal population.
19
Most Aboriginal Australians have one or more of these risk factors, which are
often unrecognised. It is possible that a substantial proportion of the Aboriginal and Torres Strait
Islander population with diabetes may remain undiagnosed (and therefore untreated) and that this may
be the case at a much younger age than for other Australians. Unfortunately, the AusDiab prevalence
study was unable to report on diabetes prevalence rates in the Aboriginal or Torres Strait Islander
population, but a similar survey may soon be conducted within this population.
20
Undiagnosed diabetes has consequences. Microvascular and macrovascular complications are often
present when type 2 diabetes is diagnosed and USA surveys have shown that the level of
hyperglycaemia in previously undiagnosed people with diabetes is high enough to warrant
pharmacological therapy.
21
Late diagnosis, especially for the Aboriginal and Torres Strait Islander
population, often occurs in the presence of end stage disease, with concomitantly higher, yet younger
death rates, greater dependency on tertiary level care and higher health care costs.
53
Large scale clinical trials have demonstrated that early detection and good management of diabetes can
prevent the development or delay the progression of complications, such as myocardial infarction, eye
disease (including diabetic retinopathy) and renal failure.
22
Based on the results of such trials (see Table
3) presents the anticipated benefits of diabetes screening and management in the Aboriginal and Torres
Strait Islander population.
Screening for diabetes may lead to significant health gains. A USA study which examined the potential
for health gain arising from screening for type 2 diabetes concluded that such screening may be cost
effective if it involved screening high risk subpopulations (minorities) and commenced at a young age.
23
The US Expert Committee believed that early detection of type 2 diabetes in those at high risk was
necessary to reduce the silent burden of the disease and its complications. No cost effectiveness study
for diabetes screening has been reported in Australia.
The National Health and Medical Research Council (NHMRC) Evidence based guidelines for the
management of type 2 diabetes mellitus: primary prevention, case detection and diagnosis (2002)
recommended that diabetes screening should be offered to all Aboriginal and Torres Strait Islander
peoples aged from 35 years, but may need to be commenced at a younger age in some regions. The
document also identifies that active case detection of undiagnosed type 2 diabetes with a single risk
factor or a combination of risk factors should detect a prevalence of undiagnosed Type 2 diabetes of
5%.
24
Most Aboriginal Community Controlled Health Services and many state government primary care
providers to the Aboriginal population have already introduced diabetes screening at a younger age
(around 18 years).*
Screening for diabetes will also detect IGT and impaired fasting glucose (IFG). The latter is an important
component of the metabolic syndrome (formerly syndrome X) (see Box 4).
Box 4. Worldwide definition of metabolic syndrome
25
According to the new International Diabetes Federation definition, for a person to be defined as having
the metabolic syndrome they must have:
Central obesity (defined as waist circumference !94 cm for Europid men and !80 cm for Europid
women, with ethnicity specific values for other groups)
plus any two of the following four factors:
raised triglyceride level: !150 mg/dL (1.7 mmol/L), or specific treatment for this lipid abnormality
reduced HDL cholesterol: <40 mg/dL (1.0 mmol/L) in males and <50 mg/dL (1.3 mmol/L) in
females, or specific treatment for this lipid abnormality
raised blood pressure: systolic BP !130 or diastolic BP !85 mmHg, or treatment of previously
diagnosed hypertension
raised fasting plasma glucose (FPG) !100 mg/dL (5.6 mmol/L), or previously diagnosed type 2
diabetes. If above 5.6 mmol/L or 100 mg/dL, OGTT is strongly recommended but is not necessary
to define presence of the syndrome.
Source: International Diabetes Foundation. The IDF consensus worldwide definition of the metabolic syndrome
The diagnosis of IGT and the metabolic syndrome is important because appropriate management may
prevent progression to diabetes. IGT and IFG cannot be detected clinically yet play an important role in
cardiovascular risk assessment (see Vascular ischaemic heart disease section).
Women with a previous history of gestational diabetes are also at high risk for the development of type 2
diabetes later in life. Diabetes in these women (and in those with any other risk factors) would be
detected if a population approach to screening was adopted, especially at younger ages (see Frequency
of intervention). In populations where screening does not start at an early age, it is important that
women who have had gestational diabetes are identified and followed up regularly.
The discussion in this section has focused on early detection (secondary prevention) and management
to prevent or delay complications (tertiary prevention). However, if people can reduce obesity, increase
their physical activity and improve their diet, then diabetes can be prevented from occurring in the first
place (primary prevention).
Primary prevention for diabetes can also include screening activities to identify people with preventable
risk factors for the disease so they can be provided appropriate counselling and management. (See
Counselling and chemoprophylaxis and Vascular health.)

* Victorian Aboriginal Community Controlled Health Organisation (VACCHO) Well Persons Health Check (WPHC),
Apunipima WPHC, North Qld WPHC, NT Coordinated Care Trials, Kimberley Aboriginal Medical Services
54
Screening tests
A fasting blood glucose should be measured as the initial screening test for Type 2 diabetes, however a
random plasma glucose may be used if collection of a fasting sample is impractical. The levels of
hyperglycaemia that provide enough specificity to predict the development of microvascular
complications of diabetes have been the basis for determining the diagnostic criteria for diabetes.
26
The
Australian criteria for the diagnosis of diabetes are shown in Box 5.
With an equivocal result of fasting plasma glucose of 5.56.9 mmol/L, or random plasma glucose of
5.511.0 mmol/L, an oral GTT should be performed.
Diabetes is diagnosed if the fasting plasma glucose is !7.0 mmol/L and, in the absence of symptoms, is
confirmed on a subsequent day. A random or casual plasma glucose >11.1 mmol/L (repeated on a
subsequent day or in the presence of symptoms) is also diagnostic.
It is currently recommended that initial screening with a fasting plasma glucose (analysed by laboratory
testing) be followed by confirmatory testing with a second laboratory blood test on a separate day,
unless the plasma glucose is unequivocally elevated in the presence of obvious symptoms.
27
Strategies
to implement these recommendations will require local solutions.
BOX 5. The interpretation of venous plasma glucose test results
28
Fasting <5.5 mmol/L or
Random <5.5 mmol/L
Fasting 5.56.9 mmol/L or
Random 5.511.0 mmol/L
Fasting >7.0 mmol/L or
Random > 11.1 mmol/L
Diabetes unlikely
Offer lifestyle advice. Retest
with fasting blood glucose after
three years*
Diabetes uncertain
Perform oral GTT
Diabetes likely
Confirm with repeat laboratory
blood glucose unless diagnosis
is clinically unequivocal. Oral
GTT is not usually indicated
Interpretation of oral glucose tolerance test (GTT)
Impaired fasting glucose
Fasting !6.1 and <7.0 mmol/L
And
2-h (if measured) <7.8 mmol/L
Retest with fasting plasma
glucose after 1 year
Impaired glucose tolerance
Fasting concentration <7.0
mmol/L
And
2-h post glucose load ! 7.8 and
< 1.1 mmol/L
Retest with fasting plasma
glucose after 1 year
Diabetes mellitus
Fasting !7.0 mmol/L
Or
2-h post glucose load !11.1
mmol/L
* For the Aboriginal and Torres Strait Islander population, a pragmatic approach is to offer 2-yearly screening in line
with the Medicare Benefits Schedule health assessment (item 710)
Source: Australian Government Department of Health and Ageing. National Integrated Diabetes Program Guide for
general practitioners
Using the diabetes diagnostic level of fasting glucose for screening
Most guidelines do not distinguish between fasting glucose levels to screen, from those required to
diagnose diabetes. This issue was investigated in detail in the NHMRC Evidence based guidelines for
the management of type 2 diabetes mellitus: primary prevention, case detection and diagnosis. It was
concluded that a fasting plasma glucose cut off point of 5.5 mmol/L best defined the upper limit of
normality, and values above this indicated that further diagnostic testing was required (an oral GTT).
Applying the guideline recommended protocol of measuring fasting plasma glucose in people with risk
factors to the general Australian population would result in 77% of people with diabetes being identified
(with a specificity of 83%) and 25% of those tested would also require an oral GTT.
29
Using a random blood glucose for screening
The SANDS questioned the value of a random blood glucose as a screening tool and concluded that, if
the cut off point was 7.5 mmol/L (meaning that at this level a diagnostic oral GTT was performed), the
test would fail to diagnose 60% of those with undiagnosed diabetes. The investigators were able to
justify the use of a random blood glucose cut off point of 5.5 mmol/L in screening for diabetes,
confirming the diagnosis with an oral GTT.
30
Guidelines from the NT recommend diagnostic testing for
55
diabetes when random plasma glucose levels exceed 5.5 mmol/L (see Box 7) as do the NHMRC
Evidence based guidelines for the management of type 2 diabetes mellitus: primary prevention, case
detection and diagnosis.
Using finger prick blood glucose for screening
Finger prick testing makes use of a blood glucose meter to ascertain capillary glucose levels which
means using different diagnostic levels for diabetes (fasting level >6.1 mmol/L when using whole
blood).
31
Blood glucose meters are frequently unreliable and very few evidence based guidelines
recommend their use for screening. The advantage of using a blood glucose meter (instant feedback)
may be outweighed by the inaccuracy, poor reproducibility and the need to use venous blood samples
for other components of the well persons health check (WPHC), such as for lipid testing or other
serology. In this case, capillary testing introduces an unnecessary invasive procedure. Some guidelines
recommend a capillary level above 5.0 mmol/L requires additional diagnostic testing. However, the
NHMRC Evidence based guidelines for the management of type 2 diabetes mellitus: primary prevention,
case detection and diagnosis clearly recommended that blood glucose meters not be used to screen for
diabetes (see Box 7).
Using urine glucose testing for screening
Using this test to screen for diabetes will miss more than half of those with undiagnosed diabetes (when
compared with the GTT as the gold standard). The sensitivity of this test is too low and it is not
recommended as a screening test for diabetes.
32
Using glycated haemoglobin estimations for screening
Two considerations are relevant to this question; the use of glycated haemoglobin as a screening test
(either stand alone or combined with blood glucose measurement) and the use of glycated haemoglobin
as a test to confirm a diagnosis of suspected diabetes. Glycated haemoglobin levels are known to
correlate with the development and progression of the microvascular complications of diabetes in the
Diabetes Control and Complications Trial (DCCT) in people with type 1 diabetes, and in the Pima Indian
and Japanese populations in people with type 2 diabetes.
33,34,35,36
A role for glycated haemoglobin in
confirming a diagnosis of diabetes was supported by a meta-analysis which concluded that a glycated
haemoglobin of 7.0% was a good cut off point for defining people who were likely to have diabetes
requiring pharmacological treatment. In this context, a glycated haemoglobin of 7.0% had a 99.6%
sensitivity and 99.9% specificity in predicting diabetes based on the WHO 1985 definition.
37
However, glycated haemoglobin is not a good predictor of undiagnosed diabetes using the new WHO
1999 diagnostic criteria. While 97% of those with fasting plasma glucose (FPG) less than 6.1 mmol/L
(normal) will also have a normal glycated haemoglobin, only in 40% of those with diabetes (!7.0
mmol/L) will the glycated haemoglobin be elevated.
38
Some of the concerns that have been raised with regard to the use of glycated haemoglobin levels for
screening and diagnosis refer to its cost, the inability to define IGT and the precision required with the
test (a coefficient of variation of less than 3% may be difficult to achieve). Consequently the US Expert
Committee and NHMRC Evidence based guidelines for the management of type 2 diabetes mellitus:
primary prevention, case detection and diagnosis do not recommend the use of glycated haemoglobin
measurements to diagnose diabetes.
39,40
However, concomitant screening with blood glucose and
glycated haemoglobin measurement could be a future screening strategy and would reduce the number
of oral GTTs.
41
Further research is needed to test this strategy.
Two recently published studies have demonstrated that the development of diabetes in people with IGT
can be prevented or delayed. The Diabetes Prevention Study
42
conducted in Finland with a 3.2 year
follow up showed that individual diet and exercise intervention conducted by a dietician could reduce the
risk of diabetes by 58% (p<0.001) in a high risk population. This was achieved with 7 sessions in the first
year and regular 3 monthly sessions after that during which goals were set on how to lose weight (>5%),
decrease total fat intake to <30% of energy, decrease saturated fat intake to <10% of energy, increase
fibre intake to >15 g/1000 kj consumed and to exercise for at least 30 minutes per day. The groups were
individually given guidance to increase their exercise levels (30 minutes per day) with a combination of
endurance exercise and supervised resistance training. The control group were set goals and given
general written and oral information about diet and exercise initially and then annually but no specific
individualised programs were offered. The incidence of diabetes in the intervention group was
significantly lower than the control group (11% vs 23%).
56
The Diabetes Prevention Program was a major clinical trial conducted in the USA over 3 years in a
group of people with IGT. The intensive lifestyle intervention included instruction on a low fat diet,
exercising for 150 minutes per week and behaviour modification skills. The results showed that this
group had a 7% weight loss in the first year, sustained a 5% loss for the studys duration and maintained
30 minutes of exercise per day. A 58% reduction in the risk of developing type 2 diabetes was found
compared to the control group who received only basic diet and exercise advice. This study also
included another group which was treated with metformin which was effective in reducing the risk of
developing diabetes by approximately 30%.
43
Additional studies have also confirmed that intensive dietary and lifestyle advice can prevent diabetes:
1. Obesity
There is evidence that weight loss in those who are obese can prevent the onset of diabetes. For
example, the progression to diabetes was reduced 30-fold in severely obese subjects who had surgery
to reduce weight and were followed for an average of 4.8 years.
44
In the Aboriginal population, leanness
appears to protect against diabetes in all age groups. Remaining lean (BMI <20 kg/m
2
) can protect older
Aboriginal people from elements of the metabolic syndrome.
45
2. Diet/nutrition
The NHMRC Evidence based guidelines for the management of type 2 diabetes mellitus: primary
prevention, case detection and diagnosis recommends that dietary fat be reduced to <30% of energy
intake with saturated fat restricted to <10%. Diets of low energy density and containing a wide range of
carbohydrate foods rich in dietary fibre and of low glycaemic index (cereals, vegetables, legumes and
fruits) are also recommended to reduce the risk of type 2 diabetes.
All clients should be advised to follow the NHMRC Dietary guidelines for Australian adults (see Box 6).
46
An 8-year follow up of 335 Aboriginal adults in a remote central Australian community found that
interventions targeting nutritional factors alone are unlikely to alter trends toward increasing prevalence
of obesity and diabetes due to the limited healthy food choices available. Therefore the role of regular
physical activity needs to be emphasised in conjunction with dietary changes.
47
Box 6. Dietary guidelines for Australian adults
48
Enjoy a wide variety of vegetables, legumes and fruits:
eat plenty of vegetable, legumes and fruits
eat plenty of cereals (including breads, rice, pasta and noodles), preferably whole grain
include lean meat, fish, poultry and/or alternatives. Reduced fat varieties should be chosen
where possible
drink plenty of water.
and take care to:
limit saturated fat and moderate total fat intake
choose foods low in salt
limit your alcohol intake if you choose to drink
consume only moderate amounts of sugars and foods containing added sugars.
Prevent weight gain be physically active and eat according to your energy needs
Care for your food prepare and store it safely
Encourage and support breastfeeding
Note: Dietary guidelines for children and adolescents in Australia, incorporating the infant feeding guidelines for
health workers is available at: www7.health.gov.au/nhmrc/publications/synopses/dietsyn.htm
Source: NHMRC Dietary guidelines for Australian adults. Canberra: NHMRC, 2003
3. Physical activity
There is evidence that moderate level physical activity is protective against diabetes, even in the
absence of dietary strategies. In those at high risk for diabetes, even low level activity can be beneficial.
Furthermore, physical activity has benefits in reducing overall morbidity and mortality, even in the
absence of weight loss. NHMRC Evidence based guidelines for the management of type 2 diabetes
mellitus: primary prevention, case detection and diagnosis state that the risk of type 2 diabetes in adults
57
declines as the frequency of exercise increases to 35 times per week, that this is equally beneficial to
people of all ages and that the benefit increases with increasing levels of obesity. A 7-year follow up
study of Aboriginal people in central Australia found that an intervention program led to reductions in the
prevalence of IGT, hypercholesterolemia and smoking. The prevalence of diabetes remained
unchanged despite a significant increase in mean BMI, possibly due to changes resulting in increased
physical activity levels.
49
4. Lifestyle (combined diet and physical activity)
Marked improvements in the metabolic abnormalities of diabetes and coronary heart disease have been
found following temporary reversion to a traditional hunter-gatherer lifestyle in a group of Australian
Aborigines with diabetes.
50
The changes were associated with weight loss due to increased physical
activity and the consumption of a low fat diet.
Implementation of a healthy lifestyle program in a remote Australian Aboriginal community produced
long term improvements with reductions in body mass index, fasting plasma glucose, fasting
triglycerides and fasting insulin concentrations.
51
These long term reductions in risk factors for chronic
disease such as diabetes were due to community control and ownership over the program which
resulted in its sustainability over time.
5. Oral hypoglycaemic agents
It is now clear that some oral hypoglycaemic agents can prevent or delay the development of type 2
diabetes, however, they are less effective than lifestyle intervention. The US Diabetes Prevention
Program reported in 2002 that metformin (850 mg twice per day) reduced the incidence of diabetes over
2.8 years by 31% compared with placebo. The protective effect was such that 14 people with high
fasting or post load glucose (without diabetes) would need to be treated with metformin over 3 years to
prevent one of them developing diabetes.
52
Similar results were demonstrated in the Prevent Non-Insulin Dependent Diabetes Mellitus (STOP
NIDDM) study in which people with IGT were treated with acarbose
53
and in the Troglitazone in
Prevention of Diabetes (TRIPOD) study where women with a previous history of gestational diabetes
were treated with troglitazone.
54
Further trials are in progress, the outcomes of which may significantly
influence the value of population based screening for those with abnormal glucose tolerance.
A preventive health assessment can be used to identify lifestyle and nutritional risk factors for diabetes
and can assist client referral to intensive preventive programs (see also the other elements of vascular
disease prevention outlining the potential benefits of other brief interventions).
Given the high prevalence of diabetes at a young age in Aboriginal peoples and Torres Strait Islanders
as reported from central Australia, north Queensland and other regions, diabetes screening should
commence in early adulthood such as at age 1518 years. Diabetes screening commenced at a
younger age in some regions was recommended by the NHMRC Evidence based guidelines for the
management of type 2 diabetes mellitus: primary prevention, case detection and diagnosis while less
prevalent regions should offer annual diabetes screening to all Aboriginal peoples and Torres Strait
Islanders aged 35 years and over.
55
(A summary of screening recommendations is shown in Box 7.)
Is the frequency of newly diagnosed diabetes high enough to warrant a new screen of the Aboriginal
and Torres Strait Islander populations every year? The incidence of diabetes in the Aboriginal
population has been reported to be 10 times higher than that for the European and USA population. An
8-year follow up study of a population in remote central Australia (19871995), indicated that 2% of the
population developed diabetes every year. This contrasts with rates of 0.25% per year elsewhere.
Obesity, defined for this study as a BMI >33, increased the rate of diabetes so that every year, nearly 5
new cases of diabetes occurred for every 100 people at this weight. In younger women (1524 years)
there was a trebling in obesity prevalence and a four to five-fold increase in diabetes prevalence.
56
The
NHMRC Evidence based guidelines for the management of type 2 diabetes mellitus: primary prevention,
case detection and diagnosis reports that the average annual rate of progression of IGT to diabetes in
the Aboriginal and Torres Strait Islander population was nearly 8%. It also reported that in the
Caucasian population with normal glucose tolerance the annual rate of progression ranged from
0.60.9%. The presence of risk factors (such as obesity) increased this rate 2-fold. It recommended that
screening was warranted if it led to at least 5% of the population being newly diagnosed for diabetes.
57
Given that the average annual rate of diabetes progression in the Aboriginal population in some regional
areas has been reported as 2% and that this increases to around 58% with risk factors, there is good
reason to recommend annual diabetes screening in these regions. Other guidelines agree that
58
screening for undiagnosed diabetes through fasting glucose should be performed every 12 years (see
Box 7). The NHMRC guidelines recommend that the diabetes screening interval after the first test is
dependent on the result. Those with normal blood glucose level on first screen should be screened
again after 3 years, while those with IGT or IFG should be screened again in 1 year. A pragmatic
approach is to offer 2-yearly screening in line with the Medicare Benefits Schedule health assessment
(item 710), with annual screening after IGT or IFG is detected.
Dietary modification and physical activity should be encouraged for the prevention of diabetes in the
whole Aboriginal and Torres Strait Islander population and strategies to achieve this should commence
at an early age (after 15 years). This should be part of a preventive health assessment of the Aboriginal
and Torres Strait Islander population in the prevention of diabetes.
The Central Australian Rural Practitioners Association recommend venous blood glucose testing (fasting
preferred but random blood glucose is acceptable) as part of an annual Aboriginal and Torres Strait
Islander adult assessment from 15 years.
58
The Northern Zone Management Unit recommends diabetes
screening (fasting venous blood sample preferred) as part of the annual adult (!15 years) health check
in north Queensland. Screening of children less than 15 years is currently under consideration (G Miller,
28 November 2002). The Royal Australian College of General Practitioners recommends screening the
Indigenous Australian population for diabetes from 35 years (based on the Australian Centre for
Diabetes Strategies draft recommendations) every 3 years, preferably using a fasting blood sample
although a random sample is acceptable.
59
A summary of recommendations by other groups is
contained in Box 7.
Box 7. Recommendations for diabetes screening
INTERNATIONAL RECOMMENDATIONS
World Health Organisation, 1994
60
Suggests that opportunistic screening of high risk persons may be useful to permit earlier intervention.
Canadian Diabetes Association guidelines, 1998
61
Testing for diabetes using fasting plasma glucose should be performed every 3 years in those over 45
years. More frequent or earlier testing should be considered for people with additional specific risk
factors for diabetes (eg. Aboriginal people). Annual testing should be considered in those with a history
of impaired glucose tolerance or impaired fasting glucose.
Community based screening programs based on measuring blood glucose levels should be established
in Aboriginal communities. Urban people of Aboriginal origin should be screened for diabetes in primary
care settings. Primary prevention programs initiated by Aboriginal communities should be encouraged.
There must be recognition of, respect for and sensitivity regarding the unique language, culture and
geographic issues as they relate to diabetes care in Aboriginal communities across Canada.
US Expert Committee on the diagnosis and classification of diabetes mellitus, 1997
62
Testing for diabetes should be considered for all individuals at age 45 years and above and if normal,
should be repeated at 3 year intervals. Testing should be considered at a younger age or be carried out
more frequently in individuals who are obese, have first degree relatives with diabetes, are members of
a high risk ethnic group, have delivered a baby weighing >9 pound or have been diagnosed with
gestational diabetes mellitus, are hypertensive, have a raised high density lipoprotein cholesterol or
triglyceride or on previous testing had IGT or impaired fasting glucose.
New Zealand Society for the Study of Diabetes, 1995
63
Screening of asymptomatic individuals should only take place in primary health care centres with
facilities for the provision of ongoing care. Non-Europeans (Maori, Pacific Islanders), aged >30 years
should be screened 3-yearly. Screening should be opportunistic. The random glucose test fulfils all the
needs in the New Zealand situation, in spite of a less than ideal predictive value. Screening for
glycosuria is unacceptable and should not be conducted.
NATIONAL RECOMMENDATIONS
National Health and Medical Research Council (NHMRC) Evidence based guidelines for the
management of type 2 diabetes: case detection and diagnosis, 2001
The plasma glucose results should be interpreted as follows:
less than 5.5 mmol/L (diabetes unlikely)
7.0 mmol/L or more fasting or 11.1 mmol/L or more random (diabetes likely)
5.56.9 mmol/l fasting or 5.511.0 mmol/L random.
59
Perform an oral glucose tolerance test (GTT) (the oral GTT should be performed and interpreted
according to the 1999 Word Health Organisation [WHO] criteria).
A confirmatory test must be performed on a separate day to confirm the diagnosis in all asymptomatic
individuals whose results are suggestive of a diagnosis of diabetes.
RECOMMENDATIONS FOR ABORIGINAL AND TORRES STRAIT ISLANDER POPULATION
NHMRC Evidence based guidelines for the management of type 2 diabetes: case detection and
diagnosis, 2001
64
Although the health impact of type 2 diabetes is significant, its overall prevalence does not justify
universal testing of the entire Australian adult population. Rather, opportunistic case detection is
recommended, eg. Aboriginal and Torres Strait Islanders aged 35 years and overin some
communities, the age range for testing should be even lower.
Measure plasma glucose as the screening test in people with risk factors. This should be performed by
a laboratory (rather than a blood glucose meter) and should preferably be done on a fasting sample.
However, a random measurement may be used. Results should be interpreted according to the 1999
WHO criteria with confirmatory testing. Periodic retesting for undiagnosed diabetes is recommended by
measuring fasting plasma glucose each year for people with IGT or IFG, every 3 years for at risk people
with a negative screen, and after 1 year for those with an initial plasma glucose consistent with a
diagnosis of diabetes or IGT/IFG which is not confirmed on subsequent testing.
Guidelines, Standards and Audit Team, NT Coordinated Care Trial, 1998
65
Test for diabetes all adults 16 years and older every year unless they already have diabetes. Fasting
blood glucose is the most accurate method of diabetes screening. It may be difficult to perform and does
not allow immediate feedback. Any person with diabetes symptoms or uncertain glucometer results
should have a fasting blood glucose. Random glucometer test with finger prick in the clinic, requires
fasting blood glucose test or oral GTT if >5.5 mmol/L.
National Diabetes Strategy, 1998
66
Opportunistic screening is recommended in people with risk factors for type 2 diabetes. Population
screening should be considered in population with a high prevalence of diabetes, for example,
indigenous Australians. The preferred option for screening for type 2 diabetes is laboratory
measurement of fasting venous plasma glucose. Conduct periodic general health checks in the
indigenous Australian population to identify a range of disorders including diabetes and associated
health problems (overweight, hypertension, microalbuminuria and hyperlipidaemia) every 12 years
from 18 years.
Office for Aboriginal and Torres Strait Islander Health Systematic Review, 1998
67
Screening should be part of the periodic health examination of adult clients and be integrated with other
aspects of this examination, such as weight, serum lipids and blood pressure. An opportunistic approach
for delivery is preferred. Screening for diabetes with a fasting blood glucose in Aboriginal and Torres
Strait clients every 12 years is recommended. Screening should commence in early adulthood. The
age is dependant on issues such as local prevalence and ease of implementation. A suggested age of
commencement is at 18 years. In those clients who are unlikely to return for testing, a glycated
haemoglobin estimation may be used judiciously.
National Aboriginal Health Strategy Working Party, 1989
68
Recommend fasting glucose checks on all Aboriginal adults every 35 years. Provide facilities for
measurement of fasting blood glucose (and if necessary glucose tolerance tests) on all Aboriginal adults
every 35 years and on pregnant Aboriginal women as they present. This can be part of an individual
consultation when a person presents for other problems, or as part of voluntary community screening
programs.
60
The Aboriginal and Torres Strait Islander population has a higher risk of developing and
dying from diabetes than the general Australian population.
The prevalence of undiagnosed diabetes in the Aboriginal and Torres Strait Islander
population exceeds 5% in all those over 35 years of age. In some regions the prevalence
approaches 5% as young as 18 years of age. The prevalence of risk factors for diabetes
and impaired glucose tolerance (IGT) in this population under 35 years of age exceeds
5%.
The incidence of diabetes in the Aboriginal and Torres Strait Islander population is 10
times higher than in the general population and reaches 2% per year in those over 15
years of age in some regions (eg. central Australia).
EVIDENCE
Level of
evidence
Screening high risk population for diabetes can lead to early detection and treatment.
Early treatment of type 2 diabetes reduces morbidity from long term complications and
has been shown to be cost effective.
I
Screening for diabetes is warranted if it leads to at least 5% of the population being
diagnosed for diabetes.
V
In those at risk of diabetes, weight loss, a healthy diet and physical activity have been
shown to prevent or delay the onset of diabetes.
II
Reduction in the risk of developing diabetes occurs with increased fish consumption and
where monounsaturated fat comprises 2025% of total energy.
II
RECOMMENDATIONS
Commence screening for diabetes at age 1518 years in regions with a high prevalence
of early onset of diabetes. In regions known to have a lower prevalence of diabetes,
commence screening at 35 years of age.
V
Commence 12-monthly re-screening for diabetes in those found to have IGT or impaired
fasting glucose (IFG), or IGT/IFG which is not confirmed on a subsequent visit.
Commence re-screening 3 yearly for those with a negative screening test. A pragmatic
approach is to offer 2-yearly screening in line with the MBS health assessment (item 710)
(see Box 5).
III
Offer diabetes screening by measuring fasting venous blood glucose. A random venous
blood sample is acceptable if a fasting sample is impractical.
V
It is not recommended to screen for type 2 diabetes by using tests for glycosylated
haemoglobin or capillary screening with blood glucose meters.
III
Provide dietary advice and further support to aid consumption of a low energy density
diet with <30% total fats and <10% saturated fat and containing a wide range of
carbohydrate foods rich in dietary fibre and of low glycaemic index (cereals, vegetables,
legumes and fruits). Dietary recommendations should be consistent with the NHMRC
Dietary guidelines for Australian adults (see Box 6, and also Physical activity and
Overweight and obesity in the Vascular heath section).
II
Encourage all clients to undertake moderate intensity physical activity on most,
preferably all, days of the week to prevent diabetes (see also Physical activity and
Overweight and obesity in the Vascular heath section).
II
Promote a combined program of diet and physical activity as more effective in
maintaining weight loss than either diet or physical activity alone (see also Physical
activity and Overweight and obesity in the Vascular heath section).
II
61
Table 3. Proposed benefits of diabetes screening in the Aboriginal and Torres Strait Islander population
prevented
Prevalence of the
problem
Relative risk
reduction
(RRR)
Follow
up time
Numbers
needed
to treat
(NNT) to
prevent
one
event
Control event
rate (CER)
Aboriginal client
expected event
rate (PEER)
Adjusted NNT
(1/PEERxRRR)
Comments
Fasting
blood
glucose
(FBG) for
diagnosis
followed by
intensive
therapy with
metformin in
overweight
people who
have
diabetes.
Myocardial
infarction (MI)
(fatal or non-
fatal).
67% of Aboriginal
diabetic deaths
were related to
heart disease in
19971999.
Aboriginal people
with diabetes are
1013.5 times more
likely to die from
diabetes than non-
Indigenous
Australians.
69
36% RRR for
myocardial
infarction
70
5 years 16 73/411 (18%)
in UKPDS
71
Assume 3 times
CER, but this is
an
underestimate.
5 Five overweight Aboriginal
clients with diabetes need to
be treated intensively with
metformin over 5 years to
prevent a death from MI.
If only half of the Aboriginal
population over 15 years of
age were screened, this
would be around 115 000
people (1996 Census). If
15% had diabetes of which
half were newly diagnosed,
this would be 8625 people.

Assuming that only half of
these required oral
hypoglycaemics over the
subsequent 5 years, this
would be 4312 people, then
treatment of these would
prevent 862 MI events over 5
years.
Intensive
glycaemic
control of
diabetes
comprising
dietary, oral,
combined
oral and/or
insulin to
maintain
FBG below 6
mmol/L).
Aggregate
microvascular
(MV) end
point.
(retinal
complications
requiring laser
Rx; two-step
progression in
microalbuminu
ria; overt
proteinuria;
increase in
plasma
creatinine).
Prevalence of MV
complications
unclear.
25% RRR.
72
10
years
36 10.63%
progression in
conventional
treatment arm.
(Conventional
arm received
dietary or oral
treatment to
maintain FBG
below 15
mmol/L
without
symptoms of
hyperglycaemi
a).
Expect rates of
progression to
be higher in
Aboriginal
population. Also
the CER is
based on
conventional
treatment which
is not a true
control arm.
12 12 Aboriginal clients with
diabetes need to be treated
over 10 years to prevent a
MV end point.
Assuming 4312 people are
treated over 10 years (who
would not have received
treatment early enough
without screening), 359 MV
end points could be
prevented over 10 years.

See Burden of disease for discussion of diabetes incidence
62
prevented
Prevalence of the
problem
Relative risk
reduction
(RRR)
Follow
up time
Numbers
needed
to treat
(NNT) to
prevent
one
event
Control event
rate (CER)
Aboriginal client
expected event
rate (PEER)
Adjusted NNT
(1/PEERxRRR)
Comments
combined
oral and/or
insulin to
maintain
FBG below 6
mmol/L).
complications
requiring laser
Rx; two-step
progression in
microalbuminu
ria; overt
proteinuria;
increase in
plasma
creatinine).
arm received
dietary or oral
treatment to
maintain FBG
below 15
mmol/L
without
symptoms of
hyperglycaemi
a).
based on
conventional
treatment which
is not a true
control arm.
Assume 3 times
CER, but this is
an
underestimate.
treated over 10 years (who
would not have received
treatment early enough
without screening), 359 MV
end points could be
prevented over 10 years.
Modified from: National Aboriginal Community Controlled Health Organisation (NACCHO). Medicare rebate for the Health assessment of Aboriginal and Torres Strait Islander persons proposal to
benefit Aboriginal health. Submission to Australian Government Department of Health and Aged Care, Medicare Benefits Branch, May 2001
63

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1998.
3 Braun B, et al. Risk factors for diabetes and cardiovascular disease in young Australian aborigines:
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4 Dunstan DW, et al. The rising prevalence of diabetes and impaired glucose tolerance: the
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6 Miller G, et al. The well persons health check: a population screening program in Indigenous
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Services Epidemiology Branch, 1999.
9 De Courten M, et al, op. cit., p. 89.
10 Dunstan DW et al, op. cit.
11 Daniel M, Rowley KG, McDermott R, Mylvaganam A, O'Dea K. Diabetes incidence in an Australian
Aboriginal population: an 8-year follow-up study. Diabetes Care 1999 Dec;22(12):19938.
12 Dunstan DW, et al, op. cit.
13 De Courten M, et al, op. cit. p. 23.
14 Welborn TA, Reid CM, Marriott G. Australian Diabetes Screening Study: impaired glucose
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15 Condon J, Dempsey K. op. cit.
16 American Diabetes Association. Screening for diabetes. Diabetes Care 2002;25:S21S24.
17 Steinhart JR, Sugarman JR, Connell FA. Gestational diabetes is a herald of (Non-Insulin
Dependent Diabetes Mellitus) NIDDM in Navajo women: high rate of abnormal glucose tolerance
after gestational diabetes mellitus (GDM). Diabetes Care 1997;20(6)9437.
18 Zimmet PZ, King OM, Bjorntorp SPA. Obesity, hypertension, carbohydrate disorders and the risk of
chronic diseases. Med J Aust 1986;145:25662.
19 ODea K. Westernisation, insulin resistance and diabetes in Australian Aborigines. Med J Aust
1991;155(4):25864.
20 Weeramanthri T. Non-communicable diseases update: diabetes: new diagnostic criteria and
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21 Harris MI. Undiagnosed NIDDM: clinical and public health issues. Diabetes Care
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22 Couzos S, Metcalf S, Murray RB, ORourke S. Diabetes. In: Couzos S, Murray RB, for KAMSC.
Aboriginal primary health care: An evidence-based approach. 2nd Edn. Melbourne: Oxford
University Press, 2003.
23 Centres for Disease Control (CDC) Diabetes Cost-Effectiveness Study Group. The cost-
effectiveness of screening for type 2 diabetes: CDC Diabetes Cost-Effectiveness Study Group,
Centers for Disease Control and Prevention. JAMA 1998 Nov 25;280(20):175763.
24 NHMRC, op.cit.
25 International Diabetes Foundation. The IDF consensus worldwide definition of the metabolic
syndrome. Available at: http://www.idf.org/webdata/docs/Metac_syndrome_def.pdf. [Accessed 23
May 2005].
26 Welborn TA, Reid CM, Marriott G, op. cit.
27 NHMRC, op. cit.
64

28 Australian Government Department of Health and Ageing. National Integrated Diabetes Program
Guide for General Practitioners. Available at
http://www.commed.unsw.edu.au/cgpis/diabetes_early_detection_&_prevention.htm. [Accessed 23
May 2005].
29 ibid.
30 Welborn TA, Reid CM, Marriott G, op. cit.
31 WHO, op. cit.
32 NHMRC, R, op. cit.
33 Diabetes Control and Complications Trial (DCCT) Research Group. The effect of intensive
treatment of diabetes on the development and progression of long term complications in IDDM. N
Eng J Med 1993;329:97786.
34 McCance DR, Hanson R, Charles MA, et al, Comparison of tests for glycated haemoglobin and
fasting and two hour plasma glucose concentrations as diagnostic methods for diabetes. BMJ.
1994 May 21;308(6940):1323-8.
35 Peters AL, Davidson MB et al for Meta-Analysis Research Group on Diagnosis of Diabetes Using
Glycated Haemoglobin Levels. A clinical approach for the diagnosis of diabetes mellitus: an
analysis using glycated haemoglobin levels. JAMA 1996;276(15)124552.
36 UK Prospective Diabetes Study 33. Intensive blood-glucose control with sulphonylureas or insulin
compared with conventional treatment and the risk of complications in patients with type 2
diabetes. Lancet 1998;352:83753.
37 ibid.
38 Davidson MB, Schriger DL, Peters AL, Lorber B. Relationship between fasting plasma glucose and
glycosylated hemoglobin: potential for false-positive diagnoses of type 2 diabetes using new
diagnostic criteria. JAMA 1999 Apr 7;281(13):120310.
39 Expert Committee on Diagnosis and Classification of Diabetes Mellitus. Report of the expert
committee on the diagnosis and classification of diabetes mellitus. Diabetes Care
1997;20(7)118397.
40 NHMRC, op.cit.
41 Wiener K, Roberts NB. The relative merits of haemoglobin A1c and fasting plasma glucose as first-
line diagnostic tests for diabetes mellitus in non-pregnant subjects. Diabet Med 1998
Jul;15(7):55863.
42 Tuomilehto J, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects
with impaired glucose tolerance. New England Journal of Medicine 2001;344(18):134350.
43 Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with
lifestyle intervention or metformin. New England Journal of Medicine 2002;346(6):393403.
44 NHMRC, op cit.
45 Rowley KG et al. Insulin resistance syndrome in Australian Aboriginal people. Clin Exp Pharmacol
Physiol 1997 Sep-Oct;24(9-10):77681.
46 NHMRC. Food for health: Dietary guidelines for Australian adults. Canberra: NHMRC, 2003.
47 McDermott R, Rowley KG, Lee AJ, Knight S, ODea K. Increase in prevalence of obesity and
diabetes and decrease in plasma cholesterol in a central Australian Aboriginal community. Med J
Aust 2000;172:4804.
48 ibid.
49 Rowley KG, et al. Reduced prevalence of impaired glucose tolerance and no change in prevalence
of diabetes despite increasing BMI among Aboriginal people from a group of remote homeland
communities. Diabetes Care 2000;23(7):898904.
50 ODea K. Marked improvement in carbohydrate and lipid metabolism in diabetic Australian
Aborigines after temporary reversion to traditional lifestyle. Diabetes 1984;33:596603.
51 Rowley KG et al. Effectiveness of a community-directed healthy lifestyle program in a remote
Australian Aboriginal community. Australian and New Zealand Journal of Public Health,
2000;24(2):13644.
52 NHMRC, op. cit.
53 Chiasson JL, et al. STOP NIDDM Trial research Group. Acarbose for prevention of type 2 diabetes
mellitus: the STOP-NIDDM randomised trial. Lancet 2002;359;207277.
54 Buchanan TA, et al. Preservation of pancreatic beta-cell function and prevention of type 2 diabetes
by pharmacological treatment of insulin resistance in high-risk hispanic women. Diabetes
2002;51(9):2796803.
55 NHMRC, op. cit.
65

56 Daniel M, Rowley KG, McDermott R, Mylvaganam A, O'Dea K. Diabetes incidence in an Australian
aboriginal population. An 8-year follow-up study. Diabetes Care 1999 Dec;22(12):19938.
57 NHMRC, op. cit.
58 Central Australian Rural Practitioners Association, CARPA Standard treatment manual, 4th edn.
59 RACGP. Guidelines for preventive activities in general practice. Updated 5th Edn. Melbourne:
RACGP, 2002.
60 WHO, op. cit.
61 Meltzer S, et al. 1998 clinical practice guidelines for the management of diabetes in Canada.
Canadian Diabetes Association. CMAJ 1998;159(Suppl. 8):S129.
62 NHMRC, op. cit.
63 New Zealand Society for the Study of Diabetes. Screening for diabetes in asymptomatic
individuals. NZ Med J 1995;108(1011):4645.
64 NHMRC, op. cit.
65 Weeramanthri T, Yarmirr D, Connors C, OLeary S, Morris P as the Guidelines, Standards and
Audit Team. Northern Territory Coordinated Care Trial. Health screening and surveillance. Darwin:
Territory Health Services, 1998.
66 Colagiuri S, Colagiuri R, Ward J. National diabetes strategy and implementation plan: an initiative
of ministerial advisory committee on diabetes. Canberra: Diabetes Australia, 1998.
67 Couzos S, Metcalf S, Murray R, ORourke S, op. cit.
68 National Aboriginal Health Strategy (NAHS) Working Party. A national Aboriginal health strategy:
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69 Edwards RW, Madden R. The Health and Welfare of Australias Aboriginal and Torres Strait
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London: BMJ Publishing Group, 2001;4445.
71 UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with
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72 UK Prospective Diabetes Study 33, op. cit.
Eye health
66
ADULT HEALTH
EYE HEALTH
Authors
Professor Hugh Taylor, Centre for Eye Research Australia, University of Melbourne
Acknowledgment
The Fred Hollows Foundation
VISUAL ACUITY
Burden of disease
Studies have shown that Aboriginal and Torres Strait Islander people from more remote communities
have exceptional visual acuity. This is not the case for urban based Aboriginal people, whose vision in
the absence of eye disease approximates that of the general population. As people age, presbyopia or
difficulty with near vision is a universal development, usually apparent after 40 years.
1
A reduction in
visual acuity is often unrecognised by the individual and under reporting is common. The burden of
unmet need in Aboriginal and Torres Strait Islander populations in relation to identification of correctable
poor vision and access to glasses may be quite significant.
2
Cataracts or opacities in the lens of the eye are also a phenomenon of aging. Aboriginal people have
twice the rate of cataract of the non-Indigenous population, according to a national survey in 1980 (age
adjusted). Impairment in vision has been well described as a risk factor for falls.
3
Untreated cataracts
have been shown to be associated with increased risk of multiple falls
4
and reduced quality of life related
to social isolation and depression.
5
Approximately 26% of Aboriginal and Torres Strait Islander people
aged 50 years or more had cataracts.
6
Waiting time for cataract surgery has been reported as too long
in several regions, however, no systematic analysis of waiting times is possible.
7
In many instances, the
waiting time for cataract surgery is less than in the mainstream public system, but this may reflect
inadequate mainstream public eye surgery services.
It is unclear why Aboriginal and Torres Strait Islander people constitute a minority of those who receive
cataract operations in Australia, far below that expected based upon population ratios, yet have twice
the prevalence of cataract of the general population. Differential rates of access to specialists are the
probable explanation, however, unrecognised disease may also explain low referral rates. It is known
that cataract is often unrecognised with significant impact on morbidity in the elderly.
8
modification
Nil Yes
Snellen
chart
Nil Nil Yes
access to
glasses and
cataract
surgery
reduction of
UV-B
exposure
reduced
smoking
Eye health
67
Screening
Screening for visual acuity in the elderly has been advocated because refractive errors are readily
correctable with eyeglasses and because surgery can be used to treat cataract. A systematic review of
randomised controlled trials could not establish that visual acuity screening of the elderly in a community
setting resulted in improved vision, but visual loss was only assessed by self reporting, not by testing.
9
These findings may not be generalisable to the Aboriginal and Torres Strait Islander population in view
of the greater burden of disease.
The Snellen eye chart is widely recommended for testing visual acuity, but the E-test visual acuity charts
for near and distance vision are useful in testing elderly Aboriginal and Torres Strait Islander people who
cannot read. These charts have been extensively field tested in 32 developing countries and their use
as a screening tool confirmed. The World Health Organisation (WHO) has reported a sensitivity of 85%
and 96% specificity for distance vision.
10
The Centre for Eye Research in Australia (CERA) has recently
developed a simple kit for vision screening especially for the elderly.*
Cataracts identified through visual acuity screening can be treated with surgery. Cataract surgery can
improve vision and therefore quality of life.
11
A meta-analysis of studies reporting the outcome of
cataract surgery in more than 17 000 eyes reported that it yields excellent visual acuity.
12
A retrospective analysis of hospital records in the Northern Territory (NT) revealed that cataract surgery
had a beneficial effect on the visual acuity and quality of life of Aboriginal people.
13
However, most
Aboriginal people in this NT cohort had undergone surgery when they were legally blind. While those
with reduced visual acuity due to cataract should be assessed for surgery, this surgery should not be
delayed until the person is bilaterally legally blind.
14
Recent guidelines have confirmed that cataract
surgery is indicated when visual acuity falls to 6/12 or worse for someone who drives a motor vehicle
and when the activities of daily living are impaired.
15
Reduced ocular exposure to ultraviolet light
16,17
and not smoking
18
are protective against cataract, as
demonstrated in reviews of the epidemiological literature and the large prospective cohort study the
US Physicians Health Study. By not smoking, the relative risk of developing cataract over 13.6 years
was reduced by 36%. The relative risk of developing cataract was also reduced in those who had
ceased smoking.
Reduction of sun exposure through the use of sunglasses or other means may only be partially
preventive as exposure to sunlight only explains 10% of cataracts (the relative contribution of sun
exposure in regions such as north western Australia may be much greater). In addition, the type of lens
opacity most consistently

associated with UV-B is cortical opacity, a form which has generally

been
shown to be less visually disabling and less likely to require

surgery than other types of cataract.
Diabetes is also a strong risk factor for cataract, however, there are no controlled

studies to demonstrate
that improved treatment

of diabetes prevents or delays lens

opacity.
19
The Royal Australian College of General Practitioners (RACGP) recommends annual vision screening in
the general population aged 65 years or more using a Snellen chart.
20
CERA recommends visual acuity
screen for the general population aged 40 years or more every 5 years. If there is a high risk for eye
disease, such as diabetes or a family history of glaucoma (rare in the Aboriginal population), visual
acuity screening should be offered every 2 years (HR Taylor, February 2002).
In the absence of evidence to the contrary, screening for reduced visual acuity should be performed in
all Aboriginal and Torres Strait Islander people aged 40 years or more at least every 2 years.

* Keeffe JE. Testing chart and instructional material can be obtained by email at: jillek@unimelb.edu.au
Eye health
68
The Central Australian Rural Practitioners Association (CARPA) recommends visual acuity screening in
the Aboriginal and Torres Strait Islander population aged 50 years or more.
21
The Northern Zone
Management Unit (NZMU) has no recommendations regarding screening for visual acuity except in
those with existing diabetes or hypertension (G Miller, 28 November 2002).
The Aboriginal and Torres Strait Islander population has a higher risk of developing
cataracts than the general Australian population.
EVIDENCE
Level of
evidence
Cataract surgery may improve vision and therefore quality of life. I
Cataracts are reduced when the eyes are protected from ultraviolet light exposure. Non-
smokers have a lower rate of cataract formation. Avoidance of sun exposure by using
sunglasses is unlikely to result in large reductions in visual disability from cataract.
III
Progressive loss of vision due to cataracts has been shown to be associated with
increased risk of multiple falls.
III
RECOMMENDATIONS
Screen adults (from 40 years of age) for reduced visual acuity at least every 2 years.
The need for cataract surgery and/or correction of any refractive errors should be
identified.
V
ACTIVE TRACHOMA
Burden of disease
Trachoma is caused by repeated episodes of eye infection with chlamydia trachomatis. The conjunctival
scarring leads to contraction and eversion of the eyelid, with subsequent corneal damage from in-turned
eyelashes (entropion and trichiasis) and blindness.
22
The occurrence of blindness in adults reflects the
intensity of active disease contracted in childhood 2040 years earlier.
23
For the clinical diagnosis of
trachoma, the trachoma grading card can be accessed from WHO, available at:
http://www.who.int/pbd/trachoma/gradcard/grading.htm.
24,25
Trachoma is endemic in the Aboriginal population of northern and central Australia. Prevalence varies
between communities from 1260% of children in east Arnhem Land, NT, to the Pilbara, Western
Australia (WA). Many Aboriginal communities have, by definition, a hyperendemic level of trachoma
(prevalence greater than 20% in children aged 10 years or less). According to WHO, a prevalence of
less than 5% in a community defines a non-endemic situation and, unless the prevalence has been
reduced to this level, the disease is still of public health significance.
26
modification
Nil Yes
WHO
trachoma
grading
chart
Yes
clean
faces
Yes
community based
single dose
antibiotic treatment
(azithromycin)
repeated 612
monthly
Yes
addressing
overcrowding
access to
water
face washing
fly control
sewerage
control
access to
trichiasis
surgery
Eye health
69
In the prevention of blindness resulting from trachoma, WHO has for many years supported and
recommended the integrated approach to prevention that has been described by the acronym SAFE:
surgery to correct trichiasis; antibiotics to reduce the community reservoir of chlamydial infection; facial
cleanliness in preschool children; and environmental changes to reduce the transmission of trachoma.
WHO emphasises that these strategies form a combined intervention as part of the delivery of primary
health care.
27
The aim of trachoma treatment is to treat the identified case and to prevent reinfection within the family
by treating family contacts. In 1998, the World Health Assembly called on member states to implement
the SAFE strategy and collaborate in the WHO Alliance for the Global Elimination of Blinding
Trachoma
28
by 2020.
There is good evidence to support all components of the SAFE strategy based on randomised controlled
trials conducted in Australia and overseas.
29
Primary health care professionals have a role in
implementing the SAFE strategy in partnership with regional public health units.
In order to deliver antibiotics to reduce the community reservoir of disease, community based screening
is required. Community based screening and treatment of Aboriginal children for trachoma is indicated
annually in endemically affected communities.
30
Once identified, active trachoma requires treatment of
the family unit with azithromycin.
31
A number of randomised controlled trials have established
azithromycin to be effective in the treatment of trachoma with single dose therapy.
32
In the clinic setting, there is an absence of evidence that opportunistic examination of childrens eyes for
trachoma will improve trachoma outcomes, as it is clear that disease control is dependant on population
based interventions. However, many town based clinics will be visited by children from trachoma
affected remote areas and an index of clinical suspicion should be maintained in order to prompt for an
examination of the eyes.
The prevalence of follicular (active) trachoma in children aged 10 years or less has been used to define
the need for control programs. For example, a prevalence of >5% in children aged 19 years using the
WHO criteria for diagnosis indicates endemic trachoma requiring population based treatment. Only
children aged 19 years need to be screened (although for logistical reasons older children are usually
screened to establish endemicity, which can underestimate the burden of disease). In communities
known to have a high prevalence of infection, screening can be avoided as it may be simpler to treat the
entire community.
33
Those children found to have trachoma should be treated with a single dose of azithromycin (20 mg/kg).
If treatment is provided for the family unit, including maternal caregivers, siblings and other family
members, it is required annually. If only children are treated, high re-infection rates occur and 6-monthly
treatment programs are required.
34
Population based trachoma screening schedules may be used to link with other child health
assessments such as anaemia or nutritional assessments.
Eye health
70
Active trachoma is endemic in the Aboriginal populations of northern and central
Australia, and predominantly affects children.
EVIDENCE
Level of
evidence
Population based strategies integrated with primary health care delivery may prevent
the spread of trachoma, treat complications and eradicate the disease.
III
RECOMMENDATIONS
Where trachoma is endemic, collaborate with the regional public health unit to annually
screen children for trachoma, and treat those affected and their household contacts.
V
Perform an opportunistic eye examination as part of any child health assessment where
trachoma affects a community. If trachoma is diagnosed, contact the relevant public
health unit or primary health care service to ascertain the individuals treatment history.
V
Single dose azithromycin is the treatment of choice for active trachoma (see
Therapeutic guidelines: antibiotic for treatment instructions available at:
http://www.tg.com.au/home/index.html.
I
TRICHIASIS
Burden of disease
Trichiasis is an end stage manifestation of trachoma a result of subtarsal scarring from chronic and
repeated infections. Evidence of at least one eyelash that touches the globe or evidence of recently
removed in-turned lashes is graded as trichiasis.
35
Those with trichiasis remain at risk of developing corneal opacity and subsequent blindness. Trichiasis
is a progressive disease, with 46% of unilateral cases

becoming bilateral, 33% of minor trichiasis cases
becoming major (>5 lashes touching the globe),

and 36% of cases experiencing incident or progressive
corneal scarring

within 1 year in a 1996 longitudinal study in Africa. Active trachomatous inflammation
and additional bacterial conjunctival infections have been shown to accelerate this process.
36
Trichiasis still affects a significant proportion of the elderly Aboriginal population from northern and
central Australia. In the Kimberley region of WA, the screened prevalence of trichiasis in Aboriginal
people aged 50 years or more reported in 2001 was 2.8%.
37
In the same year, screening the population
in a desert area of central Australia revealed trachomatous scarring in 23%.
38
The National Trachoma
and Eye Health Program conducted widespread eye screening in the 1970s and found that 41% of all
eyes with trichiasis were blind. Unless specifically looked for, trichiasis will almost certainly be missed.
Trichiasis is found mostly in the Aboriginal population in people aged 50 years or more and is usually
found in women.
39
See Active trachoma.
Surgical repair of the damage caused by trichiasis can prevent blindness.
40
However, trichiasis can
recur after all forms of surgery to correct it, necessitating vigilance and possible repeat surgery.
Furthermore, surgery cannot correct some complications, such as dry eye, and symptomatic treatment
will be required.
41
Screening, treatment and improvements to the living conditions in remote Aboriginal communities will
eventually eliminate trachoma. However, trichiasis will continue to be a visible marker of childhood
disadvantage. Screening for trichiasis has long disappeared from the periodic health examination of the
non-Indigenous population. The continued burden of disease from trachoma within the Aboriginal
population, particularly in the north of Australia, the preventability of the condition, the availability of
treatment for existing and advanced disease, and waning health care provider awareness of trachoma,
all support the need to implement a systematic screening process for trichiasis in people from affected
areas.
Eye health
71
Population based screening for trichiasis in the older Aboriginal population has been conducted,
42
but
can also be implemented opportunistically. Screening for trichiasis needs to continue for at least 20
years after endemic active trachoma disappears from affected Aboriginal communities.
Blindness is established in the 5060 year age group, and therefore screening at a younger age is
recommended.
The CARPA recommends screening for trichiasis in the NT and central Australia for the Aboriginal and
Torres Strait Islander population aged 50 years or more.
43
Screening for trichiasis in north Queensland
is not recommended (G Miller, 28 November 2002).
Trichiasis affects a significant proportion of the elderly Aboriginal population (defined
as aged >50 years) in remote areas of northern and central Australia.
EVIDENCE
Level of
evidence
Trichiasis causes progressive blindness from corneal abrasions, repeated bacterial
conjunctivitis and associated inflammation.
III
Surgical repair of the damage caused by trichiasis can prevent blindness. IV
RECOMMENDATIONS
Screen for trichiasis as part of a preventive health assessment from 40 years of age if
the region is or has been endemic for trichiasis.
V
Refer for surgery when trichiasis is present. III

References
1 Taylor HR. Eye health in Aboriginal and Torres Strait Islander communities: report of a review
commissioned by the Commonwealth Minister for Health and Family Services, 1997. Available at:
http://www.iris.medoph.unimelb.edu.au/abts/abts.htm. [Accessed 28 June 2004].
2 Eye health in Aboriginal and Torres Strait Islander communities: report of a review commissioned
by the Commonwealth Minister for Health and Family Services, op. cit., p. 5761.
3 Nevitt M, et al. Risk factors for injurious falls: A prospective study. Journal of Gerontology,
1991;46:M16470.
4 Ivers R, et al. Visual impairment and falls in older adults: The Blue Mountains eye study. Journal of
the American Geriatrics Society, 1998;46:5864.
5 Taylor HR, Keeffe JE. Updates in Medicine: Ophthalmology. Med J Aust 2002;176:29.
6 Taylor HR, op. cit., p. 58.
7 OATSIH. The review of the implementation of the National Aboriginal and Torres Strait Islander Eye
Health Program, 2003.
8 United States Preventive Services Task Force (USPSTF). Guide to clinical preventive services. 2nd
edn. Report of the USPSTF. Baltimore: Williams and Wilkins,1996.
9 Smeeth L, Iliffe S. Effectiveness of screening older people for impaired vision in community setting:
systematic review of evidence from randomised controlled trials. BMJ 1998;316:6603.
10 Keeffe JE, Lovie-Kitchin JE, Maclean H, Taylor HR. A simplified screening test for identifying people
with low vision in developing countries. Bull World Health Organ 1996;74:5:52532.
11 USPSTF, op. cit.
12 Powe NR et al. Synthesis of the literature on visual acuity and complications following cataract
extraction with intraocular lens implantation: Cataract Patient Outcome Research Team. Arch
Ophthalmol 1994;112(2):23952.
Eye health
72

13 Hewitt A, Verman N, Gruen R. Visual outcomes for remote Australian Aboriginal people after
cataract surgery. Clin Experiment Ophthalmol 2001;29(2):6874.
14 Taylor HR, op. cit., p. 667.
15 OATSIH, op. cit.
16 McCarty CA, Taylor HR. A review of the epidemiologic evidence linking ultraviolet radiation and
cataracts. Dev Ophthalmol 2002;35:2131.
17 West S. Ocular ultraviolet B exposure and lens opacities: a review. J Epidemiol 1999;9(6
Suppl):S97101.
18 Christen WG, et al. Smoking cessation and risk of age-related cataract in men. JAMA
2000;284(6):7136.
19 Congdon NG. Prevention strategies for age related cataract: present limitations and future
possibilities. Br J Ophthalmol 2001;85(5):51620.
20 RACGP. Guidelines for preventive activities in general practice. 5th edn. Melbourne: RACGP, 2001.
21 Central Australian Rural Practitioners Association. CARPA Standard Treatment manual, 4th edn.
22 Schachter J. Trachoma and inclusion conjunctivitis. In: Last JM, Wallace RB. Public health and
preventive medicine. 13th edn. Connecticut: Prentice-Hall International Inc, 1992:1479.
23 Dawson CR, Schachter J. Strategies for treatment and control of blinding trachoma: cost-
effectiveness of topical or systemic antibiotics. Rev Infect Dis 1985;7:(6):76873.
24 World Health Organisation. Trachoma and other causes of blindness. Geneva: WHO, 2004.
Available at: http://www.wpro.who.int/public/policy/50TH/Ch_28.html. [Accessed 28 June 2004].
25 OATSIH, op. cit.
26 World Health Organisation. Future approaches to trachoma control. Report of a global scientific
meeting; 1996 June 1720, Geneva, Switzerland. Geneva: WHO, 1996.
27 WHO, op. cit.
28 WHO. Agenda item 20. Proceedings of the 51st World Health Assembly; 1998 May 1216; Geneva.
[Unpublished].
29 Couzos S, Taylor HR. Trachoma. In: Aboriginal primary health care: an evidence-based approach.
2nd edn. Melbourne: Oxford University Press, 2003.
30 ibid.
31 Therapeutic Guidelines. Therapeutic guidelines: antibiotic. Version 11. Victoria: Therapeutic
Guidelines Limited, 2000.
32 Mabey D, Fraser-Hurt N. Antibiotics for trachoma (Cochrane Review). In: The Cochrane Library,
Issue 2, 2002. Chichester: Wiley.
33 Couzos S, Taylor HR, op. cit.
34 Taylor HR, V Lansingh. Azithromicin: a new era for trachoma elimination? Tracking trachoma
[Editorial]. WHO Alliance for the Global Elimination of Trachoma. Issue 2, October 1999.
35 Thylefors B, Dawson CR, Jones BR, West SK, Taylor HR. A simplified system for the assessment
of trachoma and its complications. Bull World Health Organ 1987;65:4:47783.
36 Bowman RJ, et al. Longitudinal study of trachomatous trichiasis in the Gambia. Br J Ophthalmol
2002;86(3):33943.
37 Mak DB, Plant AJ. Trichiasis in Aboriginal people of the Kimberley region of Western Australia. Clin
Experiment Ophthalmol 2001;29(1):711.
38 Lansingh VC, Weih LM, Keeffe JE, Taylor HR. Assessment of trachoma prevalence in a mobile
population in Central Australia. Ophthalmic Epidemiol 2001 Jul;8(2-3):97108.
39 Taylor HR, op. cit.
40 OATSIH, op. cit.
41 Bailey R, Lietman T. The SAFE strategy for the elimination of trachoma by 2020: will it work? Bull
World Health Organ 2001;79(3):2336.
42 Mak DB, Plant AJ. Trichiasis in Aboriginal people of the Kimberley region of Western Australia. Clin
Experiment Ophthalmol 2001 Feb;29(1):711.
43 Central Australian Rural Practitioners Association. A clinical manual for primary health care
practitioners in remote and rural communities in central and northern Australia. 4th edn. Alice
Springs: CARPA, 2003.
Kidney disease prevention
73
ADULT HEALTH
KIDNEY DISEASE PREVENTION
Authors
Dr Sophie Couzos, Public Health Officer, National Aboriginal Community Controlled Organisation
Clinical Associate Professor Mark Thomas, Department Nephrology, Royal Perth Hospital
Associate Professor Tim Mathew, Medical Director, Kidney Health Australia
Acknowledgments
Dr Wendy Hoy, Professor of Medicine, Director, Centre for Chronic Disease, The University of
Queensland, Department of Medicine, School of Medicine Central Clinical Division,
Royal Brisbane Hospital
Dr Stephen McDonald, Australia and New Zealand Dialysis Registry
Australian Kidney Foundation
KIDNEY DISEASE
Burden of disease
Kidney disease in the Aboriginal population is of epidemic proportions in some regions,
1
and is
increasing all the time (Figure 2). Despite difficult access to diagnostic services, the incidence of end
stage kidney failure (ESKF) is increased in remote versus urban centres, and in northern versus
southern states.
2
A greater proportion of Aboriginal than non-Indigenous clients with ESKF have their ESKF attributed to
diabetic nephropathy (47% vs 17%) although causes are multifactorial.
3
The most significant cause is
likely to be poor socioeconomic status. The relation between area based measures of disadvantage and
the standardised incidence of ESKF for 36 Australian Aboriginal and Torres Strait Islander Commission
regions revealed a statistically significant correlation. The authors concluded that if it was possible to
improve the health of all Indigenous Australians to the level of that of the general Australian population,
87% of cases of end stage kidney disease (ESKD) could be avoided.
4
A disproportionately higher number of Aboriginal and Torres Strait Islander clients enter dialysis
programs every year. Maintenance haemodialysis is the leading cause of hospital admissions among
Indigenous Australians (26% of all episodes of care, and 44% as principal procedure in 19981999).
5
In
2000, 8% of new clients entering these programs were Aboriginal (even though 2% of the population is
Aboriginal). Within jurisdictions, 81% of new clients in the Northern Territory (NT), 19% in Western
Australia (WA), 11% in Queensland and 6% in South Australia (SA) were Aboriginal or Torres Strait
Islander.
6
The average cost per routine haemodialysis treatment has been reported as $78 600 per
client treatment year for those in the top end of Australia's NT as estimated for the financial years
19961997 and 19971998.
7
End stage kidney failure patient survival in 19912000 was worse in Indigenous Australian clients, being
60% at 5 years, compared to 85% in non-Indigenous clients (p<0.001). Similarly, Indigenous Australian
clients who received transplants had worse 5-year patient and graft survival (70% vs 82% in non-
Indigenous clients).
8
Late diagnosis reduces the effectiveness of treatment for ESKF and affects Aboriginal clients
acceptance of dialysis treatment.
9
Undiagnosed chronic kidney failure is common in the Aboriginal
population. Approximately 40% of Aboriginal clients within ESKF programs were not known to have had
74
kidney disease before presenting with kidney failure.
10
Other data also supports this situation. First,
there is a high prevalence of unrecognised proteinuria which is a marker of kidney disease and its
progression (see below) in studies involving remote Aboriginal communities. With the progression of
albuminuria, glomerular function clearly declines over time,
11
and both changes predict kidney failure.
12
It has been said that the degree of albuminuria and reduced glomerular filtration rate (GFR) represent a
large asymptomatic base to a pyramid of kidney disease, the tip of which is manifest as ESKD.
13
Second, based on data from the Australia and New Zealand Dialysis Registry, Indigenous Australians in
receipt of dialysis were twice as likely to have been late referrals than those who were non-Indigenous.
In the period 19972002, 38% (357/933) of Aboriginal and Torres Strait Islander clients on dialysis were
late referrals compared with only 23% (2125/9250) of non-Indigenous Australians (p<0.001). Late
referral is defined as clients first seen by a kidney unit or nephrologist less than 3 months before the
initiation of dialysis, and is a reasonable surrogate for undiagnosed ESKF. Indigenous Australians make
up approximately 15% of all clients who have late referrals for dialysis (SP McDonald, November 2003).
There is also evidence of racial disparity in access to treatment services. Compared with 42% of clients
aged less than 65 years in receipt of dialysis, who were on the transplantation waiting list in 2000, only
6% of Aboriginal clients (<65 years) were also on this list. Once on the waiting list, Aboriginal people are
less likely to receive a graft.
14
Overt proteinuria and microalbuminuria are markers and predictors of kidney disease and
cardiovascular disease.
Figure 2. Incident ESKD rates for Indigenous people for Australia and New Zealand
15
(not age
adjusted)
Extracted from: Australia and New Zealand dialysis and transplant registry (24th Report). ANZDATA Registry
Proteinuria as predictor of progressive kidney disease
Microalbuminuria is a recognised early phase of diabetic nephropathy and indicates leakage of protein
from the kidney. It is often not detectable by conventional dipstick tests used to pick up overt proteinuria.
It is a predictor of the progression to kidney failure in type 1 and type 2 diabetes and non-diabetic kidney
disease. Microalbuminuria is usually expressed as an albumin-creatinine ratio (ACR) between 3.434
mg/mmol (see Table 4).
Approximately 9% of clients with microalbuminuria progress to overt proteinuria per year. In those with
diabetes, the degree of proteinuria and progressively increasing proteinuria correlates strongly with the
progression of kidney failure.
16
Once overt proteinuria occurs, progressive loss of kidney function is
usually relentless, although the rate can be modified. End stage kidney failure has been known to occur
in 50% of clients with proteinuria within 7 years.
17
Elevated serum creatinine (>124 mmol/L) was present
in 41%, and 63% of type 2 diabetics, after 3 and 5 years (respectively) of persisting overt proteinuria.
18
Improving glycaemic control in type 2 diabetes can modify this process of decline, whether by insulin or
oral hypoglycaemics.
19
75
In non-diabetic kidney disease, it has been clearly established that proteinuria is a predictor of
progressive kidney function decline and that the heavier the proteinuria, the greater the annual rate of
loss of glomerular filtration.
20,21
Proteinuria as a predictor of cardiovascular disease
In diabetics and non-diabetics, new large studies have established that the presence of
microalbuminuria or overt proteinuria predicts cardiovascular disease.
22,23
The increase in cardiovascular disease is about 3-fold in microalbuminuric clients with type 1 diabetes,
compared with age- and duration-matched normoalbuminuric clients with diabetes. The increase in
cardiovascular risk is directly related to the level of proteinuria, so the more proteinuria, the higher the
cardiovascular risk.
24
In clients with type 2 diabetes, both microalbuminuria and overt proteinuria have
also been shown to be predictive of total and cardiovascular mortality and cardiovascular
morbidity.
25,26,27,28,29
There appears to be no difference between type 1 and type 2 diabetes in the
relationship between proteinuria and kidney mortality prediction.
30
Lipid abnormalities frequently accompany microalbuminuria,
31
and this has been shown for Aboriginal
populations.
32,33
Lipid abnormalities have also been shown to promote the progression of
microalbuminuria, suggesting that hyperlipidaemia may be an independent risk factor for nephropathy,
and that lipid therapy may affect kidney disease progression. A recent meta-analysis showed that lipid
therapy could decrease proteinuria and preserve GFR in clients with chronic kidney disease.
34
Microalbuminuria also appears to be a risk factor for cardiovascular events in non-diabetic subjects with
hypertension.
35,36
Proteinuria has also been shown to relate to smoking
37
and malignancy, which
suggests that proteinuria may be a general marker of chronic poor health, as well as of acute disease.
38
Microalbuminuria may legitimately be defined as an integrated marker of cardiovascular risk,
39
an
association also clearly shown in the Aboriginal population.
40,41,42
Pathologic albuminuria (micro and
overt proteinuria) was associated with 84% of all-cause natural deaths observed in an NT Aboriginal
community after a median follow up of nearly 6 years.
43
Proteinuria prevalence in the Aboriginal and Torres Strait Islander population
Many studies have shown that proteinuria is highly prevalent in the Aboriginal and Torres Strait Islander
population. An Aboriginal community screen conducted in SA in 1998 (65% of the adult population, 149
adults, 1878 years) revealed that 50% of all adults aged older than 45 years had either
microalbuminuria (ACR 3.434 mg/mmol) or overt proteinuria (>34 mg/mmol). One-quarter of adults
aged 2944 years had evidence of proteinuria. All subjects with microalbuminuria were either diabetic
(with or without hypertension) or hypertensive. Approximately 20% of those found to have
microalbuminuria, were not previously known to have this.
44
Screening of more than 90% of Tiwi
Islanders in one community in the NT in 1995, revealed that 55% had albuminuria (ACR >3.4
mg/mmol).
45
A community based risk factor survey in eight remote Aboriginal communities (1075 people) in 2000,
reported that 22% of men and 27% of women had microalbuminuria (ACR 3.433.9 mg/mmol), and
10.4% of men and 13.5% of women had overt proteinuria (ACR >34 mg/mmol).
46
In WA, all residents of a small and remote Aboriginal community were screened for overt proteinuria.
The screening revealed that 39% of this community had overt proteinuria.
47
An unpublished survey of central Australian Aboriginal communities revealed that 24% had
microalbuminuria (ACR >3.5 mg/mmol) and 11% had overt proteinuria (>34 mg/mmol). When the data
was analysed with respect to the presence or absence of diabetes, 22% of non-diabetics compared with
34% of diabetics had microalbuminuria. There was evidence of overt proteinuria in 6% of non-diabetics
compared with 36% of clients with diabetes.
In the Aboriginal population of southeastern Australia, a cross sectional survey revealed that 40% had
evidence of a raised ACR above 3.5 mg/mmol indicative of microalbuminuria. In comparison, 8% of the
non-Indigenous population surveyed in a neighbouring town had microalbuminuria. The population
samples screened were not matched, and so could not be directly compared.
48
In community surveys of
Aboriginal children, 38% had evidence of overt proteinuria.
49
The odds of having microalbuminuria or overt proteinuria, in a cohort of urban Aboriginal versus other
ethnic groups with type 2 diabetes, were found to be higher than in a cohort of Anglo-Celtic patients with
type 2 diabetes, even after correction for age, duration of diabetes and glycaemic control.
50
76
In north Queensland, a Well Persons Health Check cross sectional survey (19982000) of 2862
Indigenous Australians revealed that 30% of those aged 1534 years had overt proteinuria (!1+
dipstick).
51
In comparison, the Australian Diabetes Obesity and Lifestyle (AusDiab) Study found proteinuria (urine
protein-creatinine ratio >20 mg/mmol) in 2.5% of the general Australian study population over 25 years
of age
52
which translates to a substantial proportion at risk of future kidney impairment.
53
modification*
Nil Yes
dipstick urinalysis
albumin
creatinine ratio
(limited
indications)**
serum creatinine
(limited
indications)**
Yes
smoking
Yes
blood pressure
control (special role
of angiotensin
converting enzyme
inhibitors or
angiotensin receptor
antagonists)
Yes
overcrowding
and poor
housing
water facilities
prevention of
skin infections
* The evidence for these interventions has been discussed in other sections (see Child health)
** Not recommended for screening in the general Aboriginal or Torres Strait Islander population
See text and recommendations for when these screening tests should be used
Cigarette smoking was associated with an increased risk of ESKF in the Multiple Risk Factor
Intervention Trial which enrolled over 300 000 white men (3557 years) followed from 19731990.
54
Smoking has been recognised as a risk factor in both type 1 and type 2 diabetes, increasing the risk of
the development of nephropathy and increasing the progression of non-diabetic kidney disease.
55
There is evidence collated in a number of review articles that reduction in smoking is protective against
deterioration in kidney disease.
56,57
Advice against smoking is strongly recommended in the prevention
of chronic disease as part of a preventive health assessment of Aboriginal and Torres Strait Islander
clients (see Smoking in the Respiratory disease Non-communicable section).
Treatment with antihypertensives will prevent worsening of kidney disease both in diabetics,
58,59
and
non-diabetics.
60
Prevention of kidney disease progression in the diabetic population
A significant body of evidence supports the use of the antihypertensive angiotensin converting enzyme
inhibitors (ACEIs) and angiotensin receptor antagonists (ARA) in those with type 1 or type 2 diabetes
with overt proteinuria, in the prevention of kidney deterioration. The progression of microalbuminuria to
overt proteinuria can also be reduced by ACEIs or ARA in both hypertensive and normotensive clients
with type 1 diabetes and in hypertensive type 2 diabetics.
61,62
For this reason, annual ACR for
microalbuminuria in the diabetic population is now widely recommended.
While it may follow that the treatment of microalbuminuria with ACEIs may also prevent ESKF and
thereby reduce mortality, as yet no trial has demonstrated this in either type 1 or type 2 diabetes ACEI
or ARA therapy in all clients who are microalbuminuric with type 1 or type 2 diabetes is now
recommended, irrespective of blood pressure. The progression of diabetic nephropathy can also be
reduced by good glycaemic control.
63
77
Prevention of kidney disease progression in the non-diabetic population
The majority of Aboriginal or Torres Strait Islanders with overt proteinuria will already have evidence of
hypertension and/or diabetes. Moreover, all kidney failure develops out of a background of persistent
albuminuria in this population.
64
However, it is useful to examine how effective ACEIs are in reducing the
rate of kidney disease progression in those with proteinuria but without diabetes.
The use of ACEIs in those without diabetes, who show overt proteinuria in the presence of hypertension,
has been shown to be of benefit in reducing the development of ESKD and delaying the progression of
kidney insufficiency.
65,66,67,68,69
In those clients with overt proteinuria but without hypertension and without diabetes, there is still debate
and uncertainty on the degree of reno-protection provided by ACEIs. Few studies have reported the use
of ACEIs in normotensive non-diabetic subjects with overt proteinuria.
Trials in the Tiwi Island Aboriginal population have involved a small cohort of subjects in this group,
however, analysis of this cohort was not reported separately. ACEI therapy trialled in hypertensive and
normotensive Aboriginal subjects, with diabetes (and micro or overt albuminuria) and those without
diabetes (with overt albuminuria), as a whole showed a significant benefit compared to historical
controls. The relative risk of combined end points for kidney failure and natural death in the treatment
group was significantly reduced and half that of the control group.
70
Further analysis suggested no
survival benefit among people without overt albuminuria, or among those with GFR less than 60 mL/min.
It was concluded that in those with hypertension, or diabetes with micro or overt albuminuria, and all
people with overt albuminuria regardless of blood pressure and diabetes, rates of natural deaths can be
reduced by an estimated 50% and kidney deaths reduced by 57% after a mean follow up of 3 years of
ACEI treatment.
71
The links between cardiovascular disease and overt and microalbuminuria suggest that proteinuria
screening of the non-diabetic population may provide a mechanism for modifying the development and
progression of cardiovascular disease. No study has yet explored this.
Screening
As many Aboriginal and Torres Strait Islander clients present with previously undiagnosed kidney
failure, there is an imperative to consider screening for proteinuria and to implement recently proven
preventive interventions.
Screening for kidney disease by testing for proteinuria
Urinary protein excretion above 300 mg/24 hr is defined as overt proteinuria. The presence of dipstick
positive proteinuria (! +1 for protein) indicates overt proteinuria (equivalent to protein excretion rate of
300 mg in 24 hours
72
(see Table 4).
Table 4. Definitions of proteinuria
Test Normal Microalbuminuria Overt proteinuria
24 hour total protein <30 mg/24 hours 30299 mg/24 hours !300 mg/24 hours
Dipstick protein <30 mg/dL N/A >30 mg/dL
or ! +1 protein
Albumin-creatinine ratio <2.5 mg/mmol 2.525 mg/mmol
(males)
3.525 mg/mmol
(females)
>25 mg/mmol
Note: Due to variability in urinary albumin excretion, an abnormal result is confirmed if it is present in two of three
specimens collected within a 36 month period. Exercise within 24 hours, infection, fever, congestive heart failure,
marked hyperglycaemia, marked hypertension, pyuria, and hematuria may elevate urinary albumin excretion over
baseline values
Sources: American Diabetes Association. Diabetic nephropathy. Diabetes Care 2003;26:S94S98. Available at:
care.diabetesjournals.org/cgi/content/full/26/suppl_1/s94. [Accessed 11 June 2004] and Morgensen CE, Keane WF,
Bennett PH, Jerums G, Parving H-H, et al. Prevention of diabetic renal disease with specific reference to
microalbuminuria. The Lancet 346:10804
Commercially available dipsticks are sensitive to albumin in concentrations of 100200 mg/L. If detected
in the absence of infection, dipstick proteinuria should be quantified by a spot ACR. The Kidney Disease
Outcome Quality Initiative of the National Kidney Foundation in the USA recommends that if a urine
78
dipstick test is positive (1+ positive for protein or greater), proteinuria should be followed with a
quantitative test for albumin-creatinine ratio within 3 months. If two or more ACR tests performed 12
weeks apart are positive, persistent proteinuria is present, and the patient should be further evaluated
for chronic kidney disease.
73
Screening for microalbuminuria by estimating ACR in those clients with diabetes has been simplified
since the introduction of point of care diagnostic instrumentation.
74,75
This approach was pioneered in
the Tiwi Islander population
76
and adopted by many other units around Australia. This method of
screening for ACR has been shown to be acceptable to Aboriginal Health Workers in SA.
77
The assessment of a person with overt proteinuria involves confirmation of this finding by excluding
other causes, such as contamination or infection, and by considering the presence of risk factors, such
as hypertension, family history, the presence of unrecognised diabetes, and kidney failure. Other risk
factors for cardiovascular disease such as obesity and family history should also be noted.
Due to the lack of definitive evidence for prevention of non-diabetic kidney disease in those who are
normotensive, there is little support from numerous guideline and consensus groups for screening the
general population for proteinuria by routine urinalysis.
78,79,80,81
Within the Aboriginal and Torres Strait
Islander population, there is potential for benefit in recognising those with overt proteinuria because of
the existing and predicted burden of kidney disease. The detection of asymptomatic overt proteinuria in
any Aboriginal or Torres Strait Islander person should lead to an assessment of blood pressure,
cardiovascular status and prompt further investigations for asymptomatic chronic kidney failure.
Furthermore, anecdotal evidence suggests a substantial amount of undiagnosed kidney disease in
Aboriginal and Torres Strait Islander people who are non-diabetic and normotensive (W Hoy, June
2002). For these reasons, all Aboriginal and Torres Strait Islander clients should be offered annual
urinalysis by simple dipstick for assessment of overt proteinuria.
Until there is evidence for the prevention of kidney disease progression in those who are normotensive
with microalbuminuria (and are not diabetic), there appears to be little evidence to support screening for
microalbuminuria (as distinct from screening for overt proteinuria) in the general Aboriginal and Torres
Strait Islander population. It has yet to be shown whether, as a marker of general vascular disease and
early kidney compromise, screening this population for microalbuminuria may complement other risk
factor assessments (such as blood pressure, weight, diabetes, smoking, lipids).
Screening for kidney disease by testing for serum creatinine concentration
Although serum creatinine is a late marker of decline in kidney function, it is often used as a crude
screening or diagnostic test for kidney failure. More accurately, the measure or calculation of a GFR is
preferred for the diagnosis of this disease. For routine clinical practice, the GFR is most simply
estimated from the serum creatinine adjusted for the age, weight and sex of the client, providing the
serum creatinine is stable and the lean (ideal) weight is used. The original Cockcroft & Gault formula for
calculated GFR
82
can be simplified to the following approximation:
Calculated GFR (mL/min) = [140 age (years)] x lean weight* (kg) x 1.23 (males only)
serum creatinine (mmol/L)
*maximum adult lean weight = height (metres)
2
x 25
Using the actual weight of an obese client in the formula will produce a falsely high calculated GFR, so
an estimate of the upper limit of normal weight is used by replacing the actual weight with [height
(metres)
2
x 25]. The MDRD formula is gaining prominence in Australia and internationally as the
preferred method of estimating GFR, as it requires no body surface area measurements, and can be
routinely calculated by pathology laboratories with serum creatinine requests. A generally accepted
definition of significant chronic kidney failure is a serum creatinine >200 mmol/L or calculated GFR <60
mL/min on two occasions at least 1 month apart in the absence of acute illness.
83
Given that microalbuminuria, hypertension and overt proteinuria usually precede any fall in GFR by
years, there is little justification for assessment of serum creatinine as a primary screening test in those
without these risk factors. Most authorities recommend waiting until there is evidence of overt proteinuria
(or microalbuminuria in those with diabetes) before measuring serum creatinine and assessing GFR.
79
Due to a significant proportion of the Aboriginal and Torres Strait Islander population likely to have
unrecognised kidney disease, screening for chronic kidney failure with a serum creatinine (used to
calculate GFR) is recommended in those Aboriginal and Torres Strait Islander clients found to have any
of the following:
overt proteinuria
family history of kidney disease
diabetes with microalbuminuria.
No studies in Australia have examined if screening for kidney impairment in those who are
asymptomatic and at high risk for kidney disease improves kidney outcomes. Provided that tertiary
services are accessible to Aboriginal people and Torres Strait Islanders, there is good reason to expect
improved outcomes if screening leads to earlier diagnosis and treatment known to slow disease
progression.
As treatment of those with microalbuminuria has been shown to be effective, screening for this marker
should be performed annually in all clients with diabetes. The presence of microalbuminuria and overt
proteinuria also indicates the presence of an additional cardiovascular risk factor and lipid studies
should also be performed. A urinalysis in those with diabetes should be performed at the initial visit and
then annually. An annual serum creatinine is recommended for every person with diabetes.
In the non-diabetic Aboriginal and Torres Strait Islander population, a urinalysis using dipstick for overt
proteinuria should be conducted annually. Screening should commence in adulthood (which may be
1518 years, depending on regional screening protocols). Testing for kidney insufficiency using a serum
creatinine should be offered annually to all Aboriginal and Torres Strait Islander clients who have overt
proteinuria, a family history of kidney disease and diabetes with microalbuminuria. It is premature to
recommend routine screening for microalbuminuria in those who are not recognised as having diabetes
or hypertension.
The Central Australian Rural Practitioners Association recommends annual urinalysis for overt
proteinuria in all Aboriginal and Torres Strait Islander adults. Screening for microalbuminuria in those
without diabetes or hypertension is not recommended.
84
The Northern Zone Management Unit also recommends annual urinalysis (simple dipstick) as part of the
adult health check (!15 years) for north Queenslanders. In the presence of 1+ or more of protein, ACR
testing is recommended. The assessment of kidney function including creatinine, urea and electrolytes,
and testing for albuminuria, is required as part of management of hypertension and diabetes (G Miller,
28 November 2002).
The Australia and New Zealand Society of Nephrology Consensus Statement (1999) recommends
urinalysis for proteinuria as part of the periodic examination of Aboriginal and Torres Strait Islander
clients.
85
The Caring for Australians with renal impairment guidelines (2001) recommends screening for
overt proteinuria and kidney impairment in clients at increased risk of kidney disease (Aboriginal and
Torres Strait Islander population) in conjunction with access to referral services.
86
The Royal Australian College of General Practitioners guidelines currently lack recommendations
pertaining to the early detection of kidney disease in the fifth edition of the red book, however, they are
included in the updated sixth edition.
87
80
The Aboriginal and Torres Strait Islander population has a much higher risk of
developing chronic kidney disease and end stage kidney failure than the general
Australian population.
EVIDENCE
Level of
evidence
In Aboriginal and Torres Strait Islander clients with and without type 2 diabetes, overt
proteinuria and microalbuminuria are predictors of kidney disease and cardiovascular
disease.
II
Proteinuria has a higher prevalence in the Aboriginal population than in the general
Australian population. It may be evident from a young age (!15 years).
III
In those with type 2 diabetes, the progression of microalbuminuria to overt proteinuria
may be prevented or delayed by using antihypertensive therapy that targets the renin-
angiotensin systems.
II
In those without type 2 diabetes, the progression of kidney disease in the presence of
hypertension and/or overt proteinuria may be prevented or delayed by using
antihypertensive therapy that targets the renin-angiotensin systems.
II
With such therapy, the rate of natural death may be reduced by an estimated 50%.
Kidney deaths may be reduced by 57% in those with hypertension or in diabetics who
have progressed to micro or overt albuminuria, as well as in all other people with overt
albuminuria. This is regardless of blood pressure and blood sugar levels after a mean
treatment period of 3 years.
III
Smoking increases the risk of progression to end stage kidney failure. III
RECOMMENDATIONS
Offer testing for overt proteinuria annually by simple dipstick commencing from 1518
years of age, depending on regional/local protocols.
V
If urine dipstick test is positive (1+ positive for protein or greater) a quantitative test for
albumin-creatinine ratio (ACR) should be arranged. If two or more ACR tests performed
12 weeks apart are positive, persistent proteinuria is present and the patient should be
further evaluated for chronic kidney disease.
V
Assess microalbuminuria annually in those with diabetes. V
It is not recommended to routinely screen for microalbuminuria in those who are not
recognised as having diabetes or hypertension.
V
It is not recommended to screen for serum creatinine as part of a routine health
assessment.
V
Offer an annual serum creatinine to clients with any of the following risk factors: overt
proteinuria, a family history of kidney disease or in diabetics with microalbuminuria.
V
Provide all clients with advice against smoking (see also Smoking in the Respiratory
disease Non-communicable section).
V

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38 Stephenson JM, Kenny S, Stevens LK, Fuller JH, Lee E. WHO, op. cit.
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41 Hoy WE, et al, op. cit.
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45 Hoy W, et al. Stemming the tide: reducing cardiovascular disease and renal failure in Australian
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Aboriginal people: prevalence and associations with components of the metabolic syndrome.
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47 Gracey M et alRisk factors for ill-health in a remote desert-dwelling aboriginal community in
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48 Guest C, Ratnaike S, Larkins R. Albuminuria in Aborigines and Europids of southeastern Australia.
Med J Aust 1993;159(5):3358.
49 Van Buynder P, Gaggin J, Martin D, Pugsley D, Mathews JD. Streptococcal infection and renal
disease markers in Australian Aboriginal children. Med J Aust 1992;156(8):53740.
50 McGill M, Donnelly R, Molyneaux L, Yue D. Ethnic differences in the prevalence of hypertension
and proteinuria in NIDDM. Diabetes Res Clin Pract 1996;33:1739.
51 Miller G, McDermott R, McCulloch B, Leonard D, Arabena K, Muller R. The well persons health
check: a population screening program in Indigenous communities in north Queensland. Aust
Health Rev 2002;25(6):14051.
52 Dunstan D, et al. Diabesity and Associated Disorders in Australia 2000The Accelerating Epidemic!
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Diabetes Institute, 2001.
53 Cass A. Kidney disease: are you at risk? Med J Aust 2002;176(11):5156.
54 Klag MJ, et al. Blood pressure and end-stage renal disease in men. N Engl J Med 1996 Jan
4;334(1):138.
55 Orth SR. Smoking - a renal risk factor. Nephron 2000 Sep;86(1):1226.
56 Ritz E, Ogata H, Orth SR. Smoking: a factor promoting onset and progression of diabetic
nephropathy. Diabetes Metab 2000 Jul;26 Suppl 4:5463.
57 Curtis B, Barrett BJ, Levin A. Identifying and slowing progressive chronic renal failure. Can Fam
Physician 2001 Dec;47:25128.
58 Jerums G, et al. Long-term comparison between perindopril and nifedipine in normotensive
patients with type 1 diabetes and microalbuminuria. Am J Kidney Dis 2001;37:890.
59 Parving, HH, Lehnert, H, Brochner-Mortensen, J, et al. The effect of irbesartan on the development
of diabetic nephropathy in patients with type 2 diabetes. N Engl J Med 2001;345:870.
60 Ruggenenti P, et al, on behalf of the Gruppo Italiano Di Studi Epidemiologici in Nefrologia (GISEN),
op. cit.
61 Lewis EJ, et al. Renoprotective effect of the angiotensis-receptor antagonist irbesartan in patients
with nephropathy due to type 2 diabetes. N Engl J Med 2001;345:851.
62 Brenner BM, et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2
diabetes and nephropathy. N Engl J Med 2001;345:861.
63 UK Prospective Diabetes Study (UKPDS) Group, op. cit.
64 Hoy WE, Wang Z, Van Buynder P, Baker PR, McDonald SM, Mathews JD, op. cit.
65 Apperloo AJ, Rensma PL. Effect of Benazepril in chronic renal insufficiency. N Eng J Med
1996;335(8)5967.
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66 De Zeeuw D, Apperloo AJ, de Jong P. Management of chronic renal failure. Curr Opin Nephrol
Hypertens 1992;1:11623.
67 Maschio G, et al. Effect of the ACE inhibitor benazepril on the progression of chronic renal
insufficiency. N Eng J Med 1996;334:93945.
68 Giatras I, Lau J, Levey AS, for ACE Inhibition and Progressive Renal Disease Study Group. Effect
of ACE inhibitors on the progression of nondiabetic renal disease: a meta-analysis of randomised
trialsAnn Intern Med 1997;127:33745.
69 Kshirsagar AV, Joy MS, Hogan SL, Falk RJ, Colindres R. Effect of ACE inhibitors in diabetic and
nondiabetic chronic renal disease: a systematic overview of randomized placebo-controlled trials.
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70 Hoy WE, Baker PR, Kelly AM, Wang Z. Reducing premature death and renal failure in Australian
aboriginals. A community-based cardiovascular and renal protective program. Med J Aust 2000
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71 Hoy WE, Wang Z, Baker PR, Kelly AM. Secondary prevention of renal and cardiovascular disease:
results of a renal and cardiovascular treatment program in an Australian aboriginal community. J
Am Soc Nephrol 2003 Jul;14(7 Suppl 2):S17885.
72 Levey AS. Non-diabetic kidney disease. N Eng J Med 2002;347:19:150511.
73 Johnson CA, Levey AS, Coresh J, Levin A, Lau J, Eknoyan G. Clinical practice guidelines for
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Am Fam Physician 2004 Sep 15;70(6):10917.
74 Croal BL, et al. The clinical application of a urine albumin: creatinine ratio point-of-care device. Clin
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75 Shephard MD, Barratt LJ, Simpson-Lyttle W. Is the Bayer DCA 2000 acceptable as a screening
instrument for the early detection of renal disease? Ann Clin Biochem 1999 May;36(Pt 3):3934.
76 Hoy WE, Baker PR, Kelly AM, Wang Z, op. cit.
77 Shephard M, Brown M, Hudson M, Riessen C, Braun J. The Umoona kidney project. Aboriginal
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78 Nagai R, Wang EEL, Feldman W. Dipstick proteinuria screening of asymptomatic adults to prevent
progressive renal disease In: Canadian Task Force on the Periodic Health Examination Canadian
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79 Scottish Intercollegiate Guidelines Network. Investigation of asymptomatic proteinuria in adults: A
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84 Central Australian Rural Practitioners Association. CARPA Standard treatment manual. 4th edn.
85 Thomas M. Australia and New Zealand Society of Nephrology consensus statement delivery of
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RACGP, 2002.
Respiratory disease Communicable
84
ADULT HEALTH
RESPIRATORY DISEASE
COMMUNICABLE
Author
Acknowledgments
Associate Professor Paul Torzillo, University of Sydney, and Medical Director, Nganampa Health
Council
Centre for Disease Control (Territory Health Services), Communicable Disease Control (South
Australia), Communicable Disease Unit (Queensland), and John Mohoric from the Immunisation
Section, Communicable Diseases and Health Protection Branch, Australian Government Department of
Health and Ageing for assistance with immunisation data
INFLUENZA
Burden of disease
There is little data on the impact of influenza within the Aboriginal and Torres Strait Islander population.
However, it is known that mortality from respiratory disease is substantially higher in this population than
in the general Australian population. Respiratory disease accounted for nearly 10% of the causes of
excess Aboriginal and Torres Strait Islander deaths over the period 19971999
1
and a substantial
proportion of these deaths have been attributed to pneumonia and influenza.
2
Pneumonia and influenza
were important contributors to the higher rates of hospitalisation for respiratory diseases with nearly five
times as many as expected among Indigenous males and females in the period 19971998.
3
Defining the public health impact of influenza can be difficult as the infection can worsen cardiac, lung,
renal and metabolic disease. It has been estimated that, for each death attributed to influenza, there
may be a further eight deaths that were influenza associated.
4
Most complications from influenza occur
in the elderly, young children, those with chronic disease and debilitated individuals. As influenza
appears to affect all populations, it likely that its role in Aboriginal and Torres Strait Islander ill health is
significant.
Since January 2001, all jurisdictions have agreed that laboratory confirmed influenza should be notified
to the National Notifiable Diseases Surveillance System and appropriate legislation has been or is being
introduced in the states and territories.
5
The Australian Sentinel Practice Research Network (ASPRN)
conducts national sentinel surveillance for influenza through general practice.
6
Increased influenza
activity is usually documented in JuneSeptember, with peaks in JulyAugust.
7
There is some evidence
that influenza outbreaks in northern Australia may occur at different periods from the south, with several
peaks throughout the year. Influenza outbreaks in the 'top end' of the Northern Territory (NT) have
occurred in FebruaryMarch, well before the commencement of the vaccination period in April.
8
The influenza virus is classified into types A, B, and C which also vary according to the capacity to
cause severe disease and epidemics. Types A and B can cause epidemics, but type B is mostly an
endemic disease and less severe. Type C is associated with minor localised outbreaks. Type A
influenza pneumonia has a higher mortality rate (9%), according to meta-analysis.
9
The types are
clinically indistinguishable, and therefore can only be determined if the client is serologically tested.
Spread is by respiratory secretions and the incubation period is 1872 hours. Influenza can be
transmitted just before the clinical symptoms develop and 510 days afterwards.
10
The influenza
vaccine in current use is inactivated (ie. killed virus usually 2 type A and 1 type B) representing the
influenza viruses likely to circulate in the upcoming winter. Clients and their doctors often express
85
concern that vaccination causes influenza, despite the fact that is not possible to contract it from
inactivated virus. This probably relates to systemic adverse effects from inactivated vaccine mimicking
influenza which occur more commonly in children.

Guillain-Barre syndrome has been linked to influenza
vaccine, but exceedingly rare at one case per million people vaccinated.
11
Vaccine coverage
In 2000, a National Influenza Survey was conducted which involved interviews with over 10 000
Australians. Overall, 74% of those aged more than 65 years reported receiving influenza vaccine during
the year 2000.
12
National survey data from 2002 involving 8000 Australians aged more than 40 years
showed that 77% of those aged more than 65 years reported receiving influenza vaccine. The
proportion of Indigenous Australians who received influenza vaccine was not reported.
13
According to the National Centre for Immunisation Research and Surveillance, the uptake of influenza
vaccine in 2001 was 87% in Aboriginal and Torres Strait Islander people responding to telephone survey
aged over 65 years (28/32 people) and 23% in those aged 464 years (8/35) (P Horby, 14 May 2002).
The sample size was very small and may therefore be unrepresentative. In comparison, 32% of the
general population aged 4064 years in the influenza risk category were immunised in 2000.
In South Australia (SA), 80% of those aged >65 years reported having influenza vaccine in 2001. This
coverage has progressively risen from 55% in 1993. Coverage in those aged 1864 years was 16%.
14
Only 1.3% of respondents were Aboriginal or Torres Strait Islander. Of these, 26% (8/30) received
influenza vaccine and all were aged less than 64 years.
15
Similarly, these results may not be
representative of the Aboriginal and Torres Strait Islander population as a whole.
Over 80% of Aboriginal Community Controlled Health Services (ACCHSs) reported that they routinely
organised influenza and pneumococcal vaccination for Aboriginal clients in 19992000, but
immunisation coverage data is unavailable (G Brice, May 2002).
In 1999, in the USA, approximately 66% of the elderly (>65 years) were vaccinated in the previous year,
which exceeded the previous national objective to vaccinate >60% of persons at high risk for
complications from influenza. Vaccine coverage for those with chronic disease aged 1864 years was
32%. However, vaccine coverage for minority populations such as blacks and Hispanics lagged behind
at approximately 50% for those >65 years. The current USA national objective is to achieve vaccination
coverage for 90% of persons aged >65 years.
16
The equivalent national Australian objective is to vaccinate more than 85% of people aged >65 years
with influenza vaccine.
17
This is not a sufficient target in the Aboriginal and Torres Strait Islander
population, as very few are alive at this age (2.6% of the population compared with 12% of the
nonIndigenous population).
18
The National Performance Indicators for Aboriginal and Torres Strait
Islander Health do not specify targets for influenza vaccine coverage for this population.
19
modification*
Yes
influenza
vaccine
Nil Nil Yes
antiviral agents
Yes
overcrowding
access to health
services
Immunisation
According to a systematic review of cohort, case control and limited randomised controlled trials, there
appears to be little doubt that influenza vaccination in the elderly reduces the risk of hospitalisation,
pneumonia and mortality during influenza outbreaks when the vaccine predicts the epidemic strain.
20
Reported reductions in hospitalisation due to pneumonia varies substantially between studies, but case
control studies in those aged more than 65 years
21
and those with diabetes
22
have reported that
influenza vaccination prevents hospitalisation from pneumonia by as much as 79%. Inactivated
influenza vaccine also prevents exacerbations in clients with chronic obstructive pulmonary disease,
23
86
but there is no evidence that it can prevent exacerbations of asthma,
24
or benefit clients with cystic
fibrosis.
25
Positive cost effectiveness studies in the elderly and working adults have been conducted overseas.
26,27
The vaccine has also been reported to reduce clinical symptoms in health care workers, which may
translate into a reduction in transmission to high risk clients. In view of this, the vaccination of healthy
staff at remote community clinics where staff relief during periods of illness may be difficult to obtain has
been advocated.
28
Australian recommendations support vaccination in healthy adults capable of
transmitting influenza to those at high risk.
In healthy adults, the efficacy of influenza vaccine is estimated at 7090% in preventing or reducing the
severity of influenza illness.
29
Another systematic review reported inactivated influenza vaccine efficacy
in healthy adults aged less than 65 years as 68% (95% confidence intervals (CI): 4978%). Intranasal
live influenza vaccines reduced the number of cases of serologically confirmed influenza A by 48%
(95% CI: 2464%).
30
Chemoprophylaxis
There is good evidence to use amantadine chemoprophylaxis among high risk individuals in contact with
an index case infected with influenza A. Amantadine is 63% protective against influenza A and
rimantadine appears equally effective.
31
It is also recommended for those with contraindications to the
vaccine, such as hypersensitivity to egg protein. The drug is taken at the beginning of the influenza
season and continued daily for the duration of influenza activity in the community.
32
These agents are
also effective as treatments, but act to shorten the duration of symptoms by only 1 day.
33
Newer antiviral agents such as neuraminidase inhibitors started within 48 hours of symptom onset are
effective at preventing both influenza A and B. When compared to placebo, they were 74% effective in
preventing naturally occurring cases of clinically defined influenza, and 60% effective in preventing
cases of laboratory confirmed influenza. As a treatment, these agents shorten the duration of symptoms
by 1 day.
34
Nebulised zanamivir (Relenza) and oral oseltamivir (Tamiflu) are both available in Australia
to shorten the duration of symptoms in those with influenza (taken for 5 days). There are no current
Australian recommendations for the use of these agents as preventive agents.
However, in 2000 in the USA, oseltamivir was approved for chemoprophylactic use in those aged over
13 years, although both neuraminidase inhibitors have been shown to prevent influenza among persons
exposed to household members with influenza. USA guidelines recommend use of antiviral
chemoprophylaxis while waiting for immunity in those at high risk in an outbreak, unvaccinated workers
caring for those at high risk during outbreaks, those with immune deficiency, and all residents in
institutional influenza outbreaks regardless of vaccination status.
35
A proportion of deaths and severe infections precipitated by influenza are due to secondary infection
with bacterial pathogens. Pneumococcal vaccine, administered to high risk groups of the population, is
likely to significantly reduce the incidence of secondary infection and hence reduce morbidity and
mortality associated with influenza. High levels of pneumococcal immunisation should be achieved
during an interpandemic period.
36
Current evidence does not support a preventive effect of homeopathy
in influenza.
37
Annual influenza vaccination is recommended for the Aboriginal and Torres Strait Islander population
aged from 50 years (and other Australians aged from 65 years). Influenza and pneumococcal vaccines
can be administered at the same visit, but at different sites. Studies have confirmed that simultaneous
administration is safe and leads to similar serological responses as when given 1 month apart. The 2003
National Health and Medical Research Council (NHMRC) recommendations for influenza vaccination in
the Aboriginal and Torres Strait Islander population are shown in Box 8.
38
87
Box 8. NHMRC Recommendations for annual influenza vaccination in the Aboriginal and Torres
Strait Islander population
39
All Aboriginal and Torres Strait Islander persons aged 50+ years
Adults and children (!6 months of age) with chronic cardiac conditions including cyanotic
congenital heart disease, coronary artery disease, and congestive cardiac failure
Adults and children (!6 months of age) with chronic suppurative lung disease including
bronchiectasis, cystic fibrosis, and chronic emphysema (COPD)
Adults and children (!6 months of age) with chronic illnesses requiring medical follow up or
hospitalisation in the preceding year including diabetes mellitus, chronic metabolic diseases,
chronic renal failure, and haemoglobinopathies
Persons with immune deficiency or immunosuppression including human immunodeficiency
virus (HIV) before the development of acquired immunodeficiency syndrome (AIDS),
malignancy (including multiple myeloma, lymphoma and Hodgkin disease), long term steroid
and other immunosuppressive drug use, nephrotic syndrome, organ transplantation
Residents of nursing homes and other long term care facilities
Those who can transmit influenza to persons at high risk
Persons with severe asthma, such as those requiring frequent hospital visits
Children (aged 6 months to 10 years) on long term aspirin therapy
Pregnant women who will be in the second or third trimester during the influenza season.
Source: NHMRC. The Australian immunisation handbook, 8th edition, 2003
The Australian Government funded National Indigenous Pneumococcal and Influenza Immunisation
Program (NIPII) was introduced in 19981999 to enhance vaccine coverage. Free influenza and
pneumococcal vaccines are provided to eligible Aboriginal and Torres Strait Islanders through general
practices and ACCHSs via state and territory health authority vaccine distribution systems.
40
Eligibility
criteria for the NIPII Program are shown in Box 9. Financial incentives to clients and health care
providers are available in the delivery of childhood vaccination,
41
but no incentive scheme operates for
adult vaccination.
Box 9. National Indigenous Pneumococcal and Influenza Immunisation Program (NIPII)
Eligibility
#
All Aboriginal and Torres Strait Islander persons aged 50+ years
Aboriginal and Torres Strait Islander peoples aged 1549 years who are at high risk because
they:
! have heart, kidney or lung disease, severe asthma or diabetes, or
! have an immune compromising condition such as HIV infection or cancer, or
! are heavy drinkers, or
! are tobacco smokers (pneumococcal vaccine only), or
! are a pregnant woman who will be in her second or third trimester in the influenza season
(influenza vaccine only).
#
Northern Territory immunisation providers should refer to local guidelines
Source: National Indigenous Pneumococcal and Influenza Immunisation Program (2004) available at:
http://www.immunise.health.gov.au/indigenous.htm
Recommendations regarding influenza vaccine do not differ among regional areas within Australia and
are ratified by the NHMRC for national application.
88
Influenza and secondary pneumonia contribute to the much higher rates of
hospitalisation for respiratory diseases among Indigenous Australians. Nearly five
times as many hospitalisations as expected occurred in both sexes during the period
19971998.
EVIDENCE
Level of
evidence
Influenza vaccination in the elderly reduces the risk of hospitalisation, pneumonia
and mortality during influenza outbreaks where the vaccine has predicted the
epidemic strain.
I
In healthy adults, the efficacy of influenza vaccine in preventing or reducing the
severity of influenza illness is estimated to be around 7090%.
I
Influenza vaccination prevents hospitalisation for pneumonia in those with
exacerbations of chronic pulmonary disease and in diabetics.
I
Vaccine coverage in the Aboriginal and Torres Strait Islander population has not
been well documented, but there is some evidence that coverage is suboptimal in
those aged less than 65 years.
III
Antiviral agents are effective at reducing the severity of influenza but are not
routine substitutes for vaccination.
I
RECOMMENDATIONS
Offer annual influenza vaccination from 50 years of age.
V
Offer annual influenza vaccination to clients with chronic illness from age 6 months
(see Australian immunisation handbook, 8th edition).
V
Combine clinic based and outreach methods to enhance vaccine coverage.
Vaccination in non-traditional settings should be included.
V
PNEUMOCOCCAL PNEUMONIA
Burden of disease
The incidence of community acquired pneumonia in the Aboriginal population of Western Australia
(WA), based on hospital admissions from 19881993, was 2098/100 000 person years (4054 years)
and 1235/100 000 person years (2539 years). This means, 12% of Aboriginal peoples in these age
groups required hospitalisation for pneumonia in any given year over this period. In non-metropolitan
WA, Aboriginal children aged <1 year, the rate of hospitalisation for pneumonia was 5 per 100 person
years, and 8 per 100 person years for those aged 14 years in this period.
42
Similar rates of hospitalised
radiologically confirmed pneumonia in the first 5 years of life have been reported.
43
Pneumococcal infection is the most common cause of community acquired pneumonia and has a
significant mortality. The case fatality rate or the proportion of cases resulting in death can vary from
926% in different populations.
44
In Aboriginal populations, the contribution of pneumococcal pneumonia
to mortality is significant. The case fatality rate during 19851990 for hospitalised central Australian
Aboriginal people was 2% in those aged less than 4 years, 15% in those aged 1559 years and 40% of
those aged more than 59 years.
45
When not causing death, pneumococcal infections cause significant illness in Aboriginal people. The
true incidence is widely under reported
46
as usually only invasive disease data is collected. Under
reporting occurs because clients are treated without bacterial culture being collected and because
primary health care often avoids hospitalisation. High hospital admission rates for pneumonia in both
Aboriginal children and adults (up to 40 times higher than the non-Indigenous population aged 40 54
years) have been reported in WA.
47
In central Australia and far north Queensland, bacteraemic pneumococcal pneumonia was the most
common type of invasive pneumococcal disease (IPD) reported (comprising 77%).
48
Even though only
about 1 in 5 cases of pneumococcal pneumonia is bacteraemic, the rate of IPD in the Aboriginal and
Torres Strait Islander population far exceeds that in the non-Indigenous population and some rates have
been the highest recorded in the world. In Aboriginal children aged less than 2 years, an IPD rate of
2053/100 000 persons per year has been reported. Compared with non-Indigenous Australians,
Aboriginal children in central Australia aged under 4 years had nearly 11 times the relative risk
89
(935/100 000 persons annual rate) of IPD, while Aboriginal adults aged more than 15 years had 20
times the relative risk (160/100 000 persons annual rate).
49
In the Northern Territory (NT), 425 cases of IPD were detected over 19941998 and 77% of these were
Aboriginal people or Torres Strait Islanders, even though only 27% of the population is Indigenous.
50
In north Queensland during 19921995, IPD was over-represented in Aboriginal and Torres Strait
Islander people, accounting for 64% of cases in 9% of the population aged more than 15 years.
51
The mean age of Aboriginal people affected with IPD in the NT was younger than non-Indigenous (39
years compared with 48 years) and age of death due to IPD was also younger (41 years compared with
53 years).
52
In Victoria, the minimum estimate for incidence of IPD in the general population aged more
than 65 years was 25 per 100 000 per year (19951998).
53
In contrast, the rate of invasive
pneumococcal disease in the NT Aboriginal population aged 5065 years was 116 per 100 000 per year
(19941998)
54
and approximately 298/100 000 (19961997) in WA.
55
No other states offered a
breakdown of IPD data by Indigenous status.
The chronic diseases (diabetes, chronic lung, renal liver and cardiac disease) which are risk factors for
IPD, are very common in the Aboriginal and Torres Strait Islander population. Alcohol abuse is a
particularly prominent risk factor for pneumococcal pneumonia in Aboriginal and Torres Strait Islander
people, as reported in the NT,
56
WA
57
and north Queensland.
58
In the USA, smoking is also a prominent
risk factor for IPD in the immunocompetent population aged 1864 years,
59
which supports vaccine
coverage for all smokers in the Aboriginal and Torres Strait Islander population aged >15 years
regardless of chronic disease.
60
This is now part of the eligibility criteria for the NIPII.
Vaccine coverage
There is evidence that high pneumococcal vaccine coverage in targeted programs using the 23-valent
pneumococcal polysaccharide vaccine (23vPPV) is difficult to achieve. One study of pneumococcal
vaccine delivery, set in United Kingdom (UK) primary health care services, increased the coverage of
clients with chronic disease from 656 (3%) to 5982 (33%) after an 8-month targeted opportunistic
vaccination campaign.
61
An audit of vaccination practice in a United States of America (USA) primary
care setting in 1995 revealed that more than 60% of those eligible for influenza vaccine (>65 years)
received it in the last vaccination period, while only 30% of these clients had ever received
pneumococcal vaccine. Nearly 70% with chronic obstructive airways disease had received influenza
vaccine in the previous vaccination period, while only 43% had ever received pneumococcal vaccine.
62
This study also explored variables that explained the vaccine coverage. While knowledge of vaccine
recommendations was good, this was not enough, as a lack of physician belief in the importance of
vaccination tended to account for vaccines not being given.
In 2000, a National Australian Survey was conducted by telephone which interviewed over 10 000
Australians to determine self reported pneumococcal vaccine coverage. Overall, 15% of those aged
more than 65 years reported receiving pneumococcal vaccine in a 5-year period (19952000). Nearly
90% of those aged 4064 years and 84% of those aged more than 65 years had either not heard of the
pneumococcal vaccine or were not sure what it was for. Only six clients who received a pneumococcal
vaccine in 19952000 were Aboriginal or Torres Strait Islander and not all of them received free
vaccine.
63
According to state government surveys, pneumococcal vaccination (23vPPV) coverage in the Aboriginal
and Torres Strait Islander population has improved over recent years. In north Queensland, 96% and
73% of Indigenous adults aged >50 years received influenza and pneumococcal vaccines for the first
time respectively in 19952000. Although the Indigenous population aged 1549 years was difficult to
target (due to problems identifying risk), approximately 50% of this population received pneumococcal
vaccine for the first time in 19952000 (assuming that half of this population cohort was eligible).
64
In 1998, in the NT, pneumococcal vaccine (23vPPV) coverage in Aboriginal population aged 1549
years ranged 913% and coverage for those aged more than 50 years ranged 4673%. In 1998,
pneumococcal vaccination for those aged 1549 years in the NT was not universal. The vaccine
coverage in the cohort of 1549 year olds, with NHMRC defined risk factors, is low, with vaccination
rates varying up to 80% (V Krause, May 1999).
The Victorian State Government provided free pneumococcal vaccine (23vPPV) to the general
population aged more than 65 years since 1998, in conjunction with annual influenza vaccine program.
The cumulative population coverage of the eligible cohort over a 2-year period (19971998) was 42%.
65
90
The Australian Government funded National Indigenous Pneumococcal and Influenza Immunisation
Program introduced in 19981999 considerably strengthened efforts to enhance pneumococcal vaccine
coverage in the Aboriginal and Torres Strait Islander population. A review of the program in 2000 which
included interviews of 35 primary health care services (18 were Aboriginal Community Controlled Health
Services [ACCHSs]) to Aboriginal and Torres Strait Islander clients in every jurisdiction, found that
services were enabled to expand their activity (no longer paying for vaccines out of their own budget).
They could focus more on extending vaccine coverage, particularly to some at-risk groups who have
little contact with health services, such as heavy drinkers. In most of these services, adult immunisation
was seen as part of core business and was given opportunistically and proactively.
66
The program also
fostered collaboration to improve vaccine coverage, which is important given that general practice
divisional immunisation projects have repeatedly overlooked target groups such as Aboriginal and
Torres Strait Islander peoples.
67
In May 2001, a Childhood Pneumococcal Vaccination Program to immunise Aboriginal and Torres Strait
Islander children with the 7-valent pneumococcal conjugate vaccine (7vPCV) (Prevenar) was launched
by the Australian Government.
68
In the NT, 95% of the birth cohort from 1 April 2001 who received the 2-
month scheduled vaccines (eg. DTP) also received 7vPCV (C Selvey, April 2002). In Queensland, 70%
of an Indigenous cohort born in August/Sept 2001 (N=199) received the vaccine by 3 months of age.
Most of the failure to receive 7vPCV was attributed to general practitioners (GPs), compared to better
performance by ACCHSs and community health vaccine providers. Over 70% of general practices
(16/22) failed to provide 7vPCV to Aboriginal and Torres Strait Islander children.
69
Other jurisdictions have so far reported poor uptake (less vaccine orders for the expected birth cohort),
eg. South Australia, Victoria. This may also be related to poor identification of Indigenous status by GPs,
which has been known to be a problem in targeting vaccination, and for which guidelines have been
developed.
70
modification*
Yes
23-valent
pneumococcal
polysaccharide
vaccine (23vPPV)
7-valent
pneumococcal
conjugate vaccine
(7vPCV)
Nil Nil Nil Yes
overcrowding
access to water
Immunisation
Currently there are two type of pneumococcal vaccine marketed: the 23vPPV and the new 7vPCV. The
23vPPV is approved for use in children older than 2 years of age and adults who are at risk of IPD. The
7vPCV is approved for use in children from 6 weeks to 9 years of age.
23-valent pneumococcal polysaccharide vaccine
The 23-valent pneumococcal polysaccharide vaccination reduces mortality from pneumonia in younger
adults, particularly in populations with high attack rates. Observation studies have shown protection
against invasive pneumococcal disease.
71
However, differences in efficacy in various population groups
and settings have been reported by a number of systematic reviews of clinical trials.
A meta-analysis (search date 1991) found that, in young healthy populations (aged <55 years),
pneumococcal polysaccharide vaccination significantly protects against pneumococcal pneumonia
(7692% efficacy), however, small reductions in mortality were not statistically significant. The
combination of trials involving high risk populations (>55 years and one or more chronic medical
conditions) reported few benefits.
72
91
In case control and cohort studies, the vaccine is 5681% protective against IPD from vaccine serotypes
in immunocompetent individuals, but not in those with severe chronic disease such as alcoholism,
chronic renal failure, malignancies and other diseases.
73,74
Another meta-analysis inclusive of more recent trials found that vaccination with pneumococcal
polysaccharide vaccine reduced the risk of IPD due to pneumococcal types included in the vaccine by
83% and IPD due to all pneumococci by 73%. It significantly reduced the risk of vaccine type
pneumococcal pneumonia but effect on non-vaccine type pneumococcal pneumonia was inconsistent. It
found no evidence that the vaccine was less efficacious for the elderly, institutionalised people or those
with chronic disease.
75
A further meta-analysis concluded that there was no strong evidence for pneumococcal polysaccharide
vaccine efficacy in the elderly. However, it is valuable in high risk groups. The vaccine protected unique
populations of healthy young adults at high risk for pneumococcal infection, such as South African gold
miners and New Guinea highlanders. They were exposed to respiratory irritants (mining dust or fireplace
smoke), shared close living and sleeping quarters, which facilitates pneumococcal transmission and
increases the risk of developing pneumonia.
76
An Australian overview reported that pneumococcal polysaccharide vaccine protected against
bacteraemia, severe disease and mortality with efficacy demonstrated in young adults at high risk for
invasive disease and in the elderly immunocompetent population.
77
A significant reduction in the incidence of IPD in Aboriginal and Torres Strait Islander adults in far north
Queensland was recently demonstrated since the widespread use of 23vPPV (begun in 1995). The
annual incidence of IPD in this population was 111 (95% CI: 77154)/100 000 in 19931994 before the
vaccination program compared to 28 (95% CI: 1353)/100 000 in 19992000, after 5 years.
78
However,
a retrospective cohort study of Aboriginal adults vaccinated over 19911993 in WA compared the
hospitalisation and mortality rates of the pneumococcal vaccine vaccinated and an unvaccinated group.
No significant differences were observed in the admission rates for pneumonia and lower respiratory
tract infection between the two groups.
79
Pneumococcal vaccine is widely recommended in those with asthma due to high risk for pneumonia, but
few trials have investigated the nature of any protective effect. There appears to be little evidence to
justify routine pneumococcal vaccination in those with asthma.
80
A Cochrane collaboration systematic review concluded from non-randomised studies that
polysaccharide vaccines are effective in the reducing the incidence of invasive pneumococcal disease
among adults and the immunocompetent elderly (55 years or more). Combined results from randomised
studies failed to show that the polysaccharide pneumococcal vaccine is effective in preventing either
pneumonia or death.
81
A review on the effects of the vaccine in those with chronic obstructive airways
disease is in development.
82
In children aged less than 2 years, most data suggest that the 23-vPPV is poorly immunogenic.
83,84
This
is despite one placebo controlled trial reporting a reduced death rate from respiratory infections in
children from Papua New Guinea vaccinated from age 6 months to 5 years.
85
Vaccination in children
aged more than 2 years has been shown to be protective in other studies.
86
Vaccination is not
recommended in children aged less than 2 years by most expert bodies.
In Australia, the 23-vPPV is recommended for Aboriginal and Torres Strait Islander children as a booster
dose, at 1824 months of age, following a primary course of the 7vPCV in Aboriginal and Torres Strait
Islander children in geographic areas of high incidence.
87
Only one published study has reported on the role of maternal pneumococcal vaccination for passive
immunisation of infants. A prospective, double blind trial of pregnant women in Bangladesh (chosen
because Bangladeshi women receive tetanus toxoid vaccination at 3034 weeks gestation to stimulate
passive immunity in the prevention of neonatal tetanus) who were given 23-vPPV, showed that their
infants had protective antibody levels up to 5 months after birth.
88
To demonstrate an impact on infant
mortality and morbidity would require much larger studies, which was supported by the World Health
Organisation in 1998.
89
7-valent pneumococcal conjugate vaccine
The 7vPCV was shown to be 94% protective against invasive vaccine-type pneumococcal infections
and 89% protective against all vaccine types in a large trial (37 868 USA infants aged less than 2 years).
It was 33% protective against X-ray confirmed pneumonia.
90
The recent 7-vPCV trial in Navajo and
White Mountain Apache children (N=8292 infants) revealed that vaccination was efficacious against
92
invasive pneumococcal disease in high risk children. The vaccine was 76.8% protective against vaccine
type invasive pneumococcal infections and 54.1% against all pneumococcal serotypes.
91,92
Further clinical trials
93
and a systematic review of trials
94
are in progress. Efficacy of this vaccine
regarding the prevention of otitis media is described in the Child health section.
Pneumococcal serotypes
In far north Queensland, all pneumococci isolated from Indigenous Australians with invasive disease
were serotypes present in the current 23-vPPV.
95
This was also reported in central Australia, where
89.5% of pneumococcal isolates from Aboriginal clients were represented in the vaccine.
96
On the other
hand, the 7-vPCV will only protect against 60% of the pneumococcal isolates that have caused invasive
disease in Aboriginal and Torres Strait Islander children compared with 88% of those in non-Indigenous
children.
97,98
Vaccine safety and re-vaccination
Pneumococcal polysaccharide vaccine safety is widely accepted, although up to 50% of recipients will
experience minor and transient local pain and swelling. Adverse effects with re-vaccination are not
greater than with the initial vaccination when re-vaccination occurs about 6 years after the initial
shot.
99,100,101,102
Therefore, re-vaccination is recommended as protective antibody levels tend to diminish
in immunocompetent individuals after this period, although some may persist with protective levels for
10 years.
103,104
Re-vaccination confers levels of protective antibody comparable to primary vaccination in
those with chronic disease.
105
If re-vaccination occurs earlier than 5 years, Arthus-like reactions have
been reported with more severe local reactions and low grade fever and chills in healthy volunteers,
106
but others have reported no increased adverse effects in those revaccinated who were
splenectomised,
107
in adults and children who had renal failure,
108
or in other children at risk.
109
In Australia, pneumococcal re-vaccination before 2002 was recommended every 5 years to at-risk
groups,
110
and many Aboriginal people have received several re-vaccinations. However, in the USA,
once only administration of the vaccine in those aged >65 years and other risk groups is recommended.
Re-vaccination (after 5 years) is considered for those aged >2 years who are at continuing high risk of
pneumococcal infections (eg. Alaskan natives and certain American Indian population). In this group, no
more than two injections are considered necessary due to lack of data pertaining to safety and
protective immunity.
111
See Frequency of intervention for recent Australian recommendations.
Schemes to increase vaccine coverage
The tremendous potential for vaccination in preventing disease is mainly limited by insufficient coverage
of the target population. The chief problem associated with pneumococcal vaccine is the failure to use it.
Several meta-analyses have identified factors, which improve adult vaccination coverage. Client focused
(in person, mail or telephone), and provider focused (office reminders or nurse initiated prompts)
interventions, were both effective in increasing high risk adult (chronic disease and elderly) vaccination
in pooled analysis. Mixed strategies were also effective, and outreach was considered essential to reach
those clients who do not routinely visit a health clinic. Provider incentives and/or enhanced client access
through walk in clinics, free vaccination, satellite vaccination sites, or the scheduling of annual physicals
during vaccination periods were possible strategies for increasing client provider contact.
112
A number of studies have shown that client and provider reminder systems can increase vaccine
delivery to high risk clients at the primary health care level.
113
Methods used by general practitioners
include computerised reminder systems, vaccine stickers on client records for opportunistic vaccination,
and postcard reminders. It is important to maintain a database of those vaccinated in order to target re-
vaccination strategies, prevent vaccine wastage, prevent adverse effects due to early re-vaccination and
evaluate service delivery. Strategies used to improve vaccination coverage need to be combined with
local contextual information to be effective.
General practitioner delivery of immunisation to clients can also improve with audit and feedback. In a
systematic review of studies, audit and feedback was defined as any summary of clinical performance
gathered over a defined period of time and presented to the health care provider after collection.
Examples of strategies included annual summaries of performance to providers (eg. from registers) with
or without financial incentives, chart reviews, lists of non-immunised clients, postgraduate education
courses and lectures. A positive association between audit and feedback and improved pneumococcal
vaccination rates was demonstrated.
114
93
Standing orders are also effective at improving adult vaccination coverage and are strongly
recommended.
115
Standing orders authorise health workers or nursing staff to deliver vaccination to
client populations by protocol without direct GP involvement.
116
Interventions that enhance client access to vaccination services such as reducing out of pocket costs
(free vaccines), measures that reduce the distance from the setting to the population, convenient times,
reduced waiting hours or home visits for advice, or provision of vaccines were shown to be strongly
effective, either alone or in combination.
117
A number of adults in the USA are now receiving vaccinations in non-traditional settings (eg. public venues,
pharmacies, workplace, home) as they are more accessible and acceptable to medically under-served
populations.
118
Otherwise known as outreach vaccination, it has been a common practice in ACCHSs and
other service providers to Aboriginal and Torres Strait Islander communities.
119
However, vaccination
outside clinic settings is challenging to health care providers due to a lack of access to resuscitation facilities
in the event of anaphylaxis, and a number of other medicolegal consequences. Guidelines to assist
providers in the implementation of outreach vaccination programs are needed in Australia, and have been
developed in the USA.
120
Enhancing the adult immunisation workforce by reducing legislative barriers to
enable Aboriginal Health Workers to vaccinate has also been recommended.
121
Vaccination outside clinic
settings has its risks but they are significantly outweighed by the benefits, thereby constituting a preferable
strategy for adults who are under-served, given it has already been adopted for reaching children overdue
for immunisations in a number of jurisdictions (see Child health).
Pneumococcal vaccination to hospital in-patients can increase coverage,
122
but inadvertent
pneumococcal re-vaccination may also occur if hospitalised patients are given the vaccine without their
primary care providers being consulted.
123,124
Improving the vaccine coverage in the Aboriginal and Torres Strait Islander population requires
collaborative efforts between public health units, representative health organisations of Aboriginal and
Torres Strait Islander communities (eg. ACCHSs) and general practice.
125
This is necessary for effective
communication with clients to ensure they can access holistic primary care and free vaccine, for the
provision of transport and acceptance of programs, as several reviews of immunisation programs and
related programs fostered by the Australian Government through divisions of general practice conclude
that the Aboriginal and Torres Strait Islander population is overlooked.
126,127,128
Monitoring outcomes
Uptake of the pneumococcal vaccine needs to monitored and improved in the Aboriginal and Torres
Strait Islander population. In Australia, it has been recommended that a target of at least 80% coverage
with 23vPPV in the Aboriginal and Torres Strait Islander population aged >15 years be achieved within 5
years of the provision of a universal and publicly funded program.
129
There are currently no
pneumococcal vaccine targets specified in the Public Health Outcome Funding Agreements between
the Australian Government and state governments, or in the National Aboriginal and Torres Strait
Islander Performance Indicators.
130
Vaccination with 7vPCV is now a part of the Australian Childhood Vaccination Schedule given at ages 2,
4 and 6 months in all Aboriginal and Torres Strait Islander infants.
The 23vPPV is recommended for Aboriginal and Torres Strait Islander children aged 1824 months as a
booster dose following a primary course of the pneumococcal conjugate vaccine, in NT, central Australia
and desert and tropical regions of WA, SA and Queensland.
131
The 23vPPV is recommended for all Aboriginal and Torres Strait Islander peoples from 50 years. It is
also recommended for those aged more than 5 years at increased risk of complications from
pneumococcal disease because of chronic illness (eg. chronic cardiac, renal, pulmonary, diabetes,
alcohol related problems), including tobacco smokers.
132
The Australian Government funded National
Indigenous Pneumococcal and Influenza Immunisation Program introduced in 19981999, also funds
free 23vPPV for Aboriginal and Torres Strait Islander population aged more than 15 years who are at
high risk because of chronic disease, heavy drinking or tobacco smoking (see Box 9).
Australian re-vaccination recommendations have been revised so that all Aboriginal and Torres Strait
Islander adults aged 1549 years with risk factors (including smoking) receive a single re-vaccination 5
years after the initial dose, then again at either 50 years, or 10 years after the first re-vaccination,
whichever comes later (ie. a maximum of three doses of 23vPPV). All Aboriginal and Torres Strait
94
Islander adults who receive their first dose at or after 50 years of age should now receive a single re-
vaccination 5 years after the initial dose (ie. a maximum of two doses of 23vPPV).
133
Recommendations regarding pneumococcal vaccine are ratified by the NHMRC for national application.
The rate of invasive pneumococcal disease in the Aboriginal and Torres Strait Islander
population far exceeds that in the non-Indigenous population. Some reported rates have
been the highest ever recorded in the world. Improving vaccine coverage in this
population requires collaborative efforts between public health units, the representative
health organisations of Aboriginal and Torres Strait Islander communities (such as
Aboriginal Community Controlled Health Services) and general practice.
EVIDENCE
Level of
evidence
The 23-valent pneumococcal polysaccharide vaccine (23vPPV) significantly protects
against pneumococcal pneumonia (7692% efficacy) in young (<55 years of age) healthy
adult populations.
I
The 23vPPV is 5681% protective against invasive pneumococcal disease from vaccine
serotypes and non-vaccine serotypes in immunocompetent adult individuals.
I
The 23vPPV has been shown to reduce invasive pneumococcal disease in the Aboriginal
and Torres Strait Islander population of far north Queensland.
III
The 23vPPV may also add protection to those with severe chronic diseases such as
alcoholism, chronic renal failure, and other diseases (although there are conflicting
research findings).
III
The 7-valent pneumococcal conjugate vaccine (7vPCV) is protective against invasive
pneumococcal infections of the vaccine serotypes and reduces the total invasive
pneumococcal disease burden (from vaccine and non-vaccine pneumococcal serotypes)
for children.
II
Opportunistic vaccination and vaccination delivered through the use of client reminder
and recall systems are effective at increasing vaccine coverage.
IIII
A program coordinated with primary health care has been found to increase adult
vaccination rates. Some of the strategies used include the use of computer generated
lists of eligible clients, free vaccination, encouragement from a primary care provider,
outreach services and health promotion.
IIII
RECOMMENDATIONS
The 7vPCV is recommended for all Aboriginal and Torres Strait Islander children as part
of the Australian Standard Childhood Vaccination Schedule (see Australian immunisation
handbook, 8th edition).
V
Offer 23vPPV with a single repeat vaccination 5 years after the initial dose from 50 years
of age (see Australian immunisation handbook, 8th edition).
V
The 23vPPV is specifically recommended for Aboriginal and Torres Strait Islander clients
aged 1549 years who smoke or who have chronic illnesses (eg. chronic cardiac, renal
and pulmonary disease, diabetes and/or alcohol related problems). Re-vaccination is
required after 5 years, and again 10 years later or at 50 years of age, whichever is later
(see Australian immunisation handbook, 8th edition).
V
Combine clinic based and outreach methods to enhance vaccine coverage. Vaccination
in non-traditional settings should be included.
V

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67 Thomson J, Hilditch A, Pirkis J, Dunt D. Immunisation initiatives in general practice: Important
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72 Fine MJ, et al. Efficacy of pneumococcal vaccination in adults: a meta-analysis of randomised
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73 USPSTF, op. cit.
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75 Hutchison BG, Oxman AD, Shannon HS, Lloyd S, Altmayer CA, Thomas K. Clinical effectiveness
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76 Moore RA, Wiffen PJ, Lipsky BA. Are the pneumococcal polysaccharide vaccines effective? Meta-
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80 Sheikh A, Alves B, Dhami S. Pneumococcal vaccine for asthma (Cochrane Review). In: The
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81 Andrews R, Dear K, Holden J, Tatham D. Vaccines for preventing pneumococcal infection in
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86 Lehmann D, op. cit.
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89 WHO. Report on the meeting on maternal and neonatal pneumococcal immunisation. Geneva
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91 Reid RR. Clinical research among American Indian populations: consideration of tribal beliefs and
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92 OBrien KL, et al. Invasive disease efficacy of a 7-valent pneumococcal conjugate vaccine among
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93 Mulholland EK. Conjugate pneumococcal vaccines: an overview. Med J Aust 2000 Oct
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pneumococcal disease in children in Far North Queensland. J Paediatr Child Health 2001
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98 Krause VL, Reid SJ, Merianos A. Invasive pneumococcal disease in the Northern Territory of
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99 Rodriguez R, Dyer PD Safety of pneumococcal re-vaccination. J Gen Intern Med
1995;10(9):5112.
100 Mufson MA, Hughey DF, Turner CE, Schiffman G. Re-vaccination with pneumococcal vaccine of
elderly persons 6 years after primary vaccination. Vaccine 1991;9(6):4037.
101 Snow R, Babish JD, McBean AM. Is there any connection between a second pneumonia shot and
hospitalization among Medicare beneficiaries? Public Health Rep 1995;110(6):7205.
102 Jackson LA, et al. Safety of re-vaccination with pneumococcal polysaccharide vaccine. JAMA 1999
Jan 20;281(3):2438.
103 USPSTF, op. cit.
104 Torzillo PJ. Pneumococcal vaccine: current status. Aust NZ J Med 1993;23:28590.
105 Davidson M et al. Immunogenicity of pneumococcal re-vaccination in-patients with chronic disease.
Arch Intern Med 1994;154(19):220914.
106 Borgono JM, et al. Vaccination and re-vaccination with polyvalent pneumococcal polysaccharide
vaccines in adults and infants. Proc Soc Exp Biol Med 1978;157(1):14854.
107 Rutherford EJ, et al. Efficacy and safety of pneumococcal re-vaccination after splenectomy for
trauma. J Trauma 1995;39(3):44852.
108 Fuchshuber A, Kuhnemund O, Keuth B, Lutticken R, Michalk D, Querfeld U. Pneumococcal
vaccine in children and young adults with chronic renal disease. Nephrol Dial Transplant
1996;11(3):46873.
109 Kaplan J, Sarnaik S, Schiffman G. Re-vaccination with polyvalent pneumococcal vaccine in
children with sickle cell anemia. Am J Pediatr Hematol Oncol 1986;8(1):802.
99

110 NHMRC, op. cit.
111 Centre for Disease Control and Prevention. Prevention of pneumococcal disease:
recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb
Mortal Wkly Rep 1997;46(RR-8):124.
112 Sarnoff R, Rundall T. Meta-analysis of effectiveness of interventions to increase influenza
immunization rates among high risk population groups. Medical Care Research and Review
1999;55(4):43256.
113 Centers for Disease Control and Prevention. Vaccine preventable diseases: improving vaccination
coverage in children, adolescents and adults. A Report on Recommendations of the Task Force on
Community Preventive Services. MMWR 1999;48(RR8):115.
114 Bordley WC, Chelminski A, Margolis PA, Kraus R, Szilagyi PG, Vann JJ. The effect of audit and
feedback on immunization delivery: a systematic review. Am J Prev Med 2000 May;18(4):34350.
115 Centers for Disease Control and Prevention, op. cit.
116 Task Force on Community Preventive Services. Reviews of evidence regarding interventions to
improve vaccination coverage in children, adolescents and adults. Am J Prev Med
2000;18(1S):97140.
117 ibid.
118 Centers for Disease Control and Prevention. Adult immunisation programs in non-traditional
settings: quality standards and guidance for program evaluation: a report of the National Vaccine
Advisory Committee. MMWR 2000;49(RR-1):113.
119 Young D. Successful strategies for an adult immunisation program. Health Promot J Aust
1998;8:5961.
121 Wronski I, et al. Improving Aboriginal and TSI Childhood Immunisation. Report to the
Commonwealth Department of Health and Family Services. Queensland: Department of Public
Health and Tropical Medicine James Cook University of North Queensland, 1996.
122 Shevlin JD, Summers-Bean C, Thomas D, Whitney CG, Todd D, Ray SM. A systematic approach
for increasing pneumococcal vaccination rates at an inner-city public hospital. Am J Prev Med 2002
Feb;22(2):927.
123 McDonald P, Fiedman EHI, Banks A, Anderson R, Carman V. Pneumococcal vaccine campaign
based in general practice. BMJ 1997;314:10948.
124 Clancy CM, Gelfman S, Poses RM. A strategy to improve the utilization of pneumococcal vaccine.
J Gen Intern Med 1992;7(1):148.
125 Mandala Consulting in association with David Lowe Consulting, Jill Hardwick Consulting and
Margaret Hayes-Hampton, op. cit.
126 Thomson J, Hilditch A, Pirkis J, Dunt D. Immunisation initiatives in general practice: Important
lessons from division projects. Aust Fam Phys 1999;28(12):12907.
127 Sibthorpe B, Meihubers S, Griew R, Lyttle C, Gardner K. Aboriginal health initiatives in Divisions of
General Practice. During the move to outcomes based block grant funding 19981999. NCEPH
Discussion Paper No 17. Canberra: The Australian National University, November 1999.
128 Harris E, et al. Action on Health Inequalities through General Practice II. The role of Divisions of
General Practice. Centre for Health Equity, Training, Research and Evaluation. Sydney: University
of Melbourne and University of NSW, 2000.
129 Communicable Diseases Network Australia. Pneumococcal Working Party. Canberra:
Commonwealth Department of Health and Ageing, January 2002.
130 Commonwealth Department of Health and Ageing, op.cit.
131 NHMRC, op. cit., p. 22034.
132 ibid.
133 ibid.
Respiratory disease Non-communicable
100
ADULT HEALTH
RESPIRATORY DISEASE
NON-COMMUNICABLE
Authors
Smoking
Dr Rowena Ivers, Illawarra Aboriginal Medical Service
Dorothy Reading, Cancer Council Victoria
Chronic obstructive pulmonary disease
Dr Graeme Maguire, Community Physician, Kimberley Health Service
Acknowledgments
Dr Rowena Ivers, Illawarra Aboriginal Medical Service
Cancer Council Victoria
Australian Lung Foundation
SMOKING
Burden of disease
The prevalence of tobacco use among Aboriginal and Torres Strait Islander Australians is higher than
for other Australians. The National Aboriginal and Torres Strait Islander Survey (NATSIS) in 1994,
indicated that 54% of males and 46% of females aged 13 years or more smoked,
1
with many people
taking up smoking at an early age. By comparison, the National Drug Strategy Household Survey in
1998 reported 29% of Australian males and 24% of Australian females aged 14 years or more were
current smokers.
2
The NATSIS only included Aboriginal and Torres Strait Islander people in urban
regions but in some remote regions, the prevalence of tobacco use is as high as 83% in Aboriginal men
and 73% in Aboriginal women.
3,4
In the NATSIS, Torres Strait Islanders were less likely than Aboriginal
people to report use of tobacco. The prevalence of tobacco use among Islander men was 48%,
compared to 57% in Aboriginal men and 55% in men of both Aboriginal and Islander origin. The
prevalence of tobacco use among Islander women and women of both Aboriginal and Islander origin
was 42%, compared to 49% in Aboriginal women. Compared to other Australians, few Aboriginal and
Torres Strait Islanders had quit.
5
Aboriginal and Torres Strait Islander results from the National Health
Survey (2001) revealed that Indigenous Australian adults over 18 years (in every age group) were twice
as likely to be current smokers than non-Indigenous (51% vs 24% respectively).
6
Tobacco chewing is common in some regions, particularly central Australia. A survey of drug use
patterns in the Northern Territory (NT) revealed that in some regions, 11% of males and 38% of females
chewed tobacco.
7
The prevalence of tobacco use is also high among Aboriginal Health Workers. In a study of health
workers in South Australia (SA), 39% smoked.
8
101
Impact of smoking to Aboriginal and Torres Strait Islander health
Consistent findings from a large body of epidemiological evidence show tobacco to be a potent
carcinogen, atherogenic, and to be a prime risk factor for myocardial infarct, coronary artery,
cerebrovascular and peripheral vascular disease.
9
The use of tobacco is probably the major cause of preventable premature mortality and morbidity among
Aboriginal people.
10
The life expectancy of Aboriginal people is 1520 years less than that of the general
population,
11
with much of this difference due to high rates of cardiovascular disease, respiratory
disease and other diseases related to tobacco. If tobacco related deaths were eliminated, one study
estimated that life expectancy for men would increase from 58.5 years to 61 years, and for women
would increase from 65.3 years to 67 years. By comparison, elimination of deaths from infectious
disease would add only 0.2 years to the life expectancy of Aboriginal people.
12
Tobacco smoking may contribute to a greater proportion of deaths among Aboriginal and Torres Strait
Islander people than in the general population (up to 26% compared to 15%).
13,14
Aboriginal and Torres
Strait Islander people are hospitalised at 23 times the rate of people in the general Australian
population,
15
with many people being hospitalised for conditions related to tobacco.
Smoking results in a relative risk of developing lung cancer of 13.0 for men and 11.4 for women.
16
Lung
cancer causes 10% of all deaths in Aboriginal and Torres Strait Islander males, and 13% of deaths in
Aboriginal and Torres Strait Islander females.
17
In the NT, Aboriginal men are up to 2.2 times more likely
to die of lung cancer and Aboriginal women are up to 3.1 times more likely to die of lung cancer than
other Australians.
18
In Western Australia (WA) in the period 19931997, Aboriginal men were less likely
than non-Aboriginal men to die of lung cancer, although Aboriginal women had similar mortality rates
from lung cancer to that of non-Indigenous women.
19
The proportion of lung cancer deaths attributable
to tobacco is similar for Aboriginal and Torres Strait Islander people and the non-Indigenous population.
In Queensland in 19921995, 81% of lung cancer deaths in Aboriginal people in remote communities
were attributable to tobacco, compared to 79% of lung cancer deaths for the whole of Queensland for
the period 19921996.
20
A smoker is nearly 10 times more likely to develop chronic obstructive pulmonary disease (COPD) than
a non-smoker.
21
Aboriginal and Torres Strait Islander men are up to 4.6 times more likely to die of
COPD and Aboriginal and Torres Strait Islander women are up to 10.7 times more likely to die of COPD
than other Australians.
22,23
The proportion of deaths from chronic obstructive airways disease
attributable to tobacco is similar (75%) for Aboriginal and non-Indigenous peoples.
24
Smokers are 1.5 times more likely to develop pneumonia than non-smokers.
25
Aboriginal and Torres
Strait Islander men were up to 19.2 times more likely to die of pneumonia, and Aboriginal and Torres
Strait Islander women were up to 15.1 times more likely to die of pneumonia than other Australians.
26,27
Smokers aged less than 65 years are 2.5 times more likely to develop atherosclerosis, three times more
likely to develop ischaemic heart disease or stroke than non-smokers.
28
Cardiovascular disease is the
main cause of death among Aboriginal and Torres Strait Islander people, accounting for 27% of deaths
of males and 30% of deaths of females,
29
mainly due to ischaemic heart disease and stroke. The
proportion of deaths from cardiovascular disease that are attributable to tobacco use may be higher for
Aboriginal and Torres Strait Islander people than for the non-Indigenous population. In Queensland in
19921995, 35% of ischaemic heart disease deaths in Aboriginal people from remote communities were
attributable to tobacco, compared to 14% of ischaemic heart disease deaths for all of Queensland for
the period 19921996.
30
Aboriginal men have up to 3.2 times the risk of ischaemic heart disease and
Aboriginal women have up to 6.8 times the risk as other Australians.
31
Tobacco use contributes to increased rates of low birth weight, increased incidence of spontaneous
abortion, prematurity, stillbirth and sudden infant death syndrome (SIDS).
32
Infants of smokers weigh on
average 200 g less than the infants of non-smokers; smokers have double the risk of having a low birth
weight infant.
32
Aboriginal women are 2.8 times more likely to deliver an infant with a low birth
weight,
33,34
and the perinatal mortality rate is 23 times higher for Aboriginal infants.
35
In a Western Australian study, the risk of dying from SIDS, which has a higher prevalence in the infants
of smokers, was 3.9 times higher for Aboriginal infants than for non-Aboriginal infants.
36
Although
smoking has not been convincingly linked to a higher risk of perinatal mortality for Aboriginal infants, it is
likely that smoking contributes.
Smokers of 20 or more cigarettes per day have up to three times the risk of developing cataracts than
non-smokers or former light smokers.
37
Aboriginal people have high rates of cataract development.
38
102
Aboriginal and Torres Strait Islander people are more likely to be exposed to environmental (passive)
smoke. Aboriginal children are more likely to suffer from ear infections (see Child health) which is linked
to exposure to tobacco smoke.
39,40
Exposure to environmental smoke results in a higher risk of
respiratory disease in infants and children,
41
and Aboriginal infants are 10 times more likely than others
to be hospitalised for this reason.
42
The use of snuff and/or chewing tobacco is associated with a variety
of serious adverse effects on reproduction, longevity, the cardiovascular system and oral health.
43
However, no direct epidemiological data is available on cardiovascular morbidity and mortality in
association with smokeless tobacco use.
44
modification
Yes
pneumococcal
immunisation
(see
Respiratory
disease
Communicable)
Yes
assessment of
smoking
status
recording of
status on
medical
record
Yes
brief
counselling
health
promotion
materials
Yes
nicotine
replacement
therapy
bupropion
Yes
smoke free public
places
health promotion
and mass media
campaigns
preventing sales of
tobacco to minors
As tobacco use is related to the heavy burden of chronic disease and premature death in Aboriginal and
Torres Strait Islander people, there would be great potential for narrowing the gap between health
outcomes in Indigenous and non-Indigenous Australians, if there was a fall in the prevalence of smoking
similar to that seen in the non-Indigenous population over the past few years.
45
Meta-analysis of trials
has confirmed that the risk of lung cancer declines after smoking cessation.
46
Few interventions aimed at reducing the harm from tobacco use among Aboriginal and Torres Strait
Islander people have been evaluated. However, there is potential for reducing harm from tobacco use
by using every opportunity to counsel on cessation of smoking.

Practitioners in primary health care can
minimise missed opportunities by offering counselling during a preventive health assessment of
individuals who smoke.
47
There is good evidence from other populations that brief advice from health professionals (doctors,
nurses and others) can help approximately 6% more smokers to quit.
48,49,50
Two or 3 minutes of brief
advice can result in quit rates of approximately 5%.
51
Culturally appropriate, non-coercive methods of
counselling should be used.
52,53
Smokers should not be blamed for their smoking.
54
The use of advice on cessation given by Aboriginal Health Workers has not been evaluated, but is likely
to be effective. Some Aboriginal and Torres Strait Islander health professionals may feel uncomfortable
giving such advice to people from their community,
55
particularly if they themselves are smokers.
Barriers to the delivery of cessation advice by Aboriginal and Torres Strait Islander health professionals
include lack of staff, feeling undervalued within the health team, feeling that they do not have the
authority to advise this client, feeling that they do not have sufficient knowledge to answer questions
which may arise from counselling, or observing that the client continues to smoke despite previous
counselling. Training in the delivery of cessation advice may reduce some of these barriers. There is
good evidence that training health professionals in delivering cessation advice can reduce the
prevalence of smoking.
56
Training should be conducted for staff delivering health services to Aboriginal
and Torres Strait Islander people. Health professionals who smoke should also be offered support for
cessation.
57
Reminders to deliver cessation advice, eg. in medical records, or incorporated into computerised recall
systems, are effective in prompting health professionals to give such advice.
58,59,60
In the USA, the rate
at which physicians provide advice on smoking cessation is a measure of the quality of care of health
services.
61
Nicotine replacement therapy can improve quit rates, irrespective of the intensity of advice offered, and
should be considered an important adjunct to advice.
62
The cost of these patches may prohibit use by
Aboriginal peoples and Torres Strait Islanders. In the NT, the provision of free nicotine patches to
Indigenous Australian clients led to a 15% quit rate after 6 months compared with 1% receiving brief
103
intervention.
63
Nicotine patches, gum and inhalers are licensed for use in Australia. There is good
evidence in other populations that the antidepressant bupropion (Zyban) is effective in assisting
smokers to quit.
64
The drug doubles cessation rates compared with placebo, but there is insufficient
evidence to determine if it is more effective than nicotine replacement therapy.
65
Quit courses are more effective than self help and other less intensive interventions,
66
but mainstream
quit courses may be relatively inaccessible or inappropriate for Aboriginal and Torres Strait Islander
people.
67
There have been no evaluations of quit courses or support groups for Indigenous Australians,
but one-on-one interaction with health professionals is probably more appropriate than group therapy.
68
Similarly, the use of quit lines can improve cessation rates,
69
but Aboriginal and Torres Strait Islander
people may find mainstream quit lines to be relatively inaccessible.
The use of health promotion materials, including self help materials, may help smokers to quit, although
the evidence in unclear.
70,71
Aboriginal and Torres Strait Islander people are likely to prefer materials
that are targeted at an Indigenous audience, which use visual media or are easy to read, and include
pictures of local or well known people.
72
Aboriginal tobacco programs have used a variety of materials
including posters, videos, pamphlets, flip charts, felt boards, CD-ROM, stickers and T-shirts.
73
In 2001, the National Aboriginal Community Controlled Health Organisation (NACCHO) published a
report following consultation with Aboriginal and Torres Strait Islander people across Australia about
tobacco programs.
74
It recommended regular screening of the smoking status of Aboriginal and Torres
Strait Islander clients incorporated in a Well Person's Health Check which should prompt action and
follow up. Smokers should be provided (as a minimum) with brief advice on tobacco by health staff
trained in this area. Regular screening would allow staff to legitimately enquire about tobacco use,
regardless of their own smoking status. Smoking should be given as high a priority as other risk factors,
both by health staff and clients, when addressing health issues particularly heart disease and diabetes
in the Aboriginal and Torres Strait Islander population.
The National Health and Medical Research Council (NHMRC) guidelines to assist primary health care
providers with the delivery of advice on smoking cessation are shown in Box 10. These could be
modified for the Aboriginal and Torres Strait Islander population as appropriate (eg. use of chewing
tobacco).
104
Box 10. Guidelines for smoking cessation
75
A system for identifying all smokers and documenting tobacco use should be used in every practice.
Ask Do you smoke? and Have you ever smoked? Once the current smoker is identified, take a brief
history including:
number of cigarettes smoked per day
previous quit attempts and what happened
presence of smoking related disease.
Assess readiness to quit by asking How do you feel about your smoking at the moment? and to
determine readiness to quit in the next 30 days by asking Are you ready to quit now? Also examine
barriers to quitting, triggers for smoking, social support, implications of other health issues and
experiences with previous quit attempts. Determine stage of readiness to change to tailor brief
intervention:
not ready
unsure
ready
action
maintenance
relapse.
Assess nicotine dependence using the Fagerstrom Test for Nicotine Dependence.* In the absence of
contraindications, pharmacotherapy should be offered to all motivated smokers who have evidence of
nicotine dependence (either nicotine replacement therapy or bupropion slow release).
Advise all smokers (at least annually) to quit in a way that is:
clear and unambiguous
supportive and non-confrontational.
Assist based on the assessment process above by providing:
minimal advice and provide written information and option of referral to support service (Quitline)
GP based assistance (by GP or skilled practice staff)
GP based assistance plus coordination of assistance from other services.
Arrange follow up with all smokers after advice to quit.
* Peters MJ, Morgan LC. The pharmacotherapy of smoking cessation. Med J Aust 2002;176:48690. Available at:
http://www.mja.com.au/public/issues/176_10_200502/pet10850_fm.html
See Smoking cessation guidelines for Australian general practice for further information
Aboriginal and Torres Strait Islander people should be advised on the health effects of environmental
smoke.
76
The effects of passive smoking may not be well understood in Aboriginal populations. A
workshop report on passive smoking in Victoria in 1993 highlighted a lack of understanding among
many of the Aboriginal participants regarding the dangers of passive smoking. The report also
highlighted the difficulties encountered by Aboriginal people when trying to preserve non-smoking areas
in their dwellings and persuading family members and visitors to respect such areas.
77
However, smoking cessation interventions targeted at individuals are unlikely to be effective without
more comprehensive approaches to tobacco control. In Aboriginal and Torres Strait Islander
communities, these could include health promotion campaigns, school education about tobacco, mass
media campaigns, programs that influence the supply and sale of tobacco, and the introduction of
smoke free public places. Tobacco programs for Aboriginal and Torres Strait Islander people should be
community controlled, holistic and acknowledge the social determinants of health.
78
The Royal Australia College of General Practitioners (RACGP) recommends that all clients more than
aged 10 years should be asked at every opportunity if they smoke.
79
However, there is no evidence of
effectiveness of interventions in children. All smokers should be advised to quit.

The optimal frequency
for counselling has not been determined but repeated messages over long periods of time are
associated with the greatest success.
80
105
The Central Australian Rural Practitioners Association (CARPA) recommends that Aboriginal and Torres
Strait Islander clients be asked if they currently smoke as part of the adult health check from 15 years.
81
The Northern Zone Management Unit (NZMU) of north Queensland also recommend annual
assessment of smoking status from age 15 years as part of an adult Aboriginal and Torres Strait
Islander health assessment (G Miller, 28 November 2002). The decision to set the lower age limit at 15
years was influenced by the known risk factor profile and prevalence of chronic illness among north
Queensland Indigenous Australian populations.
82
Smoking is more prevalent among Indigenous Australians than the general population.
Indigenous Australian adults from 18 years of age are approximately twice as likely to
be current smokers than non-Indigenous adults (51% vs 24% respectively).
EVIDENCE
Level of
evidence
The use of tobacco is probably the major cause of preventable premature mortality and
morbidity among the Aboriginal and Torres Strait Islander population.
IIIIV
Two or 3 minutes of brief advice from health professionals (doctors, nurses and others)
may result in cessation of smoking rates of about 5%.
I
The delivery of brief advice on smoking cessation is likely to be effective in reducing the
prevalence of tobacco use by Aboriginal and Torres Strait Islander clients, especially
when repeated over long periods of time.
V
Those at higher risk of developing smoking related complications include: diabetics,
pregnant women, parents of babies and young children, those with mental illness, those
with other chemical dependencies, and those with cardiovascular risk factors.
III
RECOMMENDATIONS
Incorporate counselling against smoking as a brief intervention into the preventive
health assessment of all clients commencing at 10 years of age (see Box 10).
V
Advise smokers at a higher risk of developing smoking related complications and those
with smoking related disease about the benefits of quitting.
III
Advise on the adverse health effects of environmental smoke. V
Offer smokers support including self help health promotion materials and access to
cease smoking courses and, where appropriate nicotine replacement therapy or
bupropion (see Box 10).
I
Complement strategies targeted at individuals with an Indigenous community based
approach to tobacco control.
V
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
Burden of disease
Chronic obstructive pulmonary disease (COPD) was recently defined as the progressive development of
airflow limitation that is not fully reversible.
83
It includes pathology such as emphysema and chronic
bronchitis. Emphysema is abnormal permanent enlargement of the air spaces distal to the terminal
bronchioles accompanied by destruction of their walls and without obvious fibrosis. Chronic bronchitis is
chronic cough or mucous production for at least 3 months in at least 2 consecutive years when other
causes of chronic cough have been excluded. Chronic bronchitis may precede the development of
airflow limitation, and airflow limitation may precede chronic bronchitis.
84
A major objective of the World Health Organisation (WHO) Global Initiative for COPD and the Australian
and New Zealand COPD Guidelines is to increase provider and public awareness of symptoms. COPD
often remains unrecognised by individuals and undiagnosed by health providers. In a predominantly
non-Indigenous Australian population in Australia only 21% of all adults with COPD had this recognised
by their health provider and were receiving treatment.
85
Indigenous Australians data is limited, but in a
single remote community in the Northern Territory (NT) only 8% of adults from 18 years with COPD had
this recognised by local health providers.
86
The decision to seek medical advice usually occurs when
106
COPD symptoms affect lifestyle or when COPD is associated with an acute exacerbation. However, in
the presence of mild COPD (FEV1/FVC <70% but FEV1 >80% predicted), individuals may not be aware
that lung function is abnormal. COPD cannot be diagnosed on symptoms alone and requires spirometry.
Furthermore, COPD is often misdiagnosed as asthma, as symptoms are similar, but in some individuals,
it will remain difficult to differentiate the two diseases.
87
Smoking is the single most important risk factor for COPD and accounts for approximately 85% of the
risk of developing this disease.
88
Nevertheless additional factors have also been shown to contribute to
impaired optimal adult lung function, and accelerated lung function decline with age and COPD. These
comprise factors to which Indigenous Australians may be more likely to be exposed, and include
maternal tobacco consumption during pregnancy,
89,90,91,92
prematurity,
93
intra-uterine growth
impairment,
94,95
impaired growth in the first year of life, recurrent respiratory infections in childhood,
96,97
occupational dust and fume exposure,
98,99,100
environmental tobacco smoke,
101
indoor and outdoor air
pollution
102,103
and bronchial hyper-reactivity/asthma. The role of further factors including genetic
predisposition, particularly !1 antitrypsin deficiency and immune deficiencies account for very few cases
of COPD.
104,105
In the Aboriginal and Torres Strait Islander population, COPD has been reported to be more than 10
times more prevalent than in the non-Indigenous population in Western Australia (WA). As a cause of
hospital admission during 19881993 in the Aboriginal population aged 4054 years, the prevalence of
COPD was 194/100 000 person years (compared with 18/100 000 person years in the non-Aboriginal
population).
106
COPD is a significant contributor to the health disparity between Indigenous and non-
Indigenous Australians, and in the NT, is responsible for 4% of the average years of life lost after 65
years compared with non-Indigenous Australians.
107
In general, Indigenous Australians die from COPD
at an age standardised rate five times greater than non-Indigenous Australians.
108
This disparity is
particularly acute for women who die at an age standardised rate 10 times that of non-Indigenous
Australian women.
109
COPD also accounts for a higher proportion of primary health care problems
managed in Aboriginal Community Controlled Health Services (ACCHSs) compared with mainstream
general practice.
110
modification
Yes
adult
pneumococcal
and influenza
immunisation
(see
Respiratory
disease
Communicable)
Yes
spirometry (peak
flow not
recommended)
Yes
smoking
(see
Smoking)
Nil Yes
passive
smoking
occupational
smoke and
chemicals
growth
promotion/
antenatal care
housing
education
Immunisation
See Respiratory disease Communicable section.
Counselling
Smoking cessation is the single most effective way to prevent the development of airflow limitation and
reduce its progression. Interventions to cease smoking have maximal benefit for COPD if implemented
early in the course of the disease (secondary prevention) or prior to its development (primary
prevention).
111
In a resource limited environment, identifying those smokers with early COPD who may
benefit the most from more intensive smoking cessation interventions may be advocated as an
argument for screening adult tobacco smokers (see also Smoking).
107
Environmental modification
Epidemiologic studies suggest that intra-uterine growth retardation including that associated with
maternal tobacco consumption
112
, infections in early life and poor growth in the first year of life are
associated both with reduced lung function in adulthood
113
and increased risk of COPD.
114,115
Early
studies in Indigenous Australians would suggest that this is also the case in this population and
particularly reduced intra-uterine and first year growth.
116
Environmental/social factors as evidenced by
household crowding and reduced formal educational attainment, are also associated with reduced lung
function and thus respiratory reserve even in the apparent absence of COPD.
The efficacy of interventions directed at these factors as primary prevention for COPD has not been
defined. In part this is due to the difficulty in assessing interventions in which the delay between
intervention and outcome may be decades. The overall population health benefits associated with
environmental change are clear, and their similar effect on COPD development would be supported by
these epidemiologic associations.
One potential area amenable to intervention is early life, including intra-uterine and first year growth, and
maternal tobacco consumption during pregnancy. Maternal tobacco consumption is associated with
poorer lung function at birth and in childhood (independent of birth weight and gestation) suggesting in-
utero tobacco has a direct and persisting detrimental effect on lung function. While this has not been
associated with COPD, the attainment of a lower level of optimal lung function could be associated with
the earlier development of critically impaired lung function if additional factors including tobacco
consumption were to supervene.
Evidence supporting the influence of in-utero growth on adult lung function and the occurrence of COPD
has arisen largely from retrospective cohort studies. Barkers follow up study of men born in
Hertfordshire, England 19111930
117
demonstrated a relationship between birth weight and adult lung
function with FEV1 at aged 5970 years being 60 mL (95% confidence intervals (CI): 2090 mL) greater
for every increase in birth weight of 450 g. Further rates of death from COPD were greater in those with
lower birth weight. Others
118
in a similar retrospective cohort study in south India showed that lung
function fell by a similar amount with mean FEV1 falling by 90 mL (95% CI: 10160 mL) for each 450 g
decrease in birth weight controlling for age and height.
While data for Indigenous Australians is less conclusive, a recent retrospective cohort study of an
Indigenous Australian birth cohort in the NT demonstrated that for every increase in birth weight of 100
g, early adult lung function (FEV1) was 21 mL greater, and for every increase in average weight gain in
the first year, was 50 mL.
119
These associations were independent of one another, age, height, gender
and prematurity. The gain in FEV1 with increasing birth weight independent of gestation would suggest
this is a marker of intra-uterine growth rather than prematurity. Nevertheless, this increase was modest,
and would be unlikely to have a significant bearing on eventual disability and premature mortality if
COPD occurred. In contrast, the influence of small improvements in growth in the first year of life was
associated with more significant increases in FEV1.
Addressing any of these factors, except tobacco consumption, as primary prevention of COPD remains
contentious. Nevertheless, just as reducing tobacco consumption has effects on vascular disease and
malignancy separate to its effect on COPD, these early life and environmental factors are also likely to
have more far reaching effects than on COPD alone and may be additionally advocated on this basis.
Screening
The implementation of primary or secondary preventive initiatives relies first on respectively excluding or
confirming the presence of COPD. However, the diagnosis of COPD can be difficult. The diagnosis or
exclusion of COPD relies on determining if lung function is abnormal or normal and particularly whether
airflow obstruction is present or absent. Chronic respiratory symptoms can occur without significant
airflow obstruction and in turn airflow obstruction can occur in the absence or with minimal respiratory
symptoms.
The rationale for screening for COPD is based first on whether screening techniques are effective,
achievable and acceptable, and if early diagnosis allows the implementation of interventions to reduce
the subsequent development of disease, its progression or sequelae.
Screening techniques
Spirometry is integral to the diagnosis of COPD. It is relatively inexpensive in terms of consumables, but
is somewhat labour intensive. The equipment itself requires a significant capital purchase but ongoing
maintenance and thus running costs are minimal. It requires trained staff to supervise, though the level
108
of prior knowledge required is minimal. Adverse effects relating to spirometry are infrequent and include
the rare risk of a faint associated with a forced expiratory maneuver.
The WHO has briefly appraised the use of spirometry as a screening tool to identify COPD in the
general population, however, there is no data to support that screening with spirometry can improve
COPD outcomes.
120
A screening test for COPD should lead to better health outcomes (eg. reduced
morbidity/mortality) than those achieved when clients present with signs and symptoms. In the
Aboriginal and Torres Strait Islander situation, many clients will (in general) delay seeking care even
with signs and symptoms. It is likely that airflow limitation may not be recognised until it is severe,
although few studies have reported on this issue. Lung function in Aboriginal adults was 20% less than
that in non-Aboriginal adults (in cross sectional survey),
121
suggesting that impairment may be
unrecognised or that factors in early life may impair the attainment of optimal adult lung function. Data in
Indigenous versus non-Indigenous populations does not suggest that Indigenous Australians are more
susceptible to an accelerated decline in lung function.
Furthermore, the diagnosis of COPD hinges on the presence of impaired lung function which in turn
assumes that lung function is significantly impaired in comparison to a healthy normal population. In
such a scenario, comparatively low levels of lung function may reflect optimal lung function for an
individual and values comparable to a normal population might reflect significant respiratory impairment.
Normal spirometry values for Indigenous,
122,123,124
and non-Indigenous
125,126,127
Australians are available
and should be utilised when interpreting lung function. Nevertheless while values at any one time may
be useful, particularly the ratio of FEV1 to FVC, in diagnosing or excluding significant airflow obstruction,
it is the accelerated age related decline in lung function and particularly FEV1 which in the final analysis
defines COPD.
In an ideal setting, serial measurement of lung function over several years that demonstrates an
accelerated decline in FEV1 greater than that compared to a healthy cohort, would more accurately
define COPD. In turn, such accelerated decline in lung function will lead to the onset of symptomatic
COPD, disability and premature mortality (see Figure 3).
128
1 normal growth and age related decline
3 impaired growth and normal age related decline
2 normal growth and accelerated age related decline
4 impaired growth and accelerated age related decline
Figure 3. Potential models of development of COPD, optimal lung function and its age related
decline required to interpret spirometry and its significance
Source: American Journal of Respiratory and Critical Care Medicine. Spirometric reference values from a sample of
the general US population, 1999
COPD related
disability/death
L
u
n
g

f
u
n
c
t
i
o
n
/
s
i
z
e
1 3 2
|--in utero--|----child----|----adult--------->
X X X
4
109
The WHO recommends spirometry in all smokers to detect early COPD amenable to treatment. Clients
who have chronic cough and sputum production with a history of exposure to risk factors (smoking,
occupational dusts and chemicals, smoke from home cooking and heating), should be tested for airflow
limitation, even if they do not have any breathlessness. A low peak flow is consistent with COPD but is
poorly specific. Every effort should be made to provide access to spirometry.
129
It has been suggested that a chest X-ray should also accompany spirometry in the routine assessment
of lung function in smokers, with the aim of excluding other conditions which may present with chronic
respiratory symptoms (tuberculosis, interstitial lung disease, bronchiectasis) and to detect lung cancer.
While the benefit of routine chest X-ray in excluding other chronic respiratory disease is unclear, a
systematic review of randomised controlled trials concluded that the evidence did not support screening
for lung cancer with chest X-ray and that frequent screening may even be harmful.
130
Effectiveness of treatment
None of the existing medications for COPD has been shown to modify the long term decline in lung
function.
131
Nevertheless, interventions have been demonstrated to reduce exacerbation frequency,
reduce disability and improve quality of life.
132
If individuals with more advanced COPD remain
unrecognised, they cannot be offered such interventions which may address these areas.
Long term oxygen therapy in people with COPD and significant hypoxemia has also been demonstrated
to prolong life.
133,134,135
While it is assumed that most clients with such advanced disease would be
known to health providers, this cannot be guaranteed. In well selected clients, long term oxygen therapy
has been demonstrated to improve survival. Immunisation, inhaled steroids and long and short acting
bronchodilators can either reduce exacerbation frequency, give a one off improvement in lung function
which may be clinically significant especially in those with advanced disease and improve quality of
life.
136
Pulmonary rehabilitation programs can improve exercise capacity, relieve breathlessness and improve
health related quality of life in clients with COPD. This has been demonstrated in a number of
systematic reviews of the research literature.
137,138,139,140,141
Management guidelines for COPD have been developed in Australia but do not address the role of
screening in this condition.
142,143
There is insufficient evidence to recommend screening the general Aboriginal and Torres Strait Islander
population for COPD using spirometry or other methods. However, the WHO recommends spirometry to
detect early COPD amenable to treatment in all smokers (see Screening techniques). Spirometry in
primary health care for case finding of COPD has been recommended on the basis of expert consensus
in smokers >45 years in the USA.
144
While interventions are available to reduce mortality and disability and improve quality of life, it is
unclear whether implementation of these in relatively asymptomatic people will be any more effective
compared with waiting until they develop symptomatic disease. Nevertheless, COPD is under-
recognised in Indigenous and non-Indigenous populations in Australia even when it is associated with
respiratory symptoms. This highlights the need to educate clients and health providers that such
symptoms may indicate underlying COPD, especially in those most at risk, particularly older people with
a history of tobacco consumption. In addition, facilities and spirometers need to be accessible to primary
health providers together with training in lung function interpretation. The role of spirometry screening in
high risk populations would warrant revisiting if such profile raising, education and improved availability
of quality spirometry cannot achieve improved recognition of advanced disease.
Health providers should assess smokers for symptoms of cough and sputum, and supplement this with
spirometry, although no optimal schedule for repeating measurements can be recommended. Individual
spirometry results may be difficult to interpret especially in early disease, and serial testing 23 years
apart may be useful to identify those individuals with an accelerated decline in lung function who are
likely to progress to symptomatic COPD.
The Central Australian Rural Practitioners Association and the Northern Zone Management Unit of north
Queensland do not currently recommend screening for spirometry as part of a preventive health
110
assessment in the Aboriginal and Torres Strait Islander population. The Royal Australian College of
General Practitioners has no recommendations for the use of spirometry as part of a preventive health
assessment in the general population.
Chronic obstructive pulmonary disease (COPD) is the progressive development of airflow
limitation that is not fully reversible. COPD is 10 times more prevalent in the Aboriginal
and Torres Strait population and may be attributed to the high rates of smoking as well as
factors in early life which reduce the level of optimal lung function.
COPD in Aboriginal and Torres Strait Islander clients is under-recognised by individuals
and their health care providers even when this is associated with significant symptoms.
EVIDENCE
Level of
evidence
Tobacco consumption is a major contributor to the development of COPD. I
Stopping people taking up smoking and getting those who do smoke to stop before the
onset of COPD is likely to be the most effective means of preventing the development of
COPD.
V
Treatment for COPD can improve the quality of life, reduce disability, and prolong life. I
RECOMMENDATIONS
Use spirometry opportunistically to assess airway obstruction in smokers and people with
recurrent episodes of acute respiratory infection and chronic respiratory symptoms as
part of a preventive health assessment. An optimal schedule for repeating measurements
cannot be recommended, however, serial testing every 2 years may be useful.
V
Educate clients that cough and sputum symptoms may indicate underlying COPD,
especially in those older people with a history of tobacco consumption. Advise that
symptoms of chronic bronchitis include chronic cough or mucous production for at least 3
months (in at least 2 consecutive years when other causes of chronic cough have been
excluded).
V
It is not recommended to screen for COPD using spirometry as part of a preventive
health assessment.
V
It is not recommended to use chest X-ray to detect lung cancer in smokers as part of a
preventive health assessment.
I

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Sexual health
116
ADULT HEALTH
SEXUAL HEALTH
Authors
Dr Steven Skov, Northern Territory Department of Health and Community Services
Dr Richard Murray, Kimberley Aboriginal Medical Services Council
Acknowledgments
Dr Jan Savage, Northern Territory Department of Health and Community Services
SEXUAL HEALTH
Burden of disease
The Aboriginal and Torres Strait Islander population bears a substantial proportion of bacterial sexually
transmitted infections (STIs) and associated complications, including infertility and adverse pregnancy
outcomes.
1
A study in 1983 found that pelvic inflammatory disease (PID) will occur in 1040% of women
infected with gonorrhoea or chlamydia if they do not receive treatment.
2,3
PID is then associated with
substantial risks of infertility and ectopic pregnancy. Fourteen percent of all admissions for Aboriginal
women to Royal Darwin Hospital were found to be for PID compared to 2% for non-Aboriginal women.
4
Thirty-two percent of women in a large, remote Northern Territory (NT) community had had at least one
clinical episode of pelvic inflammatory disease and 26% appeared to be infertile.
5
Data from clinical
audits in over 25 other remote NT communities suggested very similar rates of PID.
6
If notification data from NT, Western Australia (WA) and South Australia (SA) for 2002 are combined (in
the 5199% of cases where Indigenous status was known), Aboriginal people contributed 27% of all
genital chlamydia notifications, 69% of all gonorrhoea notifications and 79% of all syphilis notifications
while comprising only 3.9% of the population.
7
Studies from a variety of settings indicate markers of past hepatitis B infection in 3072% of Aboriginal
people and chronic hepatitis B virus (HBV) surface antigen carriage in 319%.
8,9,10,11,12,13,14
Chronic
carriage of HBV surface antigen is associated with progression to cirrhosis and carcinoma of the liver.
Hepatic carcinoma has been reported as occurring 10 times more frequently in Aboriginal people in the
NT.
15
Among non-Indigenous Australians, most hepatitis B is transmitted sexually or via injecting drug
use, but it is likely that hepatitis B infection in remote community Aboriginal people is largely acquired in
childhood (vertical transmission).
16
In NT Aboriginal women, 42% had evidence of human papilloma virus (HPV) infection according to a
polymerase chain reaction test a rate similar to that found among non-Indigenous women.
17,18
There is
little information concerning the occurrence of herpes simplex virus (HSV) in the Aboriginal population.
One study of male prisoners from New South Wales (NSW) found a prevalence of HSV-2 antibodies of
34% among Aboriginal inmates compared to 24% in non-Indigenous inmates.
19
In Australia,
donovanosis is now limited to Aboriginal populations in central and northern regions.
20
While now
uncommon, donovanosis does occur sporadically and should always be considered in the differential
diagnosis of genital ulcer disease in people who live in or have connections with remote central and
northern Australian regions.
At a national level, human immunodeficiency virus (HIV) infection among Aboriginal and Torres Strait
Islander people is reported at about the same rate as in the non-Indigenous population, but with
relatively more heterosexual transmission and a greater proportion of women infected (33.7% vs
Sexual health
117
10.1%). In 2003, the estimated HIV prevalence was 69 per 100 000 in both the Indigenous and non-
Indigenous Australian population.
21
There is substantial variation in the occurrence of STIs in different regions. State notifiable disease data
shows that there are major differences, not only between urban and remote areas, but also between
regions only small distances apart.
22,23
There are major gaps in current knowledge, with no specific data
available on the occurrence of STIs among Aboriginal and Torres Strait Islander people in large regions
of the country.
Immunisation Screening* Counselling Chemoprophylaxis Environmental
Yes
hepatitis B
Yes
STIs (eg.
gonorrhoea,
syphilis,
chlamydia)
Pap test
Yes
sexual and
reproductive
health
Yes
herpes simplex
Yes
condoms
education
access to
primary
health care
* See also Prevention of cervical cancer
The clinic visit offers an opportunity for reproductive health counselling as well as the identification of
those at high risk of STIs.
Immunisation
The only STI for which a vaccine is currently in use is hepatitis B virus infection. Neonatal studies have
confirmed that recombinant DNA hepatitis B vaccine is 66100% protective against vertical transmission
of hepatitis B from infected mothers.
24
In Australia, universal neonatal immunisation is now
recommended as part of the Australian Standard Vaccination Schedule (monovalent birth dose followed
by further doses at 2, 4 and either 6 or 12 months with combined vaccines including diphtheria, tetanus
and pertussis or Haemophilus influenzae type B vaccines).
25
Vaccination of susceptible sexual partners
of clients with acute hepatitis B infection should be offered postexposure prophylaxis with hepatitis B
immunoglobulin and hepatitis B vaccine. Partners of asymptomatic carriers of hepatitis B should be
offered protection by immunisation with hepatitis B vaccine.
26
Other vaccines against STIs are currently in development. A randomised controlled trial has reported no
evidence of effectiveness of glycoprotein vaccine against the HSV.
27
A recent randomised controlled
trial using HPV-16 virus-like particle vaccine reduced the risk of persistent HPV-16 infection after
median follow up of 17 months and prevented the development of cervical intraepithelial neoplasia. The
incidence of persistent HPV-16 infection was 3.8 per 100 woman years at risk in the placebo group and
0 per 100 woman years at risk in the vaccine group (100% efficacy; 95% confidence interval: 90100; P
<0.001). Persistent HPV was chosen as an end point as approximately

50% of cervical cancers are
associated with HPV-16 infection. Further research is required before such vaccines are widely used,
especially with multivalent

vaccines that include other common types of HPV.
28
A reproductive health assessment may include the provision of education, contraceptive needs,
promoting help seeking behaviour and screening appropriate to risk as a routine part of the well
persons health check.
Strategies to influence sexual behaviour can be targeted at the individual or the population as a whole.
While there is no evidence that reproductive health brief interventions are effective at reducing STI risk
behaviours in generalist settings,
29
this may be the only opportunity to provide clients with some
education. Interventions could include advice regarding risk, measures to reduce risk (such as the use
of condoms) and promotion of health care seeking behaviour. Higher risk clients (eg. those with an STI
or with significant risk behaviours) should be offered a more intensive, structured intervention, including
skills for negotiating safe sex, for which there is evidence of benefit.
30
As the impact of counselling for behavioural change within the clinic setting is limited, population based
health promotion as well as screening strategies to identify and treat infected individuals and their
Sexual health
118
sexual partners are necessary.
31
Educational interventions in which information regarding disease
transmission and prevention is presented alongside skill development can achieve short term increases
in reported condom use for vaginal intercourse. Information provision alone is insufficient to encourage
health behaviour change, as culturally appropriate and gender specific skills development and
motivation building is required to negotiate risk reduction with sexual partners.
32,33
Antiviral agents used prophylactically (daily maintenance therapy as well as commencing treatment at
the start of a recurrence) in those identified with genital herpes infection can reduce viral shedding. Daily
maintenance therapy can also reduce the frequency of recurrences as shown in systematic reviews of
randomised controlled trials. However, whether this treatment leads to reduced transmission of genital
herpes has not been adequately studied.
34
There is good evidence for the effectiveness of the male condom in reducing the risk of HIV in men and
women and the risk of gonorrhoea in men, but insufficient evidence to enable definitive conclusions to
be made about the effectiveness of condom use for the prevention of other STIs in men and women.
35
There are inadequacies in the available evidence and further well designed clinical studies are needed.
Nevertheless, promotion of condom use remains central to prevention strategies.
Numerous studies have investigated the effectiveness of sex education strategies in altering risky
sexual health behaviour (see Counselling and chemoprophylaxis). In studies targeting youth and school
age children (1121 years), there appears to be little evidence that sexual health education encourages
or leads to greater sexual activity among young people. The evidence indicates that safer sexual
practice among young people may be achieved through education. Outcomes evaluated included
adolescent pregnancy, abortion and birth rates, STI rates, and self reported sexual activity.
36
Another
systematic review also reported that school education programs did not hasten sexual activity in older
students. There was insufficient information on whether these programs decreased STI rates.
37
The US
Task Force on Community Preventive Services is currently reviewing population based interventions
that change health risk behaviours for the prevention of STIs.
38
Access to primary health care services is essential in the control of STIs. If it is possible to reduce the
population prevalence of infection through screening and treatment, the risk of infection from
unprotected intercourse will also be reduced. Because of their role in facilitating transmission of HIV
infection, reducing the burden of bacterial STIs is also a form of primary prevention of HIV infection and
is now considered a major aspect of HIV control programs. A systematic review confirmed that improved
STI treatment services can reduce HIV incidence in an environment characterised by an emerging HIV
epidemic (low and slowly rising prevalence), where STI treatment services are poor and where STIs are
highly prevalent.
39
Screening
A very large proportion of STIs cause either no symptoms or very mild symptoms. This is particularly
true of chlamydia, gonorrhoea and trichomonas in women, but also of a substantial proportion of these
infections in men.
40,41,42
People with mild symptoms may not realise that an STI is the cause, or may not
present to a clinic for care because of shame or a lack of access to health care services or an
appropriate practitioner. This provides a substantial rationale for offering an STI test as part of a
preventive health assessment, particularly in populations that have limited access to health care.
Principles of STI screening
There are two major but quite distinct potential benefits of STIs screening for:
the individuals involved (reduced sequelae of infection), and
the population (reduced transmission of infection).
However, achieving each of these benefits requires different approaches in terms of screening
strategies, the proportion of the population needing to be screened, and the effort and resources to be
expended in order to provide a certain level of benefit. Furthermore, the population prevalence of STIs,
geography, population values, and the resources and philosophy of the health service, all influence
decisions regarding screening. What constitutes a high prevalence of infection justifying action is a
judgment for the community and its health service to make. In many regions, health services lack the
data to make this assessment.
Sexual health
119
Health services need to be clear about the role they want STI screening to fulfil. If the principal aim is to
reduce pelvic inflammatory disease in women, there is good evidence that a screening program
restricted to women can achieve that aim among the women screened.
43
If the aim is to reduce
transmission of infection in the client population, then a more extensive and systematic population
approach will be required.
It is known that a key factor in transmission of STIs lies in the sexual and economic power relationships
between men and women.
44
Key philosophies in all STI/HIV prevention programs are to encourage all
individuals to adopt more responsible behaviour in terms of numbers of sexual partners, condom use
and health care seeking behaviour.
Screening can be made more efficient by the use of criteria to identify those at an increased risk of
infection among the general population (eg. age, recent change in sexual partner, number of sexual
partners, past history of an STI, type of contraception). Many such criteria have been found to be useful,
particularly for detecting chlamydia in women.
45,46
However, it is essential to do local research to
determine appropriate criteria.
Core group transmission is probably important in causing rates of STIs to be higher than they would
otherwise be in any population.
47
Targeting screening and education efforts to a core group with very
high rates of STIs and their immediate sexual networks is likely to have greater impact on the
community burden of disease than applying limited health resources throughout the non-core
population. While identifying and working with core groups can be difficult, persons at very high risk of
infection can sometimes be identified. Having had one (and especially more) STIs in the recent past is
the strongest predictor of acquiring another and should identify the individual as someone who might
benefit from a more intensive regimen of education and ongoing screening.
48
Substance misuse and
behavioural factors, such as having large numbers of sexual partners or commercial sex work would
also be reasonable criteria. Among such higher risk individuals, particularly in endemic areas, regimens
of regular gonorrhoea, chlamydia and syphilis testing should apply to both men and women.
Which STIs to screen for?
There is good evidence from overseas and Australia that screening strategies can reduce rates of some
bacterial infections and their sequelae,
49,50
specifically:
screening women for chlamydia in a general practice setting can reduce the incidence of PID
51
screening women for chlamydia in family planning and other public clinics can reduce the prevalence
of infection in that population
52
sustained screening of women and men for chlamydia in a wide variety of clinical and outreach
settings on a national basis has been followed by reductions in the national incidence of infection and
of hospital admissions for PID and ectopic pregnancies
53,54,55
in remote central Australian Aboriginal communities, substantial reductions in the prevalence of
gonorrhoea, chlamydia and syphilis were observed with the introduction of repeated, annual,
intensive screens for STIs performed on 70% of the population aged 1240 years (both male and
female) over a 46 week period.
56
Several international authorities now recommend screening young women for chlamydia,
57,58,59
but none
recommend screening men. The evidence for the benefit of screening women in terms of reduced
sequelae of infection is strong and comes from a wider range of settings than that for men. There are
very few studies focused on the screening of men.
In line with USA and UK recommendations,
60,61
all sexually active Australian women (both Indigenous
and non-Indigenous) aged less than 25 years should be offered annual chlamydia screening. Given that
it is likely that in many regions Aboriginal women experience a prevalence of gonorrhoea that is at least
as high as that which warrants chlamydia screening in other populations, there is a good case for a
gonorrhoea screening test to be added to chlamydia screening for Aboriginal women. Screening beyond
25 years or even 39 years may be indicated according to local STI data.
62
The issue of routine screening of men is more difficult. The US Preventive Services Task Force states
that there is insufficient evidence either for or against the screening of men.
63
However, screening
women only may promote gender inequality and undermine universal messages regarding responsible
sexual practices and health care seeking behaviours. It is not known what impact this may have on the
success of a population based prevention program. Also, the level of asymptomatic infection among
men varies high rates of asymptomatic (or tolerated) STI among Aboriginal men in central Australia
have been reported and this may reflect barriers in access to care.
64
For these reasons, routine
screening of Aboriginal and Torres Strait Islander men as well as women may be considered in some
regions, particularly of those with hyperendemic disease or barriers in access to curative care.
Sexual health
120
Using ethnicity as an indicator of the need for screening is a difficult and potentially divisive and
stigmatising. It should only be considered in the presence of good supportive data, the likelihood of a
clear benefit to the individuals and community. Community leaders and members must be involved in,
and consent to, the decision to screen.
It is not useful to screen for all STIs during a preventive health assessment unless there are symptoms
of infection. For example, there is no role for HSV screening in asymptomatic persons. Pap test
programs will detect some HPV infection, but there is no place at this time for using other tests to screen
for HPV.
65
Screening for hepatitis B may be considered in populations with high endemicity as there are now
feasible, effective treatments for chronic carriers and immunisation can be offered to susceptible sexual
partners and household contacts. However, there are substantial costs and workload implications that
would need to be weighed against the mostly marginal gains in prevention of complications. In most
settings, screening for hepatitis B is best conducted as part of antenatal programs with neonatal
immunisation being the most appropriate population based approach for long term control of hepatitis B
(see Immunisation).
Screening for HIV infection of asymptomatic people with no specific history of risk is not recommended,
with the exception of pregnant women.
66
Screening for trichomonas infection has recently been advocated because of the high prevalence in
remote Aboriginal communities.
67
Some evidence suggests that trichomonas infection is associated with
complications including adverse pregnancy outcomes such as prematurity, low birth weight infants,
premature delivery of small-for-gestational-age infants and enhanced transmission of HIV. No Australian
studies have examined the association of trichomonal infection and adverse pregnancy outcomes.
Overseas studies of trichomonal infection during pregnancy have found a 3040% increase in risk of
premature labour, premature rupture of membranes and low birth weight, even after controlling for other
recognised risk factors.
68
However, other infections such as chlamydia and bacterial vaginoses are also
associated with these outcomes.
69
There is also a lack of evidence supporting treatment of trichomonas
to improve pregnancy outcome. A controlled treatment trial in the USA found that treatment of
trichomonas with metronidazole, while achieving parasitological cure in 93% of asymptomatic
participants, failed to improve pregnancy outcome and, in fact, appeared to contribute to poor
outcome.
70
There have not been any large, well designed studies that can inform if trichomonas treatment can
prevent HIV infection. In Australia, where a very low HIV prevalence and high STI rates exist, there is
insufficient evidence to conclude that treatment of trichomonas would have an effect on HIV incidence.
71
Antenatal screening for syphilis is universally recommended in early pregnancy,
72,73,74
and is critical for
preventing congenital syphilis. Syphilis tests should be repeated in the third trimester and at delivery in
areas of high endemicity or for women at increased individual risk.
75,76
Antenatal screening for
chlamydia is recommended at least once and the addition of gonorrhoea testing is recommended for
those at higher risk
77
or in regions of high endemicity.
Those individuals considered to be at increased risk of infection (eg. STI in past year, substance abuse,
multiple sexual partners, new sexual partner) should be offered syphilis serology testing regardless of
age and consideration should be given to opportunistic testing when they present to the health service
for other reasons.
For populations with high endemicity, syphilis serology screening of men and women is supported.
78,79
While practical implementation is a challenge in some areas, testing can be incorporated into a
preventive health assessment or regular review for chronic disease management.
Intensive, mass screening (or treatment alone) for gonorrhoea, chlamydia and syphilis has been shown
to be effective in areas of high endemicity
80,81,82
but is usually only practical in discrete geographical
populations (eg. remote Aboriginal communities) or identifiable risk groups such as sex workers.
83
Planning, adequate resources for follow up, an understanding of disease epidemiology and full
community involvement and consent are necessary.
84
Testing
Nucleic acid amplification (NAA) tests on either endocervical specimens (obtained at the same time as
Pap test) or self obtained vaginal specimens (a swab or tampon) are highly sensitive and specific.
85,86
NAA tests on female urine specimens are less sensitive, particularly for gonorrhoea detection.
87,88
While
Sexual health
121
vaginal specimens are to be preferred, urine tests are still very useful if vaginal specimens are
impractical. In asymptomatic men, NAA tests for chlamydia and gonorrhoea using first pass urine
samples are preferred.
Given the minimally invasive nature of tests now available and ease of treatment, there are benefits for
both individuals and populations in offering screening tests for some bacterial STIs, particularly in areas
where rates of infection are high. Achieving a reduction in rates of infection at a population level requires
a systematic approach involving good population coverage, sustaining the program over some years,
good treatment, follow up, and partner notification. Screening protocols should be based on an
understanding of the regional prevalence of infection, local resources and the acceptability of testing to
clients. In the absence of good local data, testing for STIs as part of a preventive health assessment
may provide some of the information needed to inform further refinement of screening protocols.
Sexual and reproductive health counselling should be offered annually to all Aboriginal and Torres Strait
Islander people aged 1530 years. In some regions, local data may indicate extending this age range.
Except in the case of mass screening in remote Aboriginal communities, there is little direct evidence for
any particular screening frequency. Screening frequency can be individualised according to risk. For
those at high risk, particularly younger people with a recent history of an STI, re-testing within 6 months
of treatment may be of benefit in detecting a new infection.
89,90
Screening of those at lower risk of STIs
may be conducted annually or as part of a preventive health assessment.
The Central Australian Rural Practitioners Association recommends offering annual screening for
chlamydia, gonorrhoea infection and syphilis testing to all Aboriginal and Torres Strait Islander men and
women 15 years or more as part of the adult health check. Screening for hepatitis B is only
recommended if there are facilities and capacity for management of diagnosed cases.
91
The Northern
Zone Management Unit recommends annual screening for chlamydia and gonorrhoea (polymerase
chain reaction tests) in Aboriginal and Torres Strait Islander adults aged 1540 years (and younger or
older persons at risk). Those at high risk are defined as the 1525 year age group with a history of a
recent change in partner or multiple partners (without consistent condom use by clients or their
partners). In women, specimens for testing may include self collected low vaginal swab or first void urine
or endocervical swab (in that order). In men, first void urine is preferred. Testing for syphilis (using rapid
plasma reagin) is also recommended annually in all people aged 1540 years (and younger or older
persons at risk) from a venous blood sample. Assessing for the presence of symptoms related to STI is
also recommended in this group. Symptom checks include dysuria, discharge, rash and lower
abdominal pain (in women) (G Miller, 28 November 2002).
The Royal Australian College of General Practitioners currently has no specific recommendations
pertaining to screening for STIs in the Australian population.
92
Sexual health
122
The occurrence of sexually transmitted infections (STIs) and associated complications
(including pelvic inflammatory disease [PID]) in the Aboriginal and Torres Strait
Islander population is more common than in the rest of the Australian population.
EVIDENCE
Level of
evidence
Screening may be made more efficient by the use of criteria to identify those at an
increased risk of STI (eg. harmful alcohol use, age, recent change in sexual partner,
increased number of sexual partners, past history of an STI, type of contraception).
IV
Brief advice in the clinic setting may not be effective in changing sexual behaviour, but
clients provided with culturally appropriate and gender specific counselling may achieve
short term increases in reported condom use for vaginal intercourse.
I
Screening of men as well as women for chlamydia and gonorrhoea may help reduce
population transmission and reinforce health promotion messages.
V
The hepatitis B vaccine is effective in preventing neonatal infections with hepatitis B. I
Systematic annual screening may reduce the prevalence of chlamydial and gonorrhoeal
infection in the Aboriginal and Torres Strait Islander population.
IIIII
RECOMMENDATIONS
Offer annual sexual and reproductive health counselling to all clients aged 1530 years.
Extend this age range if indicated by local data.
V
Offer screening at least every 12 years for chlamydia infection to all sexually active
women younger than 25 years to reduce likelihood of PID. Also test women for
gonorrhoea in areas where it is common. Extend screening beyond age 25 years if
indicated by local data.
IIIII
Screen at least every 12 years (may coincide with the biennial Pap tests). Offer more
frequent screening to individuals with higher risk indicators (eg. recent STI, substance
abuse, multiple partners).
IVV
Consider STI screening of men at a regional level, particularly where disease rates are
high.
V
Nucelic acid amplification (NAA) tests of either self obtained vaginal swabs (or tampons)
or endocervical swabs are recommended for screening both chlamydia and gonorrhoea
in women. Urine specimens are preferred for NAA testing of men. Wherever practicable,
culture specimens for gonorrhea should also be obtained.
V
For populations where syphilis is highly endemic, screen for syphilis in men and women
every 12 years.
IIIV
Screening is not recommended in the non-pregnant population for hepatitis B,
trichomonas vaginalis, human immunodeficiency virus, herpes simplex virus or human
papilloma virus infections.
V
A universal birth dose for hepatitis B and follow up vaccination is recommended for all
Australians as part of the Australian Standard Childhood Vaccination Schedule (see
Australian immunisation handbook).
Vaccinate susceptible sexual partners and household contacts of asymptomatic hepatitis
B carriers and sexual partners of persons with acute hepatitis B (see Australian
immunisation handbook for detailed recommendations).
V

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69 KK Holmes, et al, op. cit., 465.
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Suicide prevention
127
ADULT HEALTH
SUICIDE PREVENTION
Author
Acknowledgment
Professor Ernest Hunter, University of Queensland
SUICIDE PREVENTION
Burden of disease
Aboriginal and Torres Strait Islander deaths due to suicide have been increasing in the past two
decades and rates are higher than those in the non-Indigenous population, yet these statistics are
underestimates. In 19971999, there were 23 times more suicide deaths than expected for Aboriginal
and Torres Strait Islander males and females. The suicide rate was four times higher in 1524 year old
Aboriginal and Torres Strait Islander males (108/100 000) compared with all males in this age group.
Hospital separation rates for mental and behavioural disorders in 19981999 were 1.24.1 times higher
for Aboriginal and Torres Strait Islander males and females than rates observed for all Australians.
1
The age at which most suicides in Aboriginal and Torres Strait Islander population occur is younger than
in the general population. The proportion of Indigenous deaths in Queensland for the period 19992001
of those under the age of 35 (83%) was twice that for Queensland as a whole (42%). The suicide rate as
a whole was higher by 56% for Indigenous compared to non-Indigenous populations with the greatest
excess being for males aged 1524 years (rate ratio 3.5) and rates higher in more remote areas of the
state. In this study, hanging accounted for 90% of Indigenous deaths (compared to 41% for the state as
a whole), with firearms accounting for 5% (compared to 12% for all Queenslanders).
2
The age of
Indigenous suicides has continued to fall with a number of recent suicides under age 15 years occurring
in far north Queensland.
3
Mental and addictive disorders, frequently in co-occurrence, are the most powerful risk factors for
suicide in all age groups, associated with more than 90% of all completed suicides according to reviews
of the international literature.
4,5
Young Aboriginal people most at risk from suicide are those who have a
history of self harm and who are exposed to stressful social disruption and disadvantage.
6
Awareness of
relative deprivation, disadvantage and social exclusion from mainstream society as well as other social
mediators may influence suicidal behaviour in young Aboriginal people and Torres Strait Islanders.
7
Well known risk factors for suicide include a history of previous suicide attempts, a history of mental
illness (particularly depression), one or more emotional problems requiring professional help, low self
esteem due to chronic disease or illness, feelings of hopelessness and rage, poor interpersonal skills,
dependence on others, inability to delay gratification, having caused a pregnancy, and having used
alcohol and other drugs. Impulsivity has been widely noted in relation to Indigenous suicide with a close
association to alcohol consumption, particularly binge drinking.
8
Suicide can cluster in some Aboriginal and Torres Strait Islander communities, with obvious implications
for communities as a whole: Given the cluster occurrence of suicide and the circumstances of
Indigenous communities, this means that many people, including children, will have witnessed the
aftermath of a suicide (a hanging body) perhaps several. In this context, suicidal behaviour must
necessarily be considered communicative (in life and in death). At least in Australia, the communicative
dimension of suicidal behaviour has been influenced by historical events (the Royal Commission into
Aboriginal Deaths in Custody) and by the portrayals of hanging in Indigenous art that, wittingly or not,
associate hanging with political ends.
9
Suicide prevention
128
modification
Nil Yes
screening tools
for suicidal
symptoms in
primary care
and school
settings are
currently being
investigated
Yes
brief
intervention
Alcohol (see
Alcohol
Prevention of
problem
drinking)
Yes
antidepressant
medication
Yes
community
gatekeepers
social equity
school based
programs
Few interventions have targeted Aboriginal and Torres Strait Islander people, and as a result, prevention
studies primarily involve non-Indigenous populations. Interventions may be targeted to individuals at
high risk or population based (to young people to prevent suicidal behaviour by individuals).
Screening
Studies have investigated rates of contact with primary health care providers by individuals before they
died by suicide. In the USA, a systematic review identified that contact with primary health care services
within the year of suicide was very common (75% of victims) while 45% of victims had contact within 1
month of suicide.
10
This suggests that if primary health care intervention were effective at preventing
suicide, it would be a vital point of intervention. Given the impulsive nature of many suicides in
Aboriginal and Torres Strait Islander youth, both primary health care and alternative approaches to
suicide prevention are warranted.
Screening for suicide
The assessment and treatment of suicidal persons is important, but primary health care providers lack a
suitable screening instrument. Nevertheless, the opportunistic assessment of clients who may exhibit
risk factors for suicide has been recommended.
11,12
Assessment guides have been developed to assist
primary care providers to evaluate risk by exploring the personal difficulties faced by the client (such as
depression, mental illness, family issues including abuse, cultural factors and coping skills), access to
positive resources and supports (such as relationships, environment and lifestyle), evidence of past
suicide attempts (including in family and friends), and the existence of current suicide plans. Questioning
will not aggravate the risk of suicide but failure to fully investigate, categorise the risk and respond
appropriately may result in a suicide that could have been avoided.
13
A brief screening tool for suicidal symptoms in adolescents and young adults for use in general heath
settings has been developed in Australia. This used the suicidality subscale of the depressive symptom
inventory (a four-item self report questionnaire designed to identify the frequency and intensity of
suicidal ideation and impulses in the past 2 weeks).
14
Its value is unclear but may lie in identifying high
scorers who may not disclose suicide intentions when asked by a practitioner. The applicability of such
tools in the Aboriginal and Torres Strait Islander context is also unclear. However, some tools have been
developed specifically for this population.
15
In general, the Royal Australian College of General Practitioners guidelines and other guidelines,
recommend that primary health care providers remain aware of risk factors for suicide and evaluate risk
in young people (1424 years) by specific questioning for psychological distress and suicidal
ideation.
16,17
The confirmation of suicidal intent requires subsequent appropriate management or referral
or both. A risk assessment for an Aboriginal or Torres Strait Islander individual can be greatly improved
by the involvement of an Aboriginal or Torres Strait Islander person in the assessment process, which
should also include a family member where possible.
18
Screening for depression
Clinicians should also be alert to symptoms of depression in the prevention of suicide. In 2002, the US
Preventive Services Task Force (USPSTF), following a systematic review of the evidence evaluating
screening, recommended screening adults for depression in clinical practices that have systems in
Suicide prevention
129
place to assure accurate diagnosis, effective treatment and follow up.
19
The USPSTF found good
evidence that screening improves the accurate identification of depressed patients in primary health
care settings and concluded that the benefits of screening are likely to outweigh any potential harms.
Several depression screening instruments are available and most are easy to use. Simply asking two
questions about depressed mood and anhedonia ...are as effective as longer instruments[and]
appear to detect a majority of depressed patients. These two questions are: over the past 2 weeks
have you felt little interest or pleasure in doing things? Over the past 2 weeks, have you felt down or
depressed or hopeless? The USPSTF concluded that clinicians can choose the method that best fits
their personal preference and the population and practice setting. The evidence was insufficient to
recommend for or against routine screening of children or adolescents for depression. It was noted that
clinicians should remain alert for signs of depression in younger patients.
In Australia, psychiatrists from the University of Melbourne have reviewed depressive and anxiety
disorders in primary care.
20
They commented that screening tests for depression are simply
questionnaires with a score that predicts diagnosis. They recommend a simple screening test that is
similar to the recommendation of the USPSTF. The NHMRC in 1997 produced guidelines for the
detection and assessment of depression in people aged 1320 years.
21
These have since been
rescinded as of December 2004.
Screening items for depression and self harm have been incorporated into health check protocols for
Indigenous populations in a number of regions including the Northern Territory and north Queensland.
Screening for problem drinking is also recommended (see Alcohol Prevention of problem drinking).
Biological markers of suicide risk have also been explored. Low cholesterol (from natural means or
reduced by medication) has been implicated as a marker of suicide risk through epidemiologic and
animal studies,
22
but application to clinical practice requires further investigation.
A number of studies in non-Indigenous populations have examined the use of antidepressant
medication in the prevention of suicide and self harm. A recent systematic review of 11 randomised
controlled trials intended to examine the impact of such medication on death (in those with both
schizophrenia and depression). However, suicide or other deaths were not reported by any of the trials
as an outcome, due to the uncommon occurrence.
23
Another systematic review included 20 studies examining outpatient and in-patient psychosocial
interventions (of which three were pharmacotherapy) for the prevention of suicide. Most studies found
no difference between intervention and control groups. Antidepressants were ineffective in the
prevention of suicide. The most important conclusion drawn from this review of treatment studies was
that it is unclear how death by suicide among individuals seeking help with suicidal behaviour or
disorders associated with suicidal behaviour can be reduced.
24
This is not to say that antidepressant
medications have no place, as a number of systematic reviews have confirmed they are effective in the
treatment of depression.
25
A further systematic review had the same conclusion with no clear evidence of a reduction in repeated
suicide attempts with interventions that sought to increase compliance with aftercare, or which
guaranteed in-patient shelter in the event of an emergency or psychosocial crisis. Only cognitive
behavioural therapy appeared to significantly reduce the incidence of repeated suicide attempts.
26
The Royal New Zealand College of General Practitioners commissioned a systematic review of the
evidence for the recognition, management and prevention of adolescent suicidal behaviour by primary
care practitioners.
27
Cognitive behavioural therapy and group support was found to be most effective at
preventing suicidal behaviour among young people. An appreciation of cultural factors was clearly
important in both population based and individually targeted interventions.
The most effective forms of psychosocial and physical treatments for self harm remain unclear. A
systematic review of 23 trials reported a trend towards reduced repetition of deliberate self harm
following problem solving therapy compared with standard aftercare. Reduced repetition of self harm
was also observed following the provision of an emergency contact card in addition to standard care,
compared with standard aftercare alone. However, variability in standard aftercare of clients at risk of
repeating deliberate self harm in different countries and regions may influence the relative effectiveness
of such interventions. Other effective interventions included depot use of neuroleptic medication (the
presence of psychosis can increase the risk of suicide) but this intervention should be subjected to
further evaluation. There was no evidence that antidepressants were effective in preventing repetition of
self harm, however, newer drugs (particularly the selective serotonin reuptake inhibitors) require
Suicide prevention
130
investigation and their relative safety in overdose compared to older antidepressants makes them a
preferable first option for self harm vulnerable depressed patients.
28
Importantly, it was reported that
assertive outreach for poorly compliant clients appeared to be a necessary component in maximising
the delivery of any treatment for self harm.
29
Interventions designed to reduce or eliminate alcohol consumption or prevent hazardous use of alcohol
(reported in the international literature) have been evaluated for their impact on the prevention of suicide
and injuries. A systematic review of interventions for problem drinking reported reduced suicide
attempts, domestic violence, falls, drinking related injuries, and injury hospitalisations and deaths, with
reductions ranging 2765%.
30
A systematic review examined the effect of exercise and found that it improved depression.
31
Clearly,
more studies are required in the Aboriginal and Torres Strait Islander context given that few remote
communities have access to recreational facilities (see Vascular health Physical activity).
Suicide prevention strategies must also incorporate community based initiatives that are driven by the
community. Indigenous suicide is not evenly distributed and tends to be concentrated over time in
particular settings. Taking into account the widespread experience of adversity (and risk) among
teenagers and young adults, these facts suggest the importance of the community at risk rather than the
individual at risk in conceptualising intervention.
32
A range of culturally appropriate community based interventions was implemented in Aboriginal
communities on the south coast of NSW. The main focus was to recruit members of the Aboriginal
community who had contact with youth who would identify and support people at risk of suicide and
enhance their access to treatment. Such gatekeeper training empowered Aboriginal communities and
was acceptable to them.
33
Further work is examining if this program enhanced the identification of at-risk
individuals and if referral to treatment and support services was enhanced (D Frank, 14 November
2002).
School based preventive programs for suicide prevention have become common in the USA, although
there is some evidence that they are ineffective and may cause harm.
34
A systematic review from
Canada confirmed that there is insufficient evidence to either support or not support curriculum based
suicide prevention programs in schools and that the risk of harm has not been adequately assessed in
studies to enable a clear judgment.
35
In addition, interventions that influence access to means of suicide, such as reducing the availability of
dangerous medications and removing access to guns
36
and jumping points,
37
are believed to lower the
risk of suicide.
While Australian guidelines recommend that primary health care providers remain vigilant for suicidal
risk factors in people aged 1425 years through opportunistic assessment (by asking questions about
depression and suicidal ideation), the need for repeat assessments is unclear.
The Central Australian Rural Practitioners Association recommends that an Aboriginal and Torres Strait
Islander annual health check should include a general inquiry about life and psychological distress.
38
The Northern Zone Management Unit recommends such enquiries commence at 15 years and be
delivered opportunistically (G Miller, 28 November 2002).
The American Medical Association recommends that all adolescents (1121 years) should be asked
annually about behaviours or emotions that indicate recurrent or severe depression or risk of suicide, in
conjunction with other elements of an adolescent health assessment (eg. screening for alcohol use,
sexually transmitted infections).
39
Suicide prevention
131
In both males and females, death rates due to suicide are 23 times higher among
Aboriginal and Torres Strait Islander peoples than among non-Indigenous Australians.
Most of the suicides occur in people aged 1529 years.
EVIDENCE
Level of
evidence
Increased suicide rates are known to be associated with a range of psychiatric
disorders. There are effective pharmacological treatments for some of these conditions,
particularly for unipolar and bipolar depressive disorders and schizophrenia. However,
these treatments have not been shown to be associated with a reduction in suicide
rates at a population level.
I
A number of psychosocial and cognitive interventions have been shown to be
associated with a reduction in suicidal behaviour among young people. However, these
have not been shown to be associated with a reduction in suicide rates at a population
level.
I
Interventions designed to reduce or eliminate alcohol consumption may lead to a
reduction in suicide attempts.
I
There is no optimal screening method to assess suicidal ideation. Direct questioning
may identify clients who are at risk of suicide and self harm.
IV
Screening adults for depression improves the accurate identification of depressed
patients in primary health care settings and the benefits of screening are likely to
outweigh any potential harms. Screening is recommended in clinical practices that have
systems in place to assure accurate diagnosis, effective treatment, and follow up.
I
The utility of screening instruments for suicidal ideation currently incorporated into
Indigenous health check protocols and school based screening needs further validation.
IV
RECOMMENDATIONS
Evaluate suicide risk by assessing young Aboriginal and Torres Strait Islander clients
for psychological distress opportunistically from 15 years of age. Clinical markers
include their mood and wellbeing. Use specific questioning of those found to be at risk
to identify suicidal ideation. Refer those at risk of self harm to appropriate medical
support and counselling services (see also recommendations in Alcohol Prevention of
problem drinking and refer to the RACGP red book for specific questions on suicidal
ideation).
V
Include a family member in suicide risk assessment of an Aboriginal or Torres Strait
Islander person where possible.
V
Provided effective treatment and follow up are offered to those found to have
depression, screen adults for symptoms of depression by asking clients if:
Over the past 2 weeks, have you felt little interest or pleasure in doing things? and
Over the past 2 weeks, have you felt down or depressed or hopeless?
I

References
1 Edwards RW, Madden R. The health and welfare of Australias Aboriginal and Torres Strait Islander
peoples. Canberra: ABS, 2001;745.
2 De Leo D, Heller T. Suicide in Queensland 19992001. Australian Institute for Suicide Research and
Prevention. Brisbane: Griffith University, 2005.
3 Hunter E. The protracted dawning of the Bran Nue Dae: Aboriginal suicide in social context. In:
Chandler M, Lalonde C, Lightfoot C, eds. A global perspective on problems of identity and suicide in
indigenous minority youth. Mahwah, NJ: Lawrence Erlbaum Associates, 2005 (in press).
4 Moscicki EK. Identification of suicide risk factors using epidemiologic studies. Psychiatr Clin North
Am 1997 Sep;20(3):499517.
5 Harris EC, Barraclough B. Suicide as an outcome for mental disorders: a meta-analysis. Br J
Psychiatry 1997 Mar;170:20528.
6 Parker R, Ben-Tovim DI, op. cit.
7 Hunter E, Harvey D. Indigenous suicide in Australia, New Zealand, Canada and the United States.
Emerg Med (Fremantle) 2002 Mar;14(1):1423.
8 ibid.
9 ibid.
Suicide prevention
132

10 Luoma JB, Martin CE, Pearson JL. Contact with mental health and primary care providers before
suicide: a review of the evidence. Am J Psychiatry 2002 Jun;159(6):90916.
11 Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in
general practice. 5th edn. Melbourne: RACGP, 2001.
12 RNZCGP. Guidelines for primary care providers: detection and management of young people at risk
of suicide, 1999. Available at: http://www.rnzcgp.org.nz/standard_guidelines.php. [Accessed 28 June
2004].
13 ibid.
14 Joiner TE Jr, Pfaff JJ, Acres JG. A brief screening tool for suicidal symptoms in adolescents and
young adults in general health settings: reliability and validity data from the Australian National
General Practice Youth Suicide Prevention Project. Behav Res Ther 2002 Apr;40(4):47181.
15 Westerman, TG. The Westerman Aboriginal Symptom Checklist for Youth (WASCY): a measure to
identify cultural resilience in Aboriginal youth (aged 1317) and risk of suicide, depression and
anxiety. Unpublished doctoral dissertation. WA: Curtin University of Technology, 2002. See also
Proceedings of the Mental Health Promotion and Illness Prevention Symposium, Burswood
Convention Centre, Perth, 1819 March 2002. Available at:
http://www.health.wa.gov.au/mentalhealth/symposium/index.html. [Accessed 28 June 2004].
16 RACGP, op. cit.
17 United States Preventative Services Task Force (USPSTF). Screening for suicide risk. In: Guide to
clinical preventive health services. Baltimore: Williams and Wilkins, 1996; 54754.
18 Delaney P, Raphael B, Wooding S. Suicide and self harm. In: Aboriginal primary health care: an
evidence-based approach, 2nd edn, Melbourne: Oxford University Press, 2003.
19 USPSTF. Screening for depression, 2002. Available at:
http://www.ahrq.gov/clinic/uspstf/uspsdepr.htm. [Accessed 28 June 2004].
20 Ellen SR, Norman TR, Burrows GD. MJA practice essentials. 3. Assessment of anxiety and
depression in primary care. Med J Aust 1997 Sep 15;167(6):328-33.
21 NHMRC. Depression in young people. Clinical practice guidelines. Commonwealth of Australia,
Canberra 1997. Available at: http://www.nhmrc.gov.au/rescinded/pdf/cp37.pdf. [Accessed 9 June
2005].
22 Kaplan JR, Muldoon MF, Manuck SB, Mann JJ. Assessing the observed relationship between low
cholesterol and violence-related mortality. Implications for suicide risk. Ann N Y Acad Sci 1997 Dec
29;836:5780.
23 Whitehead C, Moss S, Cardno A, Lewis G. Anti-depressants for people with both schizophrenia and
depression (Cochrane Review). In: The Cochrane Library, Issue 2, 2002. Chichester: Wiley.
24 Linehan MM. Behavioral treatments of suicidal behaviors: definitional obfuscation and treatment
outcomes. Ann N Y Acad Sci 1997;836:30228.
25 Geddes J, Butler R. Depressive Disorders. In: Clinical evidence Issue 7. London: BMJ Publishing
Group, 2002;86972.
26 van der Sande R, Buskens E, Allart E, van der Graaf Y, van Engeland H. Psychosocial intervention
following suicide attempt: a systematic review of treatment interventions. Acta Psychiatr Scand
1997;96(1):4350.
27 Hider P. Youth suicide prevention by primary healthcare professionals: a critical appraisal of the
literature. Christchurch: The Clearing House for Health Outcomes and Health Technology
Assessment, 1998;1115.
28 Australian and New Zealand clinical practice guidelines for the management of adult deliberate self-
harm. Aust NZ J Psychiatry 38(11/12):86884.
29 Hawton K, et al. Psychosocial and pharmacological treatments for deliberate self harm (Cochrane
30 Dinh-Zarr T, DiGuiseppi C, Heitman E, Roberts I. Interventions for preventing injuries in problem
drinkers (Cochrane Review). In: The Cochrane Library, Issue 2, 2002.
31 Geddes J, Butler R, op. cit.
32 Hunter E, Reser J, Baird M, Reser P. An analysis of suicide in indigenous communities of North
Queensland: the historical, cultural and symbolic landscape. Canberra: the Commonwealth
Department of Health and Aged Care, 1999.
33 Capp K, Deane FP, Lambert G. Suicide prevention in Aboriginal communities: application of
community gatekeeper training. Aust N Z J Public Health 2001 Aug;25(4):31521.
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133

34 Ploeg J, Ciliska D, Dobbins M, Hayward S, Thomas H, Underwood J.A. Systematic overview of
adolescent suicide prevention programs. Can J Public Health 1996 SepOct;87(5):31924.
35 Guo B, Harstall C. Efficacy of suicide prevention programs for children and youth, 2002. Available at:
http://www.ahfmr.ab.ca/hta/hta-publications/ reports/suicide_prevention.pdf. [Accessed 28 June
2004].
36 Conwell Y, Duberstein PR, Connor K, Eberly S, Cox C, Caine ED. Access to firearms and risk for
suicide in middle-aged and older adults. Am J Geriatr Psychiatry 2002 JulAug;10(4):40716.
37 Gunnell D, Nowers M. Suicide by jumping. Acta Psychiatr Scand 1997 Jul;96(1):16.
38 CARPA Standard Treatment Manual Reference Group. CARPA Standard treatment manual. 4th
edn. Alice Springs: CAPRA, 2003.
39 American Medical Association. Guidelines for adolescent preventive services (GAPS). Arch Pediatr
Adolesc Med 1997 Feb;151(2):1238.
Vascular health
134
ADULT HEALTH
VASCULAR HEALTH
Authors
Dr Andrew Boyden, Medical Affairs Manager, National Heart Foundation of Australia
Susan Anderson, National Manager, Food Information Program, National Heart Foundation of Australia
Dominique Cadilhac, Head, Public Health Division, National Stroke Research Institute
Professor Graeme Hankey, Neurologist, Royal Perth Hospital
Dr Erin Lalor, Chief Executive Officer, National Stroke Foundation
Acknowledgments
Professor Lindon Wing, Professor Andrew Tonkin, Professor Joe Hung, Dr Michael Stowasser,
Associate Professor David Sullivan, National Vascular Disease Prevention Partnership, National Heart
Foundation of Australia, National Stroke Foundation
BLOOD PRESSURE
Burden of disease
Hypertension is a risk factor for cerebrovascular disease, ischaemic heart disease, peripheral vascular
disease and kidney disease, with increasing risk as blood pressure (BP) increases and is a major
contributor to the overall burden of disease in Australia.
1
Cardiovascular disease (CVD) is the leading cause of death among the Aboriginal and Torres Strait
Islander population (both male and female) and the rate was three times higher than that for non-
Indigenous Australians in 19971999. Cardiovascular disease explains over 30% of the excess deaths
in the Aboriginal and Torres Strait Islander population and accounts for the highest proportion of excess
deaths. Over half (57%) of these deaths were due to ischaemic heart disease (heart attack, angina), and
a further 18% were due to cerebrovascular disease (stroke). Aboriginal and Torres Strait Islander people
also have an earlier onset of disease so that those aged 2554 years are 712 times more likely to die
from cardiovascular (CV) causes than other Australians.
2
According to various cross sectional surveys that have been conducted in the Australian general
population, there has been a decline in the proportion of the population with high BP (and/or receiving
antihypertensive treatment) over the period from 1980 to 19992000. For men aged 2564 years, this
proportion fell from 45% to 22% and for women 29% to 16%.
3
There is no national data available in relation to BP levels in Australian Aboriginal peoples and Torres
Strait Islanders.
4
However, the 2001 National Health Survey revealed that the onset of hypertension
occurred at least 10 years earlier than for non-Indigenous Australians (based on self reporting of
hypertension) with increases apparent from age 15 years (Figure 4).
5
Vascular health
135
Figure 4. Persons reporting hypertension from the 2001 National Health Survey. Australian
Bureau of Statistics. Reproduced with permission
A prevalence survey of the Kimberley Aboriginal population conducted in 1989 showed that the
prevalence of hypertension was 23 times higher than among Caucasian Australians. In particular,
hypertension in Aboriginal men was apparent at less than 30 years of age. The survey also found that
many Aboriginal people with hypertension remained undiagnosed or poorly controlled. Approximately
80% of those found to be hypertensive were previously undiagnosed. Of those previously recognised as
hypertensive, only in about one-third was the condition effectively controlled.
6
A survey of two country
towns in southeastern Australia has found that hypertension was more prevalent in those of Aboriginal
descent than in people of European descent.
7
A study conducted within an urban Aboriginal community setting found that in the 2564 year old age
group, 27% of males and 26% of females had hypertension. The study showed high levels of risk for
CVD, with 83% of participants at high or highest risk by National Heart Foundation of Australia (NHFA)
criteria. Fifteen percent of men and 6% of women had an absolute risk >15% of a cardiovascular event
within 10 years.
8
The Australian Institute of Health and Welfare (AIHW) reported in 2004 that 2000/100
000 or 2% of Aboriginal and Torres Strait Islander peoples aged 3544 years were hospitalised for heart
stroke and vascular related diseases in 20012002. The average risk for hospitalisation for CV related
disease is at least 2% by the time an Aboriginal or Torres Strait Islander person reaches 35 years.
9
This
is the same level of absolute risk for a CV event as a person with diabetes alone.
10
The Queensland Well Persons Health Check cross sectional population survey conducted in
19982000 (Indigenous Australians >13 years) screened over 3000 people for hypertension. In those
aged 1534 years, 17% of males and 5% of females had hypertension, whereas nearly 50% of those
aged 35 years had hypertension.
11
There is evidence that hypertension and ischaemic heart disease were less common in Aboriginal
populations in the past. In 19511957, the systolic BP in Aboriginal people described as semi-tribal
was less than that seen in prevalence surveys after the 1970s.
12
Hypertension is very common in those with diabetes, thought to be twice that in those without diabetes
and is one component of the insulin resistance or metabolic syndrome, which is common in Aboriginal
populations (see Diabetes prevention and early detection section). Also, it has been shown that
hypertension in clients with diabetes is associated with accelerated progression of both microvascular
(retinopathy and nephropathy) and macrovascular (chronic heart disease, stroke, peripheral vascular
disease) complications.
13
Low socioeconomic status (SES) is also linked with higher mortality rates from hypertension related
diseases such as coronary heart disease (CHD), hypertensive heart disease, stroke and end stage
kidney failure.
14
Hypertension is clearly associated with lower SES, but the magnitude of the difference is only small with
age adjusted mean systolic BP differences of about 23 mmHg between the highest and lowest SES
Vascular health
136
groups. There is little evidence that adverse psychosocial factors associated with low SES cause
chronic elevations in BP.
15
modification*
Nil Yes
blood
pressure
Yes
weight loss
physical activity
low saturated fat,
high fruit and
vegetable diet
moderate alcohol
intake
salt restriction
with high BP
Yes
antihypertensive
medication
Yes
access to
recreational
facilities
psychosocial
mediators
* See Physical activity
Screening
Hypertension is defined as systolic BP of 140 mmHg or greater and/or a diastolic BP of 90 mmHg or
greater, in people who are not taking antihypertensive medication. The diagnosis of hypertension should
be based on multiple BP measurements taken on several separate occasions.
16
Screening for hypertension involves measuring BP with a view towards subsequent lowering of BP.
There is good evidence that the early detection and management of hypertension can prevent CV
morbidity and mortality
17
(see below). The higher prevalence of undiagnosed hypertension, CV morbidity
and early age of onset of hypertension related disease in the Aboriginal and Torres Strait Islander
population supports targeting preventive activities towards this population.
Lowering of BP is effective in reducing stroke incidence and mortality in those with hypertension.
Treatment of hypertension also decreases mortality from CHD in clients with high BP.

The effectiveness
of drug therapy to lower BP and reduce fatal and non-fatal stroke, cardiac events and total mortality has
been demonstrated in a number of systematic reviews of randomised controlled trials.
18,19,20
An overview
showed that lowering BP by 1012 mmHg systolic and 56 mmHg diastolic on average, reduces the
relative risk of stroke by about 40% and of coronary disease by approximately 15%. This relative
reduction in risk is similar, whatever the BP before treatment and the absolute risk of CVD.
21
Lifestyle factors are strongly associated with BP control and an epidemiological association between BP
and excessive alcohol consumption, obesity and cholesterol levels has been reported for one Aboriginal
population.
22
At three or more standard drinks of alcohol per day, studies have consistently shown that
BP increases in direct proportion to alcohol intake, and reducing heavy alcohol consumption will reduce
BP. At lower levels of drinking, the findings are less consistent.
23,24
A recent randomised controlled trial
in the United States (US) showed that dietary sodium restriction in combination with a diet rich in
vegetables, fruits, and low fat dairy products, can lower systolic BP. The effects of sodium restriction
were observed in participants with and in those without hypertension, African Americans and those of
other races, and women and men.
25
However, meta-analysis of trials did not demonstrate significant BP
reduction from salt restriction in those with or without hypertension.
26
Other meta-analysis in
hypertensive subjects showed that sodium reduction reduces systolic blood pressure (SBP) in the
general population by a small amount, but the effect is greater among older, previously hypertensive
subjects.
27
A more recent meta-analysis involving 58 trials of hypertensive persons, showed that
reduced sodium intake (mean reduction of 6.7 g/day for 28 days) dropped SBP by 3.9 mmHg (95% CI:
3.04.8 mmHg) and diastolic blood pressure (DBP) by 1.9 mmHg (95% CI: 1.32.5 mmHg). In 56 trials
of normotensive persons, the effect of reduced sodium intake on SBP was 1.2 mmHg (95% CI: 0.61.8
mmHg) and on DBP was 0.26 mmHg (95% CI: -0.30.9 mmHg). The trials involved subjects aged
2373 years. The results did not support a general recommendation to reduce sodium intake but
reduced sodium intake may be used as a supplementary treatment in hypertension.
28
These results
have evoked criticism because the trials were of too short duration, or because dietary sodium intake
was not lowered sufficiently in the study populations.
29
Vascular health
137
Other lifestyle factors also have important preventive implications. Weight loss and increase in physical
activity have been shown to improve BP control in systematic reviews,
30
but their effects on CV
morbidity and mortality are unknown.
31
The effectiveness of counselling in persuading people to use
these means has not been adequately shown, particularly in the long term. However, even modest
improvements from counselling in primary care could have large public health benefits.
A large randomised controlled trial confirmed that a low saturated and total fat, high fruit and vegetable
diet results in modest reductions in BP.
32,33
Stress management to lower BP has been examined in a number of trials, but meta-analysis did not
confirm a significant reduction.
34
Mediating psychosocial causes of CVD is particularly relevant in
Aboriginal and Torres Strait Islander population in view of the much greater relative deprivation.
The minimum recommended BP screening interval for adults who are not being treated for hypertension
varies according to the initial BP reading. Generally, for those without significant related comorbidities
(eg. diabetes, chronic kidney disease or overt proteinuria), the re-screening intervals should be 2 years
when the initial reading is normal and 1 year when the initial reading is high-normal (see Table 5).
However, many Aboriginal and Torres Strait Islander people have a high absolute risk for a CV event,
the same as for a person with diabetes alone. Coexisting risk factors such as family history of CVD,
smoking, obesity, as well as comorbidity, indicate more frequent BP screening in this population,
commencing at an early age. The RACGP red book identifies Indigenous Australians as those at high
risk for CVD.
35
Testing the BP of Aboriginal people and Torres Strait Islanders at least every 12 months is
recommended in view of the red book recommendation for those with multiple risk factors. It is
important to minimise missed opportunities to screen as clinic visits may be infrequent.
Table 5. Suggested follow up for untreated individuals (!18 years) in relation to various ranges of
blood pressure
36
Systolic (mmHg) Diastolic (mmHg) Action
<120 <80 normal blood pressure (BP) re-check in 2 years
120139 8089 high-normal BP re-check in 1 year. Offer lifestyle advice
140159 9099 confirm within 2 months lifestyle advice
160179 100109 evaluate or refer within 1 month lifestyle advice
>180 >110 evaluate and refer within 1 week (or immediately depending on
clinical situation)
NB: If systolic and diastolic categories are different, allow recommendations for shorter follow up (eg. BP 160/86
evaluate or refer within 1 month)
recommend annual assessment of BP as part of an adult preventive health assessment in all Aboriginal
and Torres Strait Islanders more than 15 years of age. The Royal Australian College of General
Practitioners recommends that BP in the general population should be measured from 18 years, at least
every 2 years. The college also recommends that BP be measured annually in those with multiple risk
factors and every 6 months in those with diabetes or end organ damage.
37
Vascular health
138
The Aboriginal and Torres Strait Islander population has a much higher risk of
developing cardiovascular disease (CVD) and at an earlier age of onset than the
general Australian population. Ischaemic heart disease (also known as coronary heart
disease [CHD]) is a major contributor to mortality and morbidity in this population.
There is also evidence that hypertension is more common, is present from a young
age, and often unrecognised in the Aboriginal and Torres Strait Islander population.
EVIDENCE
Level of
evidence
Treatment of hypertension decreases mortality from CHD and stroke in clients with high
blood pressure (BP).
I
Modification of the following risk factors can reduce BP:
reduction of heavy alcohol consumption
weight loss
an increase in physical activity
reduction in sodium intake may be used as a supplementary treatment in those
with hypertension
smoking.
I
I
I
I
I
The effectiveness of counselling to persuade people to modify risk factors as part of a
preventive health assessment has not been adequately shown, particularly not in the
long term. However, even modest modifications in risk factors resulting from counselling
delivered in the primary health care setting could have large overall public health
benefits.
V
RECOMMENDATIONS
Measure BP of adults (>18 years of age) at every visit (ensuring BP has been
measured at least annually). Screening may commence earlier (from 15 years) in
regions known to have a high prevalence of hypertension from this age. Screen 6-
monthly for those with diabetes or target organ damage.
Follow up those with raised BP detected through screening (see Table 5 for frequency).
V
Provide appropriate counselling to promote physical activity, a healthy diet, moderation
in alcohol consumption and weight control every time a BP is measured in order to
encourage clients to modify risk factors for the primary prevention of hypertension.
V
PHYSICAL ACTIVITY
Burden of disease
The joint Centers for Disease Control and American College of Sports Medicine recommendations have
adopted the following definition of physical activity: any bodily movement produced by skeletal muscles
that results in energy expenditure.
38
Indeed, the majority of health benefits can be gained by performing
physical activities outside of formal exercise programs.
39
Exercise is a subset of physical activity that is
planned, structured, repetitive and purposive for recreation, leisure or fitness.
The current low level of physical activity in the Australian community is of great concern. Only about
46% of the adult Australian population undertakes sufficient physical activity for health benefits.
40
In
1995, 40% of the Aboriginal and Torres Strait Islander population reported no leisure time activity
compared to 34% of non-Indigenous Australians. This is particularly the case in female Indigenous
Australians where physical inactivity was reported in 42% compared to 38% of Indigenous males.
41
The
2001 National Health Survey revealed that no exercise or low level of exercise was reported by 70% of
both Indigenous and non-Indigenous Australians (in the 2 weeks before interview) and this proportion
had not changed since 1995.
42
The Queensland Well Persons Health Check Survey (19982000)
reported that around 60% of Indigenous Australians more than 15 years had reported inadequate levels
of physical activity in the preceding week.
43
The rising focus on overweight and obesity has also given rise to greater focus on physical activity.
44
Lack of physical activity is a major risk factor in heart, blood vessel disease and diabetes and evidence
of the cardio-protective role for physical activity is compelling.
45
Vascular health
139
modification
Nil Yes
enquiry for
levels of
activity
Yes
advice and
resources
according to
individuals
readiness for
change
Nil Yes
community sport
and leisure
infrastructure to
encourage
increased
participation
Screening
Ascertaining the level of physical activity undertaken by clients within a primary health care setting is
necessary in order to tailor specific information on the role and barriers to physical activity. Such an
enquiry may not necessarily be defined as screening although this term is used here, as it is part of a
process to identify a potentially unrecognised risk factor.
Recent large scale trials have made it very clear that physical activity can prevent diabetes.
46,47,48,49
Regular physical activity increases insulin sensitivity and improves glucose tolerance, in a range of
ethnic groups.
50
It has beneficial effects on the risk factors associated with the metabolic syndrome, so
that it may prevent cardiovascular disease (CVD). The effect of physical activity in overweight
individuals has been shown to be beneficial even if they remain overweight.
Morbidity and mortality have been shown in prospective cohort studies to be lower in individuals who are
physically active even if they remain overweight, possibly because of normalisation of metabolic
profiles.
51
The concept of metabolic fitness as opposed to physical fitness has been used to describe
the accrued benefits of intermittent physical activity.
Moderate to high levels of physical activity reduce the risk of non-fatal and fatal coronary heart disease
(CHD) and stroke as shown in several systematic reviews of observational studies.
52
A large case
control study has shown that physical activity was protective against the development of acute
myocardial infarction in clients with diabetes as well as other risk factors. Importantly, although a dose-
risk relationship was evident, the protection exerted by moderate intensity exercise was similar to that
from vigorous exercise.
53
This is an important point, as moderate intensity activities are more likely to be
sustainable in the long term. It is believed that intermittent activity also confers substantial benefits, so
activity can be spread over the day. Indeed, the majority of health benefits can be gained by performing
physical activities outside of formal exercise programs.
54
Physical activity can increase the risk for sudden death, but this risk in the individual is outweighed by
the benefits.
55
Healthy Aboriginal sportsmen aged 1537 years in the Northern Territory (NT) had a 40
times higher risk of sudden death than their non-Indigenous counterparts in Victoria in a cases series
from 19821996.
56
All deaths occurred in the hottest time of the year, and were attributable to
underlying ischaemic heart disease. However, heat stroke can cause myocardial injury through diffuse
microvascular thrombosis.
57
Clinical discretion is required in applying physical activity recommendations
to Aboriginal and Torres Strait Islander clients with pre-existing CHD.
Counselling
There has been very little research conducted on either the determinants of physical activity or
interventions specific to the indigenous Australian population.
There is some evidence from systematic reviews that health provider counselling can increase the
physical activity of asymptomatic and sedentary people. Interventions that encourage moderate rather
than vigorous activity and do not require attendance at a special facility were more successful. Brief
advice from a clinician has been reported to lead to short term improvement in activity, but intensive and
prolonged advice may be more effective.
58
A USA systematic review concluded there was insufficient
evidence to determine whether counselling patients in primary care settings to promote physical activity
led to sustained increases in physical activity. The review included trials that tested 35 minute
counselling sessions in the context of a routine clinical visit.
59
However, linking primary care advice with
individually tailored physical activity regimens and with community based programs may enhance the
effectiveness of primary health care counselling.
60,61
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Many behavioural and attitudinal factors that influence the motivation for and ability to sustain physical
activity have been identified. These may vary by social experiences, cultural background, physical
disability and health status. It is reported that physical activity will be more likely to be initiated and
maintained if the individual perceives a net benefit, chooses an enjoyable activity, feels competent doing
it, can access it on a regular basis, can incorporate it into a daily schedule, feels that it does not
generate financial or social costs that he/she is unwilling to bear, and experiences a minimum of
negative consequences (eg. injury, negative peer pressure).
62
An electronic intervention tool assisting general practitioners (GPs) to undertake assessment of physical
activity, provide an activity prescription and patient information has recently been developed in
Australia,
63
as well as a population health guide for GPs.
64
It is unclear what the optimal strategies are for enhancing physical activity in the Aboriginal and Torres
Strait Islander population, but it is very likely that the effectiveness of counselling will be influenced just
as much by factors such as who delivers the counselling as by the social, cultural and environmental
determinants of reduced opportunities for activity.
Successful counselling is not effective without environmental supports that enable any sustainable
improvements in physical activity. A United States (US) systematic review reported that people will
become more physically active in response to the creation of (or improved) access to places for physical
activity.
65
A summary of interventions for which there was good evidence is shown in Box 11.
Box 11. Recommendations for interventions to increase physical activity issued by the Task
Force on Community Preventive Services (US)
Informational approaches:
Community wide campaigns (eg. community events, mass media communication)
Point of decision prompts to encourage using stairs (eg. posters in stairwells).
Behavioural and social approaches:
School based physical education
Social support interventions in community settings (eg. setting up a buddy system or contracting
with another person to complete specified limits of physical activity)
Individually adapted health behaviour change (eg. individually tailoring programs, goal setting,
readiness for change).
Environmental and policy approach:
Creation of or enhanced access to places for physical activity combined with informational outreach
activities (eg. building facilities, walking trails, reducing fees to facilities).
Modified from: The Task Force on Community Preventive Services. Guide to community preventive services (The
community guide). Available at: http://www.thecommunityguide.org/pa/default.htm
In many remote and rural Aboriginal communities, community infrastructure surveys have shown
facilities for sporting and recreational activities are lacking. Surveys in remote Aboriginal communities
have reported that Aboriginal people view recreational facilities as a big priority. The Western Australia
(WA) Environmental Health Needs Survey of 1997 of Aboriginal and Torres Strait Islander Commission
(ATSIC) regions reported, for example, the Wunan ATSIC region comprising a large number of
Aboriginal communities in desert regions, that ranked the need for recreational facilities second highest
after road access to and from communities.
66
The Active Australia initiative is a unique collaboration between the sport, recreation, health, local
government, education and business sectors in recognition of the physical and social and emotional
health enhancing effect of moderate level regular physical activity.
67
Initiatives pertaining to the
Aboriginal and Torres Strait Islander populations are linked to the joint ATSIC and Australian Sports
Commission Australian Government Program for the delivery of Indigenous sport and recreation,
namely the national Indigenous Sport Program (ISP). The program was developed to meet the sporting
needs of Aboriginal and Torres Strait Islanders by encouraging access and equity with mainstream
sporting development and specific Indigenous sporting initiatives. The ISP aims to improve Aboriginal
and Torres Strait Islander participation in sport and recreation and comprises 53 Indigenous sport
development officers in each state and territory working within ATSIC regions.
68
For Aboriginal people, strategies that build on connectedness to land, values pertaining to the extended
family and elders, or identifiable role models may suggest suitable activities. Also important are the
physical and social environments that support incidental activity which is done as part of daily life.
People are more likely to participate in physical activity that provides a pleasant environment and
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141
opportunities for social contact.
69
Health providers have a role in linking health advice with locally
appropriate community sport and recreation programs.
The Centre for Aboriginal Economic Policy and Research has reviewed evidence in relation to the social
benefits of youth programs that integrate recreational facilities with education and community
development (Indigenous learning communities). A similar model in the US reported substantial
reduction in substance misuse, violence, improved school attendance and performance.
70
Research in
the NT is currently investigating the social impact of sport and recreational facilities in Aboriginal
communities (G Brennan, 2002).
An Aboriginal community in the Kimberley region of WA initiated a program promoting healthy lifestyle
and after 4 years there were improved reports of uptake of physical activity and lowering of fat and
sugar intake. The modest but important outcomes reflect the importance of environmental change such
as store management and access to recreational facilities. The need to target the young and the
importance of enabling community control to mediate psychosocial determinants of chronic disease is
also a key message.
71
Further research into the determinants of physical activity (barriers and facilitators) including the trialling
of targeted prevention/intervention strategies aimed at promoting increased physical activity among the
Indigenous Australian population is urgently needed.
72
An enquiry regarding the levels of physical activity of Aboriginal and Torres Strait Islander clients should
be part of a regular preventive health assessment. The Australian Governments National physical
activity guidelines for Australians
73
recommend that people include 30 minutes or more of moderate
intensity physical activity (such as brisk walking) on most, if not all, days of the week. These 30 minutes
can be accumulated in shorter bouts such as three 10-minute walks. While this level of moderate
physical activity is recommended for health benefit, more vigorous or sustained levels of activity (for
those who are able and want to do it) can confer additional benefit in terms of cardiovascular health and
weight loss.
Moderate intensity physical activity (at least 30 minutes every day) is recommended by Central
Australian Rural Practitioners Association and the Northern Zone Management Unit (from 15 years)
based on the National physical activity guidelines for Australians as part of an annual adult health
check.
74
The Royal Australian College of General Practitioners recommends exercise counselling be
provided to all children and adults, tailored to their health status and personal lifestyles.
75
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There is some evidence that the Aboriginal and Torres Strait Islander population has a
lower level of physical activity than the general population, however, access to
recreational facilities is poor in many Aboriginal communities. Surveys from remote
Aboriginal communities have reported that recreational facilities are regarded as a
priority.
EVIDENCE
Levels of
evidence
Lack of physical activity is a major risk factor in heart and blood vessel disease and
diabetes.
I
Physical activity can prevent diabetes. I
Moderate to high levels of physical activity reduce the risk of non-fatal and fatal
coronary heart disease (CHD) and stroke.
I
Brief interventions within primary health care that are not linked to more intensive
programs may not increase the physical activity of asymptomatic and sedentary people.
I
Creating and enhancing access to places for physical activity may improve uptake of
physical activity.
I
Counselling for physical activity is not effective without environmental supports to
sustain or enable physical activity. In many remote and rural Aboriginal communities,
community infrastructure surveys have shown that facilities for sporting and recreational
activities are lacking. People are more likely to participate in physical activity where
there is a pleasant environment and opportunities for social contact.
III
RECOMMENDATIONS
Enquire into the levels of physical activity as part of a regular preventive health
assessment. Recommend moderate intensity physical activity (such as brisk walking) of
30 minutes or more on most, if not all, days of the week. The total 30 minutes may be
accumulated in shorter bouts, such as three 10-minute walks. Advise that, while this
level of activity is recommended for health benefit, more vigorous or sustained levels of
activity (for those who are able and choose to) can confer additional benefit in terms of
cardiovascular health and weight loss.
II
Advise that increasing physical activity does not necessarily require participation in
structured exercise programs, as health benefits can be gained by increasing the
physical activity of everyday life.
V
Recommend both increased physical activity and modification of food intake for the
management of clients who are overweight and obese. Advise that physical activity
confers metabolic benefits even with a small degree of weight loss (see Obesity and
overweight).
III
Facilitate improvements in physical activity by linking health advice with locally available
and appropriate Aboriginal community sport and recreation programs as well as social
support programs (such as group activities).
V
CHOLESTEROL AND LIPIDS
Burden of disease
In the general Australian population, average total blood cholesterol levels have declined slightly since
1980. In 19992000 approximately 50% of both men and women aged 25 years and over in the general
Australian population, had a total blood cholesterol level above 5.5 mmol/L.
76
There are no national data on blood lipid levels among Aboriginal and Torres Strait Islander peoples,
although some regional data shows that abnormalities are highly prevalent in some northern Australian
Aboriginal populations and can occur at an early age.
77,78
Lipid abnormalities accompany the risk factor
clustering that occurs in the metabolic syndrome. Clustering of hypertriglyceridaemia and low levels of
high density lipoprotein cholesterol (HDL-C) levels is more prevalent in Australian Aboriginal peoples
and Torres Strait Islanders than in the general population.
79
Despite these observations, lipid levels recorded in surveys have been variable depending on the
population studied. For example, a cross sectional survey of an Aboriginal community in central
Australia reported that high total cholesterol levels were apparent from age 2025 years in both men
and women. Of those less than 35 years, 48% of men had total cholesterol levels >5.5 mmol/L,
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143
compared with 68% of men more than 35 years.
80
On the other hand, in a survey of two country towns
in southeastern Australia, the mean total cholesterol levels were higher and low density lipoprotein
cholesterol (LDL-C) levels lower, in people of European descent compared with those of Aboriginal
descent. However, in the same population triglyceride levels were higher in the Aboriginal group
surveyed.
81
The north Queensland Well Persons Health Check Survey (19982000) revealed that 62% of
Indigenous Australians more than 15 years had dyslipidaemia (total cholesterol >5.5 mmol/L and/or
triglycerides >2.0 mmol/L and/or HDL !1 mmol/L and /or LDL "3.5 mmol/L). Of those aged 1534 years,
56% had evidence of dyslipidaemia, as did 77% of men and 67% of women more than 35 years.
82
modification
Nil Yes
serum lipids
Yes
low saturated fat,
high fruit and
vegetable diet
Yes
lipid lowering
therapy
Yes
(see Overweight
and obesity)
The evidence supporting a beneficial effect of lipid lowering in cardiovascular disease (CVD) prevention
has been reviewed recently in Australia and this section is derived from this review.
83
There is good evidence to show that low density lipoproteins are atherogenic and that high density
lipoproteins have a direct protective effect against the development of atherosclerosis. Additionally,
epidemiological data have shown a curvilinear relationship between levels of LDL-C and total
cholesterol (TC) and risk of coronary heart disease (CHD). Furthermore, the concentration of HDL-C is a
strong negative predictor of CHD risk. The relationship between CHD risk and plasma triglyceride has
been more controversial than for cholesterol, although most now also regard this as being independently
related to CHD risk.
Although the risk of death from CHD is increased when the blood cholesterol is elevated, individual total
cholesterol levels are a poor predictor of risk. Whereas lipid levels on their own make only a relatively
small difference to CHD risk, when combined with other risk factors they are very important. The more
risk factors present including diabetes, smoking, family history, hypertension, obesity, and physical
inactivity, the greater the absolute risk and the stronger the indication to detect and treat high blood
cholesterol, as those at highest risk have the most to benefit from lipid modification strategies.
84
Healthy eating and lifestyle interventions
A comprehensive review of the relationship between dietary fat intake and CVD by the National Heart
Foundation Australia (NHFA) found that there was good evidence that an increase in the consumption of
saturated fatty acids is associated with an increase in risk of CHD. Replacing a proportion of saturated
fatty acids with n-6 polyunsaturated fatty acids to achieve a ratio of polyunsaturated to saturated fatty
acids of greater than one will reduce the risk of CHD.
85
Saturated fatty acids raise serum total cholesterol and LDL-C and are the key dietary determinant of
serum cholesterol.
86,87,88,89,90,91
Saturated fatty acids raise HDL-C when they replace carbohydrate in the
diet.
92 ,93,94
Increasing all fats including saturated fatty acids at the expense of carbohydrate, decrease
the fasting concentration of triglycerides.
95
N-6 polyunsaturated fatty acids have been consistently
shown to lower serum total cholesterol and LDL-C and have the greatest triglyceride lowering effect.
96,97
Dietary cholesterol increases total cholesterol and LDL-C but substantially less so than saturated fatty
acids.
98
The DASH (Dietary Approaches to Stop Hypertension) Study in the USA reported significantly reduced
levels of LDL-C and total cholesterol after 8 weeks of a diet low in saturated fat, total fat, cholesterol and
high in fruit and vegetables, when compared with controls. African Americans comprised 60% of the
study group and results did not differ by race.
99
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144
To reduce the risk of CVD, the NHFAs dietary fat recommendations are:
saturated and trans fatty acids together contribute no more than 8% of total energy intake n-6
polyunsaturated fatty acids contribute 810% of total energy intake plant n-3 polyunsaturated fatty
acid intakes be at least 2 g per day at least two fish (preferably oily fish) meals per week are
consumed
a proportion of saturated fatty acids should be replaced by monounsaturated fatty acids as strategy
for reducing the intake of saturated fatty acids, and
people at high risk of heart disease should restrict their intake of cholesterol rich foods.
100
Dietary modelling shows that the emphasis of food based recommendations to achieve the NHFAs
dietary fat guidelines should be on fat modification.
101
The NHMRC Dietary guidelines for Australian adults (summarised in Box 12 below) also recommend fat
modification. See chapter 1.6 in these guidelines for a discussion of the evidence and suggestions for
practices that can be incorporated in everyday life to optimise the fat profile of the diet.
Box 12. Dietary guidelines for Australian adults
102
Enjoy a wide variety of vegetables, legumes and fruits:
eat plenty of vegetable, legumes and fruits
eat plenty of cereals (including breads, rice, pasta and noodles), preferably whole grain
include lean meat, fish, poultry and/or alternatives. Reduced fat varieties should be chosen where
possible
drink plenty of water.
and take care to:
limit saturated fat and moderate total fat intake
choose foods low in salt
limit your alcohol intake if you choose to drink
consume only moderate amounts of sugars and foods containing added sugars.
Prevent weight gain be physically active and eat according to your energy needs
Care for your food prepare and store it safely
Encourage and support breastfeeding
Note: Dietary guidelines for children and adolescents in Australia, incorporating the infant feeding guidelines for
health workers is available at: www7.health.gov.au/nhmrc/publications/synopses/dietsyn.htm
Source: NHMRC Dietary guidelines for Australian adults. Canberra: NHMRC, 2003
The NHFA has also made practical recommendations for dietary changes to improve in a patient
brochure published on its website.
103
These recommendations include advice that intakes of cheese and
ice-cream should be limited to twice per week, and takeaways, cakes and snacks each limited to once
per week.
Other lifestyle risk factors include overweight and obesity and excessive alcohol consumption. Alcohol
consumption (30 g/day) can increase triglyceride levels as shown in meta-analysis of studies involving
healthy men and women who were not dependent on alcohol.
104
Hypertrigylceridaemia has been linked
with the metabolic syndrome, and is now recognised from meta-analyses to be an independent risk
factor for CVD.
105
People with elevated plasma triglyceride levels should be advised to limit their alcohol
intake.
106
A number of meta-analyses concluded that exercise training produced small but favourable
modifications to blood lipids in previously sedentary adults.
107 ,108
A randomised controlled trial recently
showed that exercise can favourably alter lipoproteins even with minimal changes in body weight in
those who were overweight (mean body mass index [BMI] maintained at 29). Lipoprotein improvements
were related to the amount of exercise undertaken and not to the intensity of training. A high amount of
regular exercise comprised the caloric equivalent of 28 km per week of moderate intensity jogging pace
and this had the greatest effect on reducing low density lipoproteins.
109
Therefore the keys to achieving
and maintaining a healthy weight are to enjoy regular moderate intensity physical activity (see Physical
activity) and change eating habits to modify energy intake.
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145
Lipid lowering drugs
The value of cholesterol lowering agents has been demonstrated in both primary and secondary
prevention of CHD.
Several meta-analyses of large randomised controlled trials using HMG CoA reductase inhibitors
(statins) have demonstrated that cholesterol reduction in those without known CVD (primary
prevention) clearly reduced CHD events and cardiovascular (CV) mortality, but not all cause mortality
nor mortality from coronary events.
110
Lipid lowering agents are even more effective in those with known CHD and at high risk for an
ischaemic event (secondary prevention) in the prevention of further coronary events. Several systematic
reviews and large subsequent trials have shown that lowering cholesterol in people at high risk of
ischaemic coronary events substantially reduces the risk of overall mortality, CV mortality, and non-fatal
coronary events. Systematic reviews have established that statins offer the most effective type of
treatment for reducing cholesterol and CV risk.
111
In combined primary and secondary prevention studies statins reduced major coronary events and all
cause mortality.
112
Recent studies have also demonstrated the benefits of fibrates. These trials have
also shown that these interventions are safe.
113
From many studies in primary prevention and in those with pre-existing CHD, a 1.0 mmol/L reduction in
total cholesterol translates into about a 20% reduction in risk of future coronary events.
114
There is evidence that lipid modification prevents stroke in people with known CHD, although its role in
the prevention of stroke in people without CHD, or in the prevention of further stroke remains
unresolved.
115
The large British Heart Protection Study (BHPS) recently demonstrated that lipid
modification with a statin prevents further vascular events including ischaemic stroke in those with
cerebrovascular disease at baseline.
116
In those with both type 2 diabetes and with known CHD, there is good evidence that lipid modifying
therapy markedly reduces the risk of further CHD events. Many trials have not been adequately
powered to clearly determine the effect of lipid lowering in those with type 2 diabetes for the primary
prevention of CHD. However, studies (SENDCAP and BHPS) show statistically significant reduction of
CV outcomes (anterior myocardial infarction [AMI] or ischaemia) in healthy subjects with diabetes
following lipid lowering.
117,118,119
Screening
Evidence based guidelines agree that persons with clinically evident CHD and others at high absolute
risk of CHD are likely to derive benefit from reducing elevated cholesterol levels, especially in those with
sufficient life expectancy to realise these benefits.
120
Therefore, it is believed that correcting the lipid
abnormalities detected by screening in high risk groups will lead to a gain in life expectancy. In persons
with a high risk for CHD, cholesterol screening and subsequent reduction of serum cholesterol levels
has the potential to be highly cost effective.
121
However, screening for lipid abnormalities in the general
population is a controversial issue and this is reflected in varied recommendations worldwide.
In Australia, mass screening for lipid levels in the general Australian population, regardless of age, is not
currently recommended. However, regular lipid testing is recommended for all adult Aboriginal and
Torres Strait Islander peoples because, as a group, they are at such high risk of CVD by virtue of non-
lipid coronary risk factors. These include the high frequency of CV risk factors (smoking, family history,
hypertension, obesity, and physical inactivity), and the contribution of CVD to mortality in Aboriginal and
Torres Strait Islander men and women. Prospective cohort studies such as the Framingham study have
shown that the more risk factors present, the greater the absolute risk and the stronger the indication to
detect and treat high blood cholesterol
122,123
(see Ischaemic heart disease).
Testing should begin at an earlier age than that recommended for the general Australian population.
This is due to the earlier age of onset of CHD and of dyslipidaemia (see Blood pressure). It is
recommended that plasma total cholesterol, triglycerides and HDL-C levels should be measured and
LDL-C levels calculated. These tests require a fasting blood sample, with individuals having taken only
water for the previous 12 hours.
In addition to the earlier age of onset of CVD in the Aboriginal and Torres Strait Islander population, the
Australian Institute of Health and Welfare reported in 2004 that 2000/100 000 or 2% of Aboriginal and
Torres Strait Islander peoples aged 3544 years were hospitalised for heart stroke and vascular related
diseases in 20012002. The average risk for hospitalisation for CV related disease is at least 2% by the
time an Aboriginal person reaches 35 years.
124
In Sweden, it was considered cost effective to initiate
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146
lipid lowering treatment if the 5 year CHD risk exceeded 2.4% for men aged 35 years, 2.0% for women
aged 35 years, 4.6% for men aged 50 years and 10.4% for men aged 70 years.
125
This suggests that
the Aboriginal and Torres Strait Islander population more than 35 years of age should be eligible to
commence lipid lowering therapy on the basis of this risk factor alone.
Laboratories should ideally measure lipid levels or general practices accredited by the National
Association of Testing Authorities, as this indicates satisfactory compliance with the standards required
to ensure reliability of these measurements.
126
On the other hand, the use of point of care testing in the
remote setting offers benefits such as prompt client feedback and reduction of problems associated with
long distance transport. The analysers themselves are capable of robust performance, but variation in
operator technique, consumables and adequacy of finger prick samples may undermine performance.
Where resources permit, an ideal compromise can be struck by collecting a venous sample for
measurement in an accredited laboratory, while using an aliquot for point of care testing to provide an
interim result. Quality control issues are important considerations for any use of finger prick tests in
Aboriginal and Torres Strait Islander communities. Management should not depend on finger prick
measurements alone.
Screening children
In order to screen for familial hypercholesterolaemia and familial combined hyperlipidaemia, Australian
guidelines state that clinical and laboratory assessment of CV risk factors, including LDL and HDL-C
levels, should be considered, particularly for children in families in which there is a history of premature
onset of CHD (<60 years in a first degree relative).
127
However, given the high prevalence of CHD of
premature onset within Australian Aboriginal communities, this criterion may not be particularly
discriminating in terms of identifying individuals who carry the additional risk of genetic lipid disorders,
within these communities. Nevertheless, this does draw attention to the need to identify children from
relatively high risk families within the communities so that they can be offered preventive lifestyle
interventions, control of obesity, diabetes, hypertension and/or management of dyslipidaemia at an
earlier age than would otherwise be accessed.
The NHFA recommends that all adults at high risk of CVD should have lipid levels measured at least
annually as part of ongoing assessment and management of this risk. Aboriginal and Torres Strait
Islander peoples are noted to be at high absolute risk of CHD and therefore this recommendation
applies to all adult Aboriginal and Torres Strait Islanders (from 18 years).
128
The RACGP red book
129
recommends 5-yearly lipid screening commencing at 45 years of age. For
those at higher risk of CVD, screening is recommended from 18 years of age. Healthy individuals who
have other CVD risk factors (smoking, hypertension, overweight), first-degree relatives with premature
CVD, or a high (10-15% or more) absolute risk of a CV event in the next 5 years should be screened
based on cholesterol level and level of absolute risk for CVD. Individuals with known diabetes, impaired
glucose tolerance, existing CVD or familial lipid abnormalities should be screened annually.
The Central Australian Rural Practitioners Association recommends screening for cholesterol every 5
years in Aboriginal and Torres Strait Islanders in the NT and central Australia aged 2575 years (non-
Indigenous Australians should be screened at age 4575 years every 5 years). Annual lipid screening is
recommended for people with established blood vessel disease (stroke, heart attack or angina,
peripheral vascular disease), chronic kidney impairment, diabetes, or two or more risk factors (such as
smoking, hypertension, family history of heart attack, overweight, lack of exercise).
130
The Northern
Zone Management Unit recommends screening for hyperlipidaemia in all people with established
chronic diseases (kidney, including microalbuminuria, CHD, other atherosclerotic vascular disease,
hypertension, and diabetes) (G Miller, 28 November 2002).
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147
There is evidence that there is a higher rate of dyslipidaemia in the Aboriginal and
Torres Strait Islander population than in the general Australian population.
EVIDENCE
Level of
evidence
Lowering cholesterol in clients with known coronary heart disease (CHD) reduces risk for
overall mortality, cardiovascular mortality, and non-fatal coronary events.
I
In those without known CHD, lowering cholesterol reduces the risk of cardiac events, but
may not prolong life unless the risk of a cardiac event is high (generally it is in Aboriginal
and Torres Strait Islander peoples. See Blood pressure).
I
Lowering cholesterol in clients with known cardiac disease reduces the risk of stroke. I
Lowering cholesterol in clients with type 2 diabetes (with or without known CHD) reduces
risk of cardiovascular (CV) outcomes such as acute myocardial infarction or angina.
II
A diet low in saturated fat, total fat, cholesterol and high in fruit and vegetables will
reduce the risk of dyslipidaemia.
II
The benefit of lowering cholesterol is greatest in people with the highest baseline risk of
an ischaemic cardiac event. The individuals risk for a cardiac event should influence
decisions on the management of dyslipidaemia.
I
CV risk factors include diabetes, kidney disease, smoking, family history of
cardiovascular disease (CVD), obesity, physical inactivity, and hypertension. The more
risk factors present, the higher the CV risk.
I
RECOMMENDATIONS
Ascertain CV risk status every 12 years, commencing at age 18 years (see Ischaemic
heart disease for advice on ascertaining CV risk. A risk table is available in Appendix 1).
V
Provide dietary recommendations consistent with the National Health and Medical
Research Council Dietary guidelines for Australian adults (see Box 12).
IIIV
Commence lipid screening at 18 years of age and continue annually thereafter. V
Screen lipid status in individuals using fasting blood samples for total plasma cholesterol,
HDL-C and LDL-C levels and triglycerides.
III
Those whose cholesterol levels are raised but who are at low to moderate absolute risk
of CVD should be given dietary and other lifestyle advice, and monitored more closely
over the next year (see also Overweight and obesity, Physical activity, Smoking in the
Respiratory disease Non-communicable section, and Alcohol Prevention of problem
drinking section). Refer to the RACGP red book for recommendations on when to
consider drug treatment for high cholesterol levels.
I
OVERWEIGHT AND OBESITY
Burden of disease
Obesity is an independent risk factor for morbidity and mortality related to coronary heart disease
(CHD).
131,132,133,134
It is associated with risk factors for CHD such as hypertension, type 2 diabetes,
alterations of homeostatic variables, hypertriglyceridaemia and reduced HDL levels.
135,136
There are many factors implicated as a cause of weight gain, including genetic, metabolic, psychosocial
and environmental influences.
137
It has been argued that the dramatic increase in the prevalence of
obesity is primarily due to environmental factors, particularly sedentary lifestyle and consumption of
energy dense diets.
The age adjusted proportion of overweight Aboriginal and Torres Strait Islander men (62%) is little
different from all Australian men (62%). However, from data collected in 1994 almost 25% of Indigenous
Australian males were obese, a rate somewhat higher than that for all Australian men (18%). Almost
60% of Indigenous Australian women were overweight compared to a rate of 49% among all Australian
women. Rates of obesity among Indigenous Australian women were higher at 28% compared with 18%
for all Australian women.
138
A National Health and Medical Research Council (NHMRC) review of Aboriginal and Torres Strait
Islander nutrition described Aboriginal diets as high in saturated fats and sugar, and low in fruit and
vegetables, and that this pattern is reflected in the pioneer foods that Aboriginal people had been
forced to adopt. In all remote communities studied, the intake of fats and sugars was in excess of that
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148
for the Australian population overall.
139
In one remote community, 34% of the caloric intake was from fat
and 10% from protein. However, the carbohydrate consumed was of poor quality, with 30% from refined
sugars (nearly half of which was white sugar) and 26% from complex carbohydrate.
140
The National
Aboriginal and Torres Strait Islander Survey in 1994 estimated that 48% of people aged more than 13
years had a moderate to high sugar consumption and 27% had a moderate to high fat consumption.
141
In one cross sectional survey, the use of dripping to fry foods was more common among rural than
urban Aboriginal or European people.
142
The NHMRC overview revealed that bush foods contribute only
a small proportion of nutrients in many areas, despite a significant preference for them.
Access to a healthy food supply is a major problem for many Aboriginal and Torres Strait Islander
communities. The governmental quarantine restrictions in the Torres Strait have affected traditional food
production, resulting in increased dependence on food from southern producers at increased cost and
markedly decreased quality. In addition, the amount of fruit and vegetables available per person per day
on two islands in 1993 was less than that consumed by the average Australian.
143
Only a very limited
variety of food is offered in remote community stores, relative to larger rural towns and urban centres.
Perishable items such as dairy foods, fruit and vegetables are frequently in short supply.
144
Remoteness results in higher food prices. Numerous surveys have reported significant food price
differentials in remote towns and especially in more remote outstation Aboriginal and Torres Strait
Islander communities from metropolitan regions. Furthermore, many newer Aboriginal communities do
not have a store, which presents additional problems. This may have impacted on unsatisfactory dietary
practices in Aboriginal people which is particularly relevant to the health of children and pregnant
women.
145
In urban regions, food access is affected by low income and inadequate transport.
146
The 1994 National Aboriginal and Torres Strait Islander Survey revealed that 29% of Aboriginal and
Torres Strait Islander persons more than 15 years worried about going without food. Those from rural
areas, and those from households where no one was working or there were one or more dependent
children, were the most inclined to worry.
147
modification
Nil Yes
weight
measurement
body mass
index
waist
circumference
Yes
dietary
advice
physical
activity
advice
Yes
anorectics
drugs that reduce
fat absorption and
selective serotonin
re-uptake inhibitors
Yes
food supply
community
stores
food transport
subsidies
Screening
There is consensus that the periodic health examination of adults in the general population should
include a regular assessment of weight. This is based on the potential public health benefits of even
minor levels of weight loss in those found to be obese who act on advice to lose weight. The test is
simple and inexpensive to implement.
Measures of obesity and overweight
The body mass index (BMI) is the method recommended by the World Health Organisation (WHO)
International Obesity Task Force for determining overweight and obesity.
148
The BMI is a height to
weight ratio calculated as weight (kg) divided by height (m
2
). A BMI of 18.524.9 is normal, 25.029.9 is
classified as overweight, and 30.0 and over is indicative of obesity. While there are currently no cut off
points validated for Aboriginal and Torres Strait Islanders, a BMI cut off point of 22.0 may be more
appropriate as indicative of overweight than 25.0.
149
The BMI is easy to determine and non-invasive, however, it is not sensitive to unusual body fat
distributions or high muscle mass. As a result, the waist-hip ratio (WHR) or waist circumference (WC)
have been used as markers of overweight and recommended for determining obesity related
comorbidities.
Vascular health
149
Waist circumference is recommended for determining obesity related comorbidities and appears easier
to measure (especially by clients themselves).
150
Increased risk of cardiovascular disease (CVD) has
been defined to occur at a waist circumference of "94 cm in men and "80 cm in women.
151
Waist
circumference is measured at a level half way between the superior iliac crest and the rib cage in the
mid-axillary line and not at the maximum point or the umbilicus.
152
Abdominal obesity is often measured as the WHR, calculated as the ratio of waist and hip
measurements: WHR = waist circumference (cm)/hip circumference (cm). The cut off points that may
define increased risk of CVD and all cause mortality range from 0.9 to 1.0 for men and 0.8 to 0.9 for
women.
153
In Australia, cut off points of 0.9 for men and 0.8 for women have generally been adopted.
154
However, the proportion of men and women above these cut off points vary according to the site of
measurement of both waist and hip circumferences, indicating the need for standardisation of
measurement protocols and critical assessment of the cut off levels.
155
The WHO considers that WHR is a useful research tool but that individuals at risk of obesity related
disease can be identified using waist circumference as the initial screening tool.
156
The NHMRC
recommends that for those who wish to be measured, a combination of BMI and waist circumference, or
weight and waist circumference, should be used.
157
Together these can be used as a measure of
relative changes in body fatness over time, and can also be used in assessment of risk of metabolic
complications such as diabetes and CVD (see Table 6).
Table 6. Combining measures to assess obesity and disease risk* in Australian adults
158,159
Disease risk (relative to normal measures) Classification Body mass index
(kg/m
2
) Waist circumference
Men 94102 cm
Women 8088 cm
Waist circumference
Men >102 cm
Women >88 cm
Underweight <18.5 - -
Healthy weight 18.524.9 - Increased
Overweight 25.029.9 Increased High
Obesity 30.039.9 High to very high Very high
Severe obesity >40 Extremely high Extremely high
* Risk of type 2 diabetes and cardiovascular disease
Sources: NHMRC. Clinical practice guidelines for the management of overweight and obesity in adults, 2003, and
Overweight and obesity in adults and in children and adolescents: a guide for general practitioners, 2003
Central obesity as a marker of cardiovascular risk
Central weight distribution appears better linked with excess CV risk than the BMI. Excess body fat
deposited in the abdominal region appears to be associated with increased CV risk in a number of
populations based cross sectional surveys. Waist circumference in both men and women was the
measure most highly correlated with blood pressure (BP) and plasma lipids.
160
Both WHR and WC were
independently predictive of CHD (myocardial infarction or coronary vascularisation) in men and CHD
(non-fatal myocardial infarction or CHD death) in women in prospective cohort studies of men and
women.
161,162
Larger than expected waist circumference (free of the influence of overall heaviness) is
associated with an increased risk of hypertension
163
and type 2 diabetes in women.
164,165
However, in a large cohort of American Indians, central distribution of obesity (waist) was no more
closely related to CHD and its risk factors than was generalised obesity (BMI).
166
Other analyses
showed that the US cut off for waist circumference ("102 cm for men and "88 cm for women) was
sensitive enough to predict comorbidity such as type 2 diabetes in women, but not hypertension in
overweight (BMI 2530) White, Black and Hispanic Americans.
167
Whether the WHR or BMI is a better
indicator of type 2 diabetes risk can vary according to ethnicity. In addition, threshold values for WC can
be population specific.
168
It is unclear what direct contribution weight screening makes to effecting weight loss and to subsequent
morbidity and mortality.
169
Evidence for the benefit of weight loss in disease control is substantial in relation to diseases such as
diabetes.
170
However, there appear to be no randomised controlled trials investigating the effect of
weight loss on mortality.
171
It is difficult to attribute mortality benefits from weight loss in those with
obesity related disease, as weight loss may be unintentional (eg. obesity related cancers).
172
There is evidence from systematic reviews that weight loss can lead to reductions in BP
173
and evidence
from meta-analysis of studies that weight loss can reduce lipids.
174
Vascular health
150
Counselling to promote healthy eating is widely recommended in clinical guidelines.
175,176,177 178 179
Encouraging clients to eat healthier has been shown to change dietary intake according to several
systematic reviews and subsequent trials. A combination of advice on diet and exercise is more effective
than either diet or exercise alone.
180
A low energy diet is the most effective intervention for weight loss.
Further systematic reviews have also shown that weight maintenance programs that involve family
support, or multiple reinforcing strategies (self help peer groups, self management techniques) are also
effective at reducing regain of weight or creating further weight loss.
181
Physical activity is clearly critical in weight loss and maintenance. More weight loss is achieved when
energy intake is reduced along with increased physical activity.
182
Adults should be advised to reduce
their energy intake and increase their energy expenditure.
A recent review of dietary fat and body weight by the National Heart Foundation Australia (NHFA)
indicates that without energy restriction, dietary fat reduction alone will not achieve weight loss in
overweight and obese individuals.
183
Although fat restriction contributes to calorie restriction by reducing
the energy density of the diet (energy density is a measure of the energy provided by a set weight of a
given food or diet, and is determined by the macronutrient carbohydrate, protein, fat, fibre, water and
alcohol composition), the evidence suggests that a dietary fat intake of 3035% energy does not seem
to be associated with excess energy intake. Overall, the effect of dietary fat was small compared to
other risk factors for overweight and obesity, such as physical activity level.
184
Dietary modelling carried out by the NHFA show that reducing the intake of saturated fatty acids tends
also to reduce the total dietary fat intake and thus energy density of the diet. Although energy density
appears to be a major determinant of energy intake, further research is required to determine the
relative effectiveness of manipulating the dietary fat, fibre and water content of foods on reducing the
energy density of the overall diet and whether such strategies are useful for achieving weight loss in
overweight and obese individuals and weight maintenance.
185,186,187,188,189
Food recommendations should be based on an eating pattern which includes a higher proportion of
vegetables, fruit, grain based foods and regular intake of fish, legumes, nuts/seeds, margarine spreads,
a variety of oils, low fat dairy foods and lean meat. Reducing the intake of foods that are high in
saturated fat and high in energy density, such as full fat dairy products, takeaway meals, pastries,
snacks and cakes is recommended.
190
See Box 12 for the NHMRC Dietary guidelines for Australian
adults.
191
The NHMRC Dietary guidelines for Australian adults are pertinent to Aboriginal and Torres Strait
Islander peoples with the addition of two additional recommendations:
Choose store foods that are most like traditional bush foods
Enjoy traditional bush foods whenever possible.
Medications such as appetite suppressants (anorectics), selective serotonin reuptake inhibitors and
reversible long acting inhibitors of gastrointestinal lipases (eg. orlistat to reduce fat absorption) are
effective at achieving weight loss in the short term (up to 9 months).
192
A collection of Aboriginal and Torres Strait Islander community nutrition strategies has been compiled
and summarised by Aboriginal Health Workers (AHWs),
193
or can be extracted from the Australian
Indigenous Healthinfonet.
194
Strategies include school based nutrition education programs, guidelines
for remote store managers, programs for AHWs, teaching manuals, and workshops for AHWs and bush
tucker teachers. Other examples include cooking classes and community based programs that aim to
promote behavioural change through the use of theatre.
Recognition of traditional informal learning strategies is essential for successful health promotion within
Aboriginal populations. Diabetes education camps, such as those for urban Koori people from Victoria,
were described as successful because of the involvement of family members as well as those with
diabetes, with the emphasis on participation.
195,196
The involvement of family or community in programs for lifestyle modification is believed to be an
integral requirement for success in diabetes management for Aboriginal and Torres Strait Islander
populations,
197,198
and is the underlying theme for most Aboriginal and Torres Strait Islander nutrition
strategies. It is extremely difficult for one member of a large extended family to dramatically change diet
Vascular health
151
or stop smoking when everyone else is eating a poor diet and smoking.
199
A clients household must be
involved in dietary and weight loss strategies to improve adherence.
200
Few weight loss or dietary intervention programs for Aboriginal and Torres Strait Islander populations
have been formally evaluated and reported in the published literature. The health promotion of
appropriate diet combined with physical activity in several Aboriginal communities in central Australia
was associated with reduced rates of glucose intolerance over a 7-year intervening period. However,
mean BMI increased significantly rising from 22.8 in 1998 to 24.2 in 1995.
201
In the Kimberley, Western
Australia (WA), involvement in diet and/or exercise strategies was associated with protection from
increases in plasma glucose after 4 years. The mean BMI rose by 1.6 kg/m
2
in those aged 1534 years,
but did not change in those >35 years.
202
An often repeated reason for a lack of success of prevention programs is the failure to incorporate an
intersectoral approach which includes environmental changes to make it easier for clients to incorporate
healthy eating and physical activity into their lives. Sustained behavioural change also depends on
concomitant environmental supports. This is particularly important for Aboriginal and Torres Strait
Islander populations, where a lack of facilities and barriers to accessing facilities are more prevalent.
Food supply
The National Aboriginal Health Strategy (NAHS) recognised the inequity in access to healthy food and
recommended that an adequate range of fresh foods which are low in fat, refined sugars and salt but
high in fibre be available to all Aboriginal people at prices comparable to those in metropolitan areas.
The NAHS also acknowledged that freight subsidies would be necessary.
203
Poor food supply in remote and rural areas continually undermines efforts to address the poor nutrition
and health status of Aboriginal and Torres Strait Islander peoples. Community store and takeaway food
is often nutritionally poor. In many communities community stores are frequently the only source of food
(except for traditional food sources). Therefore, they are an essential service and need to be supported
for this role in the health of the community.
204
Lack of knowledge and adherence to food safety practices during transport, storage and handling of
food can lead to poor food quality, and lack of appropriate cooking and refrigeration are barriers to a
safe and healthy household food supply. Lack of banking and credit facilities in some communities is an
important issue in terms of management of money for the community and the individual.
In recent years, strategies have been introduced to improve remote store food supply, including store
food and nutrition policies, and improved training and management of stores through training and
education, store charters outlining consumers and store operators rights and obligations. However,
coordinated action across all governments is required to improve the range, quality, variety and cost of
food supplies to remote and rural indigenous communities.
205
Community store reforms
The Arnhem Land Progress Association (ALPA), a retail cooperative owned by Northern Territory (NT)
Aboriginal communities, provides 100% freight subsided fruit and vegetables to communities (offset by
increased cigarette prices). This means that the price of fruit and vegetables is set at Darwin prices. The
policy also supports the replacement of certain foods with healthier choices and encourages stocks of
nutritious foods alongside other lines. An evaluation after 3 years of implementation, found the policy
had a significant impact on the consumption of food items which were subsidised, such as fruit and
vegetables (doubling intake per person per day). The communities that stocked the greatest variety
tended to have the highest per capita intake of fruit and vegetables.
206
Store managers can also significantly influence community store food choices. Although Aboriginal
involvement is increasing through employment, management is still generally under the control of non-
Indigenous people, and there is a high turnover in managers which results in variations in food ordering
patterns. It has been recommended that, if Aboriginal and Torres Strait Islander communities were to
take control of factors affecting their health and to bring about sustainable improvements, they would
need to address their dependency on non-Indigenous resource holders, like store managers, which may
preclude community preference and nutritional needs.
207
A NT Aboriginal community developed a strategy in 1989 to encourage consumption of healthy food
through control of store food choices. Reported outcomes included increased fruit and vegetable
supplies and sales, increases in folate levels, and improved blood lipid levels with reduced dietary fat
intake. Over the 12-month intervention period, there was a small decrease in BMI which correlated with
a decrease in total energy intake and the proportion of energy derived from fat. There were decreases in
systolic and diastolic BP, but no significant change in the status of glucose tolerance or any change in
Vascular health
152
insulin sensitivity in the community.
208
After 3 years, the program had produced lasting improvements in
the dietary intake of most target foods (including fruit and vegetables and wholegrain bread).
209
However, the effect of food prices on dietary intake was not controlled. The follow up study did note that
other communities had also shown dietary improvements and that the ALPA nutrition policy (which
includes subsidy of fruit and vegetables) may have contributed.
The National Aboriginal and Torres Strait Islander Nutrition Strategy and Action Plan outlines the
government strategy for addressing nutritional issues.
210
The optimal frequency of weight assessments is unclear. However, most clinical guidelines recommend
regular and opportunistic assessment of weight, BMI and waist circumference for the delivery of regular
preventive advice. Some guidelines have recommended that BMI be measured in clients as the initial
assessment of overweight and obesity, followed by waist circumference as an adjunct to the
assessment of cardiovascular (CV) risk factors such as lipids, blood pressure, diabetes and smoking
status.
211
The National Vascular Disease Prevention Alliance recommends that those with
overweight/obesity have BMI or waist circumference measured every 6 months.
212
Further information on screening, clinical assessment and management of overweight and obesity can
be found in NHMRC Overweight and obesity in adults: a guide for general practitioners (2003).
Threshold values for BMI, WC and WHR are unclear for the Aboriginal and Torres Strait Islander
population. The Central Australian Rural Practitioners Association recommends a BMI 18.524.9 is
normal based on the revised WHO recommendations.
213
The importance of this is mainly for
epidemiological purposes. Some people have a normal BMI, but an unhealthy collection of fat in their
abdomen (thin with a fat belly). People with a waist circumference of more than 100 cm for men and 90
cm for women should be encouraged to lose weight, as if they were overweight. Measurement of a
WHR is not recommended, as it can be difficult to perform
214
.
The Northern Zone Management Unit recommends BMI measurement annually as part of an adult
health check ("15 years) for north Queensland. A healthy BMI is defined as 18.524.9. Annual waist
circumference measurement is also recommended (with normal defined as <94 cm in men and <80 cm
in women), as is an assessment of dietary intake (dietary recall and quantification of fruit and vegetable
intake over 24 hours) (G Miller, 28 November 2002). The Royal Australian College of General
Practitioners recommend an initial assessment of BMI with repeated measures every 2 years
commencing from 12 years in those clients who appear to be overweight or underweight. This is to be
accompanied by a WC measurement in those with an elevated BMI >25.
215
Vascular health
153
There is evidence that rates of obesity in the Aboriginal and Torres Strait Islander
population are higher than in the general Australian population.
EVIDENCE
Level of
evidence
Obesity is an independent risk factor for morbidity and mortality related to cardiac
disease.
III
Without energy restriction, dietary fat reduction alone will not achieve weight loss in
overweight or obese individuals. A reduction in total energy intake remains the main
mechanism by which dietary weight loss may occur.
I
Weight loss can lead to reductions in blood pressure and serum lipids. I
Measures of central obesity such as waist-hip ratio or waist circumference (WC) are
independent markers of increased cardiovascular risk. However, threshold values for
these measures can be population specific.
III
Evidence for the benefit of weight loss in diabetes control is substantial. I
Encouraging clients to eat healthier foods may improve dietary intake. Advice on a
combination of diet and exercise is more effective than either diet or exercise alone.
I
Counselling may not be effective without family and environmental supports that provide
the framework for any sustainable improvements in physical activity and dietary
practices.
V
There is evidence that Aboriginal and Torres Strait Islander communities in remote
regions face significant access barriers to nutritious and affordable food.
III
Food subsidies and healthy food store policies in Aboriginal communities can lead to
increased consumption of healthy food.
III
Medications to effect weight loss (such as anorectics and others) are effective at
achieving weight loss in the short term.
I
RECOMMENDATIONS
Offer measurement of weight, body mass index (BMI) and WC as part of a preventive
health assessment.
V
Use a combination of BMI and WC measures to assess level of risk for type 2 diabetes
and cardiovascular disease, based on threshold values for the general population as
values for the Aboriginal and Torres Strait Islander population are unclear (see Table 6).
III
Offer measurement of WC every 6 months in the presence of overweight or obesity. V
Provide advice on diet and physical activity to those found to be overweight or obese,
consistent with the National Health and Medical Research Council (NHMRC) Clinical
practice guidelines for the management of overweight and obesity.
III
Seek the support of family members to assist in achieving weight loss. Assess obstacles
such as barriers to food supply and consumer options from community stores in each
individual case.
V
Provide advice on physical activity as a component of every weight loss program (see
also Physical activity).
III
Provide dietary recommendations consistent with the NHMRC Dietary guidelines for
Australian adults (see Box 12).
III
ISCHAEMIC HEART DISEASE
Burden of disease
Diseases of the cardiovascular (CV) system are the biggest single cause of deaths and of excess
deaths for the Aboriginal and Torres Strait Islander population.
216
Deaths from coronary heart disease
were 23 times as high among Indigenous Australians as among non-Indigenous Australians in
19961998, with this ratio increasing to 68 times for those in the 2564 year age group.
217,218
The CV death rate for Aboriginal and Torres Strait Islander males aged 3544 years is the same as the
CV death rate in non-Indigenous males aged 5564 years (19962000). Death rates due to CV disease
for Aboriginal and Torres Strait Islander females are also similar to the rates for non-Indigenous people
who are at least 20 years older (see Table 7).
219
Vascular health
154
Table 7. Age specific cardiovascular disease death rates by Indigenous status and rate ratios for
WA, SA, and NT (19962000)
Indigenous rate* Non-Indigenous rate* Rate ratio** Age
group
Males Females Males Females Males Females
<25 10 6 1 1 8.2 6.6
2534 90 48 8 4 12.0 13.2
3544 311 142 24 8 12.8 17.2
4554 698 362 77 25 9.0 14.8
5564 1184 679 262 94 4.5 7.2
6574 2336 1832 939 446 2.5 4.1
75+ 4355 3723 3843 3385 1.1 1.1
* Rates are per 100 000 people
** The rate ratio is the Indigenous rate divided by the non-Indigenous rate
Source: Derived from data provided by the AIHW National Cardiovascular Disease Database and ABS low-series
population projections. Numbers have not been adjusted for the under-enumeration of Indigenous people in death
registrations. As a result, the Indigenous rates and Indigenous:non-Indigenous rate ratios are likely to be under-
estimated by up to 30%
The Australian Institute of Health and Welfare reported in 2004 that 2000/100 000 or 2% of Aboriginal
and Torres Strait Islander peoples aged 3544 years were hospitalised for heart stroke and vascular
related diseases in 20012002. The average risk for hospitalisation for CV related disease is at least 2%
by the time an Aboriginal or Torres Strait Islander person reaches 35 years.
220
The prevalence of undiagnosed ischaemic heart disease (IHD) in the Aboriginal and Torres Strait
Islander population may also be quite high. This is supported by an electrocardiography (ECG)
screening survey undertaken in one Kimberley, Western Australia (WA) population. ECG Q-wave
abnormalities usually taken to be consistent with myocardial infarction (Minnesota coding 1.11.2) were
present in 6.1% of the Aboriginal male population. When additional ECG abnormalities indicative of IHD
were considered, they were more prevalent in the Aboriginal population than had been found for the
Busselton Caucasian population in 1966. Electrocardiography evidence of IHD and infarct was
significantly associated with systolic hypertension in both male and female Aboriginal people
surveyed.
221
There is evidence that the prevalence of undiagnosed coronary heart disease (CHD) even in young
Aboriginal people (<37 years) is high.
222
The rate of autopsy examined sudden death attributable to IHD
was 5.5 times higher for Aboriginal people than for non-Indigenous people in the Northern Territory
(NT).
223
Ischaemic heart disease in the Aboriginal and Torres Strait Islander population may remain untreated for
a number of reasons. In a NT study examining hospital emergency data over 12 months (1 January
1996 31 December 1996), Aboriginal people with myocardial infarction significantly delayed
presentation to hospital emergency departments (significantly greater than non-Indigenous population)
and were younger (by an average of 13 years).
224
Delays in Aboriginal and Torres Strait Islander peoples seeking medical care have been well
documented and are related to a number of socioeconomic and historical factors as well as poor
accessibility and inappropriateness of services.
225
Many Aboriginal and Torres Strait Islander people
avoid or delay accessing mainstream health services,
226,227,228
and delay treatment until very sick which
may be too late.
229,230
(See also Blood pressure for more information regarding burden of cardiovascular
disease [CVD].)
Vascular health
155
modification
Nil Yes
absolute CV risk
assessment
electrocardi-
ography not
recommended
serological
markers not
recommended
Yes
physical
activity
nutrition
smoking
(see
relevant
sections)
Yes
aspirin
lipid lowering
drugs
Yes
timely access
to primary
health care
services
recreational
facilities (see
Physical
activity)
This section describes the evidence supporting the use of screening tests especially through absolute
CV risk assessments and primary prevention of CHD with aspirin. All efforts to detect CV risk factors
and unrecognised CVD presupposes that interventions will prevent disease and deaths. The
effectiveness of modifications in CV risk factors through brief intervention within primary health care or
other means has been described in other sections (physical activity, obesity, kidney disease prevention
and smoking). The effectiveness of treatment of IHD and CV risk factors in the Aboriginal and Torres
Strait Islander population has been described elsewhere.
231
Of critical importance is the strong evidence
that clients who present with ischaemic cardiac symptoms within 12 hours of onset will benefit from
administration of thrombolytic therapy.
232
The effectiveness of treatment of IHD in the Aboriginal and
Torres Strait Islander population has been described elsewhere.
233
This section describes the use of
screening tests and primary prevention of CHD with aspirin.
Screening
Absolute cardiovascular risk assessment
The determination of the absolute risk of CV disease for each client is now widely
recommended
234,235,236
in order to implement effective prevention strategies. However, few studies have
evaluated if communicating global CV risk assessments to clients is an effective aid to influencing
behaviour or adherence to treatment such as aspirin, lipid lowering or antihypertensive medication.
237
An estimate of a persons absolute risk of a CV event
!
over 5 years is possible through the use of tables
developed for this purpose
238
which are accessible on the internet.
239
The overall goal of a CV risk
assessment is to achieve a 5-year CV risk of less than 15%.
240
Aboriginal and Torres Strait Islander clients should be assessed for CVD risk as part of a preventive
health assessment in order to identify risk factors and implement primary prevention. However, the
Framingham population (Caucasian and of European origin) was used to develop absolute risk tables.
The rates of CV disease in these populations are lower than those observed in the Aboriginal and
Torres Strait Islander population at any given age.
Moreover, risk assessment tables do not take into account a range of CV risk factors that are more
prevalent in the Aboriginal and Torres Strait Islander population. These include: BMI >30, first degree
male relatives with CVD (<55 years), first degree female relatives with CVD (<65 years), central obesity,
lack of physical activity, psychosocial stress, and insulin resistance (may be impaired fasting glucose or
impaired glucose tolerance). These factors independently contribute to CV risk and denote a greater risk
than summation of major risk factors in risk assessment tables.
241
Microalbuminuria and overt proteinuria are also independent predictors of CVD and highly prevalent in
the Aboriginal and Torres Strait Islander population. In a remote NT Aboriginal community,
microalbuminuria was found to be independently associated with double the risk of CHD. This makes
microalbuminuria a useful indicator of primary CHD risk, in addition to the conventional risk factors
already described (see also Kidney disease prevention).
242
Low birth weight also appears to predict an increase in CV risk factors (such as hypertension, diabetes
and hypercholesterolemia) in adulthood, as shown in a Swedish population based cohort study of men

! A CV event is defined as new angina, myocardial infarction, coronary death, stroke, transient ischaemic attack,
congestive cardiac failure, and peripheral vascular disease
Vascular health
156
followed until aged 80 years. In this study, the same hazard ratios persisted when only birth weights
from term births were used.
243
A high CV risk score in adulthood following a low birth weight has also
been reported in Aboriginal people.
244
Further cross sectional studies in progress in a NT Aboriginal
community have shown a strong inverse relationship of birth weight with systolic blood pressure and
diabetes (W Hoy, 10 August 2004). In Aboriginal Australians, the contribution of low birth weight to adult
CHD risk is likely to be much more significant than for other Australians given the high prevalence of low
birth weight in Aboriginal Australians (see Child health section).
As conventional CV risk assessment tables do not take these independent risk factors into account, and
in view of their high prevalence in the Aboriginal and Torres Strait Islander population (and low
prevalence in the populations used to derive the tables), they seriously underestimate CV risk in the
Aboriginal and Torres Strait Islander population. A recent analysis of the Framingham CHD risk
estimates applied to an Aboriginal cohort from a remote community in the NT found that the actual
number of CHD events was 2.5 times higher than that predicted when the cohort was followed up over a
period of around 10 years.
245
There is some evidence that the baseline absolute CHD risk can differ in other populations (eg. higher in
south Asians and lower in Japanese), although the relative contributions of individual risk factors to total
risk appear to be similar among all populations.
246
Estimates of a persons relative risk of a CV event are
also accessible and may be useful across populations.
247
Certain clients have very high risk for a CV event and this can be determined by history alone without
using the risk assessment tables. The absolute risk for a CV event is very high (>20% in 5 years) for
clients with existing symptomatic cardiovascular disease or history of a CV event (angina, anterior
myocardial infarction [AMI], angioplasty, coronary artery bypass grafts, transient ischaemic attack (TIA),
ischaemic stroke or peripheral vascular disease). People with diabetes who have overt proteinuria
(diabetic nephropathy) and those with hereditary lipid anomalies also have a very high absolute risk for
CV disease (>20% in 5 years).
248,249
Maori and Pacific Islanders have higher rates of CVD and at earlier ages than the rest of the population,
similar to the Aboriginal and Torres Strait Islander population. Despite the underestimation of CV risk for
these population groups, the New Zealand Guidelines Group have recommended conventional CV risk
assessment tables still be used, provided corrections to the score are made. It is recommended that CV
risk assessment commence 10 years earlier than for the general population (ie. from 35 years instead of
45 years). However, the nature of the cohort data means that risk assessment tables are not applicable
to people less than 40 years. As a consequence, it is recommended that when using the tables, risk
scores for people in these population groups should be moved up one risk category (ie. an increase of
5% CV risk over 5 years). Clients with a CV risk above 15% in 5 years should have an annual CV risk
assessment, otherwise 5 yearly assessments are indicated.
250
The New Zealand Guidelines Group also recommended that those with diabetes and microalbuminuria
should have their CV risk measured and be moved up one risk category (5% increase in risk). However,
the Australian National Prescribing Service have categorised diabetics with microalbuminuria as having
a > 20% risk over 5 years (the same as those with overt proteinuria).
251
They reasoned that few
diabetics with microalbuminuria would have lipid profiles and BP low enough to put them under 15% CV
risk. Once the 5% risk correction was made, this would place most of these clients in the >20% risk
category anyway.
There is currently insufficient information on which to base recommendations regarding the corrections
needed if conventional CV risk assessment tables are used to estimate CV risk in Indigenous
Australians. There is also an absence of Australian guidelines on this issue, although the National
Vascular Disease Prevention Alliance of Non-Government Organisations is currently considering this
matter. The similarities in CV risk between Indigenous Australians and the Maori population, suggests
that GPs should adopt similar approaches as recommended by the New Zealand Guidelines Group to
assess the CV risk of Aboriginal and Torres Strait Islander clients.
However, the issue is complicated given a recent study showed that Aboriginal womens risk of CHD is
not significantly lower than Aboriginal men. As the study was conducted in a remote NT Aboriginal
community involving nearly 900 people, the authors reported that it is not clear why the female
protective effect did not exist in this population. It remains to be verified whether the female
disadvantage is a general phenomenon in other Australian Aboriginal populations.
252,253
This suggests
that the CV risk assessment tables for females should not be used for Aboriginal women. Applying the
conventional tables to Aboriginal females will underestimate the risk of CHD. The observed CHD rate
was 30 times the predicted rate, when recently applied to a NT cohort of Aboriginal women.
254
Vascular health
157
The issue is made more complex by the possibility of substantial regional variations in the CV risk profile
of the Aboriginal and Torres Strait Islander population, not unlike that reported for end stage kidney
disease.
255
Electrocardiography
Electrocardiography is the principal screening test for IHD used by primary health care providers. The
sensitivity of Q-wave abnormalities on ECG with the Minnesota codings for myocardial infarction (MI)
has been reported as 43% with a specificity of 94%, using autopsy proven MI as the gold standard in a
10-year prospective Japanese survey. With a low population prevalence of IHD, the use of an ECG as a
screening test has a very low positive predictive value of 0.5% (very few who test positive will actually
have the disease).
256
In the Aboriginal population, using the prevalence estimate of 6% (the prevalence
may well be higher in a population of those with diabetes), the positive predictive value of an ECG even
for screening purposes is 31%.
257
Routine ECG screening has not been recommended in a number of clinical guidelines.
258
Whether the
general adult Aboriginal population should be offered ECG screening as part of a preventive health
assessment has not previously been explored.
While the initial assessment of target organ damage in Aboriginal and Torres Strait Islander clients with
diabetes should include an ECG because of the risk of silent ischaemia and high prevalence of pre-
existing CHD,
259
there is insufficient evidence to recommend an ECG as part of a preventive health
assessment for the Aboriginal and Torres Strait Islander population as a whole.
Serological markers of CV risk
There are around 250 or so risk factors reported for CHD, some of which include serological risk factors
such as elevated homocysteine (an amino acid), elevated lipoprotein (a)
260
and C-reactive protein.
261
Raised levels of homocysteine in the blood have been shown to be associated with increased risk of
coronary, cerebral and peripheral vascular disease. This relationship seems to be particularly marked in
those with vascular disease not explained by conventional risk factors.
262
Risk estimates have been
shown to be higher in cross sectional than in prospective studies.
263,264
The summary odds ratio linking
homocysteine to CHD in 26 case control studies was 1.7 (95% CI: 1.51.9) in a systematic review.
265
Raised homocysteine may promote atherosclerosis by promoting smooth muscle growth, endothelial
dysfunction and possibly thrombosis.
266
Few studies have reported the prevalence of raised homocysteine levels in the Australian population. A
cross sectional survey involving 365 urban Aboriginal people and Torres Strait Islanders in Queensland
reported high plasma levels of homocysteine in 24% of subjects (mean age 42 years) which were are
associated with a history of vascular disease, smoking, and folate and vitamin B12 nutritional
deficiency.
267
While it is known that folate supplementation reduces homocysteine levels in most
subjects, and this raises a potential therapeutic option particularly for individuals who have raised
homocysteine and vascular disease,
268,269
there is currently no data from randomised controlled trials
that demonstrate benefits of folate or vitamin B supplementation in the prevention of CVD, although
trials are in progress. A number of nutrition intervention programs in Aboriginal communities have
reported successful elevation of folate and vitamin B levels. A diet rich in fruit and vegetables will
elevate folate levels.
270
Management of lipoprotein (a) may favourably influence atherosclerotic progression, but further
research to establish benefit is necessary.
271
Similarly, more data regarding the clinical usefulness of C-
reactive protein assessments is needed.
272
No clinical practice guidelines currently recommend these or other serological markers of CHD risk, as
targets of therapy. Screening for homocysteine, C-reactive protein or other serological markers as part
of the preventive health assessment of Aboriginal and Torres Strait Islander population is not currently
recommended.
Chemoprophylaxis
Aspirin
For people with known CVD, the substantial benefits of aspirin in terms of preventing further events and
reducing mortality are well established.
273,274,275
Aspirin reduces the risk of thrombosis within blood
vessels but its use is associated with side effects including minor gastric bleeding, an increased
tendency to bruising, allergic reactions and a slightly increased risk of more significant bleeding
(haemorrhagic stroke, major gastrointestinal bleeding).
276
Contraindications to its use such as active
Vascular health
158
peptic ulceration, allergy to aspirin or other non-steroidal anti-inflammatory drugs and bleeding disorders
still need to be considered before prescribing in this group.
The use of aspirin for the primary prevention of CVD is more controversial. Most of the large studies on
which recommendations are based have been conducted in middle aged male populations and no
studies have assessed specifically the use of aspirin within the Aboriginal and Torres Strait Islander
population. In relation to prevention in those without manifest CVD, a meta-analysis provided a risk
benefit summary according to levels of CHD risk (see Table 8) and concluded that aspirin is probably
beneficial for those at high-risk of CHD in a 5-year period. It also examined rates of haemorrhagic
strokes and gastrointestinal bleeding secondary to the use of aspirin.
277
Table 8. Estimated benefits and harms of aspirin therapy for patients at different levels of risk for
CHD events*
Outcome Estimated 5-year risk for CHD events at baseline
1% 3% 5%
Effect on all cause
mortality
No change No change No change
CHD events avoided (n) 3 (14) 8 (412) 14 (620)
Haemorrhagic strokes
precipitated (n)
1 (02) 1 (02) 1 (02)
Major gastrointestinal
bleeding events
precipitated (n)
3 (24) 3 (24) 3 (24)
* Estimates based on 1000 patients receiving aspirin for 5 years and a relative risk reduction of 28% for CHD events
in those who received aspirin. CHD events = non-fatal acute myocardial infarction, fatal CHD. Values in
parentheses are 95% CIs. The following caveats apply to these estimates:
Reduction in CHD risk may be smaller in women, but data is limited
For elderly persons, absolute risk for hemorrhagic stroke and major gastrointestinal bleeding may be 23
times higher in patients receiving aspirin. However, aspirin may provide benefit in elderly persons by
reducing ischemic stroke, the incidence of which increases with age. Aspirin does not appear to improve
incidence of ischemic stroke in middle aged patients
Risk for hemorrhagic stroke may be greater with larger doses of aspirin
Aspirin may not prevent myocardial infarction in patients with uncontrolled hypertension (systolic BP >150
mmHg)
Long term outcomes (>57 years) are unknown
Patients at high risk ("10% 5-year risk) may derive greater benefit from aspirin, including a 1520% reduction
in ischemic stroke and all cause mortality, because their risk is similar to that of patients with known CHD.
Extracted from: Aspirin for the primary prevention of cardiovascular events: a summary of the evidence for the US
Preventive Services Task Force, 2002
It was concluded that aspirin appears to reduce the risk of future CHD in patients with well controlled
hypertension.
278
Data in relation to aspirin use in diabetics is limited because the proportion of diabetics in the major
studies has been small. However, based on the analysis of available information, the US Preventive
Services review suggested that diabetics benefit at least as much as non-diabetics from the use of
aspirin.
279
Australian recommendations are that people with type 2 diabetes who do not have
contraindications should be considered for prophylactic aspirin therapy (75325 mg/day).
280
A review of trials that studied aspirin doses over the range of 75325 mg/day has concluded that no
greater clinical benefit in terms of CVD prevention is achieved with dosage above the range of 75160
mg/day, with gastrointestinal bleeding and peptic ulceration side effects lowest at 75 mg.
281
National Health Foundation of Australia guidelines state that it is reasonable to use low dose aspirin in
those hypertensive patients whose BP is well controlled, and who are at high risk for CHD and are not
particularly at risk of gastrointestinal or other bleeding.
282
The New Zealand Guidelines Group
recommends that everyone with a 5-year cardiovascular risk greater than 15%, should be started on low
dose aspirin (75150 mg/day) if there are no contraindications.
283
The use of aspirin does not substitute for the management of existing risk factors such as tobacco use,
obesity, physical inactivity, dyslipidaemia, hypertension, or metabolic syndrome. Before aspirin is
prescribed for primary prevention, the overall risks to the individual should be considered, efforts should
be made to alter risk factors and the person should be fully aware of the advantages and disadvantages
of therapy.
284
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159
Lipid lowering drugs
The evidence underpinning the use of lipid lowering drugs in the primary and secondary prevention of
CHD has been described elsewhere (see Cholesterol and lipids section). The determination of the
absolute risk of CVD for each client is now widely recommended as a mechanism to better target the
prescription of lipid lowering drugs.
The Pharmaceutical Benefits Advisory Committee (PBAC) has recently reviewed prescribing restrictions
for lipid lowering drugs under the General Statement for Lipid Lowering Drugs Prescribed as
Pharmaceutical Benefits. The outcome of the review was not released at the time of writing. The PBAC
was advised by an expert forum on 29 April 2004 that Aboriginal and Torres Strait Islander clients:
have a distinct CV risk profile which require specific provisions in the criteria used to approve PBS
subsidy for lipid lowering drugs
with diabetes should be eligible for PBS subsidy of these lipid lowering drugs at any cholesterol
level in recognition that the risk for CV events is considered to be equivallent to that of patients
with symptomatic CHD
without any conventional CV risk factors should be eligible for Pharmaceutical Benefits Scheme
(PBS) subsidy of these lipid lowering drugs, if the total cholesterol level is >6.5 mmol/L, in
recognition that the risk for CV events is considered to be similar to other risk factors (A Platona,
10 August 2004).
The advice to the PBAC was made in view of existing CV risk tables underestimating CV risk in
Aboriginal and Torres Strait Islander clients. If the PBS restricted access to lipid lowering drugs based
on conventional risk assessment tables for all Australians, then Aboriginal and Torres Strait Islander
clients would be at risk of under treatment.
To achieve parity with other elements of a preventive health assessment, a CV risk assessment of an
Aboriginal or Torres Strait Islander client should be repeated 12 yearly and commence from age 35
years in both males and females.
Conventional CV risk assessment tables could mislead practitioners by underestimating risk in
Aboriginal and Torres Strait Islander clients. In the near future, Aboriginal cohort studies in progress
may better inform if CV risk estimates should be doubled, increased by 5% or if the charts should be
used by projecting upward by aged 20 years.
As in those with a past history of CV events, all Aboriginal and Torres Strait Islander clients with
diabetes, microalbuminuria (>3.4 mg/mmol or >30 mg/day) or overt proteinuria, should be considered at
high risk for CVD (>20% risk over 5 years).
The Australian National Prescribing Service has adapted the New Zealand Guidelines Group risk charts
with an Australian recommendation to increase CV risk level by one colour category for Aboriginal and
Torres Strait Islander clients.
285
The Central Australian Rural Practitioners Association recommend that
a preventive health assessment for vascular disease prevention in the Aboriginal and Torres Strait
Islander population include assessment for family history of illness such as diabetes, heart or kidney
disease, any specific symptoms of heart disease, and lifestyle questioning including smoking, exercise
and nutrition.
286
Recommendations for a structured CV risk assessment as part of an adult health check
are currently lacking from north Queensland (Northern Zone Management Unit and in RACGP
guidelines. An ECG as part of an adult health check in north Queensland is not recommended (G Miller,
28 November 2002).
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160
Deaths from coronary heart disease (CHD) were 23 times as high among Indigenous
Australians than in non-Indigenous Australians in 19961998, with this ratio increasing to
68 times for those in the 2564 year age group. Death rates due to cardiovascular disease
(CVD) for the Aboriginal and Torres Strait Islander population are similar to non-
Indigenous people who are at least 20 years older.
EVIDENCE
Level of
evidence
It is possible to estimate a persons absolute statistical risk over 5 years of a
cardiovascular (CV) event (eg. new angina, myocardial infarction, coronary death, stroke
or transient ischaemic attack [TIA]). This may be done through the use of risk
assessment tables (see Appendix 1) developed from longitudinal cohort studies for this
purpose. The CV risk assessment tables are also available at:
http://www.nzgg.org.nz/guidelines/0035/CVD_Risk_Chart.pdf. The tables use information
on sex, age, smoking status, the presence of diabetes, blood pressure and lipid status to
assess risk.
A calculator to estimate risk of CV related death is available at:
http://www.riskscore.org.uk/calculator.html.
III
Conventional absolute CV risk assessment tools will underestimate absolute CV risk
status in Aboriginal and Torres Strait Islander clients. This is because of under
representation of high risk population groups in cohort studies, and a range of CV risk
factors which are not accounted for in the tools, but which are highly prevalent in the
Aboriginal and Torres Strait Islander population.
V
In those with existing symptomatic CVD or history of a CV event (angina, anterior
myocardial infarction, angioplasty, coronary artery bypass grafts, TIA, ischaemic stroke
or peripheral vascular disease), the absolute risk for further events is very high (>20% in
5 years) and the risk assessment charts no longer apply. CV risk is determined by history
alone.
III
Risk assessment tables may underestimate risk in certain groups: those with body mass
index >30, those with first degree male relatives with CVD aged less than 55 years, those
with first degree female relatives with CVD aged less than 65 years, those with central
obesity, those lacking of physical activity, in cases of psychosocial stress, and those with
impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT). The lack of data
on the quantitative contribution of these additional risk factors means that clinical
judgment is required to estimate an individuals incremental CV risk.
V
A cohort study in the Northern Territory showed that Aboriginal womens risk of CHD is
not significantly lower than Aboriginal men. This suggests that conventional CV risk
assessment tables for females are invalid when applied to Aboriginal women.
III
There is good evidence that aspirin should be commenced in those who have already
experienced a CV event (this is an example of secondary prevention). However, many
will also have pre-existing contraindications to aspirin use. Contraindications to the use of
aspirin include peptic ulceration, bleeding disorders and allergy to aspirin or other non-
steroidal anti-inflammatory drugs.
I
Clients at high risk of CVD ("10% over 5 years risk) may derive a benefit from aspirin,
including a 1520% reduction in ischaemic stroke and all-cause mortality, because their
risk is similar to that of clients with known CVD. This is an example of primary prevention.
I
There is evidence that the Aboriginal and Torres Strait Islander population may not be
accessing timely treatment for ischaemic heart disease (IHD).
IV
An elevated blood level of homocysteine is a marker of risk for CHD but the benefit of
testing for homocysteine as part of a preventive health assessment has not been
established.
I
Elevated levels of homocysteine have been reported in Aboriginal and Torres Strait
Islander peoples with risk factors for vascular disease.
III
RECOMMENDATIONS
Inform clients that the overall goal of a CV risk assessment is to achieve a 5-year CV risk
of less than 15% through appropriate management.
V
Inform clients with a past history of CVD and/or diabetes with microalbuminuria or overt
proteinuria of their high risk for a CV event (>20% over 5 years) and the need for
appropriate lifestyle and medication management.
III
Assess for individual CV risk status from 18 years of age by determining a previous
relevant diagnosis or by the presence of the following: diabetes, hypertension, family
history of early CV events (<55 years of age), hyperlipidaemia, overt proteinuria,
smoking, obesity (especially centralised) and sedentary lifestyle. Repeat assessments
every 12 years.
V
Vascular health
161
smoking, obesity (especially centralised) and sedentary lifestyle. Repeat assessments
every 12 years.
If conventional CV risk assessment tables (see Appendix 1) are used to ascertain an
individual CV risk score in Aboriginal and Torres Strait Islander clients, the following
corrections should be considered:
tables can be used from age 35 years
tables for females may not apply to Aboriginal women
adjust the CV risk upwards. Clinical judgment is required to estimate the incremental
cardiovascular risk incurred.
V
It is not recommended to conduct an electrocardiograph as a screening test for IHD. V
It is not recommended to measure homocysteine levels as part of a routine preventive
health assessment.
V
Offer appropriate and individualised advice to all clients who are at high risk, or who have
a history of CV events (see above). Include descriptions of the symptoms of IHD and the
vital importance of medical attention in the first few hours of such symptoms.
V
Provide advice related to the reduction of lifestyle risk factors (see Overweight and
obesity, Physical activity, Smoking in the Respiratory disease Non-communicable
section, and Alcohol Prevention of problem drinking section).
III
Consider low dose aspirin therapy (75 mg/day) in well controlled hypertensive clients who
are at high risk for CHD (especially if there has been a previous CV event and/or the 5
year CV risk is greater than 15%).
V
STROKE PREVENTION
Burden of disease
Stroke is a significant public health problem in the Aboriginal and Torres Strait Islander population, as
indicated by data from Western Australia (WA), South Australia (SA) and the Northern Territory (NT).
287
Although precise estimates of the incidence and prevalence of stroke in this population are not known,
there is reasonable data about outcome.
The stroke mortality rate is significantly higher in Aboriginal populations than in non-Indigenous groups
making it one of the most serious of the vascular diseases for this population. In 19941996 in WA, SA
and the NT, the age standardised Aboriginal mortality rates from stroke were 2.4 and 2.2 times higher
than for non-Indigenous males and females respectively.
288
The mortality rate associated with stroke
among Aboriginal and Torres Strait Islanders was twice the rate of non-Indigenous people in 19961998
and in younger people (2564 years) the mortality rates were up to eight times higher.
289
Stroke also affects Aboriginal and Torres Strait Islander peoples earlier than those from a non-
Indigenous background. In the Aboriginal and Torres Strait Islander population, the 4564 year age
group represents the section of the community who are most affected by stroke. The age group most
affected in the non-Indigenous population consists of those people over 65 years, with a median age of
stroke of 76 years.
290,291
A 5-year retrospective review of Aboriginal patients with stroke in a Perth
teaching hospital (19881992) indicated the mean age of the patients was 53 years and 41% had
diabetes. The prevalence of other modifiable risk factors was relatively high (hypertension 40%,
smoking 67%, hypercholesterolaemia 60%, alcohol abuse 49% and atrial fibrillation (AF) 22%).
292
Risk factors for stroke
Many of the risk factors for stroke are common to the other vascular diseases such as coronary heart
disease (CHD) and peripheral arterial disease. Therefore, several stroke prevention strategies are the
same as for other vascular disease (eg. smoking cessation, BP and cholesterol lowering, and diabetes
control). However, AF and transient ischaemic attack (TIA) (mini strokes where symptoms do not last
longer than 24 hours) are important indicators of increased risk of stroke.
Atrial fibrillation is responsible for up to 20% of all ischaemic strokes. It is prevalent in approximately 2%
of the general population and approximately 5% of people older than 65 years.
293,294
For individuals with
AF, the risk of stroke averages 5% per year, which is 56 times greater than for those with a normal
heart rhythm of the same age.
295
The prevalence of AF in the Aboriginal and Torres Strait Islander
community is not clear although the prevalence of major causes of AF (ischaemic heart disease [IHD],
hypertension, rheumatic heart disease and diabetes) is higher in this population. Although studies from
the United States of race ethnic differences in stroke risk factors have reported that Caucasians had a
Vascular health
162
greater prevalence of AF than African Americans and Caribbean Hispanics, this may be due to the
greater longevity of Caucasians. However, it suggests that ethnic differences do exist and are important
in the planning and targeting of prevention programs for stroke.
296
Although TIAs of the brain and eye result in neurological deficits which resolve within 24 hours, they are
associated with an increased risk for stroke of approximately 1012% in the first year after a TIA.
297
In
addition, the risk of a coronary event following a TIA is increased 35% per year.
298,299
The incidence of
TIA in the general population is about 50 per 100 000.
300
The incidence of TIA in the Aboriginal and
Torres Strait Islander community is unclear. However, given the high rates of stroke incidence and
mortality compared with non-Indigenous people, the rates of TIA would be expected to follow a similar
pattern.
Preventive interventions for AF and TIA are provided below. Preventive measures related to the other
vascular risk factors hypertension, smoking, diabetes, physical inactivity, hypercholesterolaemia, and
alcohol consumption are discussed elsewhere.
modification
Nil Yes
interview and
assessment
AF
check pulse
12 lead ECG
TIA
clinical history
Yes
modifiable
risk factors
(see relevant
sections)
Yes
AF
anticoagulant (high
to moderate risk)
aspirin (low risk)
TIA
treat causal risk
factors antiplatelet
therapy
Nil
Preventive interventions for stroke associated with diet, physical activity and smoking are similar to
those for heart disease.
Screening
Atrial fibrillation
Screening for AF requires simple palpation of the radial artery pulse to document pulse rate followed by
electrocardiogram to confirm that the cause of the irregular pulse is AF.
Management of AF aims to identify and treat the underlying cause, control heart rate, restore and
maintain sinus rhythm and prevent stroke.
301
Not all strokes are caused by AF, but effective screening,
diagnosis and management of AF may prevent up to 10% of all strokes.
302
In the Aboriginal population,
about one-fifth of all strokes are attributable to AF,
303
and rheumatic heart disease (which can cause AF)
is highly prevalent in this population.
304
Although most strokes in the Aboriginal and Torres Strait
Islander population occur at a younger age and are related to chronic disease such as diabetes,
smoking and hypertension, clinical vigilance for AF is warranted in those over 40 years of age given that
most strokes occur after this age.
Transient ischaemic attacks
It is possible for health care providers to screen clients for a history of a previous TIA. This requires
providers to elicit a history of the sudden loss of focal neurological or monocular function, which is
thought to be due to a lack of blood supply to a part of the brain or eye, and which recovers within 24
hours. The sensitivity and specificity of such a history is dependent on client recollection, the prevalence
of TIA in the population and the skills of the examiner. It has been suggested that questions should elicit
symptoms of funny turns or dizzy spells, weakness or numbness in arms or legs, speech
disturbances, double vision and vertigo.
305
Screening for neck bruits or for asymptomatic carotid artery
stenosis is not recommended.
306
There is good evidence that stroke can be prevented if TIA is identified and preventive treatment is
delivered (see Chemoprophylaxis). Health care providers may target questions to those with high risk
Vascular health
163
such as clients with previous myocardial infarction or other cardiac disease, peripheral vascular disease,
hypertension or multiple lifestyle risk factors.
Appropriate questioning (for symptoms of TIA) of high risk Aboriginal and Torres Strait Islander clients
with chronic disease (such as those with diabetes, poorly controlled hypertension, chronic kidney failure
or a combination of vascular risk factors including overt proteinuria), may detect clients who have had a
TIA. It is unclear if such screening can detect more cases of TIA or earlier TIA than cases presenting
spontaneously. To justify screening for symptoms of TIA in the Aboriginal or Torres Strait Islander
population would require evidence that clients are unlikely to report such symptoms to health care
providers. Although no studies have examined this issue, Aboriginal and Torres Strait Islander clients
are socioeconomically disadvantaged and have reduced access to health care services, suggesting that
awareness of and reporting of TIA symptoms may not occur.
Chemoprophylaxis
Atrial fibrillation
People who have AF for more than 48 hours are usually considered for anticoagulant therapy and
strategies to restore normal heart rhythm.
307,308
Dose adjusted oral anticoagulants (to maintain an
international normalised ratio of 2.03.0) are effective in reducing the risk of stroke in individuals with
non-valvular AF by two-thirds
309,310
and the use of aspirin reduces the risk of stroke by one fifth.
311
The
decision to treat chronic AF with anticoagulants needs to consider the risks of thromboembolism and
haemorrhage.
312
Transient ischaemic attacks
Effective treatment for clients with TIA include:
control of causal vascular risk factors using dietary and lifestyle modification, antihypertensive
medication and lipid lowering therapy
antiplatelet therapy
anticoagulant therapy for clients with embolism from the heart
carotid endarterectomy for clients with severe carotid stenosis on the symptomatic side.
313
Aspirin is the treatment of first choice for clients with TIA.
314
When given to individuals with a history of
TIA or stroke, it reduces the relative risk of stroke by about 13%.
315
Compared with aspirin, clopidogrel
reduces the risk of stroke and other important vascular events from about 6.0% (aspirin) to 5.4%
(clopidogrel) per year, a relative risk reduction (RRR) of 10% (95% CI: 317%) and absolute risk
reduction (ARR) of 0.6%.
316
The combination of aspirin and dipyridamole reduces the risk of stroke from
about 6.0% (aspirin) to 5.1% per year, a RRR of 15% (95% CI: 526%).
317
The effect of aspirin in those without prior evidence of CVD in the primary prevention of stroke is unclear
(from meta-analysis of large clinical trials).
318
There is no evidence for the benefit of anticoagulants in people with TIA due to arterial
atherothromboembolism.
319
However, it is an effective treatment in the prevention of stroke in TIA clients
with embolism from the heart.
Carotid endarterectomy reduces the relative risk of stroke by 48% in people with severe symptomatic
carotid stenosis (7099% stenosis), and by 27% in people with moderate symptomatic carotid stenosis
(5070% stenosis). Among people with lesser degrees of symptomatic stenosis, the benefits of carotid
endarterectomy are much lower and outweighed by the risks.
320
NHMRC guidelines recommend that a carotid endarterectomy should be considered in those with
symptomatic carotid artery stenosis of 7999%.
321
Frequency of the intervention
There is an absence of evidence to support routine screening for TIA in the Aboriginal and Torres Strait
Islander population, but health care providers should ensure clients at high risk of TIA and stroke are
informed of warning signs and symptoms at regular intervals. Advice should be provided
opportunistically at every visit and/or at least once per year.
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164
Neither the Central Australian Rural Practitioners Association or the Northern Zone Management Unit
have recommendations pertaining to assessment of AF or TIA in the Aboriginal and Torres Strait
Islander population.
The Aboriginal and Torres Strait Islander population has a higher age standardised
death rate from stroke. There is an earlier age of onset of stroke, by more than 20 years,
compared with the general Australian population.
EVIDENCE
Level of
evidence
Individuals with atrial fibrillation (AF) have a 56 times higher risk of stroke than those
with normal sinus rhythm. Those who have had a transient ischaemic attack (TIA) have
an increased risk of stroke and an increased risk of a subsequent coronary event.
III
The prevalence of AF in the Aboriginal community is not clear. However, the prevalence
of major causes of AF, such as IHD, hypertension, rheumatic heart disease and diabetes
is higher in this population.
N/A
Oral anticoagulants and aspirin are effective in reducing the risk of stroke in those with
AF.
I
Antiplatelet therapy such as aspirin prevents further stroke in those with a history of TIA
or stroke. It is unclear if this treatment prevents stroke in those without such a history.
I
Those at high risk for a TIA and stroke include those who have had any of the following:
a previous myocardial infarction or other form of cardiac disease, peripheral vascular
disease, hypertension, hyperlipidaemia, diabetes or those with multiple lifestyle risk
factors (eg. smoking, alcohol abuse, overweight, and lack of exercise).
III
RECOMMENDATIONS
Screen for hypertension, smoking, alcohol consumption, overweight and obesity, and
level of physical activity (see Blood pressure, Overweight and obesity, Physical activity,
Smoking in the Respiratory disease Non-communicable section, and Alcohol
Prevention of problem drinking, for details).
IIII
Screen for AF among individuals who are more than 40 years of age in conjunction with
blood pressure measurements. Screen for AF by asking about irregular palpitations, and
feeling the regularity of the rhythm of the radial artery pulse. Confirm an irregular pulse
rate with an electrocardiograph and a medical consultation.
V
Screen for TIA every 12 months in those over 40 years of age by asking about the signs
and symptoms including funny turns or dizzy spells, weakness or numbness in the
arms or legs, speech disturbances, double vision and vertigo.
V
Consider anticoagulation in patients with documented TIAs due to AF. Use antiplatelet
therapy where TIAs are due to arterial disease.
I
Optimise management of chronic diseases and other factors that increase risk of stroke. IIII
References

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facts 2001. AIHW Cat. no. CVD 13. Cardiovascular Disease Series No.14. Canberra: AIHW,
National Heart Foundation of Australia, National Stroke Foundation of Australia, 2001.
2 Edwards RW, Madden R. The Health and Welfare of Australias Aboriginal and Torres Strait
Islander peoples. Canberra: Australian Bureau of Statistics, 2001.
3 AIHW, op. cit.
4 ibid.
5 Australian Bureau of Statistics (ABS). National Health Survey: Aboriginal and Torres Strait Islander
Results Australia, 2001. Cat. no. 4715. Canberra: ABS, 2002.
6 Smith R, et al. Prevalence of hypertension in Kimberley Aborigines and its relationship to ischaemic
heart disease: an age-stratified random survey. Med J Aust 1992;156:55762.
7 Guest CS, ODea K, Larkins RG. Blood pressure, lipids and other risk factors for cardiovascular
disease in Aborigines and persons of European descent of South Eastern Australia. Aust J Public
Health 1994;18(1):7986.
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221 Smith R, et al. Prevalence of hypertension in Kimberley Aborigines and its relationship to ischaemic
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222 Young MC, Fricker PA, Thompson NJ, Lee KA, op. cit.
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229 Stamp KM, Duckett SJ, Fisher DA. Hospital use for potentially preventable conditions in Aboriginal
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230 Devitt J, McMasters A. Living on medicine: social and cultural dimensions of ESRD among Aboriginal
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231 Walsh W, Ring I, Brown A, Boyden A, Couzos S. Ischaemic Heart Disease. In: Couzos S, Murray
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232 NHFA. Reperfusion therapy for acute myocardial infarction: guidelines, 2001. Available at:
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233 Walsh W, Ring I, Brown A, Boyden A, Couzos S. Ischaemic Heart Disease. In: Couzos S, Murray
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234 Whitworth JA; World Health Organization, International Society of Hypertension Writing Group.
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235 European Society of Hypertension Guidelines Committee. European Society of Cardiology
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236 Williams B, et al. BHS guidelines working party, for the British Hypertension Society. British
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237 Sheridan S, Pignone M, Mulrow C. Framingham-based tools to calculate the global risk of coronary
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238 Jackson R. Updated New Zealand cardiovascular disease risk-benefit prediction guide. BMJ 2000;
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239 New Zealand Guidelines Group. Management of mildly raised blood pressure in New Zealand:
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240 New Zealand Guidelines Group. The Assessment and Management of Cardiovascular risk.
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241 Grundy SM, et al. Assessment of cardiovascular risk by use of multiple-risk-factor assessment
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American College of Cardiology. Circulation. 1999. Available at:
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242 Wang Z, Hoy WE. Albuminuria and Incident Coronary Heart Disease in an Aboriginal Community.
[Abstract] Department of Medicine, University of Qld. Personal Communication, August 2004.
243 Eriksson M, Wallander MA, Krakau I, Wedel H, Svardsudd K. Birth weight and cardiovascular risk
factors in a cohort followed until 80 years of age: the study of men born in 1913. J Intern Med
2004;255(2):23646.
244 Hoy W, et al. Stemming the tide: reducing cardiovascular disease and renal failure in Australian
Aborigines. Aust N Z J Med 1999;Jun;29(3):4803.
245 Wang Z, Hoy WE. Is the Framingham coronary heart disease absolute risk function applicable to
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246 Grundy SM, et al, op. cit.
247 ibid.
248 New Zealand Guidelines Group, op. cit.
249 New Zealand Guidelines Group, 1995, op. cit.
251 National Prescribing Service. Cardiovascular risk calculator. Available at:
http://www.nps.org.au/resources/Patient_Materials/nz_cardiovascular_risk_calculator.pdf.
252 Wang Z, Hoy WE. Association between diabetes and coronary heart disease in Aboriginal people:
are women disadvantaged? Med J Aust. 2004 May 17;180(10):50811.
253 Wang Z, Hoy WE. Cardiovascular risk among urban Aboriginal people. Med J Aust. 2003 Nov
17;179(10):557.
254 Wang Z, Hoy WE, op. cit.
255 Cass A, Cunningham J, Wang Z, Hoy W. Regional variation in the incidence of end-stage renal
disease in Indigenous Australians. Med J Aust 2001;175(1):247.
256 Hiyoshi Y, Omae T, Hirota Y, Takeshita M, Ueda K, Katsuki S. Clinicopathological study of the
heart and coronary arteries of autopsied cases from the community of Hisayama during a 10-year
period: part V: comparison of autopsy findings with electrocardiograms: Q.QS items of the
Minnesota code. Am J Epidemiol 1985;121:90613.
257 Bayes T. Studies in the history of probability and statistics: IX: Thomas Bayess essay towards
solving a problem in the doctrine of chances. Biometrika 1958;45:296315.
258 Hayward RSA, Steinberg EP, Ford DE, Roizen MF, Riach KW. Preventive care guidelines: 1991.
Ann Intern Med 1991;114:75883.
259 Couzos S, Murray R, Metcalf S, ORourke S for the KAMSC, op. cit.
260 Danesh J, Collins R, Peto R. Lipoprotein(a) and CHD. Meta-analysis of prospective studies.
Circulation 2000 Sep 5;102(10):10825.
261 Mosca L. C-reactive protein: to screen or not to screen? N Engl J Med 2002 Nov 14;347(20):16157.
262 National Heart Foundation of Australia. Homocysteine and cardiovascular risk, 1997. Available at:
http://www.heartfoundation.com.au/index.cfm?page=41. [Accessed 23 June 2004].
263 Wood D, et al. Prevention of CHD in clinical practice. Recommendations of the Second Joint Task Force
of European and other Societies on Coronary Prevention. European Heart Journal 1998;19:1434503.
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264 Wood D. Established and emerging cardiovascular risk factors. American Heart Journal
2001;141:S49S57.
265 Ford ES, Smith SJ, Stroup DF, Steinberg KK, Mueller PW, Thacker SB. Homocyst(e)ine and
cardiovascular disease: a systematic review of the evidence with special emphasis on case-control
studies and nested case-control studies. Int J Epidemiol 2002 Feb;31(1):5970.
266 Guthikonda S, Haynes WG. Homocysteine as a novel risk factor for atherosclerosis. Curr Opin
Cardiol 1999;14:28391.
267 Shaw JT, et al. Plasma homocysteine levels in indigenous Australians. Med J Aust 1999 Jan
4;170(1):1922.
268 NHFA, op. cit.
269 Rene Malinow M, Bostom SG, Krauss RM. Homocyst (e)ine, diet and cardiovascular diseases: a
statement for healthcare professionals from the nutrition committee. American Heart Association.
Circulation 1999;99:17882.
271 Ballantyne CM, Herd JA, Dunn JK, Jones PH, Farmer JA, Gotto AM Jr. Effects of lipid lowering therapy
on progression of coronary and carotid artery disease. Curr Opin Lipidol 1997 Dec;8(6):35461.
272 Mosca L, op cit.
273 Hung J for the National Heart Foundation of Australia. Aspirin for cardiovascular disease
prevention. MJA 2003;179(3):147-152.
274 Hayden M, Pignone M, Phillips, Mulrow C. Aspirin for the primary prevention of cardiovascular
events: a summary of the evidence for the US Preventive Services Task Force. Ann Intern Med
2002;136:161172.
275 Antiplatelet Trialists Collaboration. Collaborative overview of randomised trials of antiplatelet
therapy - I: prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy
in various categories of patients. BMJ 1994;308:81106.
276 Hung J for the National Heart Foundation of Australia, op. cit.
277 Hayden M, Pignone M, Phillips C, Mulrow C. Aspirin for the primary prevention of cardiovascular
events: a summary of the evidence for the US Preventive Services Task Force. Ann Intern Med
2002; 136:16172.
278 Hayden M, Pignone M, Phillips, Mulrow C, op. cit.
279 ibid.
280 Australian Centre for Diabetes Strategies. National evidence based guidelines for the management of type
2 diabetes: prevention and detection of macrovascular disease. Canberra: NHMRC, 2004. Available at:
http://www.diabetes.net.au/PDF/update_04_2004/macrovascular.pdf. [Accessed 12 August 2004].
281 Wood D, et al. Prevention of CHD in clinical practice. Recommendations of the Second Joint Task Force of
European and other Societies on Coronary Prevention. European Heart Journal 1998;19:14341503.
282 National Heart Foundation of Australia. Hypertension management guide for doctors 2004, 2004.
Available at: http://www.heartfoundation.com.au/index.cfm?page=36. [Accessed 23 June 2004].
284 NHMRC. Preventive interventions in primary health care: cardiovascular disease and cancer: report
of the assessment of preventive activities in the health care system initiative: December 1996.
Canberra: Commonwealth of Australia, 1997.
285 National Prescribing Service. Cardiovascular risk calculator. Available at:
http://www.nps.org.au/resources/Patient_Materials/nz_cardiovascular_risk_calculator.pdf.
286 CARPA STM Reference Group, op cit.
287 Australian Institute of Health and Welfare. Heart, stroke and vascular diseases: Australian facts,
2001. AIHW Cat. no. Coronary Heart Disease 13. Cardiovascular Disease Series No. 14.Canberra:
AIHW, National Heart Foundation of Australia, National Stroke Foundation of Australia, 2001.
288 Thomson N, Winter J, Pumphrey M. Review of the state of knowledge of cardiovascular disease
among Aboriginal and Torres Strait Islander populations, 1999. Available at:
http://www.healthinfonet.ecu.edu.au/html/html_health/reports/cardio-review.pdf. [Accessed 23 June 2004].
289 AIHW, op. cit.
290 ibid.
291 Jamrozik K, Broadhurst RJ, Lai N, Hankey GJ, Burvill PW, Anderson CS. Trends in the incidence,
severity, and short term outcome of stroke in Perth, Western Australia. Stroke 1999
Oct;30(10):210511.
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292 Crowley P, Hankey GJ. Stroke among Australian Aboriginals in Perth, WA, 1988-1992. Aust N Z J
Med 1995 Feb;25(1):55.
293 Lake FR, et al. Atrial fibrillation and mortality in an elderly population. Aust N Z J Med 1989;19:321326.
294 Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the
Framingham study. Stroke 1991;22:9838.
295 ibid.
296 Sacco RL, et al. Race-ethnic disparities in the impact of stroke risk factors: the northern Manhattan
stroke study. Stroke 2001;32:172531.
297 Hankey GJ, Slattery JM, Warlow CP. The prognosis of hospital-referred transient ischaemic
attacks. J Neurol Neurosurg & Psychiatry 1991;54:793802.
298 ibid.
299 Hankey GJ, Warlow, C. Transient ischaemic attacks of the brain and eye. London: WB
Saunders/Balliere Tindall, 1994.
300 ibid.
301 Hankey GJ. Non-valvular atrial fibrillation and stroke prevention. Med J Aust 2001;174:2349.
302 Sandercock PAG, Warlow CP, Jones LN, Starkey I. Pre-disposing factors for cerebral infarction:
the Oxfordshire Community Stroke Project. BMJ 1989;298:7580.
303 Crowley P, Hankey GJ, op. cit.
304 Carapetis, JR et al. Cumulative incidence of rheumatic fever in an endemic region: a guide to the
susceptibility of the population? Epidemiol Infect 2000:124: 23944.
305 RACGP, op. cit.
306 United States Preventive Services Task Force. Guide to clinical preventive services. 2nd edn.
Baltimore: Williams and Wilkins, 1996.
307 Hankey GJ, op. cit.
308 ibid.
309 Benavente O, Hart R, Koudstaal P, Laupacis A, McBride R. Oral anticoagulants in preventing
stroke with non-valvular atrial fibrillation and no previous history of stroke or transient ischaemic
attack (Cochrane Review). In: The Cochrane Library, Issue 1, 2002. Chichester: Wiley.
310 Koudstaal PJ. Anticoagulants for preventing stroke in patients with nonrheumatic atrial fibrillation
and a history of stroke or transient ischaemic attacks (Cochrane Review). In: The Cochrane
311 Hart RG, Benavente O, McBride R, Pearce LA. Antithrombotic therapy to prevent stroke in patients
with atrial fibrillation: a meta-analysis. Ann Intern Med 1999;131:492501.
312 Hankey GJ, op. cit.
313 Hankey GJ, Warlow C, op. cit.
314 McCabe DJ, Brown MM. Prevention of ischaemic stroke antiplatelets. BMJ 2000;56(2):51025.
315 Antiplatelet Trialists Collaboration. Collaborative overview of randomised trials of antiplatelet
therapy-I: prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in
various categories of patients. BMJ 1994;308:81106.
316 Hankey GJ, Sudlow CLM, Dunbabin DW. Thienopyridines or aspirin to prevent stroke and other
serious vascular events in patients at high risk of vascular disease. Stroke 2000;31:177984.
317 Diener HC, Cunha L, Forbes C, Sivenius J, Smets P, Lowenthal A. European Stroke Prevention Study 2:
dipyridamole and acetylsalicyclic acid in the secondary prevention of stroke. J Neurol Sci 1996;143:113.
318 Sudlow C. Primary prevention of cardiovascular disorders. In: Clinical Evidence. Issue 6. London:
BMJ Publishing Group, 2002;1012.
319 Liu M, Counsell C, Sandercock P. Anticoagulants for preventing recurrence following ischaemic
stroke or transient ischaemic attack (Cochrane Review). In: The Cochrane Library, Issue 1, 2002.
Chichester: Wiley.
320 Cina CS, Clase CM Haynes RB. Carotid endarterectomy for symptomatic carotid stenosis
321 NHMRC. Clinical practice guidelines: prevention of stroke. Cat no. 9609377. Canberra: AGPS, 1996.
Child health
176
CHILD HEALTH
Authors
Professor David Brewster, Clinical Dean, Northern Territory Clinical School, Flinders University,
Royal Darwin Hospital
Acknowledgments
Dr Peter Morris, Head, Ear Health and Education Unit, Infectious Diseases Divisions, Menzies School of
Health Research
Professor Tim Mathew, Director, Australian Kidney Foundation
Dr Jonathan C Craig, Senior Lecturer (Clinical Epidemiology), Staff Specialist (Paediatric Nephrology)
Coordinating Editor (Cochrane Renal Group), University of Sydney
Dr Jenny Reath, The Royal Australian College of General Practitioners
This section provides evidence and recommendations related to conditions that have a higher
prevalence or potential impact on Aboriginal and Torres Strait Islander children. It is not intended to
provide an exhaustive set of recommendations for this group. The RACGP red book should be
referenced for other preventive activities that are appropriate for this age group.
ANAEMIA
Burden of disease
Iron deficiency anaemia in children is generally defined as a haemoglobin <110 g/L (with a microcytic,
hypochromic picture after the exclusion of haemoglobinopathies). Children may also be classified as
iron deficient without anaemia on the basis of decreased serum ferritin (10 !g/L), or a decreased mean
cell volume (MCV) (<72 fL), or some combination of these.
1
There is a lack of systematic data on the prevalence of anaemia in Indigenous and non-Indigenous
Australian children. In many Aboriginal communities, the burden of iron deficiency anaemia remains
significant. Screening of children in a coastal Aboriginal community in 1992 revealed a significant
prevalence of iron deficiency anaemia. In the 514 year age group, 79% had iron deficiency anaemia
and 93% demonstrated hookworm infection. In those younger than 5 years, 72% were anaemic. Most of
the anaemia could be attributed to hookworm infestation, but there was indirect evidence that an
inadequate dietary intake of iron may have contributed.
2
In the East Kimberley, Western Australia (WA),
7% of children aged younger than 5 years who participated in a health department screen in 1986 were
anaemic (haemoglobin less than 110 g/L) and 10% had significant intestinal parasites. Of these aged 5
years or more, 13% were anaemic and 24% had significant intestinal parasites.
3
A review of hookworm
infection in Australia reported the persistence of infection in the Kimberley and in the Northern Territory
(NT), but significantly reduced levels in Queensland meant that screening programs were disbanded in
1991.
4
Reductions in hookworm prevalence in the Kimberley and NT since these reports suggest that
hookworm is no longer an important cause of iron deficiency anaemia in Aboriginal children (see
Counselling and chemoprophylaxis).
A total of 774 school age Aboriginal children from 11 remote communities in the NT were screened in
1993. The prevalence of anaemia reached 39%.
5
In a cohort of 408 Aboriginal children admitted to
Royal Darwin Hospital, 55% had microcytosis (MCV <72 fL) with a blood film suggestive of iron
deficiency and 35% were anaemic (haemoglobin <110 g/L). The comparable figures for non-Aboriginal
children were 16% and 6% respectively.
Community anaemia prevalence studies in the NT have reported even higher rates of anaemia (>30%)
based on capillary haemoglobins, but these frequently give inaccurate results. If iron deficiency anaemia
were defined as microcytosis with a haemoglobin <110 g/L, then about 27% of Aboriginal children in
hospital have iron deficiency anaemia compared to 8.5% of non-Aboriginal children.
6
The high
prevalence of infections makes ferritin levels difficult to interpret in remote areas.
Child health
177
A high prevalence of iron deficiency anaemia has also been documented in Canadian Aboriginal
children aged 624 months.
7
In contrast, 6% of otherwise healthy Caucasian children aged 624 months in Adelaide, South Australia,
had iron deficiency anaemia (haemoglobin <110 g/L in association with serum ferritin <15 !g/L),
8
and
3% of preschool children (23 years) from Sydney, New South Wales, had iron deficiency anaemia.
9
Types of preventive intervention for iron deficiency anaemia
modification
Nil Yes
venous
haemoglobin,
mean cell
volume
capillary
haemoglobin
(point-of-care
testing)
soluble
transferrin
receptor
Yes
dietary advice
(earlier
weaning diet)
health
education
Yes
iron
supplementation
(eg. fortified foods,
oral* or
intramuscular iron)
deworming
(albendazole for
hookworm)
Yes
housing and
overcrowding
* Compliance with prescribed oral iron is poor
10
Iron deficiency anaemia has been correlated with poor cognitive function and delay in psychomotor
development, especially when it occurs in children younger than 2 years. However, iron deficiency is
associated with socioeconomic disadvantage and this may be a confounder.
11
Screening
Numerous guidelines over the past decade have recommended screening children for anaemia and
many health services screen children using capillary blood samples. Testing capillary haemoglobin
(using the haemoglobinometer known as Hemacue) frequently gives inaccurately low readings in the
field due to technical problems. However, if used correctly (using a cut off for anaemia of <110 g/L Hb)
the clinical sensitivity and specificity using Hemocue on capillary blood samples can reach 95% and
100% compared with laboratory Coulter testing of venous blood samples. Pre-analytical factors such as
inappropriate mixing of samples before analysis can adversely affect the reliability of results.
12
Provided
good training and quality control is monitored, point-of-care testing should correlate well with laboratory
tests.
13
A venous specimen for full blood count and thin film in neonates (dorsum of hand) is, however, more
accurate and no more painful than a capillary specimen.
14
Thumb pricks have been shown not to be too
stressful in young children.
15
The accurate diagnosis of iron deficiency is based upon a venous
haemoglobin, MCV, and thin film.
16
A serum ferritin gives falsely elevated values in Aboriginal children due to infection (ferritin is an acute
phase reactant) and is unreliable even in a community setting. The soluble transferrin receptor
measures tissue iron unaffected by infection
17,18
and its use is currently being evaluated in Aboriginal
children at Royal Darwin Hospital.
Anaemia is often subclinical, particularly in the Aboriginal and Torres Strait Islander population, where
under-reporting is common. The diagnosis of anaemia can be a useful tool for health promotion,
including the provision of treatment and preventive advice.
Child health
178
A systematic review examining the relationship between developmental delay and iron deficiency in
children younger than 3 years could find no convincing evidence that administration of iron improved
childrens scores on tests of psychomotor development within 611 days of receiving intramuscular
supplements or commencing oral iron supplements. However, the effects of longer periods of iron
therapy on psychomotor development in children with iron deficiency anaemia remain unclear. The
small number of children studied also means the results should be interpreted with caution.
19
A further
review on the impact of iron in children with iron deficiency anaemia aged younger than 1 year is due to
be completed soon.
20
There has been a significant reduction in the prevalence of hookworm due to the use of albendazole in
Aboriginal communities over recent years. The implementation of 6-monthly and annual treatments with
albendazole for children younger than 15 years and for adults, as well as environmental health
improvements, reduced the prevalence of hookworm in Kimberley Aboriginal communities dramatically
in 19921999. Anaemia prevalence in children significantly decreased at that time, despite the lack of
population based iron supplementation.
21
A Cochrane review confirmed that single or repeated chemotherapeutic treatment of helminth infections
(including albendazole) in children has been shown to have small effects in weight gain (0.1 kg
[0.040.17] after a year follow up) and improvement in other anthropometric measures. There appeared
to be no evidence of improvement in cognitive performance in children treated with chemotherapeutic
anthelmintic agents.
22
In view of the high prevalence of iron deficiency in Aboriginal community children, effort should be
directed toward preventing iron deficiency by ensuring an adequate iron intake in the diet and targeting
at-risk children (eg. low birth weight, twins, failure to thrive (FTT), late introduction of solids, poor
weaning diet, high burden of disease). The major risk factor for iron deficiency is an inadequate weaning
diet in partially breastfed children aged 424 months, which is also a major risk factor for FTT.
The effectiveness of counselling strategies and culture-specific education programs to promote healthy
dietary practices in the weaning and postweaning period for infants aged up to 1 year was examined in
a systematic review.
23
No one type of strategy was more effective than another. Lectures in clinical
settings did not affect growth or biochemical indices of nutrition, but compliance was poor. Regular
contact with peer supporters throughout the first year of the childs life was shown to delay the
introduction of unmodified cows milk and improve the overall quality of the diet at 1 year. Issues that are
important to mothers locally should be the foundation for the development of appropriate strategies to
promote better infant feeding practices.
Although many Aboriginal mothers in remote Aboriginal communities continue breastfeeding to about 18
months,
24
they may not introduce iron rich solids by 46 months in sufficient amounts to supply iron and
growth needs. It is also likely that the high burden of disease and tropical enteropathy syndrome result
in greater requirements and less absorption (see Growth failure). An important risk factor for iron
deficiency in all settings is low birth weight, particularly in preterm infants and twins.
25
Programs that aim to improve nutritional status of children through food and iron supplements have
been described as programs that mitigate the effects of poverty on children.
26
Examples include the
United States Women Infant Child (WIP) Program and school nutrition programs in the United Kingdom
(UK). The WIC Program has helped reduce the prevalence of iron deficiency anaemia in infants and
children. Similar programs do not currently exist in Australia.
There is an absence of evidence to suggest an optimal screening schedule for anaemia in children that
explains the variability in recommendations from expert groups. Aboriginal infants at high risk of iron
deficiency anaemia, such as those from remote Aboriginal communities, should be offered routine
haemoglobin measurements at least at 9 and 18 months.
Northern Territory guidelines recommend 6-monthly testing for haemoglobin to 3 years in Aboriginal
children.
27
The Northern Zone Management Unit in north Queensland also recommends capillary
screening in this age group and this recommendation has been incorporated in the newly established
North Queensland child growth assessment and action guidelines. The assessment of haemoglobin,
Child health
179
MCV and film (and iron studies if required) is a required part of diagnostic workup of children with
conditions in which anaemia is a causal or aggravating factor or a complication or both.
28
The Centre for Community Health (2001) does not recommend routine screening for anaemia in
Australian children. However, there was fair evidence to recommend that health professionals maintain
a high level of vigilance for iron deficiency and iron deficiency anaemia in children (particularly among
children from low socioeconomic areas), and that iron status be assessed based on risk factors. These
include uncorrected iron deficiency in the mother during pregnancy, prematurity, age <24 months,
introduction of cows milk as the main milk source before 12 months, and consumption of >600 mL of
cows milk per day.
29
The American Academy of Pediatrics recommends screening for anaemia at 912 months with
additional screening 15 years for clients at risk.
30
For those not breastfed, the use of iron fortified infant
formulas is recommended until at least 12 months. Iron supplementation from about 4 months

is
recommended for exclusively breastfed term infants.
The UK Working Party on Child Health Surveillance (1996)
31
did not recommend universal screening for
iron deficiency anaemia. However, it was recommended that haemoglobin should be checked in any
infant whose diet is causing concern and iron supplementation for low birth weight infants (small for
gestational age) should be given. The continuation of existing childhood screening for anaemia in
localities with severe socioeconomic deprivation was also recommended.
Aboriginal and Torres Strait Islander preschool and school age children (from 5 years)
from remote communities have a much higher documented prevalence of iron
deficiency anaemia than non-Indigenous children.
EVIDENCE
Level of
evidence
Iron deficiency anaemia may cause developmental delay in children (psychomotor and
cognitive). It is unclear if this effect is a confounder (eg. due to social deprivation
through poverty).
III
Strategies to prevent anaemia by improving iron availability in the diet include the early
introduction of iron rich solids during the weaning period.
III
Government funded nutritional support programs for socioeconomically disadvantaged
populations may reduce the prevalence of iron deficiency anaemia.
II
In areas with a high prevalence and in children with a heavy burden of parasites,
antihelminth treatment may improve weight gain.
I
Screening using capillary or venous blood samples may confirm iron deficiency
anaemia in children. Provided there is good training and quality control, point-of-care
testing may correlate well with the laboratory testing.
III
Educational strategies alone are insufficient to reduce the prevalence of iron deficiency
anaemia in Aboriginal and Torres Strait Islander children.
V
RECOMMENDATIONS
Include screening for anaemia in the preventive health assessment of high risk children.
These include twins, those with low birth weight, failure to thrive, or recurrent infections.
Check venous or capillary haemoglobin, mean cell volume, and blood film by age 69
months and repeat at 18 months.
V
Develop counselling and education strategies to promote healthy infant feeding
practices locally.
V
Link child health assessments to nutritional and environmental support programs. V
Child health
180
GROWTH FAILURE
Burden of disease
Aboriginal and Torres Strait Islander children suffer higher rates of malnutrition and failure to thrive
(FTT) than non-Aboriginal children and this has been recognised for many years.
32
Failure to thrive is a
descriptive term, not a diagnosis. It refers to the failure of growth to meet the potential expected for a
child of that age.
33
It is used to describe children with growth failure in industrialised countries like
Australia, and refers to faltering of weight gain below the third centile for age on growth charts. In the
developing world, the term malnutrition is more common, which classifies underweight children into
wasted (acute malnutrition or low weight for height) and stunted (chronic malnutrition or low height for
age), including severe nutritional illnesses such as marasmus and kwashiorkor.
Low birth weight may arise from prematurity or faltered growth in-utero (growth retardation). Children
may fail to thrive after birth, whether their birth weight was low or normal. Over the period, 19982000,
the mean national rate of low birth weight (less than 2.5 kg) for Indigenous Australians was 13%, varying
from 12% in New South Wales (NSW) to 14% in the Northern Territory (NT), and 1718% in South
Australia (SA), and the Australian Capital Territory (ACT), which compares to 6.5% for non-Indigenous
mothers. The two-times greater incidence of low birth weight babies born to Indigenous Australian
mothers compared with non-Indigenous mothers remains unchanged since 1991.
34
Over the period 19731990, there was little change in the mean weight of Aboriginal infants from remote
communities. From age 6 months to 2 years, mean weights have remained below the 30th centile.
35,36,37
Although there is considerable variation between remote communities in the NT, the Top End Growth
Assessment for Action project in October 2001 reported rates of underweight children by region as
1423% (compared to an expected rate of 3%), including wasting in 918%, stunting in 1114% and
anaemia in 2940% of Aboriginal children under 5 years, with peak rates of malnutrition affecting the
1823 month age group.
38
It has been said that international relief agencies regard a prevalence of
wasting in children of more than 8% as a nutritional emergency.
39
Malnutrition in infancy can reduce head circumference, as demonstrated in several studies from Africa,
India and the USA.
40,41,42
Malnutrition has also been linked with microcephaly in Aboriginal infants.
43
It is
not entirely clear whether microcephaly resulting from growth failure in infancy has an effect on
intellectual function and, if so, whether this is reversible. However, there is some evidence that head
circumference increases, and can catch up to normal, when nutritional deprivation ceases,
44,45
and that
head circumference in malnourished children is not linked to intellectual dysfunction.
46
Many cases of malnutrition are precipitated by diarrhoea. Aboriginal children have a high burden of
diarrhoeal disease, particularly those from remote Aboriginal communities, with resultant high rates of
hospital admission. Aboriginal children are admitted to hospital at 1.5 times the national average in
infancy and 1.3 times in children aged 14 years.
47
Rotavirus infection epidemics occur periodically
(notably in 2001) and Aboriginal and Torres Strait Islander children in the NT have severe
manifestations of osmotic diarrhoea and acidosis, which contribute to the high morbidity of diarrhoeal
disease.
48
From a community perspective, most diarrhoea has only a transient impact on nutritional status due to
the potential for catch up growth during convalescence. A child who is malnourished is more prone to
infections, further impairing nutritional status by depressing appetite and increasing demand on reserves
of protein and energy. In the community context, promoting catch up growth after diarrhoeal disease will
break the malnutrition-infection cycle. Thus, Aboriginal community children with such a high burden of
diarrhoeal disease may not demonstrate the expected catch up growth between episodes unless a
special effort is made to increase their intake of weaning foods during convalescence.
Child health
181
Types of preventive interventions for growth failure
modification
Australian
Standard
Vaccination
Schedule*
growth
monitoring
(weight, height,
head
circumference)
clinical follow
up of low birth
weight infants
dietary
advice
family
support
health
education
breastfeeding
promotion
supplementary
feeding
programs
micronutrient
supplements
(eg. zinc, vitamin
A)
personal
hygiene (eg.
hand washing,
nappy
disposal, food
preparation)
housing (eg.
overcrowding)
water and
sanitation
food (eg.
prices,
availability of
fresh fruit and
vegetables)
* All children, including those with growth failure, should be vaccinated in accordance with the Australian Standard
Vaccination Schedule (see Vaccine preventable diseases)
Observational studies have shown that antenatal care can prevent maternal and perinatal mortality and
improve pregnancy outcomes.
49
The aim of antenatal care is to undertake risk assessment and health
promotion and deliver medical and psychosocial interventions. The World Health Organisation (WHO)
recognises the importance of antenatal care in the prevention of adverse perinatal outcomes and has
endorsed 10 principles to underpin such care. These principles state that care should be culturally
appropriate, holistic and family centred.
50
There is some evidence that culturally appropriate antenatal
care programs can reduce the incidence of low birth weight infants in the Aboriginal and Torres Strait
Islander population.
51,52,53
The regular review of infants after birth has been recommended for several reasons to:
immunise with currently available vaccines against important childhood communicable diseases
monitor growth for early identification of growth failure and to implement therapy for improvement in
growth outcomes
provide health education and counselling to reduce risk of disease.
Screening
Routine growth monitoring is a key component of the at-risk approach to infant and child health services.
It aims to identify infant feeding difficulties, ill health, social deprivation (leading to poor nutrition) and
poor weight gain due to psychosocial causes. It has come under scrutiny in recent years in both the
developing and industrialised worlds, and has been criticised as a waste of valuable time and a cause of
unnecessary parental anxiety despite United Nations Childrens Fund (UNICEF) recommendations for
increased frequency of growth monitoring in children from developing countries (monthly to 18 months).
The Nyeri Declaration on Growth Promotion for Child Development
54
expressed concern that weighing
and charting millions of children in the developing world had not been followed by appropriate action.
The outcome of growth monitoring may include improvements in morbidity (such as malnutrition or
hospital admissions) or in maternal nutritional knowledge and satisfaction. However, two recent
systematic reviews have found no reliable evidence of a benefit from growth monitoring.
55,56
This could
be more related to poor documentation than to ineffectiveness, but growth monitoring must be
accompanied by action for it to be effective.
The Cochrane review concluded there was insufficient evidence that routine growth monitoring is of
benefit to child health in both developing and developed country settings. Growth monitoring was
defined as the regular recording of a childs weight, coupled with some specified remedial actions if the
weight was abnormal in some way. It grouped remedial actions such as counselling of the mother
(which may be aided by the growth chart), the provision of nutritional supplements and treatment and
investigation for disease (which may require referral to a specialist or social support). All actions can be
Child health
182
implemented through primary health care. Despite widespread implementation of growth monitoring and
remedial actions, very few studies had evaluated outcomes. Only two studies from developing countries
met quality criteria for the review.
57
The evidence for and against routine child health assessments for the Australian population has also
recently been reviewed in two reports
58,59
and is not duplicated here.

Both reports emphasised the key
position of primary health care workers to detect early signs of health problems in childhood in order to
facilitate interventions. There was insufficient evidence to make a recommendation for or against
screening for height in childhood. This was mainly because screening leads to large numbers of
referrals of short-normal children. The cause of short stature can usually be ascertained clinically (eg.
coeliac and chronic kidney disease). Turner syndrome and growth hormone deficiency were reported to
be the only conditions with few symptoms.
60
The reports did not note that nutritional deprivation, which
can be asymptomatic, is the primary reason for growth monitoring in Aboriginal children.
There was also insufficient evidence to make a recommendation for or against screening for FTT in all
Australian children. The review from the Centre for Community Child Health in Victoria found that
screening might be beneficial if systematic early detection of FTT led to management that avoided
subsequent adverse outcomes. Despite this, abandoning growth assessments was not advocated.
Routine weight monitoring at birth, 68 weeks and 812 months was recommended as part of routine
clinical care.
Despite the lack of evidence, the continuation of neonatal and 6-week examinations was advocated for
congenital heart disease, developmental dysplasia of the hip and undescended testes. The need to
promote strategies to improve attendance at the 6-week postnatal check by disadvantaged groups was
stressed. There was good evidence that well-child group visits (where mothers and children attend as a
group, often in specific clinic or community health settings) are effective in improving child health
outcomes. There appeared to be fair evidence against screening children for developmental problems,
hypertension or iron deficiency or for screening urinalysis in healthy children. A variety of reasons were
given, including the potential for harm outweighing benefits as well as failure to fulfil WHO screening
criteria.
61,62
The measurement of head circumference is intended to aid in the detection of hydrocephalus (and other
less common causes of a large head, such as subdural effusion and dysmorphic syndromes) and
microcephaly. An absolute cut off point cannot define microcephaly, although the second centile has
been used, but measurements well below this are compatible with normal intellect. If detected, there is
no specific treatment. There appears to be no justification for repeated measures of head
circumference. Developmental screening using either parental questionnaire or the Denver
Developmental Screening Test is not recommended because of poor predictive validity. The correct
identification of preschool children with developmental delay does not seem to improve their progress or
behaviour in the long term and does not justify the investment of professional time.
63
Aboriginal Health Workers have advocated identifying children at risk of child abuse as part of well-child
visits. A recent systematic review concluded there was good evidence that structured home visits,
particularly by nurses, to disadvantaged families (during the perinatal period extending to infancy), can
prevent child abuse and neglect. However, screening for children at risk or perpetrators of maltreatment
was not recommended due to the potential for harm outweighing the benefits.
64
Annual measurements of weight and height in Aboriginal schoolchildren (aged 5 years or more) are also
not recommended. A review of school screening from 11 remote Aboriginal communities in the NT found
that all children with stunting and wasting were already known to have poor growth before school
entry.
65
Twenty-one percent of the children measured (410 years) were malnourished (weight/age
below 2 Z-scores), with 51.4% stunted, 40.7% wasted and 7.9% both wasted and stunted.
66
The mean
age (range) of onset of growth faltering was 6.6 (3.512) months for stunting and 8.9 (7.518) months
for wasting.
In contrast to the targeted approach of growth monitoring and counselling, population approaches
attempt to modify risk factors for the whole population, eg. by subsidising certain foods, providing food
supplements to school children or pregnant mothers and health education programs (diet, hygiene).
These programs are expensive but like immunisations can be highly effective in improving health
outcomes. Most of these initiatives are components of the National Aboriginal and Torres Strait Islander
Nutrition Strategy and Action Plan.
67
The provision of food supplements to disadvantaged populations, through the US WIC Program for
example, has reduced the incidence of low birth weight infants
68
and infant deaths,
69
led to higher mean
Child health
183
birth weights
70
and a greater likelihood of receiving prenatal care. Child health improvements attributed
to the program included reduced rates of iron deficiency anaemia,
71
increased rates of breastfeeding at
6 months, and improved growth rates.
72
Furthermore, foods provided by WIC were not associated with
increased rates of overweight in preschool aged children.
73
A Cochrane review confirmed that balanced protein/energy supplementation in pregnancy results in
modest increases in maternal weight gain and foetal growth. Food supplementation also appears to
reduce the risk of stillbirth and neonatal death and the incidence of small-for-gestational-age infants.
74
Reviews of other programs did not find evidence for a benefit from antenatal food supplements or
nutritional advice.
75,76,77
There is little doubt that community supplementary feeding is more effective in improving malnutrition
during the vulnerable weaning period (418 months) than hospital admission or health education.
Supplementary feeding is an effective intervention to prevent malnutrition and reduce the prevalence of
persistent diarrhoea, whereas diarrhoeal disease control activities are of less proven effectiveness.
78
The use of food handouts to supplement the nutrition of Aboriginal children has been used in the past.
Free food supplements were provided to Aboriginal children with FTT in Aboriginal controlled nutrition
programs in Sydney in the 1970s.
79
The main constraints were limited funding (from Freedom From
Hunger), limited attendance at nutrition classes due to transport difficulties, poor food buying patterns
(fast foods, flour, white bread, sugar, tea and camp pie) that were not nutritionally optimal, and personal
problems of families (eg. low income, binge drinking) that could not be addressed by such programs.
There is political resistance to provision of food supplements because of the handout mentality and risk
of increasing dependency. There is no equivalent WIC food supplementation program in Australia,
although there are national and state based nutrition strategies largely responsible for community
education. Alternative schemes such as initiatives in the United Kingdom have emphasised the
importance of food supplementation to improve the health of disadvantaged school children, eg. free
provision of fruit.
80
No such program exists on a large scale in Australia.
Nutrition education needs to develop approaches that empower community members to make
appropriate choices, using both scientific and cultural knowledge.
81
A South African study carried out the
only reported randomised trial on the effectiveness of nutrition education in the rehabilitation of
malnourished children.
82
The children in the study were followed up for 12 months and received home
based appropriate nutrition education during 68 visits. Although the nutrition knowledge of caretakers
in the study group was better than controls, there were no differences in nutritional status between the
two groups despite a detailed evaluation. Possible explanations for this negative finding are that the
Hawthorne effect of home visits to the control group minimised the differences, that improved
knowledge did not change behavioural practices, or that dire poverty made subjects unable to put
educational advice into practice. The authors concluded that nutrition education per se was not an
important factor in preventing relapses of malnutrition. Newer approaches to nutrition education have
been undertaken that stress behavioural changes based on the reality in which malnourished families
are living.
83
The benefits of breastfeeding in Aboriginal and Torres Strait Islander child growth have been well
established and widely recommended.
84
There is a theoretical risk, however, that breast milk alone may
be insufficient to satisfy the infants energy requirements beyond 4 months. A Cochrane review
demonstrated no apparent risks in recommending, as a general policy, exclusive breastfeeding for the
first 6 months of life in either developing and developed country settings.
85
Environmental modification
A review of 144 intervention studies of improved water supply, sanitation and/or hygiene practices
reported median reductions in prevalence of 26% for diarrhoea, 29% for roundworms, 27% for trachoma
(eyes), and 4% for hookworm.
86
Studies most likely to show a positive health impact were integrated
projects in communities with high childhood mortality rates using good study design. The issue of study
design has featured prominently in the water and sanitation literature, particularly since a 1983 review
found serious methodological problems in nearly all published studies to date.
87
Programs cannot simply
be transplanted from one setting to another without adaptation to local circumstances.
88
There is a need
for integrated interventions fostering community motivation, organisation and program flexibility,
including hygiene education.
89
In the NT, a before and after study evaluating the impact of housing and sewerage improvements in a
large central Australian Aboriginal community on child health found that after 3 years there were no
significant changes in weight, height, prevalence of trachoma, scabies, skin sores, or clinic and hospital
use. The great mobility of people between communities made it difficult to demonstrate a health impact.
Moreover, most of the housing remained below standards suggested in the national Indigenous housing
Child health
184
guidelines. The link between housing and health is not likely to be simple, but rather mediated through a
number of complex social and behavioural factors.
90
The provision of health hardware may be outside the scope of primary health care but promotion of
environmental health is not.
91
Health assessments within a primary health care setting may identify
opportunities for individual referral to relevant agencies for socioeconomic support, white goods and
housing. They may also promote the implementation of population programs reviewing basic health
infrastructure, such as water access and sewage control.
The standard American paediatric textbook recommends that children have routine supervisory health
visits with weight, height and head circumference measured at 1, 2, 4, 6, 9, 12 and 15 months, weight
and height measured at 18 months, and annually from 25 years.
92
On the other hand, the UK Working
Party on Child Health Surveillance (UKWPCHS) 1996
93
and UK consensus meeting recommended that
infants need only be weighed at birth and with immunisations and surveillance checks, only those
causing clinical concern should be weighed and measured thereafter.
94
In settings where only mild
malnutrition is seen, weight for age alone may be the most appropriate anthropometric index.
95
Head
circumference measures were recommended at 68 weeks only, unless there were concerns. At 68
weeks, length should be measured in any infant with low birth weight (less than 2500 g) and in any
infant whose health, growth or feeding pattern is causing concern. Height measures were recommended
at 1824 months, 3.5 years, 5 years and 79 years.
96
In the NT, the Growth Assessment Action Program recommends approximately monthly weighing of
Aboriginal children in the first 3 years and then 6-monthly weighing to school entry. It also recommends
length/height measurements approximately 6-monthly to school entry and head circumference
measurements three times in the first 6 months.
97
Given that the critical period for linear growth is in the
first 2 years of life, growth monitoring needs to focus on this age group and follow up at-risk children
closely.
The Northern Zone Management Unit in north Queensland recommends growth monitoring all children
from birth to 3 years. Weight and length (at length >90 cm, height should be measured) is measured
every 2 weeks from birth to 2 months and every month from 2 months to 3 years. If after the second
year growth is normal, 3-monthly assessments are recommended. Children still considered to be at risk
of growth failure after 3 years should continue to have 3-monthly weight and height measurements.
Head circumference measurements are recommended in all children at birth, 2, 6, 12 and 18 months (G
Miller, 28 November 2002).
A summary of Australian reviews and recommendations is shown in Box 13.
Box 13. Australian reviews and recommendations for periodic health examination of children
Centre for Community Child Health, 2001
98
Insufficient evidence to make a recommendation for or against screening for FTT.
Comment: while there is some evidence that systematic detection and management of FTT in the first
year of life can improve outcomes, this has yet to be put into operation within a practicable screening
system.
Recommendations: Routine weight monitoring at birth, 68 weeks and 812 months, is recommended
as part of routine clinical care.
99
Child health surveillance should be conducted opportunistically at the same time as other activities such
as immunisation (2, 4, 6, 12, 18 months and at school entry). Height, weight and head circumference
should be measured 6 times, every 36 months in infants 02 years, then height, weight, and body
mass index annually until age 5 years.
Territory Health Services, 1997
100,101
Weight screening should be conducted twice weekly from birth to 2 months, then monthly to 3 years,
then 6-monthly to 5 years. From 2 years, less frequent weight checks can be performed if the child is
growing normally. Length should be measured at 8 weeks, 6 months, 12 months, and 6-monthly to 24
months. Height should be measured thereafter to 3 years, then annually to 5 years. Head circumference
should be measured at 8 weeks and 6 months.
Child health
185
Aboriginal and Torres Strait Islander children up to age 5 years have a higher rate of
hospital admission than other Australian children. Aboriginal children from remote
communities have particularly high rates of growth failure (wasting and stunting).
The effects of malnutrition peaks in the 1823 month age group.
EVIDENCE
Level of
evidence
At present there is insufficient evidence to be confident that routine growth monitoring is
of benefit to child health in both developing and developed country settings. The
National Health and Medical Research Council considers there is insufficient evidence
to make a recommendation for or against screening for failure to thrive, but
recommends weight monitoring as part of routine clinical care.
I
There is good evidence that improved health outcomes may be obtained by remedial
action comprising nutritional supplementation to pregnant women and to disadvantaged
families with children younger than 5 years.
III
Structured home visiting, particularly by nurses, to disadvantaged families during the
perinatal period to infancy may prevent child abuse and neglect.
I
RECOMMENDATIONS
Conduct regular postnatal review of infants. Assess growth as a minimum, with the
routine immunisation schedule (age 2, 4, 6, 12 and 18 months, and at school entry).
Include weight, length, and head circumference (commencing at age 68 weeks), and
plot on the growth chart. When undertaking growth assessments, use these
opportunities to improve immunisation coverage.
V
Follow up children with growth failure using an appropriate action plan, including history,
examination, laboratory results, relevant advice, and home visits.
V
Routine measurement of height and weight of school age children (from 5 years) is not
recommended. Weight, diet, and physical activity should be assessed opportunistically.
V
Routine formal developmental screening is not recommended. Assess children with risk
factors (including prematurity, convulsions, microcephaly, or possible foetal alcohol
syndrome) for developmental delay by age 9 months.
V
Screening for children who are at risk of abuse is not recommended. Where available,
refer disadvantaged families to a home visitation program to help prevent child abuse
and neglect.
I
Supplement clinic interventions with population based programs in order to improve the
nutrition and growth of Aboriginal and Torres Strait Islander children (see Types of
interventions in the Growth failure section).
V
Use health assessments performed in a primary health care setting to identify any
opportunities for individual referral. This may include referral to relevant agencies for
socioeconomic support, white goods and housing.
V
HEARING LOSS
Burden of disease
Ear infections are very common in Aboriginal and Torres Strait Islander children and the chronic and
suppurative consequences represent a major public health problem. One type of chronic infection is
otitis media with effusion (OME), which is common in Aboriginal children. In one study in the Northern
Territory (NT), 95% of Aboriginal infants aged 68 weeks had OME compared to 30% among non-
Aboriginal infants.
102
Otitis media with effusion is a fluctuating disease and point prevalence may be
difficult to interpret. In a USA study, 20% of days over the first year of life were associated with OME.
Rates were higher in black infants.
103
No comparative cumulative rates have been reported in Aboriginal
children, but there is some evidence they may be much higher.
104
Other forms of chronic otitis media (OM) include chronic suppurative otitis media (CSOM) which is
highly prevalent in rural and remote Aboriginal communities
105
(prevalence up to 60% has been
reported).
106
These infections occur predominantly in Aboriginal children and cause hearing loss during
the critical period of child development. Some effects may be lifelong.
Total or partial hearing loss was more likely to be reported by Aboriginal and Torres Strait Islander
peoples than non-Aboriginal people in the 2001 National Health Survey in all age groups from infancy to
55 years. In Indigenous Australian children aged 014 years, 7% reported hearing loss compared with
Child health
186
2% of the non-Indigenous population. Of those aged 1545 years, 911% reported hearing loss
compared with 39% of non-Indigenous Australians. Problems related to the ear, including hearing loss
(15%), were among the most commonly reported long term health conditions by Aboriginal and Torres
Strait Islander peoples (after eyesight (29%) and asthma (16%).
107
A detailed review of the burden of suffering in relation to chronic OM and hearing impairment in
Aboriginal populations was recently released.
108
Various ways to prevent and detect hearing loss in children are shown below.
modification*
Yes
pneumococcal
vaccines
Yes
neonatal
screening
parental
questionnaires
pneumatic
otoscopy or
tympanometry
audiometry
(more than 3
years)
Yes
parental
vigilance
developmental
milestones
Yes
breastfeeding
prophylactic
antibiotics for
recurrent OM
Yes
socioeconomic
disadvantage
overcrowding
passive
smoking
* Evidence for these interventions is discussed in detail elsewhere
109
(see also Growth failure)
The control of OM in Aboriginal populations through early detection, monitoring and delivery of
appropriate preventive, and curative and rehabilitative treatments may minimise the impact of hearing
loss.
Immunisation
Immunisation with pneumococcal conjugate vaccine
There is some evidence that the 7-valent pneumococcal conjugate vaccine given during infancy can
prevent OM. A summary of trials reporting vaccine efficacy on OM episodes is shown in Table 9.
Vaccine efficacy in preventing OM episodes (generally defined as a clinic visit with diagnosis of any type
of OM in the follow up time of the study) failed to reach statistical significance in two large trials. A
reduction in AOM episodes overall by 7% is not a very large decrease more than 90% of children will
still get OM due to non-vaccine type pneumococcal infections and other bacterial causes.
The vaccine appears to offer some protection against spontaneous tympanic membrane perforation
(acute suppurative OM) caused by vaccine-type pneumococci (48% or 65% relative risk reduction), but
no trial reported on the effect of the vaccine on overall rates of perforation. It is unclear if the vaccine will
reduce overall rates of acute suppurative OM given that 40% of disease due to pneumococcus in
Aboriginal children is not covered by the vaccine (ie. less than 60% of pneumococcal infections from
invasive isolates and those carried in the nasopharynx are vaccine-type).
110
There are more than 90
pneumococcal serotypes. Furthermore, another 40% of OM infections are caused by other bacteria (eg.
haemophilus, moraxella). Replacement of pneumococcal serotypes following vaccination has also been
documented in the Finnish Otitis Media Study (Table 9), which means that infection with non-vaccine
pneumococcal serotypes may increase, thereby reducing vaccine efficacy. A before and after Australian
trial investigating effects on the vaccine of OM is in progress in the NT
111
and many efficacy trials are
under way in the Netherlands (otitis prone children), South Africa, the USA, the Philippines, and the
Gambia.
The only way for vaccination to prevent initial bacterial colonisation and first episodes of OM in remote
Aboriginal children is for protection to begin within the first month of life. This could only potentially
happen with a birth dose or vaccination commenced early (at 6 weeks) or maternal immunisation with
polysaccharide or conjugate vaccine.
112
As yet, there are no data to support either approach as a
routine.
Child health
187
Mass conjugate pneumococcal vaccination in childhood has been estimated to potentially prevent more
than 1 million (out of 20 million) annual episodes of AOM in the USA.
113
The cost of achieving this is
high when most parents will not realise a benefit and this may adversely affect parental acceptance of
vaccines.
114
In November 1999, the USA Federal Drug Administration rejected the use of this vaccine
for OM.
115
A recent systematic review concluded that administering the conjugate vaccine on a large
scale to prevent AOM cannot be recommended.
116
Table 9. Summary of trials examining conjugate vaccine impact on OM in children
Trial Kaiser Permanente
(northern California)
117
Finnish Otitis Media
Study
118
Navajo Trial
119,120
Number N = 38 000 N = 1662 N = 8292 (Navajo and
White Mountain Apache
children as high risk
groups)
Relative risk
reduction
7% decrease in OM
episodes
6% reduction in AOM
episodes
15% reduction in new
OM episodes
Significance 95% CI: 4.19.7%
Statistically significant
95% CI: 416%
Not statistically significant,
possible increase in
number of episodes
95% CI: 2241%
Not statistically significant
Duration of
follow up
3-year period Up to 2 years Up to 2 years
Serotype-
specific outcome
No myringotomy
23 (17 control and 6
pneumo vaccine group)
episodes of
spontaneously draining
OM with pneumococci:
64.7% (p=0.035) point
estimate of efficacy
Myringotomy when AOM
diagnosed
34% reduction in all
pneumococcal OM (95%
CI: 2145%)
57% reduction in VT
CI: 4467%)
33% increase in non-VT
CI: 180%)
No myringotomy
50 (32 control and 18
pneumo vaccine group)
episodes of
spontaneously draining
OM with pneumococci:
47.7% (95% CI:
1275%) point estimate
of efficacy
Extracted from: Aboriginal primary health care: an evidence-based approach, 2003
Immunisation with pneumococcal polysaccharide vaccine
Most data suggests that the 23-valent pneumococcal polysaccharide vaccine (23-vPPV) is poorly
immunogenic
121
and not effective in preventing AOM in children younger than 2 years.
122,123
However,
there is evidence that the vaccine is protective against OM in children older than 2 years, including a
trial involving Aboriginal children.
124,125
In a pooled analysis, the polysaccharide vaccine is effective in
children aged 24 months or more in significantly reducing the mean number of AOM episodes per month
by 17% [rate ratio 0.833 95% CI: 0.6250.970]. The vaccine is more effective in reducing OM episodes
in children with recurrent OM. Approximately 32 children need to be vaccinated with the PPV to prevent
one child from having an AOM episode during 1 year.
126
Several experts have recommended the 23vPPV in children with recurrent OM who are older than 2
years.
127,128,129
The increasing prevalence of pneumococcal antibiotic resistance is one reason for
vaccination. Otitis media is increasingly caused by penicillin resistant pneumococci in the USA. Thirty-
one percent of pneumococcal middle ear isolates were relatively resistant and 15% were highly resistant
to penicillin in a prospective cohort of USA children.
130
Resistance to penicillin may also be a marker of
resistance to other antibiotics, as nearly 50% of pneumococcal strains with intermediate resistance to
penicillin also appeared to have intermediate resistance to ceftriaxone or cefotaxime.
131
Within the
Aboriginal population, and generally in the north of Australia, there is already an increasing level of
pneumococcal resistance to both penicillin and ceftriaxone in pneumococci isolated from clients with
invasive disease.
132
In addition, 27% of pneumococci carried in the nasopharynx of Aboriginal children
hospitalised in the NT demonstrated intermediate penicillin resistance and 34% demonstrated
intermediate ceftriaxone resistance.
133
Pneumococcal resistance may lead to the failure of empirical
antibiotic treatment for OM and serious invasive disease.
Aboriginal children continue to suffer from recurrent OM beyond 2 years, and therefore use of the
23vPPV may have an important clinical role in preventing further episodes of AOM in an otitis prone
child.
Child health
188
Screening
Screening children for hearing loss has been advocated because early intervention may prevent
language, speech and communication disorders. The earlier the impairment is detected, the greater the
potential for benefit. It is widely believed that the critical period for language acquisition is in the first 3
years of life.
134
Screening aims to detect hearing abnormalities earlier than spontaneous clinical presentation or
observation.
135
In this respect, there is an argument for regular otoscopic examination of Aboriginal
children to detect the presence of tympanic membrane perforations, as the condition may be
asymptomatic and clients may delay seeking treatment.
136
Delayed treatment has also resulted from
past clinical practice uncertainty. The delivery of ineffective interventions to populations with high of
infection has probably affected client confidence. Regular otoscopy may increase the profile of hearing
loss as many parents, particularly from developing countries, attach a low importance to hearing
impairments.
137
Perforated tympanic membranes are a result of acute or chronic suppuration and may be actively
discharging or dry. Detection is important, as most children with perforated tympanic membranes will
have hearing loss in the affected ear. Case finding can lead to parental education, treatment of infection,
and referral for surgical assessment if healing does not occur.
The early detection of AOM in Aboriginal children through opportunistic or regular otoscopic
examinations has also been advocated. Arguments in support of this include the detection of
asymptomatic OM (a feature in many Aboriginal children),
138,139
symptoms being an insensitive marker
of infection,
140
a suggestion that early antibiotic intervention prevents chronic sequelae,
141
and detection
of recurrent OM for which there is effective antibiotic prophylaxis.
142,143
The arguments against
screening for OM in Aboriginal children are based on the lack of evidence that chronic sequelae and
hearing outcomes would be better in those regularly screened than those given treatment following the
detection of OM by other means (eg. opportunistic case finding or presentation following an upper
respiratory tract infection. Screening for OME has been a core component of the New Zealand Ministry
of Health National Schedule for well-child assessments since 1991. Tympanometry is recommended at
8 months, 15 months, 3 years, and at school entry. A recent review reported a lack of evidence for or
against the continuation of the program.
144
The Canadian Taskforce on Preventive Health Care has
restated that there is insufficient evidence to include routine early screening for OME in, or exclude it
from, the periodic health examination of children up to 4 years.
145
Screening for hearing loss may detect conductive loss (from OME or chronic suppurative OM) or
sensorineural loss (from congenital disease in the neonatal period). Neonatal hearing screening was
recently reviewed in Australia and is not considered here.
146
Several authorities have recommended preschool hearing screening of children in the general and
Aboriginal population.
147,148,149,150
The use of a parental checklists during routine well-baby visits and
tympanometry is the main proposed method. Others have not agreed with preschool hearing screens in
the general population.
151 152
This is because, unlike in Aboriginal children, most hearing loss detected is
self limited and related to OME, which usually resolves spontaneously within 68 weeks. In the general
population, there is little evidence that screening for hearing loss of children of preschool or school age
leads to benefits in future language or communication performance,
153,154
and consequently screening is
not recommended. There is strong evidence that long term developmental effects of OME detected
through screening are minimal. Furthermore, as a fluctuating condition, detection would require
repeated screening. Treatment of children detected through repeated screening has been shown to
provide no long term developmental or academic benefit.
155
In contrast, there is support from other expert bodies for the opportunistic screening for OME in
Aboriginal children, with tympanometry or pneumatic otoscopy.
156
In Aboriginal populations, a subgroup
of children may experience frequent episodes of OM with prolonged periods of conductive deafness,
sometimes persisting to adulthood. Hearing screening in these instances may be beneficial. Screening
for OME using tympanometry or pneumatic otoscopy may identify the child with bilateral hearing loss
(who is too young to be tested with audiometry). Children who have bilateral effusion may be targeted
for further review, with referral for surgery if effusion is found to persist beyond 34 months.
The World Health Organisation (WHO) advised that routine hearing screening in school age children
may be beneficial provided there are attempts made to reach those who, because of hearing deficits,
may not be attending school.
157
Hearing screening at the start of the school year (age 45 years) for the
Indigenous and non-Indigenous population of northern Australia has also been supported, but annual
school screens thereafter are not recommended.
158,159
Child health
189
Hearing screening at school entry may influence the provision of sound amplification devices in
classrooms in regions with a high prevalence of conductive hearing loss. Sound field amplification
appears to significantly improve comprehension in school children aged 811 years.
160
Australian
national guidelines have been developed to assist schools and health care providers assess the need
for amplification devices and apply them in schools.
161
In spite of current uncertainties regarding benefits, preschool screening for hearing loss in the general
and the Aboriginal population is widely conducted in Australia.
162
In the UK, the most common preschool
hearing test conducted is the distraction test, performed at 69 months. It is used in almost all health
districts, with up to 90% of the child population tested. However, more cost effective options such as
neonatal screening programs are recommended for this population.
163
An Australian review concluded
that there is good evidence to recommend against distraction testing.
164
Screening tests
There is high quality evidence that the presence of OME can be reliably detected through screening
programs in children from at least 2 years (tympanometry and pneumatic otoscopy). Hearing impairment
can be reliably detected through audiometry screening programs in children from approximately 34
years,
165
including in Aboriginal children.
166
Tympanometry and pneumatic otoscopy have been found to
be predictive of hearing loss in Aboriginal children too young to be tested with pure tone audiometry,
from 7 months.
167
Parent-held record questionnaires for hearing loss behaviour have not been adequately validated.
Nevertheless, many experts agree that parental concern is often the single most important factor in the
diagnosis of hearing loss and most physicians endorse the periodic questioning of parents on hearing
issues.
168
While parental vigilance is important, it is an insensitive indicator of hearing loss.
169
The use of
standard parental questionnaires for Aboriginal parents may be problematic. The language used in the
questions may be inappropriate for many Aboriginal people and the expected behavioural changes
resulting from hearing loss are likely to differ between cultures. Further investigation on the most
appropriate questions for Aboriginal parents is required.
Rehabilitative programs
Referral processes to specialist and rehabilitative services need to be optimised in order to obtain the
full benefit of a coordinated hearing screening program. This may be facilitated through the use of a
hearing loss register. It is possible to set up such registers for Aboriginal children at relevant primary
health care services. Collaboration between screening services, schools and specialist and rehabilitative
services is necessary to ensure learning capacity in affected children is optimised (eg. sitting at the front
of the classroom, sound field amplification, teacher aides, sign language learning, access to resources
for the hearing impaired). Hearing aids given to children are more likely to be used if education,
maintenance and follow up are conducted in supportive and culturally appropriate environments.
The Commonwealth Hearing Services Program also provides free hearing assessment, rehabilitation,
supply and fitting of hearing aids for children. A recent review of this initiative found an inequitable
distribution of funds, with evidence of unmet hearing health needs in Aboriginal children and
adults.
170,171
The eligibility criteria for this program will be reviewed to increase access by Aboriginal and
Torres Strait Islander people.
172
A pooled study describing the effects of breastfeeding across six different countries confirmed that
breastfeeding for at least 3 months significantly reduced the risk of AOM.
173
Breastfeeding among
Aboriginal and Torres Strait Islander women remains high in remote Australia, but appears to be less
common, with a shorter duration in urban locations. Service providers responding to an invitation to
describe the promotion of breastfeeding to Aboriginal and Torres Strait Islander women in 1997 reported
breastfeeding messages delivered opportunistically during routine health care delivery was the most
common intervention used. Access to trained Aboriginal Health Workers and contact with peer
counsellors and grandmothers were also necessary to enhance breastfeeding practice.
174
A systematic
review confirmed that peer support programs can increase breastfeeding.
175
There is little evidence that AOM can be prevented by commencing treatment with antibiotics at the
onset of upper respiratory tract symptoms or as prophylaxis generally (as distinct from prophylaxis in
children with known recurrent OM which is effective).
176
Child health
190
Evidence that cessation of smoking favourably influences the progression of OME is lacking, even
though the association of OME and passive smoking is consistent across a variety of studies.
177
The parental role in the early detection of hearing loss is facilitated by the use of parent-held records
and developmental milestones assessed through questionnaires (see Screening tests).
Pneumococcal (conjugate) vaccination is now a part of the Australian Childhood Vaccination Schedule
given at 2, 4 and 6 months to all Aboriginal and Torres Strait Islander infants. In Australia, the 23vPPV is
recommended for Aboriginal and Torres Strait Islander children from 1824 months as a booster
schedule following the conjugate pneumococcal vaccine given in the NT, central Australia and the
desert and tropical regions of WA, SA and Queensland.
178
The optimal frequency for hearing screening is unclear, as few studies have examined these issues.
The Canadian Task Force on the Periodic Health Examination reported a randomised controlled trial
that demonstrated that the goals of well-baby care (which included the assessment of hearing using a
parental questionnaire) were achieved in a group allocated five or six visits coinciding with
immunisations, compared with a group allocated more frequent visits.
179
WHO indicates that hearing
screening in developing countries should be part of an integrated child development assessment that
includes growth, immunisation and other assessments.
180
Pneumatic otoscope and tympanometry should be available at all health centres providing care for
young children, along with programs to maximise recognition of ear disease in infancy.
181
The Central Australian Rural Practitioners Association recommends examining the ears of all Aboriginal
and Torres Strait Islander children when they present to the clinic (opportunistically). The Northern Zone
Management Unit recommends parental questionnaires regarding infants hearing responses to be
conducted at 6 weeks and 6, 12, 18, 30 and 42 months. Otoscopic examination, audiometry and
tympanometry are recommended in preschool children, and year 1 and year 7 school children.
182
Child health
191
Aboriginal and Torres Strait Islander children have a much higher rate of suppurative
otitis media (OM) and consequent chronic complications than other Australian
children.
EVIDENCE
Level of
evidence
Chronic OM in Aboriginal and Torres Strait Islander children causes prolonged periods
of hearing loss during early childhood.
IIIIV
Regular otoscopic examination is important as OM is often asymptomatic in Aboriginal
and Torres Strait Islander children. Symptoms are an insensitive marker of infection.
IIIIV
Early detection of acute otitis media is important as antibiotic prophylaxis is effective
against recurrent episodes of OM.
I
Early antibiotic intervention may prevent the chronic sequelae of OM. IV
Breastfeeding offers some protection against AOM. I
Peer support programs for breastfeeding should be encouraged. They have been
shown to enhance breastfeeding in Aboriginal and Torres Strait Islander women.
I
Sound field amplification appears to significantly improve comprehension in the school
classroom in children aged 811 years.
III
Children at high risk of hearing impairment include those from socioeconomically
deprived communities and from regions with a high prevalence of OM.
V
Pneumococcal vaccination is effective for the prevention of invasive pneumococcal
disease (see Respiratory disease Communicable). However, both conjugate and
polysaccharide vaccines are less effective for the prevention of OM.
II
RECOMMENDATIONS
Perform otoscopy regularly at primary health care well-baby checks and on children
younger than 5 years at all other opportunities. Management of OM should proceed
according to clinical practice guidelines.
183
V
Screen for hearing loss in all children younger than 5 years and in older children at high
risk of hearing impairment. Audiological screening tools that may assist in the detection
of hearing loss in younger children include simplified parental questionnaires as well as
pneumatic otoscopy or tympanometry in children older than 7 months. Management
should proceed according to clinical practice guidelines.
184
V
Conduct audiometry at or just before school entry. V
Use a preventive health assessment to promote breastfeeding. Refer women to
breastfeeding support programs if needed.
III
The 7vPCV is recommended for all Aboriginal and Torres Strait Islander children as part
of the Australian Standard Childhood Vaccination Schedule (see Immunisation in the
Respiratory disease Communicable section and Australian immunisation handbook,
8th edition).
II
KIDNEY DISEASE
Burden of disease
There is some evidence that Aboriginal children have a higher rate of urinary tract infections, urinary
calculi and glomerulonephritis than non-Aboriginal children, but systematic data on the rate of
urinary/kidney abnormalities is lacking. Urinary tract infection and failure to thrive (FTT) is the most
common presentation of urinary calculi in Aboriginal children. Most children with calculi present at a
young age (2.12.8 years on average), with kidney scarring and hypertension reported as
sequelae.
185,186
The high rate and regional variation of urinary calculi in Aboriginal children have been
reported on many occasions. Over a period of 4 years, 10 children less than 5 years were found to have
kidney stones (representing 16% of the population in that age group) in a remote central Australian
Aboriginal community. The highest rate was in children aged younger than 2 years, where 10% had
kidney stones.
187
In South Australia (SA), a hospital audit for the period 19851991 revealed that 36
Aboriginal children had been admitted with kidney stones and 70% were younger than 2 years.
188
Calculi in children cause considerable morbidity: nearly 80% of a series of Aboriginal children in SA
required major surgery and three kidneys were lost.
189
In some Aboriginal communities, a high rate of proteinuria in children has been noted. In one community
that underwent screening, nearly 8% of children had overt proteinuria and 13% had glomerular
Child health
192
haematuria. Whether this signifies an early manifestation of a continuing process of kidney insults
leading to chronic kidney failure in adulthood is unclear.
190
Another survey in the Northern Territory (NT)
reported that no children and adolescents aged 1019 years (n=52) had evidence of albuminuria.
However, 92% had markers of past group A streptococcal infection (antibodies to streptococcal M
protein). This marker was associated with proteinuria in adulthood, suggesting that childhood skin
infections had increased the risk of adult kidney disease in these children.
191
An association between childhood insults and adult proteinuria was found following examination of 472
Aboriginal people aged 215 years during acute poststreptococcal glomerulonephritis (APSGN)
epidemics in the NT. Those with overt albuminuria were six times more likely to have a history of
APSGN compared with controls (after adjustment for age and sex). This suggests that a history of
APSGN in childhood is a risk factor for albuminuria and haematuria in later life.
192
Low birth weight appears to be a predisposing factor to kidney disease in Aboriginal adults. Low birth
weight Aboriginal children from the NT had lower kidney volumes (likely to reflect lower nephron
numbers) than children with higher birth weights, after correction for current body size. Intrauterine
growth retardation appears to be associated with reduced nephron endowment.
193
Outbreaks of poststreptococcal glomerulonephritis affecting Aboriginal children in northern Australia are
common.
194,195
However, kidney insults in childhood are not unique to remote northern Aboriginal
communities. In Sydney and rural New South Wales, APSGN outbreaks were reported in 19992000,
with the highest incidences affecting Aboriginal children.
196
Very few studies have reported the prevalence of asymptomatic bacteruria (urinary tract infections) in
Aboriginal children. A screen of three Aboriginal communities revealed that 1.7% of children (517
years) had asymptomatic bacteruria.
197
This is similar to rates reported for non-Aboriginal
populations.
198
In the general Australian population, a cross sectional survey of 9355 South Australian
school children revealed 0.81% had clinically significant kidney abnormalities (urinary tract infections,
vesico-ureteric reflux, glomerular disease, kidney stones, essential hypertension, and a kidney
neoplasm).
199
modification*
Nil Nil Nil Yes
management of
skin infections
(impetigo,
scabies, fungal
can prevent
streptococcal
infections
Yes
housing and
overcrowding
to prevent
skin infections
* See Growth failure
Apart from the prevention of streptococcal infections by managing skin infections (impetigo, scabies and
fungal infections), and housing and water infrastructure,
200
it is unclear whether intervention delivered to
children manifesting early kidney damage can prevent the onset of chronic kidney failure in adulthood.
In the past, urinalysis for the general population of children was advocated mainly to identify
asymptomatic bacteruria to prevent the sequelae of pyelonephritis and kidney damage. In addition, the
aim was to identify those with underlying urinary abnormalities in order to preserve kidney function
through early intervention. However, urinalysis in childhood has largely disappeared from the periodic
health examination recommendations of several expert bodies.
Screening
A review of the outcomes of screening and treatment for asymptomatic bacteruria in girls aged 515
years revealed no impact on the rates of pyelonephritis or kidney scarring. An evaluation of the natural
history of asymptomatic bacteruria in Swedish children showed that 80% resolved spontaneously or
after antibiotics given for other reasons. The routine screening of children for asymptomatic bacteruria
was not therefore recommended.
201,202,203
Child health
193
In Japan, urinalysis screening in children is still performed and advocated by many, although there are
doubts about the benefits. Screening for urine abnormalities is believed to have facilitated the early
detection of kidney disease in children. In a case series of children with chronic progressive kidney
disease, 27% were found by routine urinalysis in schools.
204
Although many cases of kidney disease
can be detected, it is still unclear whether screening can alter the prognosis of these children, as there is
no specific treatment in most cases.
205
Some kidney diseases (such as IgA nephropathy) detected by
screening may be steroid responsive, but only about 10% progress to chronic kidney failure anyway.
206
Another follow up study of children with screen detected membranoproliferative glomerulonephritis
reported a better outcome (remission of urinary abnormalities, histological improvement) over 8 years,
suggesting that earlier detection and treatment may have an effect on prognosis. However, this report
was a case series without control groups.
207
A comparison of Japanese children with screen detected
kidney disease and with symptomatic kidney disease concluded that it is still unclear whether mass
urinary screening can alter the outcome of children with glomerulonephritis.
208
There are no published meta-analyses or systematic reviews investigating the benefits or harm of
routine urinalysis in children except where it pertains to urinary tract infections (see above). There are
no published Australian studies that prospectively assess outcomes following urine screening of
Indigenous children, but a study in SA is undertaking kidney screening in an Aboriginal population.
209
The urinalysis of Aboriginal and Torres Strait children would aim to detect asymptomatic bacteruria,
haematuria and proteinuria, which may suggest the presence of previously unknown calculi or
glomerulonephritis. However, whether screening the urine of children can prevent kidney deterioration
due to screen detected glomerulonephritis is not certain. There are no published studies that report on
the screening of Aboriginal or Torres Strait Islander children for asymptomatic kidney stones. As most
calculi occur in young children and are symptomatic, screening for haematuria at older ages may not be
of any value. In those who are younger than 3 years, the collection of urine specimens can be
problematic. Furthermore, the impact of asymptomatic bacteruria in Aboriginal and Torres Strait Islander
children may be quite low, as most are inadvertently treated with the antibiotics given for skin and other
infections.
On the other hand, urinalysis may help maintain health provider awareness of the possibility of these
conditions in Aboriginal and Torres Strait Islander children, as well as reminding parents and care givers
of the importance of symptomatic kidney disease. It may have potential for the preservation of kidney
function, but this has not yet been demonstrated. There is at present no evidence to indicate that urine
screening can cause harm, but providers may instil a sense of fear in Aboriginal and Torres Strait
Islander families when screening may not result in an intervention or treatment that can alter health
outcomes.
210
Chemoprophylaxis
A review of the prevention of glomerulonephritis in Aboriginal and Torres Strait Islander children through
the screening and treatment of impetigo and skin sores concluded there is little evidence to support the
prophylactic use of penicillin as primary prevention. The screening of Aboriginal school children for skin
infections in order to administer prophylactic penicillin to prevent APSGN has been proposed over the
years, but no controlled studies in Aboriginal populations have been conducted to evaluate this
intervention. However, when there is an outbreak of APSGN, prophylactic intramuscular benzathine
penicillin administration can prevent further cases. It is recommended prophylactic antibiotics be
administered to all those at risk, including those aged 315 years who are close contacts of cases
(regardless of the presence of skin sores) and those in the community with skin sores present when
screened.
211,212
There is little evidence to support regular urinalysis in Aboriginal children. There have been no published
Australian position statements or recommendations on this issue.
Neither the Central Australian Rural Practitioners Association or the Northern Zone Management Unit in
north Queensland have recommendations relating to urinalysis in Aboriginal children. Of those
authorities that have recommended urinalysis in children (such as American Acadamy of Pediatrics),
screening at 5 and 15 years has been suggested (with testing at the latter age for dipstick
leucocytes).
213,214
A project team from Centre for Community Child Health in Melbourne, Victoria
recently reviewed childhood surveillance for the National Health and Medical Research Council and
Child health
194
concluded there was no evidence that screening urinalysis prevents kidney or other disease. Treating
asymptomatic bacteruria may even be harmful. Screening urinalysis was not recommended as it was
costly to the community, may result in physical and psychological costs to the clients and their families,
and has high rates of misclassification. Moreover, this team was unable to find any evidence that
measurement of blood pressure as a screening procedure during childhood improves health outcomes,
or that it is a valid or reliable screening test. They report that while it is known that hypertension in
children is linked to the disease in adulthood, there are also many questions about the validity and
reliability of blood pressure readings in children, the significance of diurnal variations, and the levels at
which to commence treatment. Implementation of screening programs to detect hypertension in well
children was not recommended.
215
The review did not examine the role of urinalysis in Aboriginal
children.
There is evidence that Indigenous children have a higher rate of urinary tract
infections, urinary calculi, and glomerulonephritis than other children.
EVIDENCE
Level of
evidence
It is unclear whether urinary screening may alter the outcome for children with
glomerulonephritis.
III
Evidence does not support regular urinalysis or blood pressure measurement for
detecting kidney disease in Indigenous children. There is a lack of evidence that those
with disease detected via screening have a better outcome than those found
symptomatically. It is unclear if harm, such as anxiety within the family, may arise from
routine urinalysis in Indigenous children.
V
RECOMMENDATION
It is not recommended that urinalysis or blood pressure be used to screen for kidney
disease in children unless there is a clinical indication.
V
VACCINE PREVENTABLE DISEASES
Burden of disease
In 2004, the National Centre for Immunisation Research and Surveillance (NCIRS) published the first
comprehensive descriptive analysis of vaccination coverage and vaccine preventable diseases (VPDs)
in the Aboriginal and Torres Strait Islander population at the national level. This confirmed that the
Aboriginal and Torres Strait Islander population experience a substantially higher burden from VPDs in
almost all instances. In addition, incomplete identification of Aboriginal and Torres Strait Islander status
tends to underestimate disease burden.
216
The report examined the following VPDs: Haemophilus
influenzae type B, hepatitis A and B, influenza and pneumonia, measles, meningococcal disease,
pertussis, and pneumococcal disease. Pneumococcal and influenza vaccination have been discussed
elsewhere (see Respiratory disease Communicable section and see also Hearing loss in this section).
Notification data for VPDs with few or no notifications in the period (diphtheria, mumps, polio, rubella,
tetanus) were not presented and are not considered here.
Invasive disease due to H. influenzae type B (Hib) in Aboriginal and Torres Strait Islander children had a
10 times higher incidence rate (notification rate over 20002002) than the non-Indigenous Australian
population, and a higher rate ratio than other VPDs. Overall, Hib cases have declined markedly since
vaccination began in 1993. In the 20002002 period, a total of 47 cases of Hib disease were notified in
children less than 5 years. Almost 50% of these cases were in Aboriginal and Torres Strait Islander
children. Regional variations in immunisation coverage may be a reason for increasing disparity in Hib
disease rates.
Aboriginal and Torres Strait Islander children have a higher burden of hepatitis A infection than non-
Indigenous children, with an incidence rate ratio of 2.9 for the period 20002002 (Table 10). Several
deaths of Aboriginal and Torres Strait Islander children due to fulminant hepatitis A infection have been
reported, making it the most frequent infectious cause of death in Indigenous preschool children in north
Queensland since 1993 (excluding pneumococcal disease).
217
Consequently, in 1999, far north
Queensland introduced routine hepatitis A vaccination of Aboriginal and Torres Strait Islander children
from age 18 months using a two dose schedule at 18 months and 2 years, and a catch up program of
two doses, 6 months apart, up to age 6 years. This program has been very successful in the region and
Child health
195
there have been no notifications of hepatitis A in this population since June 2000. Hepatitis A seems to
have been eradicated from Aboriginal and Torres Strait Islander communities in north Queensland very
soon after the vaccination program began.
218
Following a recommendation from the Australian Technical
Advisory Group on immunisation, hepatitis A vaccination for all Aboriginal and Torres Strait Islander
children in high risk areas will be implemented from 1 November 2005.
Rates of hepatitis B infection in Aboriginal Australians were very high in the 1990s, at which time a
targeted approach to hepatitis B vaccination existed. For example, 46.9% of Aboriginal primary school
age children tested positive for hepatitis B virus in the Northern Territory (NT) in 1989.
219
The national
universal infant vaccination program for hepatitis B commenced in 2000, together with a program
targeting adolescents. There have been no notified or hospitalised cases of hepatitis B in Indigenous
Australian children aged 04 years over the period 19992002. This reflects the success of both the
universal infant hepatitis B vaccination program and antenatal programs. However, new cases of
hepatitis B infection are still occurring in Aboriginal and Torres Strait Islander adolescents aged 1524
years at rates four times higher than the general population (Table 10). Of those infected with hepatitis B
virus at birth, 90% will develop chronic hepatitis. Of these, 25% will progress to liver cirrhosis or
hepatocellular carcinoma.
Measles was associated with high levels of morbidity among Aboriginal and Torres Strait Islander
children in the past, but this is no longer the case, with very low rates of notification and no excess rates
of infection when compared with non-Indigenous children (Table 10).
Notification or hospitalisation rates for meningococcal infections are two times higher in Aboriginal and
Torres Strait Islanders than in the non-Indigenous Australian population (Table 10). The greatest
differential disease burden is evident in children aged 04 years, with a rate ratio of Indigenous to other
notifications of 3.5. Based on outbreak reports, meningococcal infections in the Aboriginal and Torres
Strait Islander population are more likely to be serogroup B disease in the youngest children. The
conjugate meningococcal C vaccine was introduced into the ASVS for all children in 2003.
Overall notification rates for pertussis infections do not appear to differ between the Aboriginal and
Torres Strait Islander and non-Indigenous population (Table 10), however, the notification rate among
children aged 04 years was twice that of the non-Indigenous population. Despite long standing
vaccination programs, these differential rates suggest suboptimal vaccine coverage.
Table 10. Summary of notification or hospitalisation rates of vaccine preventable diseases in
Australia 20002002*
220
Notification or hospitalisation rates (all
ages)
Indigenous age group with peak

incidence
Disease
Indigenous Other
Incidence rate ratio

Age
group
Notification or
hospitalisation rate
Invasive Hib disease 1.2 0.1 9.7 04 10.0
Hepatitis A 9.1 3.1 2.9 04 37.1
Hepatitis B 7.2 1.6 4.4 1524 14.1
Influenza
49.3 17.1 2.9 04 127.3

Measles 0.2 0.4 0.6
Meningococcal
disease
7.2 3.4 2.1 04 50.7
Pertussis 41.8 46.9 0.9 04 89.7
Pneumococcal
disease
44.7 9.9 4.5 04 87.0
* Notifications (New South Wales, Northern Territory, South Australia and Western Australia only) where the date of
onset was 1 January 2000 31 December 2002, except for pneumococcal disease which is from 1 January 2001
31 December 2002
Notifications per 100 000 population (unless otherwise specified), age standardised to the Australian Bureau of
Statistics Australian estimated population 2001
Includes records where Indigenous status was not stated
Influenza data are hospitalisations (all states and territories) where the month of separation was 1 July 1999 30
June 2002
Source: National Centre for Immunisation Research and Surveillance. Vaccine preventable diseases and vaccination
coverage in Aboriginal and Torres Strait Islander people, Australia 19992002, 2004
Child health
196
Types of preventive interventions for vaccine preventable diseases in
children
modification
Yes
Australian
Standard
Vaccination
Schedule
Yes
Antenatal
hepatitis B
virus screening
Nil Yes
Refer to NHMRC
Australian
immunisation
handbook, 8th
edition
Yes
(See Growth
failure)
Immunisation
The National Health and Medical Research Council (NHMRC) has developed the Australian Standard
Vaccination Schedule (ASVS) for all Australians.
221
In order to ensure that Aboriginal and Torres Strait
Islander children can benefit from immunisation, the preventive health assessment must include the
assessment of individual immunisation coverage.
Over the past decade, there have been substantial improvements in the immunisation coverage of
Australian children. However, the immunisation coverage of Aboriginal and Torres Strait Islander
children may still be suboptimal. The NHMRC established a target of greater than 90% immunisation
coverage of Australian children at 2 years for all diseases specified in the schedule by the year 2000.
222
As at 31 December 2004, the national immunisation coverage for children, based on the Australian
Childhood Immunisation Register (ACIR), was 91.2% (at 1215 months) and 91.7% (at 2427 months)
fully immunised.
223
The ACIR cannot at present report accurately on the immunisation coverage of Aboriginal and Torres
Strait Islander children as not all Aboriginal and Torres Strait Islander children are registered on the
ACIR, and those who are, may not identify as Indigenous. The NCIRS analysis of the register data in
2004 indicated that 82% of children aged 1 year recorded as Aboriginal or Torres Strait Islander were
fully vaccinated, a rate 9% below that for non-Indigenous children. By age 2 years, coverage in
Aboriginal and Torres Strait Islander children increased to 90.9%, a rate 0.4% below that of non-
Indigenous children. Using the National Health Survey data (2001), coverage for Aboriginal and Torres
Strait Islander children aged 26 years was estimated 917% lower than non-Indigenous children for
individual vaccines.
224
Urban regions with a high proportion of Aboriginal residents have been shown to be significantly
associated with lower immunisation coverage of children when ACIR data was correlated with
socioeconomic indicators in 1999.
225
Most recently, an evaluation of the ACIR, using a proxy indicator
for Aboriginal and Torres Strait Islander status, concluded that Aboriginal and Torres Strait Islander
immunisation coverage is 17% lower, with the biggest gaps in urban areas.
226
Reasons for suboptimal coverage are unclear. However, despite significant federal investment in
immunisation incentives to general practitioners (GPs) $26 million annually in 19981999
227
several
reviews of immunisation programs and related programs fostered by the Australian Government through
divisions of general practice have concluded that Aboriginal and Torres Strait Islander populations are
overlooked.
228,229,230
Interventions to improve vaccine uptake have been reviewed by the Centres for Disease Control in the
USA.
231
There is good evidence for the effectiveness of a range of strategies, including appropriate
client reminder and recall, multicomponent interventions (such as client education, expanded clinic
hours, reduced distance from vaccination settings to the population, reduced out of pocket costs, home
visits), and school vaccination policies, demonstrated in a range of high risk population subgroups.
There is also good evidence for the effectiveness of vaccination reminders (manual or computerised) to
health professionals as part of client assessment. In this way, standing orders are also effective, but
most studies have examined their use in adult vaccination. Standing orders authorise health workers or
nursing staff to deliver vaccination to client populations by protocol without direct GP involvement.
Home based vaccinations have also been shown in a Victorian trial to improve coverage in children
behind in their vaccination schedule,
232
and to improve vaccination coverage of Aboriginal and Torres
Child health
197
Strait Islander children in a Cairns based program in north Queensland.
233
Neither trial discussed risks
of adverse events in the non-clinic setting.
While there was insufficient evidence to assess the effectiveness of client or family incentives for
improving vaccination coverage, an Australian appraisal of the maternity immunisation allowance
(maternal payment for child vaccination introduced in 1998) found a significant association between
immunisation status of children and parental reports on the influence of the payments.
234
It is unclear if
this incentive payment is accessible to Aboriginal and Torres Strait Islander women and this requires
further investigation.
See also Schemes to increase vaccine coverage in Pneumococcal pneumonia in the Respiratory
disease Communicable section.
Screening
There is little evidence in support of screening for the majority of VPDs described in this section. Outside
of antenatal care, there are currently no Australian guidelines on whether screening for hepatitis B
infection should be offered to all Aboriginal and Torres Strait Islander peoples.
A 2004 review of 703 hepatitis B surface antigen positive patients attending a Melbourne liver clinic
concluded that screening should be offered to people born in, or with parents born in areas of high
endemicity.
235
The US Preventive Services Task Force in 2004 strongly recommended screening for
hepatitis B virus infection in pregnant women at their first antenatal visit.
236
The American Association
for the Study of Liver Diseases practice guidelines updated in September 2003, state that screening for
hepatitis B should occur in pregnant women, children born in hyperendemic areas and family members
of hepatitis B virus infected persons.
237
There is good evidence of the effectiveness of prophylaxis for those exposed to certain VPDs in
specified circumstances. This has been reviewed by the NHMRC in the Australian immunisation
handbook, 8th

edition.
238
In particular, the NHMRC has recommendations pertaining to the
administration of:
normal human immunoglobulin to close contacts of hepatitis A cases
normal human immunoglobulin or immediate vaccination using MMR vaccine for contacts of
patients with confirmed or suspected measles
hepatitis B immunoglobulin as postexposure prophylaxis for non-immune individuals exposed to a
hepatitis B surface antigen positive person
antibiotics as chemoprophylaxis for meningococcal contacts and for the elimination of
nasopharyngeal carriage of Neisseria meningitidis
antibiotics as chemoprophylaxis for contacts of pertussis cases
antibiotics as chemoprophylaxis for contacts of a child with invasive H. influenzae type B infection.
Primary care providers should also be aware of the importance of their role in working with their local
public health units for interventions such as contact tracing and disease notification.
Aboriginal and Torres Strait Islander children should be immunised in accordance with the ASVS (Table
11). There are two diseases in the schedule with vaccination requirements specific to Aboriginal and
Torres Strait Islander children. These are:
Hib infection where the PRP-OMP vaccine is preferred in Aboriginal and Torres Strait Islander
children, and
Pneumococcal infections for which 23vPPV is recommended as a booster dose between age 18
months and 2 years, following a primary course with the 7-valent pneumococcal conjugate vaccine
recommended for all children.
The ASVS shown in Table 11 is recommended by the NHMRC in the current Australian immunisation
handbook, 8th edition. There may be variability in vaccines recommended or funded, depending on the
state or territory in which the vaccinations are being given.
From 1 November 2005, there will be a single schedule the National Immunisation Program Schedule
(NIPS). It will incorporate all the current ASVS vaccines, apart from the 50 year old adult diphtheria and
Child health
198
tetanus booster (which is not funded through the NIPS). The NIPS will also include vaccination for
hepatitis A for Aboriginal and Torres Strait Islander children in high risk jurisdictions (Western Australia,
Queensland, South Australia and Northern Territory).
Table 11. The Australian Standard Vaccination Schedule, 2003
Age Vaccine
Birth Hepatitis B
1
2 mths Hepatitis B
2,3
DTPa Hib
1,2
IPV 7vPCV
4mths Hepatitis B
2,3
DTPa Hib
1,2
IPV 7vPCV
6 mths Hepatitis B
2
DTPa Hib
1
IPV 7vPCV
12 mths Hepatitis B
3
Hib
1,2
MMR MenCCV
18 mths VZV
2 yrs
23vPPV
1
4 yrs DTPa IPV MMR
1013 yrs Hepatitis B
4
VZV
1
1517 yrs dTpa
Schedule key
Hepatitis B
1
Monovalent hepatitis B vaccine
Hepatitis B
2
Hepatitis B vaccine given as either monovalent vaccine or in combination with
DTPa, three doses at 2,4 and 6 months in addition to the birth dose for a total of
four doses
Hepatitis B
3
Hepatitis B vaccine in combination with Hib (PRP-OMP), three doses at 2,4 and
12 months in addition to the birth dose for a total of four doses
Hepatitis B
4
Hepatitis B vaccine for children aged1013 years who have not received a
primary course
Hib
1
PRP-T, HbOC (non-Indigenous children)
Hib
2
PRP-OMP (all children)
23vPPV
1
Pneumococcal polysaccharide vaccine (Aboriginal and Torres Strait Islander
children only). This dose can be given between 18 months and 2 years of age
(refer to state/territory public health units for recommended age for
administration)
VZV
1
Vaccination only for children with a negative history of varicella disease or
vaccination
Vaccine key
Hepatitis B Hepatitis B vaccine
DTPa Diphtheria-tetanus-acellular pertussis infant/child formulation
dTpa Adult/adolescent formulation diphtheria-tetanus-acellular pertussis vaccine
Hib
Haemophilus influenzae type b (Hib) vaccine PRP-OMP, PRP-T, HbOC (as
monovalent or in combination)
IPV Inactivated poliomyelitis vaccine (in combination)
MMR Measles-mumps-rubella vaccine
VZV Varicella-zoster vaccine
7vPCV 7-valent pneumococcal conjugate vaccine
23vPPV 23-valent pneumococcal polysaccharide vaccine
MenCCV Meningococcal C conjugate vaccine
Notes*
Aboriginal and Torres Strait Islander children receive three doses of PRP-OMP vaccine
Non-Indigenous children can receive three doses of PRP-OMP vaccine or four doses of PRP-T or HbOC vaccine.
(Mixing Hib schedules is not recommended. Infants starting with PRP-OMP should continue with PRP-OMP)
Adolescent hepatitis B and VZV are not required if a primary vaccination course has been given in early childhood
Access to the pneumococcal conjugate vaccine is provided to the following groups; all Aboriginal and Torres Strait
Islander children up to age 2 years, Aboriginal children in central Australia up to age 5 years, non-Indigenous children
in central Australia up to age 2 years, and all children under 5 years with medical risk factors that predispose them to
high rates or high severity of pneumococcal infection
IPV is preferred to OPV, subject to the availability of IPV or IPV-combination vaccines but both IPV and OPV are
acceptable for use in the ASVS
* incorporating changes approved by NHMRC in 2004
Source: NHMRC, Australian immunisation handbook, 8th edition, 2003
Child health
199
All states and territories recommend the implementation of the ASVS in the NHMRC Australian
immunisation handbook, 8th edition. Hepatitis A vaccine is currently recommended and funded for all
Aboriginal and Torres Strait Islander children in north Queensland from age 18 months to 6 years (first
dose at 18 months with the second 6 months later).
239
Aboriginal and Torres Strait Islander children have a higher incident rate of vaccine
preventable diseases than non-Indigenous Australian children.
EVIDENCE
Level of
evidence
National aggregate data indicate that immunisation coverage in Aboriginal and Torres
Strait Islander children is suboptimal relative to non-Indigenous children.
III
The National Health and Medical Research Council Australian immunisation handbook,
8th edition, identifies two diseases with vaccination requirements specific to Aboriginal
and Torres Strait Islander children: Hib infections (PRP-OMP vaccine preferred) and
pneumococcal infections (booster dose with pneumococcal polysaccharide vaccine
[23vPPV] following primary course with the conjugate pneumococcal vaccine [7vPCV]).
V
Interventions effective at improving vaccine uptake include mechanisms that enhance
opportunities for the delivery of vaccination, eg. recall systems and provider reminders,
prompting at all clinic visits. Multicomponent interventions include client education,
expanded medical clinic hours, reduction in distance from vaccination settings to the
population (eg. home vaccination), reduced cost to individuals, and combining
vaccination and nutritional programs.
IIII
RECOMMENDATIONS
Conduct regular postnatal review of all infants and complete the Australian Standard
Vaccination Schedule.
V
Use reminders, checklists or computerised prompts during every clinic visit to remind
parents and staff about immunisations needed at that visit.
V
Use growth or nutritional assessments as an opportunity to improve immunisation
coverage.
V
Supplement clinic interventions with population based programs in order to improve
immunisation coverage. Consider local promotional activities and home visits for the
delivery of vaccinations.
V
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174 Engeler T, et al, op. cit.
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177 ibid.
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239 ibid.
Appendix
209
People at very high risk (>20% over 5 years) determined clinically
People who have had a previous cardiovascular event (angina, myocardial infarction, angioplasty, coronary artery bypass
grafts, transient ischaemic attack, ischaemic stroke or peripheral vascular disease)
People with genetic lipid disorders (familial hypercholesterolaemia, familial defective ApoB and familial combined
dyslipidaemia)
People with diabetes and overt nephropathy (albumin:creatinine ratio >30 mg/mmol) or diabetes and other renal disease.
Where CV risk is determined using the Framingham risk equation and tables
The following groups should be moved up one risk category (5%), as their cardiovascular risk may be underestimated in the
Framingham risk equation:
people with a family history of premature coronary heart disease or ischaemic stroke in a rst-degree male relative before the
age of 55 years or a rst-degree female relative before the age of 65 years
Mori
Paci c peoples or people from the Indian subcontinent
people with both diabetes and microalbuminuria
people who have had type 2 diabetes for more than 10 years or who have an HbA1c consistently greater than 8% people
with the metabolic syndrome.
These adjustments should be made once only for people who have more than one criteria (the maximum adjustment is 5%).
Where risk factor levels are extreme
If blood pressure is consistently greater than 170/100 mm Hg or total cholesterol greater than 8 mmol/L or TC:HDL ratio
greater than 8 the person is classi ed at least at high risk (>15%) and should receive speci c lifestyle advice and medication
to lower their risk, irrespective of their calculated cardiovascular risk
For age greater than 75 years the 5 year cardiovascular risk is greater than 15% in nearly all individuals.
The above tables have been reproduced with permission of the New Zealand Guidelines Group, www.nzgg.org.nz.
APPENDIX CARDIOVASCULAR RISK TABLES

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Evidence base to a preventive

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this would be 8625 people.

Indigenous age group with peak

Incidence rate ratio

49.3 17.1 2.9 04 127.3

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