Evidence base to a preventive health assessment in

Transcription

National guide to
a preventive health
assessment for
Aboriginal and
Torres Strait
Islander people
Second edition
National guide to a preventive health assessment for Aboriginal
and Torres Strait Islander people, second edition
Recommended citation
NACCHO/RACGP. National guide to a preventive health assessment for Aboriginal and
Torres Strait Islander people. 2nd edn. South Melbourne: The RACGP, 2012.
Disclaimer
The information set out in this publication is current at the date of first
publication and is intended for use as a guide of a general nature only and
may or may not be relevant to particular patients or circumstances. Nor
is this publication exhaustive of the subject matter. Persons implementing
any recommendations contained in this publication must exercise their
own independent skill or judgement or seek appropriate professional
advice relevant to their own particular circumstances when so doing.
Compliance with any recommendations cannot of itself guarantee
discharge of the duty of care owed to patients and others coming into
contact with the health professional and the premises from which the
health professional operates.
While the text is directed to health professionals possessing appropriate
qualifications and skills in ascertaining and discharging their professional
(including legal) duties, it is not to be regarded as clinical advice and,
in particular, is no substitute for a full examination and consideration of
medical history in reaching a diagnosis and treatment based on accepted
clinical practices.
Accordingly The Royal Australian College of General Practitioners
and its employees and agents shall have no liability (including without
limitation liability by reason of negligence) to any users of the information
contained in this publication for any loss or damage (consequential
or otherwise), cost or expense incurred or arising by reason of any
person using or relying on the information contained in this publication
and whether caused by reason of any error, negligent act, omission or
misrepresentation in the information.
Artwork by Dreamtime Public Relations and commissioned by,
and used for, NACCHO purposes
Published by:
The Royal Australian College of General Practitioners
College House
1 Palmerston Crescent
South Melbourne VIC 3205 Australia
Tel 03 8699 0414
Fax 03 8699 0400
www.racgp.org.au
ISBN: 978-0-86906-341-5
© The Royal Australian College of General Practitioners, 2012. All rights reserved.
National guide to a preventive health assessment for Aboriginal and Torres Strait Islander people
Acknowledgements
The National guide to a preventive health assessment for Aboriginal and Torres
Strait Islander people, second edition, is a collaborative effort of the National
Aboriginal Community Controlled Health Organisation (NACCHO) and The Royal
Australian College of General Practitioners (RACGP).
Project management
Dr Sophie Couzos, Public Health Medical Officer, National Aboriginal
Community Controlled Health Organisation
Ms Lauren Cordwell, Manager, the RACGP National Faculty of Aboriginal and
Torres Strait Islander Health
Clinical editor
Dr David Peiris, The George Institute for Global Health, on behalf of NACCHO,
Tharawal Aboriginal Corporation
Project coordination
Ms Jill Dixon, National Advisor, the RACGP National Faculty of Aboriginal and
Torres Strait Islander Health
Ms Nikola Merzliakov, Projects and Community Relationships Coordinator,
the RACGP National Faculty of Aboriginal and Torres Strait Islander Health
Editorial committee
Dr David Peiris, Dr Sophie Couzos and Dr Tim Senior
Authors
Dr Penny Abbott, Aboriginal Medical Service Western Sydney
Professor Anne Chang, Menzies School of Health Research
Dr Justin Coleman, Inala Indigenous Health Service
Dr Sophie Couzos, National Aboriginal Community Controlled Health Organisation
Dr Emma Fitzsimons, Danila Dilba Health Service
Dr Gabrielle Hall, locum general practitioner, Aboriginal Community Controlled
Health Services
Dr Jenny James, Aboriginal Medical Service Western Sydney
Dr Nadia Lusis, Victorian Aboriginal Community Controlled Health Organisation
Dr Sandra Meihubers, dental public health consultant
Dr Jacki Mein, Apunipima Cape York Health Council
Dr Annapurna Nori, Nunkuwarrin Yunti
Dr David Peiris, The George Institute for Global Health, on behalf of NACCHO,
Tharawal Aboriginal Corporation
Dr Eileen Rafter, Wuchopperen Health Service
Dr Tim Senior, Tharawal Aboriginal Corporation
Professor Tim Usherwood, University of Sydney
Dr Nicolette de Zoete, Kimberley Aboriginal Medical Services Council
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ii
Reviewers
The following people and organisations contributed information that was used in
the National guide to a preventive health assessment for Aboriginal and Torres
Strait Islander people and/or reviewed various drafts of this publication which
were addressed by authors and the Editorial Committee.
Expert reviewers
Professor Bruce Armstrong
Professor David Atkinson
Professor Malcolm Battersby
Dr Alex Brown
Professor Jonathan Carapetis
Associate Professor Wendy Cavilla
Dr Vijenti Chandra
Professor Anne Chang
Professor Stephen Colagiuri
Associate Professor Kate Conigrave
Mrs Patricia Delaney
Dr Elizabeth Denney-Wilson
Professor Gregory Dore
Dr Ben Ewald
Dr Hasantha Gunesekara
Dr Rowena Ivers
Dr Warren Jennings
Associate Professor Amanda Leach
Dr Dina LoGiudice
Dr Vivienne Manessis
Associate Professor Peter Morris
Professor Kaye Roberts-Thomson
Professor Sherry Saggers
Dr Steven Skov
Professor Hugh Taylor
Associate Professor David Thomas
Associate Professor Mark Thomas
Professor Andrew Tonkin
Mr James Ward
Organisational reviewers
Professor David Atkinson, Australian College of Rural and Remote Medicine and
Kimberley Aboriginal Medical Services Council
Professor Bob Batey, Australasian Society for HIV Medicine
Dr Stephen Carbone, Victorian Aboriginal Community Controlled Health
Organisation
Dr Sophie Couzos, NACCHO
Mr William Darbishire, The Australian Lung Foundation
Mr Brian Dooley, Heart Support Australia
Editorial Committee. Queensland Health, Royal Flying Doctor Service of
Australia (Queensland Section) and Apunipima Cape York Health Council.
Chronic Disease Guidelines. 3rd edition, 2010
Editorial Committee. Queensland Health, Royal Flying Doctor Service of
Australia (Queensland Section). Primary Clinical Care Manual. 7th edition, 2011
Healthcare and Education Committee, Diabetes Australia
Dr Robert Grenfell, National Heart Foundation of Australia
Professor David Johnson, Caring for Australasians with Renal Impairment
Dr Erin Lalor, National Stroke Foundation and National Vascular Disease
Prevention Alliance
Associate Professor Tim Mathew, Kidney Health Australia
Dr Liz Moore, Aboriginal Medical Services Alliance Northern Territory
Ms Paula Murray, Asthma Foundation
Dr Cathy Pell, Australasian Society for HIV Medicine
Professor David Roder, Cancer Council Australia
Ms Janet Struber, Central Australian Rural Practitioners Association
Dr Katie Panaretto, Queensland Aboriginal and Islander Health Council
Adult and child preventive health lifecycle charts
Ms Nikola Merzliakov, the RACGP
The Royal Australian College of General Practitioners Project
Reference Group
The following people participated in Project Reference Group meetings to direct
the implementation of the project:
Ms Dea Delaney Thiele (chair), NACCHO
Ms Donna Ah Chee (chair), NACCHO
Dr Sophie Couzos, NACCHO
Dr David Peiris, The George Institute for Global Health on behalf of NACCHO
Associate Professor Brad Murphy, the RACGP National Faculty of Aboriginal
and Torres Strait Islander Health
Professor Mark Harris, University of New South Wales
Dr Joy Eshpeter, Office for Aboriginal and Torres Strait Islander Health
Dr Kerryn Coleman, Office for Aboriginal and Torres Strait Islander Health
Dr Nadia Lusis, Victorian Aboriginal Community Controlled Health Organisation
Dr John Daniels, Redfern Aboriginal Medical Service
Dr Jiri Rada, the RACGP Foundation
Professor David Atkinson, Kimberley Aboriginal Medical Service Council and
Australian College of Rural and Remote Medicine
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Ms Lauren Cordwell, the RACGP National Faculty of Aboriginal and Torres Strait
Islander Health
Ms Jill Dixon, the RACGP National Faculty of Aboriginal and Torres Strait
Islander Health
Ms Nikola Merzliakov, the RACGP National Faculty of Aboriginal and Torres
Strait Islander Health
Endorsement and support
NACCHO and the RACGP acknowledge the following:
Ms Donna Ah Chee (Chief Executive Officer, NACCHO)
Ms Dea Thiele (former Chief Executive Officer, NACCHO)
Mr Justin Mohamed (Chair, NACCHO)
NACCHO Board of Directors
The RACGP National Faculty of Aboriginal and Torres Strait Islander Health Board
The RACGP National Standing Committee – Quality Care
The RACGP Council
Australian College of Rural and Remote Medicine
NACCHO and the RACGP acknowledge the contribution made by the
following RACGP staff:
Ms Jill Dixon, National Advisor, National Faculty of Aboriginal and Torres Strait
Islander Health
Ms Helen Bolger-Harris, Manager, Clinical Improvement Unit
Mr Stephan Groombridge, Program Manager, Quality Care
Ms Nikola Merzliakov, Projects and Community Relationships Coordinator,
National Faculty of Aboriginal and Torres Strait Islander Health
Ms Denese Warmington, Managing Editor, Publications Unit
Mr Jason Farrugia, Senior Graphic Designer, Publications Unit
Ms Morgan Liotta, Production Coordinator, Publications Unit
Sponsors
The Australian Government Department of Health and Ageing, Office for
Aboriginal and Torres Strait Islander Health
Contents
Foreword1
Introduction2
Methodology7
15
What’s new in the second edition?
19
Chapter 1: Lifestyle
Overview20
Smoking21
Recommendations
24
Overweight/obesity27
Recommendations
30
33
Physical activity
Recommendations
36
Alcohol37
Recommendations
39
Gambling43
Recommendations
45
52
Chapter 2: Child health
Immunisation53
Recommendations
55
Anaemia56
Recommendations
58
60
Growth failure
Recommendations
64
66
Childhood kidney disease
Recommendations
68
76
Chapter 3: The health of young people
Overview77
Psychosocial79
Recommendations
79
80
Unplanned pregnancy
Recommendations
82
84
Illicit drug use
Recommendations
88
96
Chapter 4: Dental health
Overview97
Recommendations
99
103
Chapter 5: Rheumatic heart disease
Overview104
Recommendations
111
114
Chapter 6: Eye health
115
Visual acuity
Recommendations
117
118
Trachoma and trichiasis
Recommendations
120
123
Chapter 7: Hearing loss
Overview124
125
Preventive interventions
Recommendations
131
Chapter 8: Sexual health and bloodborne viruses
138
Overview139
Recommendations
149
Chapter 9: Antenatal care
158
Overview159
Recommendations
168
Chapter 10: Mental health
Prevention of depression
Recommendations
Prevention of suicide
Recommendations
178
179
183
184
186
Chapter 11 : Respiratory health
188
Pneumococcal disease prevention
189
Recommendations
191
Influenza prevention
192
Recommendations
194
Asthma195
Recommendations
197
Chronic obstructive pulmonary disease
198
Recommendations
200
Bronchiectasis and chronic suppurative lung disease
202
Recommendations
205
213
Chapter 12: Cardiovascular disease prevention
Overview214
Recommendations
216
Chapter 13: Chronic kidney disease prevention and management
221
Overview222
Recommendations
225
Chapter 14: Type 2 diabetes prevention and early detection
229
Overview230
Recommendations
235
Chapter 15: Prevention and early detection of cancer
239
Overview240
241
Prevention of cervical cancer
Recommendations
242
244
Prevention and early detection of liver (hepatocellular) cancer
Recommendations
245
Prevention and early detection of breast cancer
247
Recommendations
249
252
Prevention and early detection of colorectal (bowel) cancer
Recommendations
254
256
Early detection of prostate cancer
Recommendations
256
Chapter 16: Preventive health for the elderly
262
Overview263
Osteoporosis264
Recommendations
267
Falls269
Recommendations
270
Dementia272
Recommendations
274
Appendix 1
277
Appendix 2
279
Foreword
It is my pleasure to release the second edition of the National guide to a
preventive health assessment for Aboriginal and Torres Strait Islander people
for use throughout Australia. This valuable resource is the product of intense
research by authors with experience within Aboriginal Community Controlled
Health Services, and by the continued collaboration between the National
Aboriginal Community Controlled Health Organisation (NACCHO) and The Royal
Australian College of General Practitioners (RACGP).
The prevention of disease is a core element of primary healthcare. For over
four decades, Aboriginal Community Controlled Health Services have provided
comprehensive and culturally appropriate primary healthcare to Aboriginal and
Torres Strait Islander people. They know what works and how services must be
delivered to reach those who are most vulnerable.
The National guide to a preventive health assessment for Aboriginal and Torres
Strait Islander people will assist health providers in unlocking the health system
– the socioeconomic, geographical and health literacy barriers that prevent
many Aboriginal and Torres Strait Islander people from accessing the services
and the opportunities to be healthy to the same extent as other Australians.
Supported by the latest national and international evidence and good practice
points, the guide will assist health providers to maximise the opportunity for the
prevention of disease at each clinic visit, and inform the set-up of information
management systems for prevention of disease throughout a patient’s lifespan.
The National guide to a preventive health assessment for Aboriginal and
Torres Strait Islander people was conceived and started by NACCHO in 2001
and went on to be supported by the RACGP from 2002. The first edition was
published in 2005 and has proven to be widely used by health services and
health policy makers to inform best practice in preventing disease in Aboriginal
and Torres Strait Islander populations. This second edition has been significantly
updated and improved, with appraisal and endorsement from peak bodies
across Australia.
On behalf of the NACCHO Board of Directors, I wish to acknowledge the
efforts of the RACGP, who worked with NACCHO to update this resource and
commend the National guide to a preventive health assessment for Aboriginal
and Torres Strait Islander people. I encourage health providers to implement
its recommendations to bring about significant improvements in health service
access and health status for the Aboriginal and Torres Strait Islander population.
Mr Justin Mohamed, Chair
National Aboriginal Community Controlled Health Organisation
May 2012
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2
Introduction
The review and updating of the first (2005) edition of the National guide to a
(‘National Guide’) is a joint initiative of the National Aboriginal Community
Controlled Health Organisation (NACCHO) and The Royal Australian College of
General Practitioners (RACGP) National Faculty of Aboriginal and Torres Strait
Islander Health. The National Guide is a practical resource intended for all health
professionals delivering primary healthcare to Aboriginal and/or Torres Strait
Islander people. Its purpose is to provide GPs and other health professionals with
an accessible, user-friendly guide to best practice in preventive healthcare for
Aboriginal and Torres Strait Islander patients.
This second edition of the National Guide comprises:
• the National Guide, which contains evidence statements, recommendations, risk
calculation tables and an outline of the development of the guide
• the evidence base: the collection of evidence underpinning the guide and
recommendations (electronic only) (see the Methodology section ‘Searching the
evidence base and drafting recommendations’)
• a child and adult lifecycle summary chart listing activities recommended at each
age group.
The National Guide is available on the NACCHO and the RACGP websites at www.
naccho.org.au and at www.racgp.org.au/aboriginalhealth/nationalguide.
The National Guide is being integrated into clinical software over time to support
primary healthcare professionals to implement best practice by providing them
with accessible, accurate and up-to-date preventive health information relevant to
Aboriginal and Torres Strait Islander people. For further information contact the
RACGP National Faculty of Aboriginal and Torres Strait Islander Health on 03 8699
0499 or email aboriginalhealth@racgp.org.au.
Purpose
The National Guide is intended for all health professionals delivering primary
healthcare to the Aboriginal and Torres Strait Islander population. This includes
general practitioners (GPs), Aboriginal and Torres Strait Islander health workers,
nurses and those specialists with a role in delivering primary healthcare. The
National Guide makes specific recommendations regarding the elements of a
preventive health assessment across the lifecycle of the Aboriginal and Torres Strait
Islander population.
The aim of the National Guide is to provide an up-to-date, evidence-based national
resource that can help inform health providers and policy makers on a defined set
of activities that are of particular relevance to Aboriginal and Torres Strait Islander
people.
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. The health status of
Torres Strait Islander people is very similar to that of the Aboriginal population, and
the information in the National Guide can be applied to both population groups.
How to use the guide
Using the recommendations
All health professionals delivering primary healthcare to Aboriginal and/or
Torres Strait Islander patients should use the recommendations to enhance the
clinical care they provide. The National Guide aims to complement the RACGP
Guidelines for preventive activities in general practice (the ‘red book’) by dealing
with health issues that are specific to the Aboriginal and Torres Strait Islander
population.
Cross referencing with the RACGP red book
The chosen subject areas in the National Guide represent the key health issues
that are amenable to primary healthcare 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. urinary incontinence), GPs are encouraged to cross-reference with the red
book, which is available on the RACGP website at www.racgp.org.au/guidelines/
redbook. The red book is a synthesis of evidence-based guidelines from Australian
and international sources and provides recommendations for everyday use in
general practice.
Using local guidelines
Healthcare providers (particularly in regional and remote areas) are also
encouraged to refer to local guidelines, where 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 only appropriate for an elderly
Aboriginal patient who was raised in a trachoma endemic area (see Chapter 6:
Eye health). Consequently, many recommendations highlight the importance of
clinical discretion in decision making.
Appraising current preventive practice
Healthcare 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 patients. Providers may also benefit by appraising certain screening
activities for which there are ‘good practice points’ (ie. expert opinion based
recommendations but little current evidence). Inappropriate preventive
interventions may draw resources away from activities known to improve the
health of the Aboriginal and Torres Strait Islander population, such as risk factor
modification and immunisation programs.
Why preventive health assessments are necessary
A systematic and comprehensive approach to prevention
There is strong evidence that the delivery of clinical preventive health services
improves health outcomes. These services include immunisation, screening for
asymptomatic disease, chemoprophylaxis (using medication to prevent the onset
of disease), counselling and other ways to encourage patient behavioural change,
as well as primary healthcare influences over environmental factors.
See the Methodology section ‘Developing recommendations’.
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4
Opportunity to improve Aboriginal and Torres Strait Islander health equality
Primary care providers often miss opportunities for the prevention of chronic
disease and associated complications in the Aboriginal and Torres Strait
Islander population, and miss opportunities to identify if patients are of
Aboriginal and/or Torres Strait Islander origin.
Health service utilisation data indicate that Aboriginal and Torres Strait Islander
people are high users of publicly provided services such as public hospitals and
community health services and low users of medical, pharmaceutical, dental
and other health services that are, for the most part, privately provided.1
Overall, in 2008–09, the potentially preventable hospitalisation rate for Aboriginal
and Torres Strait Islander people (14 564 per 100 000 population) was 4.9 times
the rate for other Australians (2956 per 100 000).2 Potentially preventive chronic
diseases and injury are conditions causing the greatest proportion of excess
deaths for Aboriginal and Torres Strait Islander people.3
Despite the overall health needs being higher for Aboriginal and Torres Strait
Islander people, in 2008–09, average Medicare Benefits Schedule (MBS)
expenditure per person was $363 for Aboriginal and Torres Strait Islander
people and $621 for non-Indigenous Australians, a ratio of 0.58.1 The average
Pharmaceutical Benefits Schedule (PBS) expenditure per person was $250
for Aboriginal and Torres Strait Islander people and $338 for non-Indigenous
Australians, a ratio of 0.74.1
When preventive opportunities are missed, this can lead 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.2 Consequent
life expectancy is much lower – Aboriginal and Torres Strait Islander males
in 2005–07 had a life expectancy of 67 years, 11.5 years fewer than nonIndigenous males2 (based on the Australian Bureau of Statistics revised ‘direct
method’ to account for the under-identification of Aboriginal and Torres Strait
Islander deaths adopted in 2009).
Return on investment
Many chronic diseases within the Aboriginal and Torres Strait Islander
population are unrecognised by patients. 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 patient’ while the patient 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 comorbidities in patients who
already have a chronic disease.
The preventive approach to health has shown return on investment in nonIndigenous Australians, especially federal expenditure on immunisation, public
health campaigns and the incorporation of preventive measures into primary
care.4 Aboriginal and Torres Strait Islander people have a significant capacity
to benefit from preventive healthcare. Given the reduced access to preventive
healthcare by Aboriginal and Torres Strait Islander people and the huge burden
of undiagnosed disease, effort needs to focus on measures to ensure that
Aboriginal and Torres Strait Islander patients who are symptomatic of disease,
as well as those who do not yet know they have disease (subclinical), have
access to help.
Identifying Aboriginal and Torres Strait Islander patients
Implementing preventive health assessments requires healthcare providers to
identify the target population. Research shows that where general practices
take systematic action to improve their identification processes, there is
a corresponding increase in the number of correctly identified patients.5
Identifying Aboriginal and Torres Strait Islander status is a necessary
precondition for participating in the Closing the Gap initiative, agreed by the
Australian Government and the Council of Australian Governments in 2008.6
Without practice awareness, a patient who is of Aboriginal and/or Torres Strait
Islander origin cannot benefit from the measures in the Australian Government’s
Indigenous Chronic Disease Package.6 These include key measures available
under the Practice Incentives Program Indigenous Health Incentive and PBS
Co-payment Measure. For more information see www.medicareaustralia.gov.au/
provider/incentives/pip/forms-guides.jsp#N10068.
The RACGP paper, Identification of Aboriginal and Torres Strait Islander
people in Australian general practice, assists health professionals in identifying
Aboriginal and Torres Strait Islander patients; this is available at www.racgp.org.
au/aboriginalhealth.5
All health professionals have an important role in facilitating the identification of
Aboriginal and Torres Strait Islander patients. In order for a person to identify as
being Aboriginal and/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. Several guidelines
have been developed to assist GPs with this issue.5,7,8
Implementing preventive health interventions
Most preventive interventions are efficiently delivered opportunistically in the clinical
encounter where primary healthcare services are available. Others are delivered
through integrated approaches between primary healthcare providers and other
services such as in the planning and delivery of breast cancer screening.
Using multiple strategies
Implementing preventive health assessment and interventions ideally involves
strategies for both patients and healthcare providers. Usually multiple strategies
are most effective, as exemplified by those used to increase adult vaccination
(see Chapter 11: Respiratory health). 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 patient
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 patient in recognition of
the interdependence of many risk factors and determinants of disease.
Undertaking interventions
A preventive health assessment should be undertaken by healthcare providers
who have the capacity to undertake, or to arrange for, appropriate management
5
6
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.
Appropriate health policies
A supportive health policy is critical to implementing a preventive health
assessment. Examples include financial incentives and workforce support. Those
who have been screened need to be treated, so an effective screening program
will increase the demand for care, yet many health services for Aboriginal and
Torres Strait Islander people are under-resourced. Plans to reduce premature
and excess Aboriginal and Torres Strait Islander morbidity and mortality need to
include investment in the management of previously unrecognised diseases.
Medicare and the Practice Incentives Program Indigenous Health Incentive
General practitioners may undertake preventive activities recommended in the
National Guide as part of their usual consultations. Medicare benefits are payable
for a medical examination or test on a symptomless patient by that patient’s 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.
Medicare rebates for preventive health assessments are available for all Aboriginal
and/or Torres Strait Islander people of any age through an annual health
assessment (Medicare Item 715). General practitioners are advised to check the
requirements in the current online MBS before claiming these items. They need to
be aware of, and comply with, the requirements of the specific MBS descriptors
when providing services. The National Guide contains advice on almost all
elements of the requirements to claim this rebate.
Other MBS rebates can support preventive health assessments of the Aboriginal
and Torres Strait Islander population, including:
• telehealth rebates (eg. item 2100)
• follow up assessments by allied health professionals including Aboriginal and
Torres Strait Islander health workers (AHWs) across Australia (eg. item 81300) or
AHWs in the Northern Territory only or practice nurses (eg. item 10987)*
• follow up of GP management plans by AHWs across Australia (eg. item 10950)
or AHWs in the Northern Territory only (eg. item 10997)*
• immunisation by AHWs in the Northern Territory only (eg. item 10988)*
• antenatal services in RRMA 3–7 areas by AHWs in the Northern Territory only*
(or midwives/nurses) (eg. 16400).
In addition, preventive health assessments can be supported through ‘CTG’
scripts, which provide copayment relief for PBS prescriptions for patients who
identify as Aboriginal and/or Torres Strait Islander. Health services can also receive
incentive payments for identifying Aboriginal and/or Torres Strait Islander patients
and offering these patients a health assessment. The Practice Incentives Program
is outlined at www.medicareaustralia.gov.au/provider/incentives/pip/index.jsp.
* Check MBS eligibility requirements. The Australian Health Practitioner Regulation Agency is
currently nationally registering Aboriginal and Torres Strait Islander health practitioners, which may
affect the eligibility of AHWs (those not registered as ‘practitioners’) to claim MBS rebates, while
broadening eligibility for practitioners.
Methodology
The review and updating of the first (2005) edition of the National guide to a
was undertaken by NACCHO and the RACGP in 2010, and funded by the Office
for Aboriginal and Torres Strait Islander Health. It was led by a project executive
whose role was to coordinate all aspects of the project including liaison with the
funder, convening a project reference group, commissioning a clinical editor,
commissioning authors to develop chapter drafts for specific topic areas,
coordinating expert individual and organisational reviews, formatting and editing
the final version, seeking endorsement and developing print and electronic
strategies for dissemination. The role of the project reference group was to
contribute to and clarify the overall scope of the National Guide, provide advice
regarding its development, periodically appraise the content of draft chapters,
and provide advice regarding its dissemination. The project reference group
included representation from NACCHO, the RACGP, the Office for Aboriginal
and Torres Strait Islander Health, the Australian College of Rural and Remote
Medicine and selected Aboriginal Community Controlled Health Services and
GP representatives.
The development of the second edition comprised three stages:
• Review of the first edition of the National Guide
• Evidence review and formulation of recommendations
• Editorial review, expert review and stakeholder consultation.
Review of the first edition
A formal review of the first edition of the National Guide was conducted
to determine current usage and how the structure, content and modes of
dissemination could be improved. An online survey involving 86 healthcare
practitioners – comprising GPs, nurses and AHWs – was conducted in
September 2010. Following this, 11 key informant interviews were conducted
with a purposive sample to gain a more in-depth understanding of ways
to improve the National Guide. A diverse sample was sought to include
representatives from Aboriginal Community Controlled Health Services, other
Aboriginal health services, general practices and government departments
working in urban, rural and remote settings. Some key findings from this
consultation process are summarised below.
Use of the National Guide varied considerably, with staff from Aboriginal
Community Controlled Health Services reporting greatest usage. A range of
health professionals accessed the National Guide including GPs, public health
medical officers, practice nurses and AHWs. The National Guide was used
for clinical care, teaching, developing policies and guidelines for best practice,
general information, designing health practice protocols, and developing
research and quality improvement questions. Features that made the National
Guide easy to use included the summary charts, layout and provision of
evidence for recommendations and its use as a resource when explaining
health issues with staff, patients, students and trainees. The main barriers
to use included general lack of awareness of the National Guide, out-of-date
recommendations, excessively ‘busy’ charts and summaries, and a lack of
electronic integration with clinical software.
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8
Suggestions to improve the content included:
• provision of more regular updates
• a summary of disease burden data
• practical actions that primary care practitioners can undertake to improve
access to best practice care, including activities that can be undertaken by
non-medical staff.
Formatting suggestions included:
• the provision of practice points
• arranging the content in themes
• evidence of recommendations to be provided in a full reference document.
It was generally considered important that the National Guide be accessible in
a range of formats to enhance accessibility. Both print and electronic versions
were considered necessary. Incorporation into clinical software was frequently
suggested as an effective publication method. Respondents also felt that greater
awareness of the National Guide could be attained through public presentation
opportunities and a targeted marking strategy to various primary care
stakeholders. While most respondents considered it important to have a separate
preventive health guide for Aboriginal and Torres Strait Islander people, a number
of people recommended greater consistency in recommendations between it and
the RACGP Guidelines for preventive activities in general practice (‘red book’).9
Evidence review and formulation of recommendations
Defining the scope
The review of the first edition of the National Guide underscored the importance
of providing practical recommendations to primary care practitioners in the
prevention of disease affecting Aboriginal and Torres Strait Islander people.
The focus is on health issues that were preventable and amenable to primary
healthcare intervention and contributed greatly to the morbidity and mortality of
Aboriginal and Torres Strait Islander people. Existing topic areas from the first
edition were reviewed by the project reference group and all were considered
appropriate for inclusion in the second edition. It was agreed that the following
new topics would also be included: antenatal care, adolescent health, rheumatic
heart disease prevention, asthma, depression prevention, bronchiectasis and
the health of older people.
Despite its breadth, for mainly practical reasons related to time and resource
constraints, it was not possible to include a number of other important
preventive health issues. Examples include genetic testing, pre-conception
counselling, certain cancers and urinary incontinence. Readers are therefore
encouraged to consult other preventive health guides for advice in these areas.
Preventive activities are typically classified as:10
Primary prevention, which avoids the development of a disease. Populationbased health promotion activities are examples of primary preventive measures.
Secondary prevention, which focuses on early disease detection and
implementation of interventions to prevent disease progression and emergence
of symptoms.
Tertiary prevention, which reduces the negative impact of an already
established disease by restoring function and reducing disease-related
complications.
The emphasis of the National Guide was on primary prevention activities.
Additionally, for some topic areas, it was considered important to include
secondary prevention activities if these were considered effective, feasible to
implement and able to make a substantial contribution to reduction in overall
disease burden. For example, it is well established that a large number of
cardiovascular disease (CVD) events occur in people who have had a prior event
and consequently secondary prevention interventions targeting this group play
a key role in reducing overall CVD-related disease burden. Thus, a pragmatic
approach was taken for each topic area to determine if any secondary
prevention activities should be included. This was facilitated by regular
communication between authors, editors, the project reference group and, at
the later stages, expert reviewers.
Developing recommendations
Preventive interventions were:
• classified according to their type and assessed for their effectiveness based
on critical review of established guidelines and empirical literature (see
‘appraisal process’)
• assessed for whether the evidence base informing them was considered
generalisable to an Aboriginal and Torres Strait Islander healthcare context
• assessed for whether they were feasible to implement in a primary healthcare
setting.
Classification of preventive interventions
Interventions were classified into five categories to ensure a systematic and
comprehensive approach to prevention.11
• Immunisation involves the administration of vaccines to prevent the onset of
infectious disease.
• Screening involves the systematic detection and management of disease
before symptoms develop. Screening is warranted when management of the
disease in the preclinical phase confers benefits beyond those from when
the person becomes symptomatic and seeks clinical help. Examples include
screening for diabetes, cancer, osteoporosis and high cardiovascular risk.
• Behavioural interventions involve any interventions that target the actions
a person may take for the purpose of promoting or maintaining health (eg.
physical activity), or brief interventions, for example, to support smoking
cessation or safe sex.
• Chemoprophylaxis involves the use of medication to prevent the onset
of disease or reduce the risk of acquiring disease: for example, use of
angiotensin converting enzyme inhibitors to prevent kidney disease and the
use of antiviral drugs to prevent influenza.
• Environmental influences include community and public health focused
structural interventions that are considered relevant to primary care
practitioners either via direct implementation or via involvement in peripheral
activities such as advocacy and liaison with other agencies. It also includes
systems based interventions conducted in the health service. Examples
9
10
include community based programs to ensure improved food supply, school
based interventions, implementation of systematic recall and reminder system,
advocacy to government stakeholders for local/regional liquor licencing
regulations, and involvement of the health service in social marketing activities.
Generalisability of recommendations to an Aboriginal and
Torres Strait Islander health context
The National Guide was developed with the view that there had to be specific
evidence against generalising national and international recommendations,
before interventions were deemed not to apply to Aboriginal and Torres Strait
Islander populations. Further, the vast heterogeneity of Aboriginal and Torres
Strait Islander populations means that statements based purely on genetic
predisposition to disease are generally unhelpful. Individual predisposing risk
factors such as family history and genetic markers may, however, be relevant.
Factors to consider when assessing whether the evidence was valid for
application in the Aboriginal and Torres Strait Islander health context included:
• differences in prevalence of disease/risk factors for Aboriginal and Torres
Strait Islander populations that may influence the population benefits, costeffectiveness of the intervention, and predictive value of screening tests
• whether sociocultural factors might predicate a different approach
• whether the effectiveness of the intervention is known to exhibit wide variation
depending on geographical region.
Relevance and applicability to primary healthcare
Interventions were also assessed for the context of service delivery in which
they would be principally implemented. Some preventive activities, although
clearly linked to improved health outcomes, were omitted because they are
generally implemented outside the primary healthcare context. Examples
include screening for tuberculosis, interventions to increase workforce
participation and housing and education initiatives.
Other considerations influencing whether recommendations were suitable
for primary healthcare included whether the information was useful for
clinical decision making, particularly for areas where there is clinical practice
uncertainty or where the issue is considered contentious or controversial.
Searching the evidence base and drafting recommendations
The evidence base for the National Guide was informed primarily by national
and international evidence-based guidelines. Published guidelines from several
national and international guideline developer groups were sourced. Where
Australian guidelines were being updated or newly developed, the guideline
developers were contacted to review the most current drafts.
The following guideline developers groups/repositories were reviewed:
• Australian National Health and Medical Research Council (NHMRC) guidelines
portal12
• UK National Institute for Health and Clinical Excellence (NICE)13
• New Zealand Guidelines Group (NZGG)14
• Scottish Intercollegiate Guidelines Network (SIGN)15
• US Preventive Services Task Force (USPTF)16
• US Agency for Healthcare Research and Quality.17
Clinical practice guidelines developed by non-government organisations
were also reviewed. Examples included the RACGP Guidelines for preventive
activities in general practice,9 the Central Australian Rural Practitioners’
Association manual18 and the Therapeutic Guidelines.19
Where existing or newly developed guidelines were considered insufficient for
particular topic areas, systematic reviews and meta-analyses of the primary
research literature were reviewed. In the absence of these studies, or where the
scope was considered insufficient, authors were instructed to conduct literature
reviews of empirical research where relevant. Empirical literature searches
focused on studies published from June 2005 (the date of completion of
evidence reviews for the first edition) to December 2011. In the absence of any
empirical research, authors sought to source expert opinion statements to guide
best practice recommendations. The following sources were used to search
for empirical literature: Cochrane Database of Systematic Reviews, MEDLINE,
Informit, Australian Indigenous Health Infonet, evidence reviews from the British
Medical Journal’s Clinical Evidence and Dynamed, and the USA Centers for
Disease Control.
Authors were instructed to objectively examine the evidence and summarise
the recommendation, critically appraise the source of the recommendation,
assign the level and strength of evidence (see below) and record the relevant
references (see below). To update chapters from the first edition authors
were provided with documents outlining the evidence base used for the
relevant chapter draft.10 They were then asked to review the evidence to
identify whether existing recommendations remained appropriate, whether
any recommendations could no longer be substantiated and needed to be
deleted, and whether any additional recommendations needed to be included.
For sections not covered in the first edition, authors conducted reviews of
national and international guidelines and the empirical literature via the process
described above.
The RACGP Guidelines for preventive activities in general practice format for
providing recommendations was adapted to incorporate the five prevention
categories used to guide the scope of interventions.9 It was assumed that
the populations of interest for all recommendations in the National Guide are
Aboriginal and Torres Strait Islander people. Although a recommendation may
have been equally applicable to other populations, this was considered outside
the scope of this project. A reporting template was used to guide authors in the
format of the recommendations. An example follows.
Topic: Smoking prevention and cessation
Preventive
intervention
type
Who is at risk?
What should be done?
Screening
People aged
≥10 years
Smoking status should be
Opportunistic and
assessed for every patient over 10 as part of an annual
years of age on a regular basis
health assessment
How often?
Level/
strength of
evidence
References
IA
9,20–22
11
12
Critical appraisal and assigning the level and strength of
evidence
For guidelines that were already endorsed or developed by the following
organisations, authors were instructed to not conduct a critical appraisal
process: NHMRC, NICE, SIGN, USPSTF, NZGGG. For other guidelines, authors
were recommended to use the AGREE critical appraisal tool to assess for
guideline quality.15 For systematic reviews and randomised controlled trials the
SIGN appraisal tools were recommended.24,25
Although it was not intended that these questions be formally reported in the
National Guide, authors were provided with the following questions to assist in
the assessment of a study/guideline recommendation:
• What are the most relevant primary and secondary preventive interventions to
report in the National Guide on this topic?
• Is the intervention relevant to primary healthcare?
• For relevant interventions, what is the magnitude of effect? This may be
represented by absolute rates and number needed to treat (NNT) or harm
(NNH), or by absolute differences or differences in relative risk.
• Are the benefits/harms clinically significant?
• Is the intervention generalisable to the Aboriginal and Torres Strait Islander
population?
• Are there any caveats to implementing this intervention?
Each recommendation was graded according to the NHMRC classification
scheme for assigning level (Table 1) and strength (Table 2).26 For some
interventions there was limited evidence from which to draw conclusions on
the intervention’s effectiveness. Expert opinion was therefore considered
very important in interpreting the evidence and making judgements about
the relevance of recommendations to Aboriginal and Torres Strait Islander
health (see generalisability above). Expert opinion based recommendations
were assigned as good practice points (GPP). In determining GPP, there was
regular discussion between authors, the editors and, at the later stages of the
project, the project reference group and external experts. This process was
especially important for determining the optimal frequency of an intervention or
the age from which to commence an intervention. For example, on the basis
of disease prevalence data, many preventive interventions are recommended
to commence at an earlier age in Aboriginal and Torres Strait Islander people
than in the general population. Where needed the project reference group
was also consulted to assist writers by taking a consensus approach to
recommendations.
13
NHMRC levels of evidence and grades for recommendations
These are derived from the NHMRC Levels of evidence and grades for
recommendations for developers of guidelines (2009).26
Table 1. Level of evidence hierarchy
I
A systematic review of level II studies
II
A randomised controlled trial
III–1A pseudorandomised controlled trial (ie. alternate allocation or some
other method)
III–2A comparative study with concurrent controls:
Non-randomised, experimental trial; cohort study; case-control study;
interrupted time series with a control group
III–3A comparative study without concurrent controls:
Historical control study; two or more single arm study; interrupted time series
without a parallel control group
IV
Case series with either post-test or pre-test/post-test outcomes
Table 2. Body of evidence matrix
Component
A (Excellent)
Body of evidence
can be trusted to
guide practice
B (Good)
Body of evidence can
be trusted to guide
practice in most
situations
C (Satisfactory)
Body of evidence
provides support for
some recommendation(s)
but care should be taken
with this application
D (Poor)
Body of evidence
is weak and
recommendation
must be applied with
caution
Evidence
base*
One or more level I
studies with a low risk
of bias or several level
II studies with a low
risk of bias
One or two level II
studies with a low risk of
bias or a SR/several level
III studies with a low risk
of bias
One or two level III studies
with a low risk of bias, or
level I or II studies with a
moderate risk of bias
Level IV studies, or level
I to III studies/SRs with a
high risk of bias
Consistency†
All studies consistent
Most studies consistent
and inconsistency may
be explained
Some inconsistency
reflecting genuine
uncertainty around clinical
question
Evidence is inconsistent
Clinical impact
Very large
Substantial
Moderate
Slight or restricted
Generalisability Population/s studied in
body of evidence are
the same as the target
population for the
guideline
Population/s studied in
the body of evidence
are similar to the target
population for the
guideline
Population/s studied in body
of evidence differ to target
population for guideline but
it is clinically sensible to
apply this evidence to target
population‡
Population/s studied in
body of evidence differ
to target population and
hard to judge whether it is
sensible to generalise to
target population
Applicability
Applicable to the
Australian healthcare
context with few caveats
Probably applicable to the
Not applicable to the
Australian healthcare context Australian healthcare
with some caveats
context
Directly applicable
to the Australian
healthcare context
SR = systematic review, several = more than two studies
* Level of evidence determined from the NHMRC evidence hierarchy (Table 1)
† If there is only one study, rank this component as ‘not applicable’
‡For example, results in adults that are clinically sensible to apply to children OR psychosocial outcomes for one cancer that may be
applicable to patients with another cancer
14
Editorial review, expert review and stakeholder consultation
Authors submitted their drafts to the clinical editor, who reviewed and provided
feedback for suggested revisions. Several chapters, including those authored by
the clinical editor, were also reviewed by the public health medical officer from
NACCHO. Following this a three-member editorial team comprising the clinical
editor, the NACCHO public health medical officer and the medical advisor to
the RACGP Faculty of Aboriginal and Torres Strait Islander Health held several
meetings, each of two days duration, to review all chapter drafts.
Drafts were sent to several independent expert reviewers for appraisal. Reviewers
were given a template to complete in which they were asked the following
questions:
• Are the recommendations consistent with your knowledge of the evidence?
• If applicable to this topic, are the good practice points consistent with your
understanding?
• Where there is a deviation in the above, is that deviation acceptable within the
limits of our knowledge?
• In relation to primary prevention (and possibly secondary prevention), is there
anything that is vital to this topic that has been missed? If so, what?
• Please include any other feedback you may have on this topic.
Reviewers were also invited to make specific comments and suggested
wording changes within each topic draft. The recommended changes to
the topic draft were reviewed by the clinical editor, who then corresponded
with the author to respond to the recommendations. Members of the project
reference group and external peak body organisations were also consulted to
review chapter recommendations and their feedback was incorporated through
editorial team review. The editorial team determined the final content of the
drafts in consultation with authors. The contributing authors, external reviewers
and external peak body organisations invited to comment are listed in the
acknowledgements.
Role of the funding source and conflicts of interest
The revision and updating of the National Guide is a joint project of the
NACCHO and the RACGP National Faculty of Aboriginal and Torres Strait
Islander Health. A grant from the Australian Government Department of Health
and Ageing was provided to the RACGP, to assist in the development of the
content and to assist with the editing and dissemination process. The funding
body for this project had no involvement in the conception and design of
the National Guide, and development of the content. Australian Government
departmental representatives were invited to appraise drafts and make
recommendations to NACCHO and the RACGP for improvements and the
decision to act on these recommendations was independently made by the
editorial team. All contributing authors were asked to declare any pecuniary
or other conflicts of interest and these declarations are included in the list of
authors section. External reviewers and organisations were not funded and the
generosity of their contribution is greatly appreciated.
What’s new in the second edition?
The format of the second edition of the National Guide has been significantly
revised to give some structure to the different types of preventive activities
delivered by primary healthcare providers. All the evidence underpinning the
recommendations is included in the preamble to the recommendations, which is
available at www.racgp.org.au/aboriginalhealth/nationalguide.
The format of the National Guide is now also better aligned with the RACGP
red book. The guide aims to complement the red book by dealing with health
issues that are specific to the Aboriginal and Torres Strait Islander population.
Where issues common in the general Australian population have not been dealt
with in this National Guide (eg. urinary incontinence), health professionals are
encouraged to cross reference with the red book, which is available on the
RACGP website at www.racgp.org.au/guidelines/redbook.
New chapters
Topic
Scope
Gambling
Recommends interventions to prevent gambling related harms:
the identification and management of problem gambling and
gambling prevention strategies including community activities
The health of young
people
Focuses on three key preventive health issues for young
people: psychosocial assessment, unplanned pregnancy and
illicit drug use
Rheumatic heart
disease
Provides recommendations for all people in addition to those
with a history of acute rheumatic fever/rheumatic heart disease
and communities where Group A streptococcal infections are
common and acute rheumatic fever is prevalent
Antenatal care
Focuses on five key preventive health issues for pregnant
women: general assessment at the first antenatal visit,
smoking cessation, alcohol consumption, genitourinary and
bloodborne virus infections and nutritional assessment and
supplementation
Mental health
Focuses on screening for depression and suicide prevention
Preventive health for
the elderly
Focuses on three key preventive health issues for elderly
people: osteoporosis, falls and dementia
15
16
Key changes to existing chapters
Topic
Key changes
Smoking
New recommendations include assessing smoking status regularly,
assessing level of nicotine dependence and implementing a system to
identify all smokers and document tobacco use
Overweight/obesity
New behavioural recommendations for overweight/obese people
including assessing the risk/benefit of orlistat and bariatric surgery, and
the need to advocate for community based interventions to increase
access to healthy food
Physical activity
New behavioural recommendations for people that are insufficiently
active, have diabetes and/or cardiovascular disease. Levels of physical
activity align with the Australian National Physical Activity Guidelines 2010
Alcohol
New recommendations include screening for hazardous drinking in high
risk groups, considering screening for people 10–14 years and advising
women to limit their alcohol intake to no more than 2 standard drinks/
day if they choose to drink while breastfeeding. Health professionals to
promote community-led strategies to reduce alcohol supply
Child health
Includes a significant number of key changes under immunisation,
anaemia, growth failure and childhood kidney disease
Dental health
New recommendations include non-dental professionals undertaking oral
health reviews in addition to regular dental health professional reviews,
application of fluoride varnish for 0–5 year olds, and antibiotic prophylaxis
prior to dental procedures for people at high risk of endocarditis. Health
professionals to advocate for fluoridation of the community water supply
Eye health
New recommendations for eye examinations and visual acuity
assessments throughout the lifecycle as well as specialised assessments
for people with cataracts or diabetes. Advice for smokers and reducing
ocular exposure to UV-B light to reduce cataracts
New trachoma and trichiasis recommendations for those in trachoma
endemic areas include community screening programs, eye
examinations for adults >40 years and prevention and control strategies.
Assessing housing situations for overcrowding and providing support is
also relevant for people outside of trachoma endemic areas
Hearing loss
New recommendations include various vaccinations for children aged
<15 years and pregnant women, providing hearing screening throughout
the lifecycle, and new behavioural, chemoprophylaxis and environmental
recommendations
Sexual health and
bloodborne viruses
Adds general prevention advice that includes behavioural and
environmental recommendations and screening for chlamydia,
gonorrhoea, trichomonas vaginalis, syphilis and hepatitis B. Updated
immunisation advice has been included for hepatitis B, human papilloma
virus, hepatitis A, hepatitis C and human immunodeficiency virus
Respiratory health
This chapter focuses on five key preventive respiratory health issues:
pneumococcal disease, influenza, asthma, chronic obstructive
pulmonary disease (COPD), bronchiectasis and suppurative lung disease.
Asthma, bronchiectasis and suppurative lung disease are new topics
New recommendations for influenza prevention, encouraging good
hygiene practice and minimising exposure risk for healthcare workers.
Other changes include consideration of chemoprophylaxis for people at
high risk of influenza complications and community based strategies to
improve vaccination uptake
New recommendations for pneumococcal disease prevention include
promotion of strategies to improve pneumococcal vaccination uptake
such as reminder/recall systems and community awareness
New recommendations for COPD include offering vaccination, screening
for symptoms of COPD, discussing smoking cessation and minimising
other risk factors for COPD and pharmacotherapy to improve quality of
life
Cardiovascular disease
This chapter focuses on recommendations to determine the
absolute risk for cardiovascular disease (CVD) based on multiple risk
factor assessment for people without an established diagnosis of
cardiovascular disease. Framingham, non-Framingham risk factors and
clinically high risk conditions are presented as well as recommendations
for chemoprophylaxis. Recommendations for those with an established
diagnosis of CVD are also presented. The Australian cardiovascular risk
charts are given in Appendix 1
Chronic kidney disease
New recommendations include screening for chronic kidney disease
(CKD) risk factors for those without risk, screening for CKD with eGFR
and urinary albumin-creatinine ratio for those with a risk factor, and
supporting population-based strategies to reduce scabies and pyoderma
among children. Numerous behavioural and chemoprophylaxis
recommendations have also been included
Diabetes prevention
New recommendations include screening for diabetes from >18 years
of age in regions with high diabetes prevalence and/or with high risk
conditions, but consider an AUSDRISK assessment only in populations
with low prevalence. Behavioural recommendations focus on diet,
physical activity and breastfeeding. Pharmacotherapy is discussed for
people with a high risk condition and advocacy for community based
interventions are recommended
Cancer
Focuses on five areas for prevention and early detection of cancer:
cervical, breast, liver, prostate and bowel cancer. Liver, prostate and
bowel cancer are new topics
New recommendations for cervical cancer include promoting human
papilloma virus (HPV) vaccination and commencing Pap screening
regardless of HPV vaccination status. Other recommendations include
assessing smoking status and offering a sexual health review
New recommendations for breast cancer include discussing
familial breast cancer and breast awareness, while mammographic
screening differs depending on age and level of risk. New behavioural
recommendations cover physical activity, diet, alcohol consumption,
smoking and breastfeeding. Hormone replacement therapy and other
pharmacotherapy are discussed
17
18
References
1.
Australian Institute of Health and Welfare. Expenditure on health for Aboriginal and Torres Strait Islander people
2008–09. Health and welfare expenditure series no. 44. Cat. no. HWE 53. Canberra: AIHW, 2011.
2. Australian Institute of Health and Welfare. The health and welfare of Australia’s Aboriginal and Torres Strait
Islander people, an overview 2011. Cat. no. IHW 42. Canberra: AIHW, 2011.
3. Office for Aboriginal and Torres Strait Islander Health. Aboriginal and Torres Strait Islander Health Performance
Framework. Canberra: Department of Health and Ageing, 2010.
4. Applied Economics. Returns on investment in public health. An epidemiological and economic analysis
prepared for the Department of Health and Ageing. Canberra: Department of Health and Ageing, 2003.
5. The RACGP National Faculty of Aboriginal and Torres Strait Islander Health. Identification of Aboriginal and
Torres Strait Islander people in Australian general practice. South Melbourne: The RACGP, 2011.
6. Close the Gap is ‘a commitment made in 2008 by all Australian governments to work towards a better future for
Aboriginal and Torres Strait Islander people under the National Indigenous Reform Agreement of the Council of
Australian Governments (COAG). It aims to close the gap of Aboriginal and Torres Strait Islander disadvantage in
areas such as health, housing, education and employment’. See www.health.gov.au/tackling-chronic-disease.
7.
Kelaher M, Parry A, Day S, Paradies Y, Lawlor J, Solomon L. Improving the identification of Aboriginal and Torres
Strait Islander people in mainstream general practice. Melbourne: The Lowitja Institute, 2010.
8. Australian Institute of Health and Welfare. National best practice guidelines for collecting Indigenous status in
health data sets. Cat. no. IHW 29. Canberra: AIHW, 2010.
9. The Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice (the
red book), 7th edn. South Melbourne: The RACGP, 2009 cited 2011 October 10. Available at www.racgp.org.au/
Content/NavigationMenu/ClinicalResources/RACGPGuidelines/TheRedBook/redbook_7th_edition_May_2009.
pdf.
10. National Aboriginal Community Controlled Health Organisation. Evidence base to a preventive health
assessment in Aboriginal and Torres Strait Islander peoples. South Melbourne: The Royal Australian College of
General Practitioners, 2005.
11. Jamison DT, Mosely WH, Measham AR, Bobadilla JL (editors). Disease control priorities in developing countries:
an overview. Oxford University Press for the World Bank, 1993.
12. National Health and Medical Research Council, National Institute of Clinical Studies. Clinical practice guidelines
portal. Canberra: Australian Government Department of Health and Ageing, 2011. Cited October 2011. Available
at www.clinicalguidelines.gov.au/.
13. National Institute for Health and Clinical Excellence. Find guidance. London: National Institute for Health and
Clinical Excellence, 2011. Available at http://guidance.nice.org.uk/.
14. New Zealand Guidelines Group. Guidance library. Wellington: New Zealand Guidelines Group, 2011. Available at
www.nzgg.org.nz/search.
15. Scottish Intercollegiate Guidelines Network. Published guidelines. SIGN, 2011. Cited October 2011. Available at
www.sign.ac.uk/guidelines/index.html.
16. US Preventive Services Task Force. Recommendations. Washington DC: US Department of Health and Human
Services, 2011. Cited October 2011. Available at www.uspreventiveservicestaskforce.org/recommendations.
htm.
17. Agency for Healthcare Research and Quality. Evidence based practice. US Department of Health and Human
Services, 2011. Cited October 2011. Available at www.ahrq.gov/clinic/epcix.htm.
18. Central Australian Rural Practitioners Association. CARPA standard treatment manual, 5th edn. Alice Springs,
NT: CARPA, 2009.
19. Therapeutic Guidelines Limited. Therapeutic guidelines products. Melbourne: Therapeutic Guidelines Limited,
2011. Cited October 2011. Available at www.tg.org.au/index.php?sectionid=97.
20. Fiore MC, Jaen CR. Tobacco Use and Dependence Guideline Panel. Treating tobacco use and dependence
2008 update: clinical guideline. Rockville, MD: US Department of Health and Human Services, 2008. Cited
October 2011. Available at www.ncbi.nlm.nih.gov/books/NBK12193/.
21. Ministry of Health. New Zealand smoking cessation guidelines. Wellington: Ministry of Health, 2007.
22. US Preventive Services Task Force. Counseling and interventions to prevent tobacco use and tobacco-caused
disease in adults and pregnant women: US Preventive Services Task Force reaffirmation recommendation
statement. Annals of Internal Medicine 2009;150(8):551-5.
23. AGREE Research Trust. Appraisal of Guidelines for Research and Evaluation (AGREE) Instrument 2011. Cited
October 2011. Available at www.agreetrust.org/.
24. Scottish Intercollegiate Guidelines Network. Methodology checklist 1: systematic reviews and meta-analyses.
SIGN, 2011. Cited October 2011. Available at www.sign.ac.uk/guidelines/fulltext/50/checklist1.html.
25. Scottish Intercollegiate Guidelines Network. Methodology checklist 2: randomised controlled trials. SIGN, 2011.
Cited October 2011. Available at www.sign.ac.uk/guidelines/fulltext/50/checklist1.html.
26. National Health and Medical Research Centre. NHMRC levels of evidence and grades for recommendations for
developers of guidelines. Canberra: NHMRC, 2009. Cited October 2011. Available at www.nhmrc.gov.au/_files_
nhmrc/file/guidelines/evidence_statement_form.pdf.
Chapter 1
Lifestyle
Smoking
Author Penny Abbott
Expert reviewers Rowena Ivers, David Thomas
Overweight/obesity
Author David Peiris
Expert reviewer Elizabeth Denney-Wilson
Physical activity
Author David Peiris
Expert reviewer Ben Ewald
Alcohol
Author Penny Abbott
Expert reviewer Kate Conigrave
Gambling
Author Penny Abbott
Expert reviewer Malcolm Battersby
20
Lifestyle
Overview
This section provides recommendations for interventions to improve health
outcomes related to tobacco smoking, overweight/obesity, alcohol, physical
activity and gambling. In addition to specific tools mentioned within each
risk factor section, the ‘5As’ model is recommended to assist primary care
practitioners in a general approach to lifestyle risk factor assessment and
management. The 5As originally proposed are outlined in Table 1.1.1
Table 1.1. The 5As model for behavioural and other interventions
related to lifestyle risk factors
Assess
Ask about/assess behavioural health risk(s) and factors affecting choice of behaviour change
goals/methods
Advise
Give clear, specific, and personalised behaviour change advice, including information about
personal health harms and benefits. It recognises that the health practitioner can be a catalyst
for action and can enhance motivation for change
Agree*
Collaboratively select appropriate treatment goals and methods based on the patient’s interest
in and willingness to change the behaviour. This involves joint consideration of treatment
options, consequences and patient preferences and setting management goals
Assist
Using behaviour change techniques (self help and/or counselling), aid the patient in achieving
agreed upon goals by acquiring the skills, confidence and social/environmental supports for
behaviour change, supplemented with adjunctive medical treatments when appropriate (eg.
pharmacotherapy for tobacco dependence)
Arrange
Schedule follow up contacts (in person or by telephone) to provide ongoing assistance/support
and to adjust the treatment plan as needed, including referral to more intensive or specialised
treatment. Follow up visits often involve repeating the preceding 4As
*Some models omit the ‘Agree’ component and include an initial ‘Ask’ component in which risk factors
are identified
The 5As model was originally proposed by the US National Cancer Institute
to assist with smoking cessation counselling.2 It was then adapted by the
Canadian Taskforce on Preventive Healthcare and used by the US Public Health
Service to report on the effectiveness of interventions to support tobacco
cessation.3 It has since been adapted for use with broader preventive health
interventions that are administered in a clinical setting.1,4 The model is well
informed by systematic reviews of the evidence on behavioural interventions and
is recognised as an effective mechanism for translating evidence into practice. It
has demonstrated widespread utility in Australia and internationally.5,6
Lifestyle
Smoking
Background
Aboriginal and Torres Strait Islander people over the age of 15 years are twice
as likely to smoke as their non-Indigenous counterparts, with 45% self reporting
as current daily tobacco smokers in 2008.7 Sixty-eight percent of Aboriginal
and Torres Strait Islander children aged 0–14 years live with a smoker.8,9 With
such high prevalence rates, the use of tobacco is a major preventable cause of
premature mortality and morbidity among Aboriginal and Torres Strait Islander
people.9–11 Factors contributing to these high smoking rates include past
government policies where tobacco was included in rations and in lieu of pay,
socioeconomic disadvantage, high levels of community acceptance of smoking
and lack of access to adequately resourced tobacco control interventions.10,12,13
Those at higher risk of developing smoking related complications include those
with diabetes and other cardiovascular risk factors, pregnant women, those
with a mental illness and those with other chemical dependencies.14 Tobacco
smoking was calculated to be responsible for one-fifth of the total deaths of
Aboriginal and Torres Strait Islander people in 2003, with particularly high
mortality rates due to ischaemic heart disease, chronic obstructive pulmonary
disease and lung cancer.11 Smoking in pregnancy is linked to poorer perinatal
and child health.9 Exposure to environmental tobacco smoke is also a significant
cause of mortality and morbidity and children are particularly sensitive to its
effects.15,16
Tobacco dependence can be related to marijuana use. Young people can
initially become dependent on tobacco from mixing it with cannabis. Cannabis
addiction may complicate efforts to quit smoking tobacco.17 (See Chapter 3: The
health of young people.)
Smokeless tobacco, including native tobaccos such as pituri, has been
a historic form of nicotine delivery in Aboriginal and Torres Strait Islander
communities. The tobaccos are chewed or pasted inside the mouth. There has
been little research into the modern day use or effects of smokeless tobacco in
Aboriginal and Torres Strait Islander communities, though this is still practised,
particularly in central Australia.18,19
Interventions
Health practitioners play a vital role in the prevention of smoking and the
reduction of adverse health effects from smoking. All smokers should be
advised to stop smoking and all interested smokers should be offered
support to do so.20 General practitioners are advised to incorporate risk factor
assessment and preventive health interventions within normal consultations
whenever possible and at least annually. Such interventions are likely to involve
management of multiple risk factors including smoking.21,22 There is strong
evidence for the effectiveness of brief advice, brief interventions, cessation
counselling, proactive quitlines and pharmacotherapy in increasing quit rates in
general populations. Although there are relatively few interventions assessing
the effectiveness of these interventions for Aboriginal and Torres Strait Islander
people, there is no evidence to suggest these interventions are any less
effective.10,12,23
21
22
Lifestyle
Brief advice to quit has a small but significant effect on cessation rates.
Assuming an unassisted quit rate of 2–3%, brief advice can increase quitting by
a further 1–3%.24 Brief advice to stop smoking, which can be done in as little
as 30 seconds, probably works mainly by motivating a quit attempt and seems
to have its greatest effect in less dependent smokers.14,20,24 More effective than
brief advice alone is a ‘brief intervention’ delivered by a health professional,
which typically lasts 5–10 minutes. There are many frameworks for the structure
of brief interventions, including the commonly recommended 5As: ask, assess,
advise, assist, arrange (see the introduction to this chapter).20,21,25 Typical brief
intervention activities include screening, providing brief advice, counselling
techniques such as motivational interviewing, and recommending specialist
support and/or pharmacotherapy as required. There is a dose-response effect
to these intervention activities: the longer the duration of the person-to-person
intervention the more effective it is.26 There is no evidence that any particular
behaviour change method is more effective than another, but the basic
principles of setting a quit date, emphasising the importance of abstinence
and providing multisession support (preferably four or more sessions) are
important.20,26 Relapse prevention advice for quitters in the first year after
smoking cessation is recommended;4,26 however there is insufficient evidence to
recommend any specific relapse prevention interventions.20,27
Assessment of readiness to quit assists in planning treatment, and tailoring
interventions according to whether the patient is willing or unwilling to quit is
helpful.26 Traditionally patients have been classified into the following stages of
readiness to quit: pre-contemplation, contemplation, preparation, action and
maintenance.14 However, there is no evidence the stages of change model is any
more useful in smoking cessation than any other approach and should not limit
health professionals from using interventions such as motivational interviewing
for people who profess unwillingness to quit.20,26,28 Smoking cessation advice
should be sensitive to the patient’s preferences, needs and circumstances.
Factors consistently associated with higher abstinence rates are high motivation,
readiness to quit, moderate to high self efficacy, supportive social networks and
lower nicotine dependence. The Fagerström test for nicotine dependence is
a validated measure for assessing nicotine dependence and may be useful in
predicting relapse to smoking and guide a clinician on the intervention needed
(see Resources).14,22,28
Flexible and culturally targeted modes of delivery of smoking cessation
interventions are likely to be important to, and improve their effectiveness for,
Aboriginal and Torres Strait Islander people.12,13,30 The effect of training health
professionals to give cessation advice appears to be modest in reducing
smoking rates on an individual basis but on a population health level it is
effective.26 Treatment delivered by a range of health professionals increases
tobacco cessation rates.20,26 At the health service level, instituting a practice
system designed to identify and document tobacco use, such as a clinic
screening systems and the use of computer prompts, almost doubles the rate of
health professional intervention and results in higher rates of cessation.14,26
Referral to quitlines should be strongly considered for all smokers. There is
conflicting evidence of their effectiveness in Indigenous or minority communities;
however quitlines have been shown to be effective in many populations
worldwide and are likely to be beneficial for Aboriginal and Torres Strait Islander
people.10,12,20,21,23,26,30
Lifestyle
Self help materials are defined as resources provided to an individual
unaccompanied by any intervention provided by a health practitioner. They may
be written, internet based or other media. Self help resources appear to have
a small effect in increasing quit rates compared to no intervention.31,32 There is
no current evidence that they have an additional benefit when used alongside
other interventions such as advice from a healthcare professional or nicotine
replacement therapy (NRT). Tailoring of materials increases their benefit.31
Aboriginal and Torres Strait Islander people are likely to prefer resources that are
targeted and relevant to their community.10
Pharmacotherapies increase the effectiveness of smoking cessation counselling
and should be offered to all smokers who wish to quit, except those in whom
there are medical contraindications or insufficient evidence of effectiveness,
such as pregnant women, light smokers and adolescents.20,26,30 Nicotine
replacement therapy doubles the rate of successful quit attempts. Bupropion
and varenicline triple the rate of success, but have a greater side effect profile
than NRT.26,33 Varenicline and bupropion are not recommended for use in
pregnancy; NRT can be considered during pregnancy after discussion of the
risks and benefits.30
Smoking cessation counselling has been shown to be effective for
adolescents,26 but there is a lack of clear evidence as to the specific
interventions of most use in this group. It is recommended that interventions
that are known to be effective in adults are also offered to adolescents.20 There
is still a lack of evidence as to the effectiveness of school education programs in
reducing the uptake of smoking.34 There are several as yet unevaluated school
education programs that have been developed for Aboriginal and Torres Strait
Islander children and adolescents.10 Computer and internet cessation programs
are potential vehicles for smoking cessation programs for young people.14,32
Multicomponent community interventions appear to have some effect in
reducing uptake of tobacco use in young people.35 Mass media campaigns can
prevent the uptake of smoking by young people and work best when combined
with broader tobacco control measures such as restricting adolescents’ access
to tobacco.30,36,37
Environmental tobacco smoke (ETS), or secondhand smoke, causes asthma,
ischaemic heart disease, COPD and lung cancer in non-smokers and is linked
to multiple other diseases.38 Children are particularly susceptible to ETS, of
particular importance given the high rates of ETS exposure for Aboriginal and
Torres Strait Islander children both in utero and after birth.39 Intensive efforts to
reduce children’s exposure to secondhand smoke are required and may include
parental education and legislative initiatives.15,40
Public health initiatives are important in reducing smoking prevalence. Broad
initiatives, such as raising standards of living and improving educational and
employment opportunities, are critical to reducing smoking and the harm it
causes for Aboriginal and Torres Strait Islander people.10,12,14,41 Multicomponent
smoking cessation interventions are likely to increase abstinence rates and
should be encouraged.6,20,26 This includes key public health initiatives such as
price increases and taxation, restricting tobacco industry marketing, smokefree
regulations (smoking bans), particularly in workplaces, and mass media
campaigns.15,38,42
23
24
Lifestyle
Recommendations: Primary prevention
Preventive
intervention
type
Who is at
risk?
How often?
Level/strength References
of evidence
Screening
People aged
≥10 years
Smoking status should be
assessed for every patient
over 10 years of age on a
regular basis
Opportunistic
and as part of
an annual health
assessment
IA
20,21,26,43
Current
smokers
A system for identifying all
As part of a
smokers and documenting
systematic health
tobacco use should be used in service approach
every health service
IIB
14,26
Assess the level of nicotine
dependence to help predict
relapse to smoking and
guide intervention choice
(eg. Fagerström test: see
Resources)
GPP
22,23,44
IIIC
14,16,21,26,36,45
Behavioural
Non-smokers
Opportunistic
Advise non-smokers to limit
Opportunistic
their exposure to tobacco
smoke, especially parents of
babies, young children and
pregnant women
Parents who smoke should be
counselled not to smoke in the
house or in a confined space
such as a motor vehicle
Lifestyle
25
Recommendations: Interventions for smokers
Who is at
risk?
How often?
Behavioural
Current
smokers
All patients who smoke, regardless of
the amount they smoke and whether
they express a desire to smoke or not,
should be offered brief cessation advice
at every visit (consider using the 5As
framework – see Chapter 1: Lifestyle,
introduction)
Opportunistic at IA
every visit and
as part of an
annual health
assessment
14,20,21,26,43
Brief interventions should be adapted
to local cultural setting (see Resources:
SmokeCheck)
N/A
GPP
12,13,21,25
Smoking cessation counselling should
be offered to all people at every
opportunity, and if possible, should
comprise at least four face-to-face or
group support sessions
Opportunistic
IA
20,26,46
Consider referral to a proactive smoking Opportunistic
cessation telephone service such
as a quitline, particularly for people
with limited access to face-to-face
counselling
IIA
10,12,20,21,
23,26,30
Make available tailored self help quit
smoking materials, both print and
electronic
Opportunistic
IB
16,20,26,32,46
Within 1 week
of quitting
Then within
1 month of
abstinence
Then
opportunistic
for at least
1 year
IIC
14,20,26,27,47
IA–IIIC
16,21,43,48,49
IA
20,26,30
People
Offer follow up visits for smokers
who have
attempting to quit
stopped
smoking in
the past year
Pregnant
women who
are current
smokers
Chemoprophylaxis Current
smokers
Environmental
Offer intensive smoking cessation
counselling (see Chapter 9: Antenatal
care, for detailed recommendations)
Recommend smoking cessation
pharmacotherapies to patients
interested in quitting. First line
treatments are NRT, bupropion and
varenicline
Pregnant women may be offered NRT
if the benefits outweigh the risks (see
Chapter 9: Antenatal care)
Opportunistic
Level/
strength of
evidence
References
Preventive
intervention type
GPP
Complement the above individual
based strategies with a community
based approach to tobacco control (eg.
promotion of smoke free workplaces)
IIIC
10,50,51
Promote training of Aboriginal and
N/A
Torres Strait Islander health workers in
brief interventions for smoking cessation
to increase quit rates
GPP
10,12
26
Lifestyle
Resources
Educational and quitting resources (Centre for Excellence in Indigenous Tobacco
Control)
www.ceitc.org.au
Tobacco in Australia: a comprehensive review of the major issues in smoking and
health in Australia (Cancer Council Victoria)
www.tobaccoinaustralia.org.au
Fagerström nicotine dependency test
www.health.wa.gov.au/smokefree/docs/Fagerstrom_Test.pdf
Detailed information on tobacco resources, publications, programs and projects
(Australian Indigenous HealthInfoNet)
www.healthinfonet.ecu.edu.au/health-risks/tobacco
Brief intervention and self help resources to promote smoking cessation for Aboriginal
people (SmokeCheck)
www.smokecheck.com.au/about/resources/index.php
Medicines to help Aboriginal and Torres Strait Islander people stop smoking:
a guide for health workers
Email IndigenousTobacco@health.gov.au for a copy
Medicines to help you stop smoking: a guide for smokers
Email IndigenousTobacco@health.gov.au for a copy
Supporting smoking cessation: a guide for health professionals (RACGP)
www.racgp.org.au/guidelines/smokingcessation
National Tobacco Campaign including ‘Break the Chain’ campaign for Aboriginal and
Torres Strait Islander people and Quitline (proactive telephone support) information and
referral forms (Australian Government)
www.quitnow.gov.au/internet/quitnow/publishing.nsf/Content/home
Closing the Gap clearinghouse (AIHW)
www.aihw.gov.au/closingthegap/documents/resource_sheets/ctgc-rs04.pdf
Quitting resources (NSW Health)
www.health.nsw.gov.au/PublicHealth/healthpromotion/tobacco/cessation.asp
Internet smoking cessation programs and resources
National youth smoking website
www.OxyGen.org.au
Quitcoach
www.quitcoach.org.au.
Lifestyle
27
Overweight/obesity
Background
Obesity is a surplus of body weight due to an excess accumulation of body
fat.52 Being overweight is an independent risk factor for numerous comorbidities
associated with metabolic complications and/or the excess weight itself.53 It is
associated with other cardiovascular risk factors including insulin resistance,
blood pressure elevation, elevated triglycerides and reduced high density
lipoprotein (HDL) cholesterol levels.54
Body mass index (BMI) is an approximate measure of total body fat represented
by weight/(height in metres) squared. BMI is the recommended measure for
classifying overweight (BMI >25 kg/m2 for adults and >85th centile for children
aged 2–18 years) and obesity (BMI >30 kg/m2 for adults and >90th centile
for children aged 2–18 years).55 It is important to note, however, that these
thresholds for overweight and obesity are derived from Caucasian populations
and they may not be applicable to some Aboriginal and Torres Strait Islander
people. While there are presently no adjusted thresholds validated for Aboriginal
and Torres Strait Islander people, a BMI of 22 kg/m2 for overweight adults has
been proposed as a more accurate representation of risk, particularly in remote
populations.56
Waist circumference, as an indicator of abdominal adiposity, may be a better
predictor of obesity associated complications for Aboriginal and Torres Strait
Islander populations,56,57 and should be used in combination with BMI to
refine assessment of risk.58 Waist circumference may be easier to measure
by the patients themselves and thus an appropriate alternative measure for
self assessment and monitoring (see Resources).59 World Health Organization
guidelines provide thresholds that combine BMI and waist circumference
to assess disease risk of type 2 diabetes, elevated blood pressure and
cardiovascular disease. These are shown in Table 1.2.
Table 1.2. Combining measures to assess obesity and disease risk* in adults
Classification
Body mass index
(kg/m2)
Disease risk (relative to normal measures)
Waist circumference
Men 94–102 cm
Women 80–88 cm
Waist circumference
Men >102 cm
Women >88 cm
Underweight
<18.5
–
–
Healthy weight
18.5–24.9
–
Increased
Overweight
25.0–29.9
Increased
High
Obesity
30.0–39.9
High to very high
Very high
Severe obesity
>40
Extremely high
Extremely high
* Risk of type 2 diabetes, elevated blood pressure and cardiovascular disease
Source: NHMRC 2003a2
28
Lifestyle
The 2004–05 National Aboriginal and Torres Strait Islander Health Survey is the
most recent comprehensive survey of dietary activity and overweight/obesity. It
found Aboriginal and Torres Strait Islander males and females were 1.5 and 2 times
more likely respectively to be obese than non-Indigenous males and females.60
Further, the survey found that Aboriginal and Torres Strait Islander people were
twice as likely to report no usual daily fruit intake and seven times more likely to
report no daily vegetable intake when compared with non-Indigenous Australians.60
Poor food supply is a major barrier to addressing healthy nutrition for Aboriginal
and Torres Strait Islander people. A 2008 survey in the Northern Territory found that
55% of surveyed communities did not have access to any fresh food for extended
periods.61 In both urban and remote areas food access is affected by low income
and inadequate transport;62 overcrowding, poor housing and inadequate cooking
and food storage facilities are additional environmental factors.63 Community store
and takeaway food is often nutritionally poor and apart from traditional food sources
is the principal source of food in many areas. Even if nutritious, less energy dense
food is available it is disproportionately more expensive than energy dense food and
therefore less accessible to people on low incomes.64
Counselling to promote healthy eating is widely recommended in clinical
guidelines. Encouraging people to adopt healthier diets as part of a specific weight
management plan (which includes at a minimum targeted information, goal setting
and follow up consultations) has been shown to change dietary intake and lead
to improved health outcomes.65,66 A combination of advice on diet and exercise is
more effective than advice on either diet or exercise alone.65 A low energy diet is the
most effective intervention for weight loss.58
The Australian Dietary Guidelines for adults are highlighted in Table 1.3. Two
recommendations that may be more relevant to some Aboriginal and Torres Strait
Islander communities are also included.
Table 1.3. Dietary guidelines for Australian adults*
• Enjoy a wide variety of nutritious foods
• Eat plenty of vegetables, legumes and fruits
• Eat plenty of cereals (including breads, rice, pasta and noodles), preferably wholegrain
• Include lean meat, fish, poultry and/or alternatives
• Include milks, yoghurts, cheeses and/or alternatives. Reduced-fat varieties should be chosen,
where possible
• Drink plenty of water
• Choose store foods that are most like traditional bush foods*
• Enjoy traditional bush foods whenever possible*
• 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
Source: NHMRC 2003b28
* Recommendations specific to some Aboriginal and Torres Strait Islander communities
Lifestyle
Cognitive focused behavioural interventions include situational control and stimulus
control avoiding cues, cognitive reframing, reinforcement techniques, self recording of
calorie intake and eating behaviours, goal setting and relapse prevention strategies.
The combination of diet plus exercise plus behavioural interventions produces more
beneficial outcomes than each component in isolation.58
Orlistat is the most effective agent in the treatment of obesity and should be prescribed
in combination with a weight reducing diet and other lifestyle changes to maximise
its effectiveness. It also causes small decreases in total cholesterol, glycosylated
haemoglobin and progression to diabetes.58,66 Orlistat in combination with behavioural
interventions can lead to greater weight loss than behavioural interventions alone.66 The
most common side effects of orlistat medication are gastrointestinal and these are more
likely if the diet is high in fat. Typically treatment should only be continued beyond 12
weeks if there has been at least a 5% weight loss. The risks and benefits should therefore
be thoroughly discussed before considering adding Orlistat to behavioural interventions.
There has been one systematic review which has found that bariatric surgery,
mainly in people with a BMI ≥35 kg/m2, is an effective weight loss intervention.58,67
Bariatric surgery encompasses a range of procedures that are either restrictive
(eg. laparoscopic banding, sleeve gastrectomy), malabsorptive (eg. bilio-pancreatic
diversion) or a combination of the two. It has also been shown to reduce all-cause
mortality and have a number of other clinically significant health outcomes (eg.
improved cardiovascular risk, glycaemic control and renal function). The degree of
weight loss is influenced by the type of surgery that is performed, with malabsorptive
procedures tending to produce the greatest weight loss. One large cohort study
found that surgery is associated with some harms (wound complications, bleeding,
thromboembolism, pulmonary complications)68 and so the decision to recommend
surgery should be balanced against these harms.
There are few robust evaluations of health promotion strategies to prevent overweight/
obesity in Aboriginal and Torres Strait Islander communities. Interventions to improve
food security include school based nutrition education programs, structured
workshops, cooking classes, demonstrations and community kitchens. There is
both local and international evidence to suggest that these programs can improve
participants’ food security through developing cooking, shopping and budgeting skills
as well as reducing social isolation. Interventions that employ a peer-to-peer education
model are likely to more effective in enhancing food security.
One reason for the limited success of prevention programs is the failure to incorporate an
intersectoral approach. The National Aboriginal and Torres Strait Islander Nutrition Strategy
and Action Plan identified the following seven priority areas to build on efforts to improve
access to nutritious and affordable food across urban, rural and remote communities:
• Food supply in remote and rural communities
• Food security and socioeconomic status
• Family focused nutrition promotion
• Nutrition issues in urban areas
• The environment and household infrastructure
• Aboriginal and Torres Strait Islander nutrition workforce
• National food and nutrition information systems.
29
30
Lifestyle
More recently the National Preventative Health Strategy has stressed that
multicomponent, community based programs are critical to reducing the
obesity related disease burden experienced by Aboriginal and Torres Strait
Islander people.68 A number of environmental strategies have been introduced
to improve remote store food supply, including food production, freight
subsidies, store food and nutrition policies, improved management of stores
through training and education, store charters outlining consumers’ and store
operators’ rights and obligations, takeaway outlet interventions, food aid and
food subsidy programs, interventions to improve storage and kitchen facilities
and health education.69,70
The complexity of interventions highlights the importance of coordinated action
between health and non-health sectors to improve the range, quality, variety and
cost of food supplies to remote and rural communities. It is important primary
care practitioners are aware of the breadth and complexity of these interventions
as they may be able to play a key role in their implementation at the local level.
Recommendations: Overweight/obesity
Preventive
intervention type
Who is at risk? What should be done?
How often?
References
Level/
strength of
evidence
Screening
All people aged
<18 years
Assess BMI using age and
sex specific centile charts (see
Chapter 2: Child health and
Resources)
Opportunistic
and as part of
an annual health
assessment
GPP
58
All people aged
≥18 years
Assess BMI and waist
circumference (see Table 1.2)
Opportunistic
and as part of
an annual health
assessment
GPP
58
1B
58
Groups associated with
improved outcomes from BMI/
waist circumference monitoring
include:
• individuals seeking advice on
weight management
• those with conditions
associated with overweight/
obesity (CVD, diabetes, stroke,
gout, liver or gallbladder
disease)
Behavioural
All people aged
≥18 years
Provide brief advice to promote
healthy eating and physical
activity as per Australian
guidelines (see Table 1.1 and
Chapter 1: Physical activity)
Opportunistic
GPP
Adults with
overweight/
obesity
Develop a weight management
plan that must include:
Opportunistic
and as part of
an annual health
assessment
IB
58,65
IC
71
• targeted information as per
Australian dietary guidelines
(see Table 1.3)
• goal setting
• at least one follow up
consultation
Encourage regular self weighing
Lifestyle
Children with
overweight/
obesity
Chemoprophylaxis People aged
≥18 years with
one or more
weight related
comorbidities
present (severe
mobility
restriction,
arthritis, type 2
diabetes) and a
BMI ≥28 kg/m2
Encourage a net energy deficit
through combined dietary and
physical activity interventions
as per Australian dietary and
physical activity guidelines
IB
Consider referral to specialist
services, dietitian and/or exercise
physiologist if available
GPP
Individual or group based
psychological interventions* are
recommended in combination
with dietary and physical activity
advice
IA
58,66
IB
58
Except in severe obesity, weight
maintenance rather than weight
loss is recommended for healthy
growth and development
Recommend referral for
specialist review for children with
severe obesity
IVD
58
Assess risk/benefit of orlistat on Opportunistic
an individual basis in conjunction and as part of
with lifestyle interventions
an annual health
assessment
IA
58,66
IIC
58,67
GPP
69,70
Develop a targeted weight
management plan as for adults.
This plan must involve at least
one parent/carer and aim to
change the whole family’s
lifestyle
Opportunistic
and as part of
an annual health
assessment
Surgical
People aged
≥18 years with
one or more
weight related
comorbidities
present (as
above) and a
BMI ≥35 kg/m2
Assess risk/benefit of bariatric
surgery on an individual basis
in conjunction with lifestyle
interventions
Environmental
Communities
Advocate for multifactorial and
N/A
coordinated community based
interventions to increase access
to healthy and nutritious food (eg.
subsidised healthy food in stores)
Opportunistic
31
58,72
*Cognitive focused behavioural interventions include: situational control and stimulus control, avoiding cues to overeating, cognitive reframing
and reinforcement techniques, self recording of calorie intake and eating behaviours, goal setting and relapse prevention strategies
32
Lifestyle
Resources
Growth charts (Centers for Disease Control and Prevention)
www.cdc.gov/growthcharts/cdc_charts.htm
BMI charts (WHO)
children 5–19 years
www.who.int/growthref/who2007_bmi_for_age/en/index.html
children under 5 years
www.who.int/childgrowth/standards/bmi_for_age/en/index.html
Helpful tips for measuring waist circumference (Australian Government)
www.health.gov.au/internet/abhi/publishing.nsf/Content/
How+do+I+measure+myself-lp.
Lifestyle
Physical activity
Background
Physical activity is any bodily movement produced by skeletal muscles that
results in energy expenditure.74 This definition importantly recognises that physical
activity is not restricted to structured exercise programs. Lack of physical activity
is an independent risk factor for a range of diseases, in particular cardiovascular
disease (CVD), diabetes, some cancers and osteoporosis.75 Non-vigorous (light
or moderate) physical activity reduces the risk of all-cause mortality, with the
greatest benefits apparent in moving from no activity to low levels of activity. Two
and a half hours per week of moderate physical activity* (equivalent to 30 minutes
daily of moderate intensity activity on 5 days a week) compared with no activity
is associated with a reduction in mortality risk of 19%, while 7 hours per week
of moderate activity compared with no activity reduces mortality risk by 24%.76
Being based on self reported data, this may be an underestimate of the true
mortality benefit from physical activity. Other studies using objective measures of
physical activity expenditure have shown up to a 69% reduction in mortality in the
upper tertile of activity when compared with the lower tertile.77
By contrast with most other risk factors, physical inactivity is equally and highly
prevalent among Aboriginal and Torres Strait Islander people when compared
with non-Indigenous people. Based on 2004–05 National Health Survey and
National Aboriginal and Torres Strait Islander Health Survey data, no exercise or
low levels of exercise was reported by 75% of those aged 15 years and over in
the 2 weeks prior to interview.78,79
Interventions
There is evidence that interventions to increase physical activity can lead to
significant risk reductions in vascular disease and diabetes.80,81 Further, a health
benefit accrues to people who increase their physical activity levels, even
in the absence of weight reduction. Secondary prevention interventions for
people with diabetes and both postacute and stable CVD are also effective.82
Targeted interventions involving professional guidance and continued support
can lead to moderate short and midterm increases in self reported physical
activity, achievement of a predetermined level of physical activity and improved
cardiorespiratory fitness.83,84
The specific components of successful interventions are difficult to discern owing
to large heterogeneity in the types of interventions previously studied. When
translating clinical trial based interventions into real world settings there appears
to be a substantial reduction in the effectiveness of those interventions.85 A World
Health Organization systematic review of 67 studies examining 29 primary care
based strategies concluded that the most effective interventions need to be
moderately intensive and include three key components:86
• a
t least one session involving a health risk appraisal with a healthcare
professional, with brief negotiation or discussion to decide on reasonable,
attainable goals, and a follow up consultation with trained personnel
• support with targeted information
• linked and/or coordinated with other stakeholders such as community
sports organisations, ongoing mass media physical activity campaigns and
integration with social support measures (eg. buddy system, contracts for
exercise, group activities).87
33
34
Lifestyle
Use of pedometers has been shown to lead to an absolute short term increase
in physical activity of around 2000–2500 steps per day, reductions in blood
pressure and mild reductions in body mass index.88 Long term effects are not
known.
Environmental policies targeting the built environment, in particular increased
access to public transport, increased recreational space opportunities,
reduction in environmental barriers to physical activity and point-of-decision
prompts to increase use of stairs have been shown to be effective.86,87 Facilities
for sporting and recreational activities are lacking in many remote Aboriginal and
Torres Strait Islander communities and surveys have reported that the need for
such facilities is ranked as a high priority among community members.89 Health
promotion strategies in the school and workplace are also effective in increasing
physical activity,86,87 but have not been well studied in Aboriginal and Torres
Strait Islander community settings.
*Moderate physical activity is activity at a level that causes your heart to beat faster and some
shortness of breath, but you can still talk comfortably. Vigorous physical activity is activity at a
level that causes your heart to beat a lot faster and shortness of breath, which makes talking
difficult between deep breaths (ie. physical activity at a heart rate of 70–85% of maximum heart
rate [MHR]). MHR is calculated as 220 minus age.
Lifestyle
Table 1.4. Australian physical activity guidelines:
Recommendations by age group
Age group
Recommendation
Under 2 years
For children under 1 year supervised floor based play in safe
environments should be encouraged from birth
For children under 2 years no time watching television or using other
electronic media
2–5 years
Toddlers and preschoolers should be physically active every day for at
least 3 hours, spread throughout the day
Watching television and the use of other electronic media (DVDs,
computer and other electronic games) should be limited to less than 1
hour per day
5–12 years
At least 60 minutes (and up to several hours) of moderate to vigorous
physical activity every day
No more than 2 hours per day using electronic media for entertainment
(eg. computer games, TV, internet), particularly during daylight hours
12–18 years
At least 60 minutes of moderate to vigorous physical activity every day
No more than 2 hours per day using electronic media for entertainment
(eg. computer games, TV, internet)
18–54 years
The following 4 steps are recommended:
• Think of movement as an opportunity, not an inconvenience
• Be active every day in as many ways as you can
• Put together at least 30 minutes of moderate physical activity on most,
preferably all days. 30 minutes can be accumulated throughout the day
in 10–15 minute sessions or done in one session
• If you can, also enjoy some regular vigorous activity for extra health and
fitness
55 years and over
Older people should do some form of physical activity, no matter what
their age, weight, health problems or abilities
Older people should be active every day in as many ways as possible,
doing a range of physical activities that incorporate fitness, strength,
balance and flexibility
Older people should accumulate at least 30 minutes of moderate physical
activity on most, preferably all days. Sedentary people may need to
gradually build up to 30 minutes or more
Older people who have stopped physical activity, or who are starting a
new physical activity, should start at a level that is easily manageable
and gradually build up the recommended amount, type and frequency of
activity
Older people who continue to enjoy a lifetime of vigorous physical activity
should carry on doing so in a manner suited to their capability into
later life, provided recommended safety procedures and guidelines are
adhered to
Source: Department of Health and Ageing 201092
35
36
Lifestyle
Recommendations: Physical activity
Preventive
intervention
type
Who is at
risk?
Screening
All people
Assess current level of physical activity
Behavioural
All people
How often?
Level/
strength of
evidence
Opportunistic
IB
and
as
part
of
For patients who are insufficiently active give
targeted advice and written information. This an annual health
assessment
should include the following:
References
86,87,90
• determine existing preferred physical
activities and invite patients to propose
new activities
• ask the patient the amount/frequency
of activity they feel is achievable and
set exercise goals aiming to achieve
National Physical Activity Guideline
recommendations (see Table 1.4)
• record these goals and provide patients
with a written copy
• consider cognitive behavioural support
and follow up
• consider additional social support (eg.
buddy system, involvement in a group
activity, referral for coaching)
People with
diabetes
For sedentary people, a gradual introduction
and initial low intensity of physical activity
with slow progressions in volume and
intensity is recommended
Those on insulin should be given
individualised advice on avoiding
hypoglycaemia when exercising (eg.
adjustment of carbohydrate intake, reduction
of insulin dose, and choice of injection site)
Consider referral to an exercise physiologist
for coaching if facilities are available
Opportunistic
and as a part
of an annual
diabetes
assessment
GPP
91
People with
Those with recent acute coronary syndrome Opportunistic
cardiovascular event or revascularisation surgery (CABG,
disease
PCI) should be advised to participate in a
short period (up to 12 weeks) of supervised
exercise rehabilitation
IA
82
Those who are well compensated and
clinically stable should commence an initial
low intensity of physical activity with slow
progressions in volume and intensity
Consider referral to an exercise physiologist
for coaching if facilities are available
IIB
82
Environmental All people
Refer to appropriate community based
physical activity programs and encourage
use of public facilities that promote activity
(eg. advocate for increased availability of
sports and recreational facilities in remote
communities)
Opportunistic
IB
and as part of
an annual health
assessment
88,90
Lifestyle
Alcohol
Background
Any level of drinking alcohol can increase the risk of ill health and injury.
Alcohol is responsible for a considerable burden of death, disease and injury
in Australia. Drinking is a major factor in much of the injury resulting from road
crashes and other accidents, and in social problems such as violence, family
breakdown, child abuse and neglect. As such, alcohol related harm is not
restricted to individual drinkers but has relevance for families, bystanders and the
broader community.93 Although most surveys show that Aboriginal and Torres
Strait Islander people are less likely than the general population to drink, the
prevalence of harmful drinking and alcohol attributable injury and disease in the
Aboriginal and Torres Strait Islander population is about twice that of the nonIndigenous population.94 The rate of alcohol attributable death among Aboriginal
and Torres Strait Islander people is similarly twice that of the non-Indigenous
population.95 There is a strong association between alcohol use and associated
harms such as suicide and violence.96 Alcohol causes and exacerbates common
mental health conditions such as anxiety, depression and insomnia.94
The current Australian guidelines for healthy men and women recommend that
drinking no more than two standard drinks on any one day reduces the lifetime
risk of harm from alcohol related disease or injury.93 Every drink above this level
continues to increase the lifetime risk of both disease and injury; drinking less
frequently over a lifetime (eg. drinking weekly rather than daily), and drinking less
on each drinking occasion, reduces this risk.93 For healthy men and women,
drinking no more than four standard drinks on a single occasion reduces the
risk of alcohol related injury arising from that occasion. Not drinking is the safest
option for pregnant or breastfeeding women and for children and adolescents
under 18 years of age.93
There is clear evidence to support the effectiveness of primary care screening
in detecting at-risk levels of alcohol consumption using quantity-frequency
estimates.97 Given the late presentation of alcohol problems in many
Aboriginal and Torres Strait Islander people, active screening and detection is
recommended.97 The appropriate frequency of alcohol screening in Aboriginal
and Torres Strait Islander settings is uncertain, with no clear evidence base
to draw on. Screening can be done by a drinking history taken as part of the
routine interview. Brief questionnaires are also available as an aid to systematic
screening and can be incorporated into adult health assessments. The AUDIT
tool, comprising 10 questions that cover level of consumption, evidence of
dependence and experience of harms, is the most sensitive of the currently
available screening tools (see Resources). There is high level evidence to
support its use in the general population, although it has not been validated
specifically in the Aboriginal and Torres Strait Islander community.97,98 A shorter
version, AUDIT-Consumption (AUDIT-C), comprises the first three questions of
AUDIT and may also be used for practical purposes when time is limited. These
questions assess alcohol consumption, asking: ‘How often do you have a drink
containing alcohol?’, ‘How many drinks containing alcohol do you have on a
typical day when you are drinking?’ and ‘How often do you have six or more
drinks on one occasion?’98,100 Another structured questionnaire, the Indigenous
37
38
Lifestyle
Risk Impact Screen (IRIS), is a 13-item structured questionnaire that can be
used to help in identification of alcohol and drug problems and mental health
risks for Aboriginal and Torres Strait Islander people (see Resources).94,101–103
Several barriers to successful integration of these tools in Aboriginal and Torres
Strait Islander settings have been identified104,105 and screening tool questions
may require rephrasing to allow for cultural differences.94,102 Nevertheless it is
likely they will assist in the earlier detection of alcohol problems in Aboriginal
and Torres Strait Islander people.94,105 Indirect biological markers (such as liver
function tests) should only be used as an adjunct to other screening measures
as they have lower sensitivity and specificity in detecting people risk of alcohol
related harm than structured questionnaire approaches.97
Brief interventions for problem drinking can decrease alcohol misuse and
alcohol related harm.105 Brief interventions are particularly effective in nondependent drinkers who are drinking at risky levels, but are also useful
in dependent drinkers as a precursor to engaging them in more intensive
treatments.99,105 These treatments include measures that can be provided by
primary healthcare services, including psychosocial counselling, and where
suitable, home detoxification and use of relapse prevention medications. Other
drinkers may benefit from referral to specialist services.97
Positive outcomes in the management of problem and dependent drinking
are likely in Aboriginal and Torres Strait Islander settings if they are delivered
in a respectful and non-judgemental manner.94,104,106,107 Training is available to
increase skills in providing appropriate brief intervention.
Aboriginal and Torres Strait Islander people are acutely aware of the costs of
alcohol and there are several examples of active community engagement in
responding to alcohol misuse.9,4 This includes primary prevention activities such
as school and family education programs and programs aimed at fostering self
esteem and cultural connectedness in youth.94,108 Environmental strategies such
as reducing access to alcohol have also been used in some communities with
evidence of effect in decreasing alcohol related harm.108
Lifestyle
Recommendations: Alcohol
Level/
strength of
evidence
References
1B
97–99
I–IIIB
99,109
As part of an
annual health
assessment
1B
94,97–105
People aged
10–14 years
Consider sensitive and age
As part of an
appropriate alcohol intake
annual health
screening in aged 10–14 years
assessment
(see Chapter 3: The health of
young people)
Parental or carer involvement may
be required and referral should be
considered
IIIB
98,109,110
People with
hazardous
and harmful
drinking levels
Review for comorbid disease and As part of an
other chronic disease risk factors annual health
assessment
1A
97,111
Preventive
intervention
type
Who is at
risk?
How often?
Screening
All people
Ask about the quantity and
As part of an
aged ≥15 years frequency of alcohol consumption annual health
to detect hazardous drinkers (see assessment
Table 1.5)
Focus particularly on the following Opportunistic
high risk groups:
• adolescents and young adults
• women who are pregnant or
planning a pregnancy
• illicit drug users
• those with a family history of
alcohol dependence
• people with medical conditions
made worse by alcohol (chronic
liver disease, hypertension,
other major organ disease)
• people suffering from mental
illness made worse by alcohol
such as anxiety and depression
Consider the use of structured
questionnaires such as AUDIT,
AUDIT-C or IRIS to assess
drinking (see Resources –
these tools may require some
adaptation to local community
needs)
39
40
Lifestyle
Recommendations: Alcohol (continued)
Behavioural
Environmental
People with
hazardous
and harmful
drinking levels
Offer brief interventions. Consider
using tools such as FLAGS and
5As approach (see Table 1.1
and 1.6 and Chapter 1: Lifestyle,
introduction)
Brief interventions alone are not
sufficient for people with severe
alcohol related problems or
alcohol dependence who require
referral or extended intervention.
(Treatment specific guidelines
should be consulted in these
circumstances)
Opportunistic
and as part of
an annual health
assessment
IA
97–99
Women who
are pregnant,
breastfeeding,
seeking preconception
counselling
Advise to abstain from alcohol,
emphasising the risks to the
unborn child
Advise breastfeeding mothers
that not drinking is the safest
option, especially in the first
month postpartum. For those
choosing to drink, alcohol intake
should be limited to no more than
two standard drinks per day.
Continue to promote
breastfeeding
Pregnant women:
At first and
subsequent
antenatal visits as
appropriate
For all others
opportunistic
and as part of
an annual health
assessment
IA
93
GPP
108,112,113
Promote community led
strategies to reduce alcohol
supply including:
• advocacy for ‘dry communities’
• restrictions to liquor licensing
hours
• better policing of responsible
service of alcohol
• community development
initiatives
Lifestyle
Table 1.5. National Health and Medical Research Council guidelines for
safer alcohol use
For healthy men and women, drinking no more than two standard drinks on any day reduces the
lifetime risk of harm from alcohol related disease or injury
For healthy men and women, drinking no more than four standard drinks on a single occasion reduces
the risk of alcohol related injury arising from that occasion
For children and young people under 18 years of age, not drinking alcohol is the safest option:
• parents and carers should be advised that children under 15 years of age are at the greatest risk of
harm from drinking and that for this age group, not drinking alcohol is especially important
• for young people aged 15−17 years, the safest option is to delay the initiation of drinking for as long
as possible
Maternal alcohol consumption can harm the developing fetus or breastfed baby:
• for women who are pregnant or planning a pregnancy, not drinking is the safest option
• for women who are breastfeeding, not drinking is the safest option
Source: NHMRC 200993
Table 1.6. The FLAGS framework for brief intervention
Feedback
• Provide individualised feedback about the risks associated with continued drinking,
based on current drinking patterns, problem indicators, and health status
• Discuss the potential health problems that can arise from risky alcohol use
Listen
• Listen to the patient’s response
• This should spark a discussion of the patient’s consumption level and how it relates to
general population consumption and any false beliefs held by the patient
Advice
• Give clear advice about the importance of changing current drinking patterns and a
recommended level of consumption
• A typical 5–10 minute brief intervention should involve advice on reducing consumption
in a persuasive but non judgemental way
• Advice can be supported by self help materials, which provide information about the
potential harms of risky alcohol consumption and can provide additional motivation to
change
Goals
• Discuss the safe drinking limits and assist the patient to set specific goals for changing
patterns of consumption
• Instil optimism in the patient that his or her chosen goals can be achieved
• It is in this step, in particular, that motivation-enhancing techniques are used to
encourage patients to develop, implement and commit to plans to stop drinking
Strategies • Ask the patient to suggest some strategies for achieving these goals
• This approach emphasises the individual’s choice to reduce drinking patterns and allow
them to choose the approach best suited to their own situation
• The individual might consider setting a specific limit on alcohol consumption, learning to
recognise the antecedents of drinking, and developing skills to avoid drinking in high risk
situations, pacing one’s drinking and learning to cope with everyday problems that lead
to drinking
Source: Haber P, Lintzeris N, Proude E, Lopatko O 200997
41
42
Lifestyle
Resources
Quick reference guide to the treatment of alcohol problems: companion
document to the guidelines for the treatment of alcohol problems (Australian
Government)
www.alcohol.gov.au/internet/alcohol/publishing.nsf/Content/treat-quick
Guidelines for safer alcohol use (NHMRC)
www.health.gov.au/internet/alcohol/publishing.nsf/Content/standard
AUDIT tool (Northern Territory Government)
www.health.nt.gov.au/library/scripts/objectifyMedia.aspx?file=pdf/63/68.
pdf&siteID=1&str_title=Alcohol%20Screen%20(AUDIT)%20Tool.pdf
AUDIT-C tool
www.cqaimh.org/pdf/tool_auditc.pdf
IRIS tool (Queensland Government)
www.health.qld.gov.au/atod/prevention/iris.asp
Talking about alcohol with Aboriginal and Torres Strait Islander patients
flipchart (the flipchart includes tear off prescription pads)
www.alcohol.gov.au
Standard drink definition and calculator
www.health.gov.au/internet/alcohol/publishing.nsf/Content/standard.
Lifestyle
Gambling
Background
Gambling has been formally defined as ‘an entertainment based on staking
money on uncertain events driven by chance’.114 Gambling disorders are often
categorised in the literature into problem and pathological gambling; the latter
currently medically defined as an impulse disorder. Problem gambling is more
loosely defined,115 but in the Australian context the term problem gambling
is generally used to refer to the full continuum of gambling related harm.116
Gambling disorders are characterised by difficulties in limiting money and/or
time spent on gambling, which leads to adverse consequences for the gambler,
for others, or for the community.114
Recreational gambling takes many forms, with electronic gaming machines
(‘pokies’) and table games such as roulette and blackjack accounting for the
bulk of expenditure. The main form of gambling in Aboriginal and Torres Strait
Islander communities has traditionally been card playing. While this has been
problematic for some individuals, where ‘pokies’ have become available locally
they have replaced traditional forms of gambling, often with more harmful
consequences.114
Gambling is a significant issue for many Aboriginal and Torres Strait Islander
people, and can have serious consequences for individuals, families and
communities.117–119 Aboriginal and Torres Strait Islander people are more likely
to be regular and problem gamblers than non-Indigenous people and to start
gambling at a younger age.117,119,120 Problems that have been reported as
associated with gambling in surveys of Aboriginal and Torres Strait Islander
communities include financial hardship, social and emotional difficulties,
substance abuse and contact with the criminal justice system.117,118 Gambling
disorders are highly associated with psychiatric comorbidities, particularly
substance use disorders.115
Environmental risk factors for problem gambling include the cultural and
social normalisation of gambling, exposure to peer and family gambling and
introduction to gambling at an early age, including through family activities such
as gifting lottery tickets and involvement in sport associated gambling.120–122
Children whose parents and/or siblings have issues with problem gambling
or substance abuse are at higher risk of becoming problem gamblers.123
Adolescents who gamble are at particularly high risk for problem gambling
and develop problem gambling behaviours at 2–3 times the rate of adults.120,121
There is limited information on the early identification of adolescents with
gambling problems.121 Warning signs of adolescent problem gambling include
multiple visits to internet gaming sites, finding instant lottery tickets, excessive
interest in sports events and significant unexplained monetary outlays.122
Family cohesiveness and school connectedness may protect adolescents from
problem gambling.122
43
44
Lifestyle
Interventions
Interventions involving a broad group of stakeholders, including government,
industry and community, are important to reduce harms caused by
gambling.117,123,124 Public health interventions, such as safety controls for technology
based gambling and prevention of access to instant lottery tickets for those
under 18 years of age, may assist to reduce uptake of gambling and harms from
gambling.122,125,127 There is currently little published information internationally on
culturally specific prevention initiatives for problem gambling.123 Interventions are
likely to be more effective if they take a broad approach to preventing gambling
related harms. In Aboriginal and Torres Strait Islander communities this must
include attention to the social and environmental context of gambling, and take into
account individual community needs and promote whole of community health.117,119
The first Australian guideline on the prevention and treatment of problem
gambling has been released, with Cochrane systematic reviews to follow.116
The goal of gambling prevention activities is to encourage responsible and
non-harmful gambling activities in those who choose to gamble.123 It should be
approached by health professionals in a similar way to other risk behaviours
such as smoking and alcohol.122,123
Screening for problem gambling is not generally part of routine general practice
in Australia, despite GPs and other primary care workers being well placed to
provide early identification and intervention for problem gamblers.125,128 Primary
care workers may become more confident and effective at detecting problem
gambling through recognising that stress related medical disorders may be
a presenting complaint of a person with underlying problem gambling and
that problem gambling is commonly associated with other health problems
including substance abuse and mental health disorders.125–127 Other vulnerable
groups are the elderly, people with intellectual disability and people from poorer,
disadvantaged communities.114
There are several tools that can be used to screen for problem gambling
behaviours,115,116,125 although some are quite long and therefore, it has been
argued, impractical for primary care screening.127 Validated screening measures
are most likely to be useful in high risk groups such as those with mental health
problems, and recently released Australian clinical guidelines have a guide
to available tools.116 The EIGHT questionnaire has been used successfully
in general practice settings.129 A simple question as to whether a patient is
experiencing problems with their gambling may be as effective as more detailed
tools and more appropriate for primary care screening.127 No screening tools
have been validated for use with Aboriginal and Torres Strait Islander groups.117
Work is currently being undertaken in New South Wales to develop and test a
tool for use with Aboriginal people.130
More research is needed into screening and intervention for adolescents who
gamble.131 Most current research has been done in the context of school based
interventions.131 Given gambling behaviours begin around 12 or 13 years of age,
preventive interventions, such as school based strategies educating young people
on basic principles of gambling, should begin before then.123–132 Increasing the
awareness of teachers, parents and healthcare professionals in recognising
adolescent gambling may assist in the identification of at risk adolescents.122
Lifestyle
45
Reviews and randomised controlled trial evidence around treatment of
pathological gambling provide some evidence for the effectiveness of cognitive
behaviour therapy.133,134 There is a need for clear local referral pathways and
training of staff in Aboriginal and Torres Strait Islander health services to improve
the prevention, detection and management of problem gambling.117 Shame and
stigma may prevent Aboriginal and Torres Strait Islander people from accessing
help for gambling related problems.117
Recommendations: Gambling
Preventive
intervention type
Who is at
risk?
Screening
All people aged Consider asking patients if they
>12 years
participate in gambling activities (eg.
‘pokies’, cards, roulette, blackjack and
other table gambling, lotteries, sport
associated gambling)
For those who are gambling, screen for
problems by asking a simple question
such as: ‘Have you ever had an issue
with your gambling?’
Specific groups at risk of problem
gambling include people with stress
related medical problems, mental
health issues, substance misuse
How often?
Level/
strength of
evidence
References
Opportunistic
and as
part of an
annual health
assessment
GPP
115–117,125,127
Young people
aged 12–24
years
Consider screening young people for
gambling behaviours as part of general
screening tools such as HEEADSSS
(see Chapter 3: The health of young
people)
GPP
122
High risk
groups such as
young people
or adults with
mental health
or substance
use problems
Consider use of a validated
measurement tool for problem
gambling as part of a community based
program (see Resources)
GPP
116
Children
with parents/
siblings who
are known to
have problem
gambling
Assess the impact of family gambling
on children
GPP
122,123
Opportunistic
46
Lifestyle
Recommendations: Gambling (continued)
Behavioural
Environmental
All people
identified
with problem
gambling
Management options for problem
gambling include:
Young people
aged from 12
years
Communities
Opportunistic
GPP
115,122,125–127
Where appropriate, engage with
local school authorities and support
implementation of school based
gambling prevention strategies
Encourage teachers, parents and
healthcare professionals to be more
aware of adolescent gambling
N/A
IIIB
122,123,132,135
Adopt or support community focused
activities (eg. community campaigns)
that promote strategies to control
gambling and related harms
N/A
GPP
114,117,119
• brief treatments and motivational
interviewing aimed at promoting
behaviour change
• cognitive behavioural therapy
• treatment of coexistent and
complicating factors such as
depression and substance abuse
• referral to gambling support helplines
and websites (see Resources)
• referral to gambling treatment centres
Resources
‘Let’s talk about gambling’ (Aboriginal Health and Medical Research Council)
www.aboriginalgamblinghelp.org.au
Gambling Help Online
Counselling, information and support service for problem gambling issues, includes
contact details for local face-to-face counselling and support
www.gamblinghelponline.org.au
National problem gambling telephone counselling services
National Problem Gambling Hotline: 1800 858 858
Gamblers Anonymous: 1800 002 210
Problem Gambling Research and Treatment Centre
Guidelines for screening, assessment and treatment in problem gambling
www.med.monash.edu.au/sphc/pgrtc/guideline/index.html.
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31. Lancaster T, Stead LF. Self-help interventions for smoking cessation. Cochrane Database Syst Rev 2005;Jul
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32. Civljak M, Sheikh A, Stead LF, Car J. Internet-based interventions for smoking cessation. Cochrane
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33. Singh S, Loke YK, Spangler JG, Furberg CD. Risk of serious adverse cardiovascular events associated with
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47
48
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35. Sowden AJ, Stead LF. Community interventions for preventing smoking in young people. Cochrane
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51
Chapter 2
Child
health
Author Jenny James
Expert reviewer Hasantha Gunesekara
Child health
Immunisation
Background
Immunisation has had a powerful impact in preventing disease in Aboriginal
and Torres Strait Islander children.1,2 However, Aboriginal and Torres Strait
Islander children still have higher rates of vaccine preventable diseases1,3–6 and
decreased rates of vaccination coverage when compared to non-Indigenous
children.2,7–12 Coverage rates from universally funded vaccines are similar in
Aboriginal and Torres Strait Islander children and non-Indigenous children by
24 months of age,1 but delayed vaccination is more common in Aboriginal and
Torres Strait Islander children and fewer are fully vaccinated at 12 months of
age.1,2,7–12 Recent data from the Australian Childhood Immunisation Register
showed 91% of children Australia wide were fully vaccinated at 12 months of
age, while only 83% of Aboriginal and Torres Strait Islander children were fully
vaccinated at the same age.1
The Australian Childhood Immunisation Register coverage estimates are
reliable with regards to identifying Aboriginal and Torres Strait Islander status
of children,11 however, routine reports on immunisation coverage allow for
significant lags in immunisation. The Australian Childhood Immunisation
Register’s reporting of coverage rates at 1 year of age are based on completion
of vaccinations scheduled at age 6 months or earlier,11,12 so data on delays in
vaccination in Aboriginal and Torres Strait Islander children may underestimate
the magnitude of the problem.
Some vaccination programs are not universally applicable to all Australian
children and target Aboriginal and Torres Strait Islander children only.
Comparison of rates of immunisation coverage from universally applicable
versus targeted vaccination programs show the latter are sometimes associated
with lower rates of immunisation coverage in Aboriginal and Torres Strait Islander
children. This is reflected in low rates of coverage for hepatitis A vaccine and
23vPPV, both of which are vaccinations recommended for Aboriginal and
Torres Strait Islander children only.1,2,5,6 There is also evidence that non-vaccine
serotypes cause a disproportionate amount of disease in Aboriginal children
compared to non-Aboriginal children with regards to some vaccine preventable
diseases. This has been seen with mumps, invasive pneumococcal disease
and meningococcal disease.1,6,13 Therefore, it is likely that factors other than
immunisation coverage, such as heavy nasopharyngeal colonisation, poorer
immunologic responses and persistent nasopharyngeal carriage continue to
contribute to higher rates of vaccine and non-vaccine preventable disease in
Aboriginal and Torres Strait Islander children.6
Young Aboriginal and Torres Strait Islander adults experience a much higher rate
of invasive pneumococcal disease due to non-7vPCV serotypes.1,5 Coverage
rates for influenza and pneumococcal vaccination 23vPPV in eligible Aboriginal
and Torres Strait Islander people aged 15–49 years are low.1
The National Health and Medical Research Council Australian Immunisation
Handbook,14 9th edition, identifies no diseases in New South Wales, Victoria,
the Australian Capital Territory or Tasmania requiring specific immunisation
coverage for Aboriginal and Torres Strait Islander people up to and including
the age of 14 years. In other states and territories (health authorities should be
53
54
Child health
consulted to determine exact geographic boundaries) the following diseases
have vaccination requirements specific to Aboriginal and Torres Strait Islander
children:
• hepatitis A
• tuberculosis
• pneumococcal disease (requiring a booster dose at 18–24 months of age
with 23vPPV)
• Hib infections requiring PRP-OMP vaccine.
They have also identified two diseases requiring immunisation coverage in
Aboriginal and Torres Strait Islander people aged from 15–49 years:
• influenza with yearly vaccination recommended for all Indigenous adolescents
(and adults) in that age group
• pneumococcal disease with 23vPPV recommended for Aboriginal and Torres
Strait Islander adolescents (and adults) with a chronic disease.14
A large number of interventions can improve immunisation coverage. They can
be summarised under three categories: provider/system based interventions,
enhancing access to vaccination services, and increasing community demand
for vaccination. Effects may be increased if the interventions are administered in
combination rather than as single interventions.15
Resources
Catch-up immunisation calculator
www.health.sa.gov.au/immunisationcalculator/
Australian Immunisation Handbook
www.health.gov.au/internet/immunise/publishing.nsf/content/handbook-home.
Child health
55
Recommendations: Immunisation
Who is at
risk?
How often?
Immunisation*
All children
Conduct regular postnatal review of
all infants and offer vaccination
As per Australian IA
standard
vaccination
schedule
14
Use the catch-up schedule for all
children behind in their vaccination
schedule
Opportunistic
IA
14
Implement provider/system based
interventions: review vaccination
status at each clinic visit and make
a documented plan for the next
vaccination
Every visit
IA
16,17
Ascertain local clinic vaccination
N/A
rates via audits of health records and
Australian Childhood Immunisation
Register records
IA
16,18–20
Implement recall and reminder
systems and computer prompts
for staff and patients to address
immunisation gaps, particularly in
the first 12 months
N/A
IA
16–22
Implement an adverse events
reporting system
N/A
IA
16–22
Increase access to vaccinations via:
N/A
IA
16–20,22,23
Ongoing
IA
15,16,18,20–24
Environmental
Level/
strength of
evidence
References
Preventive
intervention
type
• fast tracking children presenting
for immunisation
• training and reminders for staff to
screen and offer vaccinations
• providing home visits and mobile
clinics for immunisation
If resources are limited, focus
particularly on vaccinations due in
the first 12 months
Increase community demand for
vaccinations by:
• promoting vaccination to parents,
child care staff, and community
workers such as Aboriginal and
Torres Strait Islander liaison
officers
• using posters and other visual
materials in public places
• personalising health records
• giving all parents/carers a record
in card or book form of their child’s
immunisation status
• commencing promotional
activities for parents of neonates
early and in places where parents
of very young babies attend
* Vaccination should be implemented according to best practice recommendations in the Australian Immunisation Handbook and state
and territory immunisation schedules
56
Child health
Anaemia
Background
This chapter reviews the evidence for the prevention of iron deficiency anaemia
(IDA).
IDA is very common in Aboriginal and Torres Strait Islander children although
data are lacking from many settings, particularly in urban areas. A prevalence of
greater than 5% is considered by the World Health Organization to be of public
health significance; the data that are available indicate rates of IDA in Aboriginal
and Torres Strait Islander children in remote Australia are significantly higher.24,25
IDA is associated with developmental delay of cognitive and psychomotor
functions. It is not clear whether the relationship is causal or associative.24,26–31
Morbidity from infectious disease is increased in iron deficient populations
because of the adverse effect of iron deficiency on the immune system. IDA
also increases the risk of heavy metal poisoning in children as iron deficient
individuals have an increased absorption capacity for other heavy metals,
including toxic metals such as lead and cadmium.32
Contributors to IDA in Aboriginal and Torres Strait Islander children are
multifactorial and may include: low birthweight, prematurity and maternal
anaemia, twin birth, poor quality and late introduction of weaning foods, high
rates of infection and tropical enteropathy syndrome associated with failure to
thrive, and cow’s milk in the first year.26,31–35 Moderate to severe infestations with
hookworm, via intestinal blood loss, can also contribute to IDA.24,33,35,36
There are different approaches to the diagnosis of IDA. Haemoglobin (Hb) levels
combined with erythrocyte indices are commonly used. Iron indices can also be
measured. Another diagnostic pathway is to measure the response in Hb to oral
iron therapy, without any measurement of iron indices. In Aboriginal and Torres
Strait Islander children, anaemia is almost always caused by iron deficiency,
and intercurrent rates of infection are high, making iron indices an unreliable
indication of current iron stores. In Aboriginal and Torres Strait Islander children,
anaemia is most commonly diagnosed by Hb and red cell indices.24,26,31,35 The
prevalence of haemoglobinopathies as a cause for microcytic anaemia is low,
but should still be considered as a possible cause, particularly in those in whom
treatment for IDA fails to show an improvement in Hb.37
There is widespread agreement that Hb limits to define anaemia should differ
according to age, gender and physiological status (eg. pregnancy), and for
babies, whether they are breast or bottle fed. However, there are differing
recommendations on the cutoff levels of haemoglobin for definition of anaemia.
The Kimberley Aboriginal Medical Services Council defines anaemia in children
aged 6–24 months as being Hb <105 g/L, and in children aged 2–11 years
as being Hb <115 g/L. The Central Australian Rural Practitioners’ Association
define anaemia in children from 6 months of age as being Hb <110 g/L. This has
implications for treatment decisions.24,26,35,38–41
Interventions
International guidelines state there is insufficient evidence to recommend
either for or against universal screening for IDA in children.28,42 However, these
guidelines draw attention to groups of children at high risk of anaemia and the
subsequent importance of clinical assessment as a means of informing
Child health
decisions about whether to screen. Some Australian guidelines recommend
screening all Aboriginal and Torres Strait Islander children.35 Screening can be
done with venous blood, but if there is good training and quality control, pointof-care testing can correlate well with the lab testing.24,35,43 Though Helicobacter
pylori infection is associated with IDA in children, benefits of mass screening are
not clear.44–46
Evidence differs with regards to whether chemoprophylaxis using oral iron
supplementation should be offered universally, without screening, to children
who are at high risk of IDA and who are older than 6 months. This is a
preventive use of iron supplementation, aimed at preventing IDA,28,31,32,34,47 as
opposed to using it only for therapeutic effect.24,26,35,48 This preventive rationale
is sometimes considered in areas where there are high prevalence rates of
anaemia in the communities of children under question.
There is good evidence to support the widespread use of multicomponent
interventions that don’t involve medicinal iron supplementation in prevention
of IDA. This includes delaying cord clamping beyond 3 minutes, which
increases iron stores from birth.49–51 Multicomponent interventions need to
be both early and often, and may also involve food based approaches, food
and formula fortification, iron supplementation, treatment for hookworm,
and integration of IDA prevention with other primary health prevention
programs such as immunisation and micronutrient supplementation for
children with failure to thrive. Interventions can be delivered through local
healthcare providers including GPs and Aboriginal and Torres Strait Islander
health workers, and through government funded nutritional supplementation
programs.24,26,31,32,34,35,47,52
There is good evidence that oral iron supplementation has a beneficial effect
on some cognitive domains in iron deficiency and IDA in children older than 6
years of age. Iron supplementation provided as ‘sprinkles’ shows promise,53-55
as it may have fewer side effects and improve adherence to daily iron
supplementation. However, this has not been borne out in all studies.56 It is not
clear whether oral iron supplementation in children with IDA younger than 6
years confers benefits on cognitive or motor development. There is considerable
variation in the populations studied, and there are no studies assessing this
outcome in Aboriginal and Torres Strait Islander communities.34,48,57
Exclusive breastfeeding until 6 months has many benefits and is currently
recommended Australia wide,52,58 however, there are concerns that this may not
provide enough iron to babies at increased risk of IDA.26,31,33 In such instances,
introduction of iron fortified weaning foods at 4 months or supplementation
with oral iron have been suggested. While IDA is often associated with failure
to thrive in Aboriginal and Torres Strait Islander children, treatment of iron
deficiency does not appear to improve growth.48,59
In children with a history of IDA, recurrence of IDA may occur. This has major
implications for long term follow up of children, highlighting the importance of
IDA prevention programs being managed not just by individual clinicians, but at
the health service level.60–62
Guidelines make strong reference to the link between poverty and poor
nutrition. In low income households nutrition counselling on its own is not
recommended. However, it may be effective if combined with government
funded nutritional support programs that remove financial barriers to improved
nutrition.31,42,47,52,63
57
58
Child health
Recommendations: Anaemia
Preventive
intervention type
Who is at risk?
How often?
Level/
strength of
evidence
References
Screening
All children aged
>6 months from
communities with
a high prevalence
of iron deficiency
anaemia (IDA)
Children in other
areas with risk
factors:
Take a nutritional history asking
about intake of iron rich foods
such as meat and fortified
cereals, leafy green vegetables
and vitamin C intake with meals
At age 6–9
months and
repeat at 18
months
GPP
28,42
Test at age 6–9 GPP
months and
repeat at 18
months
30,35
25
More frequent
testing if IDA is
diagnosed
IIC
60,61
Opportunistic
IB
26,31,52,58
• history of low
birthweight or
pre-term birth
• maternal anaemia
• twin
Perform haemoglobin (Hb) via
• failure to thrive
point-of-care capillary sample or
• chronic infections venous blood (including blood
film)*†
Behavioural
Babies born without Recommend exclusive
risk factors for IDA
breastfeeding to 6 months
(see below)
Babies born with
low birthweight
(<2500 g),
prematurity (<37
weeks) or to
mothers who had
maternal anaemia
Recommend exclusive
breastfeeding to 4 months
GPP
26,31,33
All babies
Introduce iron rich foods at
weaning. Examples include
meat (three serves per week),
fortified cereals, leafy green
vegetable, eaten with vitamin C
rich food (eg. fresh citrus fruit)
Also discuss withholding cow’s
milk until 12 months of age and
avoiding tea
IB
26,31,52,58
Consider oral iron
supplementation in consultation
with a paediatrician
GPP
35
Chemoprophylaxis Babies aged <6
months with IDA
risk factors as
above
Child health
Environmental
59
Children aged 6
months to 16 years
in areas with high
rates of hookworm
infections
Consider use of single
dose albendazole as part
of a systematic child health
surveillance program in
consultation with local public
health units
Refer to Australian Therapeutic
Guidelines for dosing regimen64
Every 6 months GPP
24,25,35,36
Children with IDA
Include children on recall
registers for regular review and
Hb repeat testing as per above
N/A
GPP
31
Communities with
a known high
prevalence of IDA
Advocate for and support
Immediately
nutritional programs that remove and ongoing
financial barriers to improved
nutrition and improve the range
and accessibility of healthy
foods alongside the food
strategies recommended above
(see Chapter 1: Lifestyle, section
on overweight/obesity)
IA
31,42,47,52,63
* Diagnose IDA using erythrocyte indices (eg. blood film, mean cell volume) and Hb levels of less than 110 g/L in children over 6 months of
age. Consult local laboratories for reference limits of Hb levels in children >2 years
†There are jurisdictional differences in the screening for anaemia (eg. Queensland and the Northern Territory) and local guidelines should
be consulted
Resource
Iron deficiency anaemia assessment, prevention and control:
a guide for programme managers (WHO)
www.who.int/nutrition/publications/en/ida_assessment_prevention_
control.pdf.
60
Child health
Growth failure
Background
Growth failure is the principal manifestation of malnutrition in children. The terms
growth failure and failure to thrive (FTT) are used interchangeably and refer
to the failure to achieve the growth potential expected for a child. The term is
usually applied when the growth crosses two or more centile lines downwards
on a standard growth chart.25 There are three different growth charts (Centers
for Disease Control, World Health Organization and National Center for Health
Statistics) used in Australia by various health authorities and medical software
companies,65 so it is important to be consistent with the chart being used and
to consider the growth parameters in the context of the health of the child.66
The most common dietary problem in Aboriginal and Torres Strait Islander
children is insufficient weaning foods from 6–24 months of age.24 In Aboriginal
and Torres Strait Islander children this usually involves a vicious cycle of
malnutrition and infection.67 In all populations it may reflect any one or a
combination of the following: multicomponent feeding difficulties (often related
to lack of food security), chronic ill health, living in a context of poor social
determinants of health or carer neglect. Some Aboriginal and Torres Strait
Islander communities continue to have paediatric populations with disturbingly
high rates of FTT, and these communities often show high rates of other
paediatric complex and chronic conditions such as chronic suppurative otitis
media, rheumatic fever, rheumatic heart disease and fetal alcohol syndrome.
Such communities may also have high rates of notifications of child abuse and
neglect, though how many of these notifications are substantiated is not clear
from the data.68
The long term health sequelae from childhood growth failure are significant.
There is evidence that intrauterine growth restriction and growth failure in early
childhood is associated with the development of obesity in later childhood
and adult cardiovascular disease.69,70 Increased risks for secondary disability
from FTT, including cognitive, neurological and psychomotor deficits persist
despite interventions. However, permanent growth retardation may be able
to be prevented with early and intensive secondary interventions once a child
has FTT. These findings underscore the importance of primary prevention of
FTT, because despite rapid and appropriate interventions in a child diagnosed
with FTT, some of the serious secondary disabilities will be unable to be
prevented.71,72 Approaches to FTT in different parts of the world share some
similarities, but need to be context specific.73 In Aboriginal and Torres Strait
Islander community settings, interventions to prevent FTT need to address the
social determinants of health, which implies improvements in areas such as
overcrowded living conditions, housing, hygiene, education and employment.
Evacuating children to hospital for tube-feeding in an attempt to achieve rapid
catch-up growth may have deleterious effects in the long term.74
Interventions
A detailed history, physical examination and assessment for psychosocial
deprivation and developmental assessment are important. In the primary
care setting, major organic disease is uncommon (<5%) and can usually be
suspected on clinical assessment and appropriate lab testing. If there is an
absence of other signs or symptoms, it is usually appropriate to embark
Child health
on a trial of improved nutrition prior to proceeding immediately to further
investigation.23,24,75 There is evidence that action plans are lacking after
identification of growth faltering in Aboriginal and Torres Strait Islander children.
This is of particular concern in areas with high staff turnover, where there are
practitioners providing services for short blocks of time. Existing systems may
not always be providing for adequate follow up of growth faltering.62
Growth monitoring is often recommended as an opportunistic activity to
undertake with usual clinical care, rather than as a specific screening tool.
This is particularly the case when growth monitoring is reviewed with regards
to its usefulness in diagnosis of FTT.76 One important systematic review67,77
recommended that growth monitoring be integrated into a broader primary
healthcare program and stressed the need for effective follow-on action. Some
guidelines recommend minimum intervals, and the current RACGP Guidelines
for preventive activities in general practice (‘red book’) recommend weight/
height/head circumference at 7 days, then at 6–8 weeks, then at 4, 6, 12 and
18 months.52,78 It makes the point that weight may need to be monitored more
frequently if there are clinical concerns. One guideline for Aboriginal and Torres
Strait Islander health settings recommends even more frequent monitoring
of weight, height and head circumference.75 Some guidelines recommend
against such regular monitoring.23 Irrespective of frequency, growth monitoring
in situations of malnutrition should be coupled with history gathering and
counselling, finding out about food intake patterns and understanding from the
caregiver’s perspectives what they feel about their child’s development and
growth. In many growth monitoring programs it has been noted that the skill
and experience necessary for such counselling are not available because use is
made of low skilled staff or volunteers. Health professionals do not often engage
in counselling because they do not receive adequate training in counselling,
are not supervised when beginning to practise it or because workloads do not
permit it.76 Interpretation of growth charts is not necessarily straightforward
either. In non-Indigenous communities, the weights of breastfed babies may fall
below two centile lines, and use of complementary formula can increase weight.
Such babies are not necessarily described as having FTT.79 Interpretation of
growth charts needs to be done with a knowledge of the health context of the
community within which a health professional works.
FTT has been associated with depressed developmental test scores.71 There is
strong evidence to support publicly funded, centre based, comprehensive early
childhood development programs for children from low income backgrounds
aged 3–5 years, based on their effectiveness in preventing delay of cognitive
development and increasing readiness to learn, but evidence is insufficient
to determine the effectiveness of early childhood programs on child health
screening outcomes.80 However, such programs may be useful as secondary
strategies to prevent some of the possible deleterious follow-on effects of FTT.
Routine developmental screening is recommended in the current edition of
the RACGP red book and is timed to coincide with growth monitoring checks
and other important interventions such as immunisations.78 Other Australian
guidelines also recommend developmental surveillance be tied in with routine
child checks rather than singled out.23 However, there is no consensus on the
correct developmental assessment tool to use with Aboriginal and Torres Strait
Islander children and none have been validated in Aboriginal and Torres Strait
Islander populations. Use of parent reporting as in ASQ or PEDS can be used,
or others administered by the health professional such as DDST.23,81
61
62
Child health
While it is important to consider neglect if a child has FTT secondary to an
inadequate diet, it is clearly difficult to distinguish between neglect and material
poverty. There is some evidence that neglect may be more common in
communities that experience poverty.82 It is useful to consider the constraints on
the parents’ or carers’ ability to meet their children’s needs within a framework
of understanding of how other people in similar circumstances have been able
to meet those needs.42,78,83 The effects of many programs to prevent neglect
are not known84,85 and outcome evaluations of child maltreatment prevention
interventions are exceedingly rare in low and middle income countries.86 A
Cochrane review showed insufficient evidence to support parenting programs as
an intervention in child abuse including neglect.87 The Triple P parenting program
is a well known multilevel program aimed at helping caregivers find solutions to
parenting and child rearing problems. If it is being considered for Aboriginal and
Torres Strait Islander families it is recommended that child health professionals
consult with their local community regarding the cultural appropriateness and
acceptability of Triple P before implementing the program, and that the program
be facilitated in partnership with an Indigenous child health worker.23
There is some evidence to suggest that home visiting helps prevent neglect,
particularly first episode neglect, and particularly when used as part of a
preventive, multicomponent package including parent education and possibly
enhanced paediatric care.85 Cost effectiveness of home visiting programs aimed
at preventing neglect has been evaluated in vulnerable families with maternal
sensitivity and infant co-operativeness being among the operational outcomes.
No author judgement was made on whether the benefits were worth the
costs.88,89 It has been suggested that interventions to prevent neglect should
focus more on the community level, for example by using media campaigns to
promote a ‘norm’. Neglect predicts future maltreatment, hence any interventions
need to be sustained and ongoing.90
There is evidence that fetal alcohol syndrome, independent of the effects of
poor nutrition, is associated with growth deficits in children. Not drinking during
pregnancy is the safest option.91,92 Brief interventions have been shown to be
effective in reducing alcohol use during pregnancy and postnatally.93
There are many studies providing evidence that providing multiple
micronutrients (MMN) to pregnant women improves birthweights of babies,
and may have other beneficial effects on pregnancy outcomes as well.
Supplementation with single nutrients does not appear to have the same effect.
Single micronutrient (MN) zinc supplementation given during pregnancy may
decrease prematurity of infants but does not increase birthweight.94
In contrast, the evidence is more mixed with regards to whether MMN given to
children in the first 2 years of life improves growth. One important systematic
review found the research evidence supported neither implementation of new
programs nor withdrawal of existing MMN supplementation programs.67,77
Study variability is large, in terms of what was given, what dose, what duration,
baseline characteristics of children, and whether MN were combined with other
strategies to enhance growth. Some studies show that MN do not improve
growth,59,63,95–97 and others show that MMN do improve growth.24,74,98–100 It has
also been noted that there is still a lack evidence of any deleterious effects of
MMN on children. It appears single MN have no effect on growth, though zinc
supplementation is recommended by some Australian experts in cases of FTT
to reduce infections, rather than to prevent growth faltering. Most evidence
states that zinc supplements given to children in the first year of life can reduce
Child health
illnesses such as respiratory infections or acute and chronic diarrhoea.97,101–103
There is evidence that zinc supplementation is of no benefit in preventing growth
faltering.67,77 There is evidence of benefit from vitamin A supplementation in
populations with moderate to severe vitamin A deficiency.67,77 Chemoprophylaxis
using deworming regimens has also been shown to confer benefit to children
living in areas known to have high rates of infestation.67,75,77 Prophylactic
albendazole appears to be well tolerated.
Nutrition education coupled with growth monitoring can improve a mother’s
knowledge of good diets, but may not translate into improved health outcomes
for a child.104 However, it has been noted to be very context specific63 and the
potential for an impact on growth appears to be greater with interventions that
combine nutritional information with provision of complementary food with or
without fortification, or increased energy density of complementary foods. There
is evidence suggesting that for nutritional counselling to be effective it should
involve52 ‘hands-on’ skills development, be tailored to the educational level
and needs of the mother’s and to family resources and include strategies for
behaviour change, and be ongoing and delivered by nutrition paraprofessionals
and/or peer supporters. One important systematic review found evidence that
effective nutrition counselling was often part of a multifaceted intervention and
involved education to not only carers, but also to community health workers
and community representatives.67,77 Parenting in an Aboriginal and Torres
Strait Islander community often includes the role of extended family and kin
and in particular acknowledges the role of grandparents in transmission of
cultural knowledge and customs, so nutritional education is best provided at
multiple levels in the community.23 Postnatal peer support programs can reduce
cessation of exclusive breastfeeding, as can face-to-face support from health
professionals, some antenatal education and postnatal home visiting support.
Written information such as leaflets is not very effective.52 In the context of
Aboriginal and Torres Strait Islander health, home visits to relay nutritional
information are recommended.24 There is evidence that if doctors improve their
knowledge and counselling skills around nutrition this may be helpful in the
prevention of FTT.24,67,78,93
Interventions attempting to favourably alter the intake of nutrients include
treating lactose intolerance. However, in cases of acute diarrhoea, there is
no benefit in using a non-lactose formula over a lactose containing formula
in the re-feeding period following rehydration in studies continued for up to 7
days. Guidelines recommend confirmation of lactose intolerance with Clinitest
tablets before treatment.75,105 There is evidence that encouraging certain eating
behaviours may be helpful in improving nutrition for children in low income
households. This includes encouraging and supporting parents and carers
to make home prepared foods for infants and young children, without adding
salt, sugar or honey; encouraging families to eat together and encouraging
parents and carers to set a good example by the food choices they make for
themselves; and advising parents and carers not to leave infants alone when
they are eating or drinking.52
There are similarities and differences in scientific versus lay perspectives on
growth. Scientific perspectives focus on the extreme ends of poor health
and look forward to adult outcomes, but lay perspectives are more focused
on framing discussions around what is normal and the current health status
of the child. This may have implications for how healthcare providers should
pitch discussions with carers of children at risk of FTT to promote maximum
engagement in preventive strategies. It has been noted that children who
63
64
Child health
are stunted may look ‘normal’, albeit young for their age. Caregivers may be
unaware that their child’s growth is very poor and that their idea of a ‘norm’ may
not reflect a healthy nutritional status.24,106,107
Food insecurity is a major problem in many remote and urban Aboriginal
and Torres Strait Islander communities (see Chapter 1: Lifestyle, overweight/
obesity). Food insecurity involves a problem with both the supply of nutritious
food, which can be limited in remote Australia, and a family’s ability to access
it. The latter may be compromised by high prices for fresh fruit and vegetables,
poverty, not having a refrigerator, lack of transport to get to the shop, and
excess expenditure on substances such as cigarettes and alcohol, and other
substances. Such problems need to be addressed by long term co-operation
and commitment of intersectoral bodies working with local communities so that
appropriate action plans can be enacted.108
Community feeding programs supply supplementary foods to children at
risk of FTT, often on a population basis, though children can be individually
targeted if there are risk factors for FTT. Food may be distributed for no cost
through childcare centres and schools, exceeding what is usually provided in
such places or given out through health services. Such programs have been
used to overcome food insecurity barriers, without the need to alter community
infrastructure. Using community feeding programs has mixed evidence, with
one systematic review67,77 stating such programs should only be relatively short
term and must be supported by the community. Another review shows support
for this approach.74
Recommendations: Growth failure
References
Level/
strength of
evidence
Preventive
intervention type
Who is at
risk?
How often?
Screening
All children
Recommend growth monitoring
(including weight, length, head
circumference, nutritional and
psychosocial assessment to
coincide with child health visits for
immunisation* (see Table 2.1)
At 2, 4, 6, 12, 18,
IA
24 and 36 months
and between 4 and
5 years
Monitor weight
more frequently if
there are concerns
Behavioural
All children
Discuss growth monitoring
Opportunistic
findings with the family, explaining
how weight gains are linked to
good health and always link the
discussion with any nutritional
intervention currently being
undertaken
Assess developmental milestones
(gross motor, fine motor, speech
and language, social interactions)
with growth monitoring checks
Consider using parent report
questionnaires and questions in
patient held record (see Chapter
7: Table 7.1)
Maintain a high index of suspicion
in children with following risk
factors: possible fetal alcohol
syndrome, microcephaly,
convulsions and prematurity
IA
At 2, 4, 6, 12, 18,
IA
24 and 36 months,
and between 4 and
5 years
52,62,67,104
24,52,67,75,77,78
24,74,106,107
25,78
Child health
65
Mothers
Promote breastfeeding by
discussing the health benefits,
use of peer support, face-to-face
health professional and postnatal
home visits
Opportunistic
IB
52
All families
Provide nutrition education
Opportunistic
counselling targeting both families
and community workers
IB
23,52,67,73,77
Counselling should focus on
behaviour change, be community
driven and integrated with other
preventive child health programs
Consider referral to a dietitian if
simple measures are not helpful
GPP
Children
in families
experiencing
socioeconomic
hardship or
psychosocial
stress
Provide home visiting support by
referral to an early intervention
program
Opportunistic
Ensure regular communication
between primary healthcare
staff and other agencies so that
nutritional support programs
are integrated with psychosocial
support
IA
67,77,85,109
GPP
Chemoprophylaxis Children living
in areas with
high rates
of helminth
infections
Recommend anti-helminth
treatment with a single dose of
albendazole
Refer to Australian Therapeutic
Guidelines for dosing regimen64
Opportunistic
IA
67,75,77
Environmental
Community food
supplementation programs may
be used short term to overcome
issues of lack of food security,
providing they have the support
of the community and are part of
a multifaceted intervention
N/A
IA
67,77
* Correction for prematurity must be made until 18 months for head circumference, 2 years for weight and 40 months for height. Measure
length if <2 years and height if >2 years. Measure head circumference until 36 months of age and body mass index (BMI) from 2 years of
age. Be sure equipment is calibrated and measurements are accurately done78
Table 2.1. Conducting a growth monitoring action plan
• Document carer concerns and the barriers they perceive to breastfeeding and healthy
nutrition
• Explore issues of finances, transport, home storage (refrigerator) availability, numbers
of people living at home, food preferences, food preparation equipment availability,
facilities to maintain hygiene and hygiene practices
• Involve the carer in finding solutions to problems, and focus on finding solutions that
are practical and context specific, paying particular attention to family needs and
resources
• Give information about appropriate weaning foods and amounts
• Consider linking the child to a team approach involving an Aboriginal and Torres Strait
Islander health worker, community nurse, family support worker and dietitian if there
are indications that the child is at risk of FTT or showing early signs of growth faltering
• Document review dates and begin next review by review of previous action plan
66
Child health
Childhood kidney disease
Background
Aboriginal and Torres Strait Islander adults have very high rates of end stage renal
disease (ESRD) and there is evidence it is increasing.4,110,111 Renal disease can start
in utero and has been linked with low birthweight.112 Aboriginal and Torres Strait
Islander children have higher rates of urinary tract infection (UTI), renal calculi and
glomerulonephritis than non-Indigenous children, though much of the current evidence
for this comes from the more remote parts of Australia. There is a lack of studies into
incidence rates of these diseases from urban areas. The vast majority of these children
will make a full clinical recovery from these renal illnesses.24,113–117
There is mixed evidence as to whether renal disease occurring in childhood contributes
to high rates of chronic kidney disease (CKD) in Aboriginal and Torres Strait Islander
adults. Risk factors for CKD seen in children, such as haematuria and proteinuria, are
often transient116,118–120 with the exception of microalbuminuria in children with prepubertal and pubertal onset diabetes.121,122 Single estimations of urinary blood and
protein in children vary according to posture, illness, exercise and time of day. Screening
urinalysis is costly to the community, may result in physical and psychological costs
to the patients and their families, and is prone to misinterpretation. Baseline CKD risk
factors are frequent in both Aboriginal and non-Aboriginal primary school aged children,
though there is evidence that, at a single test, Aboriginal children have a greater risk
of haematuria than non-Aboriginal children. Higher rates of transient haematuria may
reflect the higher incidence of transient disease seen in Indigenous children, such as
post-infectious glomerulonephritis.23,42,81,116,118,119,123,124
Though most children make an apparent full recovery from acute post-streptococcal
glomerulonephritis (APSGN), in some Aboriginal and Torres Strait Islander communities
children who had APSGN have six times greater risk of developing renal disease as
an adult. Thus it is not clear whether the link between APSGN and adult onset CKD
is causative or associative. However, the possibility of a causative link makes the
prevention of streptococcal skin disease an important issue for Aboriginal and Torres
Strait Islander children. There is good evidence that prevention and treatment of
skin infections may be helpful in prevention of APSGN. Children with skin sores and
household contacts of such children should be given targeted treatment with antiscabetics and benzathine penicillin. However, there are different recommendations
regarding the extent of chemoprophylaxis coverage that is required in the community.
At a population level, regular community based programs may be useful to screen and
treat all children in a target age group (eg. ages 0–3 years) for both scabies and infected
sores. Simultaneous treatment of the whole community to remove scabies (a common
precursor to streptococcal skin infection) followed by regular ongoing surveillance
and treatment of scabies and skin sores (at least three times per year) may prevent
streptococcal skin infections.115,120,125 There is good evidence that improvements in
housing to reduce overcrowding and promotion of regular washing for children will also
help prevent skin sores.113,117,125,126
There is a similar lack of certainty around the link between childhood UTI and adult
ESRD. It is not clear what the true rate of ESRD caused by pyelonephritic scarring/reflux
nephropathy is, nor is it clear what proportion of these people had a UTI in childhood.127
The lack of certainty surrounding this link is reflected in the recommendations, where
there is mixed evidence for the use of antibiotic prophylaxis routinely following first
time UTI. Some studies show that even in children with vesicoureteric reflux, antibiotic
prophylaxis is not superior to supportive care in preventing subsequent UTIs or renal
Child health
parenchymal injury, and in fact can produce harm.122,127 Other studies support the use
of prophylactic antibiotics following a first-time UTI at least until any imaging studies
are completed.128,129 However, asymptomatic bacteriuria in infants and children should
not be treated with prophylactic antibiotics,127 though it is reasonable to consider
antibiotic prophylaxis in infants and children who have had recurrent UTI.127 Some
behavioural and environmental preventive activities for children who have had one UTI
can decrease the chances of further UTIs. However, there is no evidence that long
term outcomes, after a first-time typical UTI, are improved by the use of investigations
in children over the age of 6 months.24,127,130
While high grade vesicoureteric reflux (VUR) is associated with kidney damage, there
is no evidence that continuous antibiotic prophylaxis in children with this condition is
effective in reducing the rate of pyelonephritis recurrence and the incidence of renal
damage in children with VUR.131–133 Some of the kidney damage caused by high
grade VUR occurs prenatally.134 Even though the incidence of VUR is increased in the
siblings and children of those with VUR, there is no evidence that screening for VUR
in these subgroups will result in any benefit as the value of identifying and treating
VUR is unproven.133 Circumcision reduces the risk of UTI in boys but has a significant
complication rate of haemorrhage and infection, so is not recommended routinely to
prevent UTIs. However, in boys with recurrent UTI or high grade VUR there may be a
possibility of a net clinical benefit from circumcision given this particular subset of boys
has a higher chance of UTI recurrence.135
Renal calculi in Aboriginal children are predominantly radiolucent uric acid stones
and present on average at 24 months of age, though some have been apparent in
children as young as 8 months. They usually occur in the upper renal tract and are
rare in children living in urban areas. They have been linked with chronic diarrhoea and
environmental induced enteropathy.114,136 There is no evidence linking childhood renal
calculi to the higher rates of ESRD seen in Aboriginal and Torres Strait Islander adults.
There is mixed evidence as to whether blood pressure screening to detect renal
disease should be performed in children. Some evidence supports screening children
yearly from the age of 3 years, and younger if there are risk factors for high blood
pressure such as obesity.123,137 However, this screening is not primarily recommended
for purposes of screening for renal disease in children, nor is it solely recommended
so that treatment can prevent renal damage: rather it is primarily targeting prevention
of cardiovascular disease. Other evidence either makes no comment about screening
for blood pressure in children,78 or supports explicit recommendations for not using
blood pressure to screen for renal disease. This is particularly so when blood pressure
screening is discussed with regards to being a marker of undiagnosed kidney disease
in children.81,116,118,119 Screening recommendations include much discussion about the
importance of taking blood pressure correctly and interpreting the findings carefully.
This includes recommendations for:
• auscultation to be used in conjunction with mercury or aneroid
sphygmomanometers rather than use of automated devices
• correct positioning of the child
• correct cuff size according to the size of the child’s arm
• being particular in interpretation of blood pressure values according to age, gender
and height
• repeat measurements of blood pressure to validate an abnormal finding followed by
referral for appropriate work-up if hypertension is confirmed.
67
68
Child health
The measurement of blood pressure in all young children has not been linked to
strong evidence of improvements in diagnosis and treatment of renal disease, and
may be problematic on different fronts. The practice of measuring blood pressure
to ensure accuracy of readings and the interpretation of values is more complicated
in children than for adults and is thus vulnerable to a fair degree of equipment and
practitioner error. It may make community based screening unnecessarily difficult,
and divert efforts into directions where the evidence of gain for the child is only
mixed and not validated for Aboriginal and Torres Strait Islander populations.
Recommendations: Childhood kidney disease
How often?
Level/
strength of
evidence
References
All children without a Routine urinalysis or blood pressure
high risk condition
screening for kidney disease is not
recommended unless there is a clinical
indication
N/A
IA
23,42,81,116,
118,119,123,124
Children living in
Check the skin for scabies and impetigo
areas with high rates and treat according to management
of infectious skin
guidelines
disease (scabies and
impetigo)
Opportunistic
and as
part of an
annual health
assessment
GPP
64,120
IB
133
Preventive
intervention
type
Who is at risk?
Screening
Children with first
episode UTI
Assess need for imaging tests based on As needed
treatment response within 48 hours and
whether atypical features are present
(see Table 2.2)
Children with
pre-pubertal and
pubertal onset
diabetes
Check albumin to creatinine ratio (ACR)
using single voided specimen, morning
specimen preferred
Behavioural
Children who have
had at least one
episode of UTI
Identify and correct predisposing factors As needed
for recurrence (including constipation,
dysfunctional elimination syndromes,
poor fluid intake and delays in voiding)
IA
127
Chemoprophylaxis
Children living in
areas with high rates
of infectious skin
impetigo)
Treat household contacts of someone
with scabies with 5% permethrin cream
if over 2 months old and sulphur 5% or
crotamiton cream if <2 months of age
In communities where there are
outbreaks of infected scabies, offer
all household contacts of people with
impetigo a single dose of benzathine
penicillin G (see Resources)
IIIC
113,117,120
Environmental
Children living in
areas with high
rates infectious skin
impetigo)
Promote good hygiene practices at
Opportunistic
home
Refer to relevant housing support
services to promote access to adequate
washing facilities and toilets
IA
113,120
Community based interventions that
use screening and immediate treatment
for skin sores and scabies in targeted
age groups should be combined with
simultaneous treatment of the whole
community for scabies (see Resources)
IA
113,117,120
5 years after
IA
diagnosis or at
age 11 years,
or at puberty
(whichever
is earlier),
then annually
thereafter
As needed
N/A
121,122
Child health
Table 2.2. Recommended imaging following first
presentation with UTI
Infants younger than 6 months
Test
Responds well to treatment
within 48 hours
Atypical
UTI*
Ultrasound during the acute infection
No
Yes
Ultrasound within 6 weeks
Yes
No
DMSA 4–6 months following the
acute infection
No
Yes
MCUG
No
Yes
within 48 hours
Atypical
UTI*
Children aged 6 months to 3 years
Test
No
Yes
No
No
acute infection
No
Yes
MCUG
No
No
within 48 hours
Atypical
UTI*
Children aged 3 years or more
Test
No
Yes
No
No
acute infection
No
No
MCUG
No
No
DMSA = dimercaptosuccinic acid scan (an intravenous radionuclide scan for assessing renal
function), MCUG = micturating cystourethrogram
*Atypical UTI features include: the patient is seriously ill, poor urine flow, abdominal or bladder
mass, raised creatinine, septicaemia, failure to respond to treatment with suitable antibiotics
within 48 hours, infection with non-E. coli organisms
†MCUG should not be performed routinely but should be considered if any of the following
features are present: dilatation on ultrasound, poor urine flow, non-E. coli infection, family
history of VUR
Source: National Collaborating Centre for Women’s and Children’s Health, 2007.127 Refer to this
resource for imaging recommendations for recurrent UTI
Resource
Guidelines for community control of scabies, skin sores and crusted scabies in the
Northern Territory (Northern Territory Department of Health and Families)
www.health.nt.gov.au/library/scripts/objectifyMedia.aspx?file=pdf/10/83.
pdf&siteID=1&str_title=Healthy+Skin+Program.pdf.
69
70
Child health
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103. Brooks WA, Santosham M, Naheed A, Goswami D, Wahed MA, Diener-West M, et al. Effect of weekly
zinc supplements on incidence of pneumonia and diarrhoea in children younger than 2 years in an
urban, low-income population in Bangladesh: randomised controlled trial. Lancet 2005;366(9490):999–
1004.
104. Panpanich R, Garner P. Growth monitoring in children. Cochrane Database Syst Rev 2000(4):CD001443.
105. National Collaborating Centre for Women’s and Children’s Health funded to produce clinical guideline
for NHS by NICE. Clinical guideline: diarrhoea and vomiting caused by gastroenteritis diagnosis,
assessment and management in children under 5 years. NCCWCH, 2009.
106. Lucas P, Arai L, Baird J, Kleijnen J, Law C, Roberts H. A systematic review of lay views about infant size
and growth. Arch Dis Child 2007;92(2):120–7.
107. Lucas PJ, Roberts HM, Baird J, Kleijnen J, Law CM. The importance of size and growth in infancy:
integrated findings from systematic reviews of scientific evidence and lay perspectives. Child Care Health
Dev 2007;33(5):635–40.
108. National Aboriginal and Torres Strait Islander Nutrition Working Party. National Aboriginal and Torres
Strait Islander Nutrition Strategy and Action Plan 2000–2010: Strategic Inter-Governmental Nutrition
Alliance of the National Public Health Partnership, 2001.
109. Queensland Health. Strategic Policy for Aboriginal and Torres Strait Islander Children and Young
People’s Health 2005–2010. Brisbane: Strategic Policy Branch, Queensland Health, 2005.
110. Australian Bureau of Statistics & Australian Institute of Health and Welfare. The health and welfare of
Australia’s Aboriginal and Torres Strait Islander peoples 2008, ABS cat no. 4704.0. Canberra: ABS,
2008. Cited October 2011. Available at www.aihw.gov.au/publications/index.cfm/title/10583.
111. Singh GR, White AV, Hoy WE. Renal ultrasound findings in an Australian Aboriginal population with high
rates of renal disease. Nephrology 2005;10(4):358–61.
112. Hoy WE, Hughson MD, Singh GR, Douglas-Denton R, Bertram JF. Reduced nephron number and
glomerulomegaly in Australian Aborigines: a group at high risk for renal disease and hypertension.
Kidney Int 2006;70:104–10.
113. Singh GR. Glomerulonephritis and managing the risks of chronic renal disease. Pediatr Clin North Am
2009;56(6):1363–82.
114. Carson PJ, Brewster DR. Unique pattern of urinary tract calculi in Australian Aboriginal children. Paediatr
Child Health 2003;39:325–8.
115. Scrace M, Koko K. An outbreak of acute post-streptococcal glomerulonephritis in remote Far North
Queensland. Aust J Rural Health 2006(4):160–3.
116. Haysom L, Williams R, Hodson EM, et al. Natural history of chronic kidney disease in Australian
Indigenous and non-Indigenous children: a 4-year population-based follow-up study. Med J Aust
2009;190(6):303–6.
117. Johnston F, Carapetis J, Patel MS, Wallace T, Spillane P, Territory Health Services Northern
Territory Australia. Evaluating the use of penicillin to control outbreaks of acute poststreptococcal
glomerulonephritis. Pediatr Infect Dis J 1999;18(4):327.
118. Haysom L, Williams R, Hodson E, et al. Risk of CKD in Australian indigenous and nonindigenous
children: a population-based cohort study. Am J Kidney Dis 2009;53(2):229–37.
119. Haysom L, Williams R, Hodson E, et al. Early chronic kidney disease in Aboriginal and non-Aboriginal
Australian children: remoteness, socioeconomic disadvantage or race? Kidney Int 2007;71(8):787–94. .
120. Centre for Disease Control Healthy Skin Programme Northern Territory. Guidelines for community
control of skin sores scabies, and crusted scabies in the Northern Territory Darwin: Northern Territory
Government, 2010. Cited October 2011. Available at www.health.nt.gov.au/library/scripts/objectifyMedia.
aspx?file=pdf/10/83.pdf&siteID=1&str_title=Healthy+Skin+Program.pdf.
Child health
121. Donaghue KC, Chiarelli F, Trotta D, Allgrove J, Dahl-Jorgensen K. ISPAD Clinical Practice Consensus
Guidelines 2006–2007. Microvascular and macrovascular complications. Pediatr Diabetes
2007;8(3):163–70.
122. Isbel N, de Looze F, Gallagher M, Glasziou P, McLeod S, McTaggart S, et al. Proteinuria CARI guidelines.
Aust Fam Physician 2005;34(11).
123. National Heart Lung and Blood Institute US Department of Health. The fourth report on the diagnosis,
evaluation, and treatment of high blood pressure in children and adolescents National High Blood
Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents.
Pediatrics 2004;114(Suppl 2):555–76.
124. Caring for Australasians with Renal Impairment. Urine protein as diagnostic test: evaluation of proteinuria
in children. Sydney: CARI, 2004. Cited October 2011. Available at www.cari.org.au/ckd_urineprot_list_
pub2004.php.
125. Zaffanello M, Cataldi L, Franchini M, Fanos V. Evidence-based treatment limitations prevent any
therapeutic recommendation for acute poststreptococcal glomerulonephritis in children. Med Sci Monit
2010;16(4):RA79–84.
126. Steer AC, Danchin MH, Carapetis JR, Centre for International Child Health University of Melbourne.
Group A streptococcal infections in children. J Paediatr Child Health 2007;43(4):203–13.
127. National Collaborating Centre for Women’s and Children’s Health. Urinary tract infection in children
diagnosis, treatment and long-term management. London: National Institute for Health and Clinical
Excellence, 2007. Cited October 2011. Available at www.nice.org.uk/nicemedia/pdf/CG54fullguideline.
pdf.
128. American Academy of Pediatrics Committee on Quality Improvement. Practice parameter: the diagnosis,
treatment, and evaluation of the initial urinary tract infection in febrile infants and young children. Elk
Grove Village, IL: American Academy of Pediatrics, 2011. Updated September 2011. Cited October 2011.
Available at http://aappolicy.aappublications.org/cgi/content/abstract/pediatrics;103/4/843.
129. Craig JC, Simpson JM, Williams GJ, et al. Antibiotic prophylaxis and recurrent urinary tract infection in
children. N Engl J Med 2009;361(18):1748–59.
130. Finnell SME, Carroll AE, Downs SM. Diagnosis and management of an initial UTI in febrile infants and
young children. Pediatrics 2011;128(3):e749-e70.
131. Pennesi M, Laura Travan L, Peratoner L, et al. Is antibiotic prophylaxis in children with vesicoureteral
reflux effective in preventing pyelonephritis and renal scars? A randomized, controlled trial. Pediatrics
2008;121(6):1489–94.
132. Keren R, Carpenter M, Greenfield S, Hoberman A, Mathews R MT, Chesney R. Is antibiotic prophylaxis
in children with vesicoureteral reflux effective in preventing pyelonephritis and renal scars? A
randomized, controlled trial. Pediatrics 2008;122(6):1409–10.
133. Skoog SJ, Peters CA, Arant BS Jr, et al. Pediatric Vesicoureteral Reflux Guidelines Panel Summary
Report: Clinical practice guidelines for screening siblings of children with vesicoureteral reflux and
neonates/infants with prenatal hydronephrosis. J Urol 2010;184(3):1145–51.
134. Zaffanello M, Franchini M, Brugnara M, Fanos V. Evaluating kidney damage from vesico-ureteral reflux in
children. Saudi J Kidney Dis Transpl 2009;20(1):57–68.
135. Singh-Grewal D, Macdessi J, Craig J. Circumcision for the prevention of urinary tract infection in boys: a
systematic review of randomised trials and observational studies. Arch Dis Child 2005;90(8):853.
136. Baldwin DN, Spencer JL, Jeffries-Stokes CA. Carbohydrate intolerance and kidney stones in children in
the Goldfields. J Paediatr Child Health 2003;39(5):381–5.
137. Cincinnati Children’s Hospital Medical Center. Best evidence statement (BESt). Blood pressure
measurement in children. Cincinnati: Cincinnati Children’s Hospital, 2009. Cited October 2011. Available
at www.guideline.gov/content.aspx?id=14293&search=hypertension#Section420.
75
Chapter 3
The health
of young
people
Author Annapurna Nori
Expert reviewer Sherry Saggers
The health of young people
Overview
In this chapter the terms ‘young people’ and ‘adolescents’ refer to people aged
12–24 years. This is consistent with the definitions used by the University of
Melbourne Centre for Adolescent Health, the NSW Centre for the Advancement
of Adolescent Health and the Australian Institute of Health and Welfare.1,2 It is
important to note that this definition differs from the World Health Organization
defined age range of 10–19 years.
The preventive health issues for young people are very broad. To narrow the
scope for the National Guide, this chapter focuses on three topics: psychosocial
assessment, the prevention of unplanned pregnancies, and illicit substance use.
Other areas relevant to youth health, in particular smoking, physical activity,
obesity, alcohol, sexual health, depression and suicide, are addressed in other
chapters.
According to the World Health Organization, ‘Nearly two thirds of premature
deaths and one-third of the total disease burden in adults are associated with
conditions or behaviours that began in youth, including tobacco use, a lack of
physical activity, unprotected sex or exposure to violence. Promoting healthy
practices during adolescence, and efforts that better protect this age group
from risks will ensure longer, more productive lives for many’.3
Young people’s specific developmental and health needs are distinct from that
of children or adults. Their sexual and reproductive health in particular tend to
be different from those of adults.4 The underlying aetiology of illness in young
people is most often psychosocial.1 Although social and economic factors can
influence health in all age groups, the adverse health outcomes for young people
are strongly influenced by family breakdown, physical/sexual abuse and neglect
and homelessness. Adolescence is a period of risk taking and experimentation,
thereby providing greater potential for adverse health outcomes. Despite this,
young people underutilise primary care, are reluctant to seek help for health
problems and seldom receive counselling about risk taking behaviours when
they do.5–7 Clinician training and charting tools are associated with increases in
rates of screening and counselling of adolescents about risky behaviours.8
An overview of the health of Aboriginal and Torres Strait
Islander young people
In the 2006 census, around 120 378 people identified as Aboriginal, Torres
Strait Islander or both in the age group 12–24 years.9 They comprise 3.4% of the
total Australian population of young people in that age range and 26.5% of the
total Aboriginal and Torres Strait Islander population.9 By contrast, young people
comprise 18% of the total Australian population. Most Aboriginal and Torres
Strait Islander young people live in major cities and inner and outer regional
areas, however, they account for over half of all young people in Australia living
in very remote areas.9
Among the general Australian youth population, the leading causes of death
and illness are accidents and injuries (unintentional and self inflicted), mental
health problems (including depression and suicide) and behavioural problems
(including illicit drug use). Half of all deaths in those aged under 19 years
are caused by injuries.10 The overall death rate and the injury death rate for
Aboriginal and Torres Strait Islander young people are four and five times
greater than for non-Indigenous young people respectively.
77
78
In 2004–05, young Aboriginal and Torres Strait Islander people aged 15–24
years were less likely to rate their health as excellent or very good, compared to
young non-Indigenous people (59% compared to 70% respectively).2 Aboriginal
and Torres Strait Islander young people were slightly more likely than nonIndigenous young people to rate their health as fair or poor (9% compared to
7%). They are more likely to experience health risk factors such as obesity,
physical inactivity, smoking, lower educational attainment and imprisonment.
Fifty percent of Aboriginal and Torres Strait Islander young people aged 18–24
years are smokers, compared to 26% of their non-Indigenous counterparts. In
the 18–24 years age group, the prevalence of a long term health condition is 1.5
times greater than for non-Indigenous young people. Hospital separations due
to mental and behavioural disorders (including substance and alcohol abuse)
are 1.6 times greater than non-Indigenous youth in several Australian states.
Among the general population in 2005, half of sexually transmissible infections
(STIs) notifications were for young people aged 12–24 years.2 In the same
period 13% of all chlamydia notifications, 64% of all gonococcal notifications
and 56% of all syphilis notifications were for Aboriginal and Torres Strait
Islander young people. Aboriginal and Torres Strait Islander youth are less
likely to access primary healthcare services and are more likely to present to
tertiary healthcare services than non-Indigenous young people. Youth friendly
primary care services that are sensitive to the administrative, financial, cultural
and psychological hurdles experienced by young people is an integral step in
providing effective preventive interventions.1,7,11,12
Note: a detailed review of unplanned pregnancy and illicit drug use
epidemiology is provided in separate sections.
Psychosocial
Background
Since the aetiology of most illness in young people is psychosocial,
a comprehensive psychosocial assessment is considered one of the
cornerstones of primary healthcare for young people. There is, however,
limited evidence on its effectiveness in improving health outcomes and current
recommendations rely on expert opinion. The HEEADSSS assessment is the
most widely recommended psychosocial assessment tool both nationally
and internationally.1,7,11,13–16 It is a systematic, structured and graded approach
and designed so that topics perceived to be non-threatening are broached
before moving to more sensitive issues. Appendix 3.1 provides a table showing
adolescent development stages. Appendix 3.2 provides the assessment
questions. HEEADSSS has been endorsed by the University of Melbourne
Centre for Adolescent Health, the NSW Centre for the Advancement of
Adolescent Health, the RACGP and state funded family planning organisations
such as Family Planning Queensland.1,17
The HEEADSSS assessment is recommended to be conducted as part of an
annual health assessment. Numerous organisations including the US Preventive
Services Task Force, the American Academy of Paediatrics and the American
Medical Association11,18 have produced guidelines recommending annual
screening of young people for high risk behaviours. In Australia, the Medicare
health assessment items for Aboriginal and Torres Strait Islander people provide
an opportunity to conduct funded annual health assessments. The Adolescent
Health GP resource kit, produced by the NSW Centre for the Advancement
of Adolescent Health and Transcultural Mental Health Centre, also provides
templates for a health assessment for young people.19
Recommendations: Psychosocial assessment
Preventive
intervention
type
How often?
of evidence
Screening
All young people Conduct a psychosocial
aged 12–24
assessment to obtain a holistic
years
assessment of health and to
determine risk factors affecting
wellbeing
Useful tools include the
HEEADSSS assessment (see
Appendix 3.2)
Opportunistic
and as part of
an annual health
assessment
GPP
1,7,11,13–18
79
80
Unplanned pregnancy
Background
In 2008, almost 19% of all births in Australia were to young women aged 15–24 years.20 In
2003, more than half of pregnancies in young women aged 15–19 years resulted in induced
abortions.21 This implies that many pregnancies in young women are unplanned events. In
addition, teenage pregnancies are associated with increased risk of pre-term births, smallfor-gestational-age babies and neonatal deaths. Teenage mothers often find it difficult to
complete their education, can be separated from the child’s father, often have less financial
resources than older mothers, and their children tend to have worse health. Children of
adolescent parents have increased risk of developmental delay, behavioural problems,
substance abuse, early sexual activity and becoming teenage parents themselves.22,23
Aboriginal and Torres Strait Islander young women are more likely to get pregnant and
smoke during pregnancy, and are at greater risk of adverse outcomes for themselves
and their babies. In 2005, the age specific fertility rate of Aboriginal and Torres Strait
Islander young women in the age group 15–19 years and in the age group 20–24 years
was 4.3 times and 2.3 times higher than for non-Indigenous young women respectively.
In 2008, 20% of Aboriginal and Torres Strait Islander mothers were teenagers compared
to 3.5% of non-Indigenous mothers.20 Aboriginal and Torres Strait Islander women of all
ages have babies with a three times higher prevalence of low birth weight, and two times
higher prevalence of pre-term deliveries. Pregnant Aboriginal and Torres Strait Islander
young women are also more likely to have fewer antenatal attendances. In 2004–05,
34% of all hospitalisations for Aboriginal and Torres Strait Islander young people were
due to pregnancy related complications. Congenital abnormalities are more prevalent
in Aboriginal and Torres Strait Islander than in non-Indigenous babies, particularly for
babies born to teenage mothers.24
Evidence of effectiveness of preventive interventions
The clinic visit can be used to engage the young person in a discussion targeting
reproductive health, or within the context of broader and more general health issues.
Indeed, commencing the consultation with a more general approach is better suited to
the needs of a young person.1 The components of routine antenatal health assessments
are outlined in Chapter 9: Antenatal care.
Screening and behavioural interventions
Experts in Australia, the USA and the UK recommend three interventions for young
people: anticipatory guidance/counselling, screening for sexual activity and at risk sexual
behaviour, and appropriate counselling for preventing unplanned pregnancies.1,11,25–28
Anticipatory or health guidance is defined as a proactive, developmentally based
counselling technique that focuses on a young person’s stage of development. It
is meant to ‘promote a better understanding of their physical growth, psychosocial
and psychosexual development, and the importance of becoming actively involved
in decisions regarding their healthcare’.11 There is a paucity of good quality studies
assessing the effectiveness of counselling on unplanned pregnancies.25,26,28,29
Consequently recommendations are generally based on expert opinion30 and suggest
that counselling should include ‘advice on how to prevent unplanned pregnancies, all
methods of reversible contraception, how to get and use emergency contraception,
and to provide supporting information in an appropriate format’.27 Parents or guardians
should also receive health guidance at least one time each during the young person’s
early, middle and late adolescence.11
Barrier methods of contraception, especially male condoms, are effective for both
pregnancy prevention and reducing risk of some STIs. While the method specific failure
rate for condoms is 2%, the typical use failure rate is around 15% due to improper and
inconsistent use.25 Condoms are recommended as a primary prevention intervention
but ongoing education with emphasis on consistent and proper use is important.
Chemoprophylaxis
Hormonal contraception includes the oral contraceptive pill (OCP) and long acting
reversible contraception (LARC), which is defined as any method that requires
administration less than once per cycle or month. Examples of hormonal LARCs
include progestogen-only injections, progestogen-only subdermal implants and
progestogen-only intrauterine devices (IUDs) while copper intrauterine devices are a
form of non-hormonal LARC. Unlike the oral contraceptive pill (OCP), effectiveness of
LARC does not depend on daily compliance. There is scant but reassuring literature
on the use of IUDs in adolescents.31 Due to the adverse but reversible effect of
progestogen-only injections on bone mineral density, this should be used cautiously as
first line contraception in young women aged under 18 years.32 Subdermal progestogen
LARCS are not known to be associated with reduced bone mineral density.32 On the
basis of extrapolated evidence, all other hormonal contraception has the same safety
and efficacy profile in young women as in adult women.
According to the 2004–05 National Aboriginal and Torres Strait Islander Household
Survey, condoms followed by the OCP were the main methods of contraception
reported by young Aboriginal and Torres Strait Islander women aged 18–24 years in
2004–05, 25% and 16% respectively. Implants and injections were reported by 6%
each. An estimated 14% of young Aboriginal and Torres Strait Islander women reported
not using any contraception.
Hormonal contraception is traditionally commenced with the onset of menses to avoid
contraceptive use during an undetected pregnancy. An alternative is immediate initiation
if pregnancy can be reliably ruled out. The advantage of this method in young women
is to improve the uptake of contraception. However, with the exception of injectable
progestogen, there is limited evidence that immediate commencement of contraception
reduces unintended pregnancies.33
Emergency contraception can decrease the chance of pregnancy. To date, however,
there is no evidence that either advance provision of, or increased access to, emergency
contraception reduces unintended pregnancies at a population level.29,34 On the
encouraging side, advance provision has not led to increased rates of STIs, increased
frequency of unprotected intercourse or changes in contraceptive methods. In particular,
women who received advance emergency contraception were as likely to use condoms
as women who did not receive this. In a study involving adolescents, experience with
emergency contraception was associated with an increased probability of condom use
and an increased perceived capacity to negotiate condom use.26 It is therefore reasonable
to support young women’s knowledge of, and access to, emergency contraception.
Environmental
There have been a few reviews of the effectiveness of primary pregnancy prevention
programs in young people. Interventions studied have been in both low and middle
income countries and high income countries. They include school based programs,
community based programs, family planning clinics, workplace programs, mass
media programs (social marketing) and health facility based programs.31,35-37 Overall,
most programs have a positive impact on knowledge and attitudes, and no impact on
sexual activity or delaying initiation of sexual intercourse. There is some evidence that
programs can be effective in increasing contraceptive use and to a much lesser extent
reducing pregnancy rates. In one systematic review of educational interventions to
inform contraceptive choice, theory based groups consistently demonstrated favourable
81
82
results. These included social cognition models (particularly social cognitive theory),
motivational interviewing and the aids risk reduction model.38 Community based
programs tend to be more effective than school based programs, and clinic based
programs more effective than non-clinic based programs. Programs in youth
friendly services can improve knowledge, increase contraceptive use and increase
use of the service. Abstinence programs were the least successful intervention.
Recommendations: Unplanned pregnancy
Who is at risk?
Screening
All young people Ask if sexually active and identify
aged 12–24 years at risk sexual behaviours (eg.
unprotected sexual intercourse:
see Chapter 8: Table 8.1)
Opportunistic and
GPP
as part of an annual
health assessment
(including
psychosocial
assessment)
1,11
Behavioural
All young people
Opportunistic and
GPP
health assessment
1,11,27
Provide anticipatory guidance*
and sexual health education,
tailoring the information according
to whether a young person is
sexually active or not (see Chapter
8: Sexual health and bloodborne
viruses)
Discussion should include the
following:
How often?
Level/
strength of
evidence
References
Preventive
intervention type
• sexual development and sexual
feelings
• prevention of unplanned
pregnancies including
abstinence
• resisting sexual and peer
pressure
• methods of reversible
contraception, access to and
use of emergency contraception
Young people
who are
considering
initiating sexual
activity or who are
sexually active
Recommend use of and/or provide Opportunistic and
IIIC
condoms
health assessment
Discuss the proper methods for
condom usage
25
Young people
engaging in risky
sexual behaviour
Use individual behaviour change
techniques such as brief
interventions (eg. information
giving, motivational interviewing)
and cognitive behavioural therapy
GPP
27
Offer or refer to theory based
pregnancy prevention/education
programs to improve knowledge
and increase contraceptive use.
Examples include social cognitive
theory,† motivational interviewing
program, AIDS risk reduction
model (see Table 3.1)
IA
31,35–38
Provide health guidance to parents At least once at
and other guardians regarding
early, middle and
youth sexual health following the
late adolescence
principles of anticipatory guidance*
GPP
11
Parents or
guardians of
young people
Opportunistic
Chemoprophylaxis Young females
who are
sexually active
or considering
initiating sexual
activity
Environmental
83
Assess suitability for and offer
hormonal contraception. Methods
include the oral contraceptive
pill and long acting reversible
contraception (ie. progestogen
only injections, progestogen only
subdermal implants, progestogen
only IUDs)
Opportunistic
IIIC
31,32
Young females
who have had
unprotected
intercourse
Conduct a detailed history to
assess the context
Discuss and recommend
emergency contraception as
necessary
Arrange for appropriate follow up
Opportunistic
IIB
26
N/A
Promote youth friendly primary
healthcare services
N/A
GPP
1
*Anticipatory guidance is a developmentally based counselling technique that focuses on a young person’s stage of development. Counselling
is focused towards gaining a better understanding of young people’s physical growth, psychosocial and psychosexual development. It
emphasises the importance of the young person becoming actively involved in decisions regarding their healthcare11
†Social cognitive theory is a learning theory based on the idea that people learn by watching what others do and do not do
Table 3.1. The AIDS risk reduction model
This model has three stages and is based on several other behaviour change
theories, including the health belief model, ‘efficacy’ theory, emotional influences and
interpersonal processes. The three stages outlined below are behaviour labelling,
commitment to change and taking action
Stage
Influences
1. R
ecognition and labelling of one’s
behaviour as high risk
• Knowledge of sexual activities associated with
HIV transmission
• Believing that one is personally susceptible to
contracting HIV
• Believing that having AIDS is undesirable
• Social norms and networking
2. Making a commitment to reduce
high risk sexual contacts and to
increase low risk activities
• Cost and benefits
• Enjoyment (eg. will the changes affect my
enjoyment of sex?)
• Response efficacy (eg. will the changes
successfully reduce my risk of HIV infection?)
• Self efficacy
• Knowledge of the health utility and enjoyability
of a sexual practice, as well as social factors
(group norms and social support), are
believed to influence an individual’s cost and
benefit and self efficacy beliefs
3. Taking action:
•information seeking
•obtaining remedies
•enacting solutions
Depending on the individual, phases
may occur concurrently or phases
may be skipped
• Social networks and problem solving choices
(self help, informal and formal help)
• Prior experiences with problems and solutions
• Level of self esteem
• Resource requirements of acquiring help
• Ability to communicate verbally with sexual
partner
• Sexual partner’s beliefs and behaviours
Source: Family Health International 200239
84
Illicit drug use
Background
Young people most commonly acquire illicit drugs through a friend,
acquaintance or relative. Curiosity, peer pressure and wanting to do something
exciting are the most common reasons for initiating illicit drug use. Reasons
for not initiating drug use are not being interested, and concerns over health,
addiction and the law. When compared with non-Indigenous people, Aboriginal
and Torres Strait Islander people are twice as likely to be recent users of illicit
drugs (25% compared to 14.7%), are more likely to engage in risky drug use and
polydrug use, experience greater drug related harm and are more likely to begin
using illicit drugs at a younger age.40–42
There are social, legal and health related harms associated with illicit drug use.
Polydrug use is not common among youth in general, but when it occurs it is
a major risk factor for subsequent drug related harm.43,44 The 2010 National
Drug Strategy Household Survey found that illicit drug users were more likely
to be diagnosed or treated for a mental illness and report high or very high
levels of psychological distress compared with those who had not used an illicit
drug in the previous 12 months.40 There was a statistically significant rise in the
proportion of recent users with a mental illness between 2007 and 2010.
Cannabis use is associated with lower educational attainment, use of other
illicit drugs and criminal offending. Regular intoxication may interrupt crucial
psychosocial development such as identity formation, and interpersonal and
occupational skill development. For Aboriginal and Torres Strait Islander young
people, there are additional harms since substance dependence further
compounds social deprivation, poverty, decreased cultural learning, alienation
and the chronic ill health cycle.45 There has been conflicting evidence that
cannabis use leads to mental health disorders. Authoritative reviews conclude
that cannabis only exacerbates symptoms and precipitates psychotic episodes
in vulnerable individuals.44 The most serious long term effect of inhalant abuse
is irreversible neurological damage leading to cognitive impairment. Prenatal
exposure is associated with low birthweight, prematurity, developmental delays,
neurobehavioral problems and physical malformations.45 There is also emerging
evidence that substance use is associated with periodontal disease.46 Risk
factors for problematic drug use are highlighted in Table 3.2. Factors that reduce
the risk of illicit drug use include a high degree of family attachment, effective
parental communication and supervision, and religious participation.
Table 3.2. Risk factors for illicit drug use
Individual influences
• Not completing secondary school
• Unemployment
• Delinquency
• Residing in remote and very remote areas
• Favourable attitudes to drug use
• Sensation seeking and adventurous personality
• Relationships with peers involved in drug use
• Low involvement in activities with adults
Family influences
• Parental conflict
• Parent-adolescent conflict
• Parental attitudes to drug use and rules around drug use
• Alcohol and drug problems in the family
Community influences
• Perceived and actual level of community drug use
• Community disadvantage and disorganisation
• Availability of drugs within the community
• Positive media portrayal of drug use
Sources: Loxley W, Toumbourou J, Stockwell T, Haines B, Scott K, Godfrey C, et al 2004 and
Australian Institute of Health and Welfare 200544,53
In the general population, the 2010 National Drug Strategy Household Survey
Data found 21.5% of young people aged 14–19 years had ever used cannabis and
15.7% had used in the previous year.40 Youth in this age group are more likely to
be recent users of cannabis than recent users of tobacco.47 In the Aboriginal and
Torres Strait Islander population cannabis is the most commonly used illicit drug,
followed by amphetamines.48 Aboriginal and Torres Strait Islander youth are also
more likely than non-Indigenous youth to smoke cannabis. Since the mid 1990s,
there has been a rapid and significant increase in cannabis use within some
Aboriginal and Torres Strait Islander communities.42 In the 2004–05 National
Aboriginal and Torres Strait Islander Health Survey, 23% of non-remote Aboriginal
and Torres Strait Islander people aged over 17 years reported using cannabis in
the previous 12 months.49 This may in part be due to increased local trafficking,
supply reduction measures to combat petrol sniffing and alcohol dependence
and the larger context of the consequences of colonisation such as social and
cultural alienation, boredom and a perceived lack of a meaningful future.42,50,51 In
the general population, approximately 9% of those who ever use cannabis will
develop dependence. Risk factors for cannabis dependency in adolescents are
earlier age of initiation and frequency of use. There is almost a fivefold increased
risk of developing dependence in those using at least weekly. Compared to adult
users, young people have higher rates of binge and opportunistic cannabis use,
shorter duration between first exposure and dependence, and shorter intervals
between first and second drug diagnosis.41
Injecting drug use prevalence is comparatively low in young people (0.3%
among 14–19 year olds and 0.9% among 20–29 year olds).40 A study
commissioned by the Aboriginal Drug and Alcohol Council of South Australia
involving an urban Aboriginal population found no significant differences
between those over 25 years and those younger than 25 years in terms of drug
85
86
use patterns. However, there is still the problem of injecting drug use and the
related harm. The report states ‘the implication of this finding is that those under
25 years may have comparatively poorer outcomes in future years compared
to their older counterparts’.52 Among the general population sources of needles
and syringes for injecting drug users are chemists (64.5%), needle and syringe
programs (37.2%), friends (25%) and hospital or doctor (14.9%).40
Young people aged 14–19 years are more likely than those in other age groups
to have used inhalants or volatile substances (prevalence 1.2%) and are more
likely to use it frequently (once or more per month).44 Seventy-five percent of
inhalant use occurs in a person’s own home or at a friends.53 The risk of inhalant
use is increased in the presence of social disadvantage and family dysfunction.
The use of inhalants by marginalised youth tends to be motivated by the need
to relieve boredom and cope with emotional distress. In some Aboriginal and
Torres Strait Islander communities, one study found that young people used
sniffing as an expression of power (eg. through its ability to provoke outrage and
to control body weight through suppressing appetite).45
The inaugural 2010 National Indigenous Drug and Alcohol Conference
recommended the following strategies to address the rising prevalence of illicit
drug use among Aboriginal and Torres Strait Islander youth:
• include in preventive health and chronic disease agendas for Aboriginal and
Torres Strait Islander people a substantial focus and specific funding for
addressing substance use
• greater resources to increase the level of ongoing training and capacity of
Aboriginal and Torres Strait Islander health workers in the substance use
sector
• greater investment for a wider variety of sports and other cultural activities for
Aboriginal and Torres Strait Islander youth.54
Evidence of effectiveness of preventive interventions
Australia is an international leader in addressing drug related problems with
the three-pronged approach of supply reduction, demand reduction and
harm reduction/minimisation. This chapter focuses on primary and secondary
prevention interventions in the domains of demand reduction and harm
minimisation. Supply reduction strategies are generally beyond the scope of
primary healthcare services and are therefore not addressed here.
Immunisation
Immunisation against hepatitis B is a harm minimisation strategy to protect
against the consequences of injecting drug use with contaminated needles.55
(See Chapter 8: Sexual health and bloodborne viruses.)
Screening
Screening can be performed to assess individuals at risk of illicit drug use or
to identify use. Illicit drug use is initiated and maintained by a complex array of
biological, cognitive, psychological and sociocultural processes. Hence, all of
these domains should be assessed. Adolescent self reporting of cannabis use
is generally reliable, but reporting of other illicit drugs may be less reliable.41
Assessment should therefore be performed in a non-judgemental manner.
In addition, illicit drug use questions are less threatening when asked in the
context of a general health interview. This is best done via a comprehensive
psychosocial assessment.1,11,41 Such assessments can either be done in
a routine manner11 or opportunistically in young people presenting with
respiratory disorders and mental health problems since these are common
among cannabis users.41 Assessment should be done in conjunction with a
psychosocial assessment (see psychosocial assessment section).
The following screening tools have been developed to identify substance use:
The CRAFFT screening tool is a behavioural health screening tool for use with
children and young people under the age of 21 years.56 It is recommended
by the American Academy of Pediatrics Committee on Substance Abuse
for use with adolescents. It consists of a series of six questions developed
to screen adolescents for high risk alcohol and other drug use disorders
simultaneously. It is a short, effective screening tool meant to assess whether
a longer conversation about the context of use, frequency, and other risks and
consequences of alcohol and other drug use is warranted. The tool can be
self administered or administered by a clinician. It has been translated into six
languages. (See Resources for links to the English versions).
The Indigenous Risk Impact Screen (IRIS) and brief intervention is a 13-item
two factor screen that assesses alcohol and other drug use and associated
mental health issues. It has been validated for use with Aboriginal and Torres
Strait Islander people aged 18 years and over and is included in the Australian
Department of Health and Ageing Alcohol treatment guidelines for Indigenous
Australians.57 In July 2009, the Australian Government extended funding for
the IRIS program to support a national training rollout. Training is a necessary
prerequisite to use of the IRIS tool.
The Substances and Choices Scale is a tool developed in New Zealand and
validated for use in people aged 13–18 years.56,58 It can also be used for repeat
measures to assess change over time.
Behavioural
The majority of problematic illicit drug use occurs in young people with high
levels of risk factors (Table 3.2). Prevention programs to prevent initiation
of illicit drug use should commence with younger children.43,44 There is
evidence supporting the implementation of drug education, especially if based
on social learning theories. Although there is limited evidence, preventive
case management tailored to a young person’s developmental needs is an
appealing approach for those with multiple risk factors for illicit drug use.44
Important aspects of this approach are to assess needs, identify relevant
services, coordinate service delivery and monitor outcomes. It requires
complex coordination across a range of service types.44 Examples include
the Multisystemic Treatment and Children at Risk programs in the USA. Key
elements of these programs include developing service delivery objectives in
consultation with the young person and their family, collaboration between
various services (eg. community health, juvenile justice, drug abuse, education),
and ongoing monitoring of progress. They typically require intensive case
management, coordinating family intervention, after school activity, mentoring,
tutoring, individual psychiatric assessment and counselling.
Brief interventions such as those which form part of the IRIS program are
supported and recommended as a culturally validated tool.59
Environmental
The legacy of colonisation and public health interventions involving forcible
isolation, incarceration and punitive measures needs to be taken into account
87
88
in addressing illicit drug use. Improved access to youth friendly primary care
services is important and has been recommended by the National Indigenous
Drug and Alcohol Committee. Youth workers also have potential to positively
impact on Aboriginal and Torres Strait Islander young people’s resilience,
although this strategy has not been formally evaluated.60
Community support and engagement is particularly important for illicit drug
use programs, because of multifactorial risks and the need for multidisciplinary
resources. Such factors are especially critical in addressing inhalant use, in
particular petrol sniffing.61 Strategies that are devised without community input
run the risk of being rejected.62 Successful community engagement strategies
include mentorship, encouraging positive school ethos, and youth sport
and recreation programs. Mentorship is aimed at developing positive social
relationships between young people and adults in order to support healthy
role modelling. This is a promising approach and warrants further research.44
Parenting programs and other family based interventions aimed at encouraging
healthy family development and reducing parent-adolescent conflict show
promise but also need further research.63-65
Successful school based drug education programs are those based on social
learning theory and which take into account causes of drug use and adolescent
developmental pathways. The Life Skills Training Program, peer education and
youth sport/recreation programs are recommended approaches that warrant
further research.44
There is strong evidence to support needle and syringe exchange programs
and supervised injection centres.66–70 (See Chapter 8: Sexual health and
bloodborne viruses.)
Recommendations: Illicit drug use
Level/
strength of
evidence
GPP
References
Assess for presence of risk factors for As part of an
illicit drug use (see Table 3.2)
annual health
assessment
GPP
1,5,7,11
Administer one of the following
Opportunistic
questionnaires to ascertain drug use:
IIIB
1,5,7,11,56–58
Preventive
intervention
type
Immunisation
Who is at risk?
How often?
All young people
aged 12–24 years
Review hepatitis B immunisation and
immune status and offer vaccination
where indicated (see Chapter 8:
Sexual health and bloodborne viruses)
As per Australian
standard
vaccination
schedule
Screening
All young people
Young people
with risk factors
for drug use (see
Table 3.2)
Behavioural
55
• CRAFFT screening tool (≤21 years)
• IRIS tool (≥18 years)
• Substances and Choice scale
(13–18 years (see Resources)
Young people
Refer for preventive case
with multiple risk
management where services are
factors for drug
available*
use (see Table 3.2)
Opportunistic
IB
44
Young people who Provide brief interventions (eg. in
are using illicit
conjunction with administration
drugs
of one of the above screening
questionnaires). (See also the 5As
framework Chapter 1: Lifestyle,
introduction)
Opportunistic
IIIB
47,57
Refer to drug education programs
Opportunistic
based on social learning theories (eg.
life skills program, peer education,
youth sport/recreation program)
IIB
44,61,62
Consider referral where appropriate
Opportunistic
to parent education programs
and family intervention therapy
to encourage healthy family
development and reduction of parentadolescent conflict
IIB
63–65
Young people who Refer to needle and syringe exchange Opportunistic
are using injecting programs where appropriate
drugs
IB
66
N/A
GPP
71–73
Promote access to community
and school based drug education
programs (based on social learning
theories)
IB
44,74
Promote youth friendly, primary
healthcare services
Support increased access to youth
workers
GPP
1,44,60,75
Support community driven illicit drug
use prevention programs (especially
valuable for inhalant abuse)
IIB
61
Support and promote community
engagement strategies such as
mentorship
IB
44
Support supervised injecting centres
IIB
67–70
Families of young
people who are
using illicit drugs
Environmental
89
Promote school completion
N/A
* Preventive case management involves the coordinated delivery of intensive services tailored to meet a range of developmental needs. It
requires intensive case management through coordinating family intervention, after school activity, mentoring, tutoring, individual psychiatric
assessment and counseling. The approach therefore will involve complex coordination across a range of service types such as health,
juvenile justice, education, and substance abuse. Key aspects are to assess needs, identify relevant services, coordinate service delivery
and monitor outcomes. The young person (and if possible the family) should be involved in developing the service delivery objectives.44 This
can be similar to developing a care plan for people with chronic conditions
Resources
CRAFFT tool for clinicians
www.ceasar-boston.org/CRAFFT/pdf/CRAFFT_English.pdf
CRAFFT tool for self administration
www.ceasar-boston.org/CRAFFT/pdf/CRAFFT_SA_English.pdf
Substances and choices scale manual
www.sacsinfo.com/docs/SACSUserManualNoPrint.pdf
Substances and choices scale questionnaires
www.sacsinfo.com/Questionnaires.html
IRIS (Indigenous risk impact screen) tool and brief intervention. The screening tool
is made available only after participation in a training workshop
www.health.qld.gov.au/atod/prevention/iris.asp.
90
Appendix 3.1. Stages of adolescent development
Early
(10–13 years)
Middle
(14–17 years)
Late
(18–21 years)
Central
question
‘Am I normal?’
‘Who am I?’
‘Where do I belong?’
‘Where am I going?’
Major
developmental
issues
• Coming to terms with
puberty
• Struggle for autonomy
commences
• Same-sex peer relationships
all important
• Mood swings
• New intellectual powers
• New sexual drives
• Experimentation and risk taking
• Relationships have self centred
quality
• Need for peer group acceptance
• Emergence of sexual identity
• Independence from parents
• Realistic body image
• Acceptance of sexual identity
• Clear educational and
vocational goals, own value
system
• Developing mutually caring and
responsible relationships
Main concerns
• Anxieties about body shape • Tensions between family and
and changes
adolescent over independence
• Comparison with peers
• Balancing demands of family and
peers
• Prone to fad behaviour and risk
taking
• Strong need for privacy
• Maintaining ethnic identity while
striving to fit in with dominant
culture
• Self responsibility
• Achieving economic
independence
• Deciding on career/vocation
options
• Developing intimate
relationships
Cognitive
development
• Still fairly concrete thinkers
• Less able to understand
subtlety
• Daydreaming common
• Difficulty identifying how
their immediate behaviour
impacts on the future
• Longer attention span
• Ability to think more abstractly
• More able to synthesise
information and apply it to
themselves
• Able to think into the future and
anticipate consequences of
their actions
• Able to think more rationally
• Concerned about individual
freedom and rights
• Able to accept more responsibility
for consequences of own behaviour
• Begins to take on greater
responsibility within family as part
of cultural identity
Source: Chown P, Kang M, Sanci L, Newnham V, Bennett DL 20081
Appendix 3.2. HEEADSSS assessment
Assessment area
Suggested questions
H – Home
Explore home situation, family life, relationships and stability
Where do you live? Who lives at home with you?
Who is in your family (parents, siblings, extended family)?
What is your/your family’s cultural background?
What language is spoken at home? Does the family have friends from outside its own cultural
group/from the same cultural group?
Do you have your own room?
Have there been any recent changes in your family/home recently (eg. moves, departures)?
How do you get along with mum and dad and other members of your family?
Are there any fights at home? If so, what do you and/or your family argue about the most?
Who are you closest to in your family?
Who could you go to if you needed help with a problem?
E – Education/
Employment
Explore sense of belonging at school/work and relationships with teachers/peers/
workmates, changes in performance
What do you like/not like about school (work)? What are you good at/not good at?
How do you get along with teachers/other students/workmates?
How do you usually perform in different subjects?
What problems do you experience at school/work?
Some young people experience bullying at school: have you ever had to put up with this?
What are your goals for future education/employment?
Any recent changes in education/employment?
E – Eating/Exercise
Explore how they look after themselves, eating and sleeping patterns
What do you usually eat for breakfast/lunch/dinner?
Sometimes when people are stressed they can overeat, or under eat: do you ever find yourself
doing either of these?
Have there been any recent changes in your weight? In your dietary habits?
What do you like/not like about your body?
If screening more specifically for eating disorders you may ask about body image, the use of
laxatives, diuretics, vomiting, excessive exercise, and rigid dietary restrictions to control weight.
What do you do for exercise?
How much exercise do you get in an average day/week?
A – Activities/peer
relationships
Explore their social and interpersonal relationships, risk taking behaviour, as well as
their attitudes about themselves
What sort of things do you do in your free time out of school/work?
What do you like to do for fun?
Who are your main friends (at school/out of school)?
Do you have friends from outside your own cultural group/from the same cultural group?
How do you get on with others your own age?
How do you think your friends would describe you?
What are some of the things you like about yourself?
What sort of things do you like to do with your friends?
How much television do you watch each night?
What’s your favourite music?
Are you involved in sports/hobbies/clubs?
91
92
Appendix 3.2. HEEADSSS assessment (continued)
D – Drug use/
cigarettes/alcohol
Explore the context of substance use (if any) and risk taking behaviours
Many young people at your age are starting to experiment with cigarettes/drugs/alcohol. Have any
of your friends tried these or other drugs like marijuana, injecting drugs, other substances?
How about you, have you tried any? If Yes, explore further
How much do you use and how often?
How do you (and your friends) take/use them? Explore safe/unsafe use, binge drinking, etc.
What effects does drug taking or smoking or alcohol have on you?
Has your use increased recently?
What sort of things do you (and your friends) do when you take drugs/drink?
How do you pay for the drugs/alcohol?
Have you had any problems as a result of your alcohol/drug use (with police, school, family,
friends)?
Do other family members take drugs/drink?
S – Sexuality
Explore their knowledge, understanding, experience, sexual orientation and sexual
practices – look for risk taking behaviour/abuse
Many young people your age become interested in romance and sometimes sexual relationships.
Have you been in any romantic relationships or been dating anyone?
Have you ever had a sexual relationship with a boy or a girl (or both)? – If Yes, explore further
(If sexually active) What do you use to protect yourself (condoms, contraception)?
What do you know about contraception and protection against STIs?
How do you feel about relationships in general or about your own sexuality?
(For older adolescents) Do you identify yourself as being heterosexual or gay, lesbian, bisexual,
transgender or questioning?
Have you ever felt pressured or uncomfortable about having sex?
S – Suicide/Self harm/ Explore risk of mental health problems, strategies for coping and available support
depression/mood
Sometimes when people feel really down they feel like hurting, or even killing themselves. Have you
ever felt that way?
Have you ever deliberately harmed or injured yourself (cutting, burning or putting yourself in unsafe
situations eg. unsafe sex)?
What prevented you from going ahead with it?
How did you try to harm/kill yourself?
What happened to you after this?
What do you do if you are feeling sad, angry or hurt?
Do you feel sad or down more than usual? How long have you felt that way?
Have you lost interest in things you usually like?
How do you feel in yourself at the moment on a scale of 1 to 10?
Who can you talk to when you’re feeling down?
How often do you feel this way?
How well do you usually sleep?
It’s normal to feel anxious in certain situations – do you ever feel very anxious, nervous or stressed
(eg. in social situations)?
Have you ever felt really anxious all of a sudden – for what particular reason?
Do you worry about your body or your weight? Do you do things to try and manage your weight
(eg. dieting)?
Sometimes, especially when feeling really stressed, people can hear or see things that others don’t
seem to hear or see. Has this ever happened to you?
Have you ever found yourself feeling really high energy or racey, or feeling like you can take on the
whole world?
S – Safety
S – Spirituality
Sunscreen protection, immunisation, bullying, abuse, traumatic experiences, risky behaviours
Beliefs, religion, What helps them relax, escape? What gives them a sense of meaning?
Sources: Goldenring J, Rosen D 2004 and Sanci L 200114,76
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53. Australian Institute of Health and Welfare. 2004 National Drug Strategy Household Survey: detailed findings.
AIHW cat. no. PHE 66. Canberra: AIHW, 2005.
54. National Indigenous Drug and Alcohol Committee. The way forward: resolutions from the Inaugural National
Indigenous Drug and Alcohol Conference. Adelaide: National Indigenous Drug and Alcohol Conference, 2010.
55. National Health and Medical Research Council. The Australian Immunisation Handbook, 9th edn. Canberra:
Commonwealth of Australia, 2008. Cited October 2011. Available at www.health.gov.au/internet/immunise/
publishing.nsf/content/handbook-home.
56. New Zealand Guidelines Group. Identification of common mental disorders and management of depression in
primary care: an evidence-based best practice guideline. Wellington: New Zealand Guidelines Group, 2008.
Cited December 2011. Available at www.depression.org.nz/ContentFiles/Media/PDF/depression_guidelines.pdf.
57. Department of Health and Ageing. Alcohol treatment guidelines for Indigenous Australians. Canberra:
Commonwealth of Australia, 2007. Cited October 2011. Available at www.alcohol.gov.au/internet/alcohol/
publishing.nsf/Content/426B5656C2395CC3CA2573360002A0EA/$File/alc-treat-guide-indig.pdf.
58. Christie G, Marsh R, Sheridan J, et al. The Substances and Choices Scale (SACS): the development and testing
of a new alcohol and other drug screening and outcome measurement instrument for young people. Addiction
2007 Sep;102(9):1390–8(9).
59. Schlesinger CM, Ober C, McCarthy MM, Watson JD, Seinen A. The development and validation of the Indigenous
Risk Impact Screen (IRIS): a 13-item screening instrument for alcohol and drug and mental health risk. Drug
Alcohol Rev 2007(26):109–17.
60. Gray D, Stearne A, Wilson M, Doyle M. Indigenous-specific alcohol and other drug interventions: continuities,
changes and areas of greatest need. National Indigenous Drug and Alcohol Committee, Australian National
Council on Drugs, 2010.
61. d’Abbs P, MacLean S. Petrol sniffing in Aboriginal communities: a review of interventions. Casuarina, NT:
Cooperative Research Centre for Aboriginal & Tropical Health, 2000. Cited October 2011. Available at www.
crcah.org.au/files/crcah_docs/Petrol%20Sniffing%20in%20Aboriginal%20Communities.pdf.
62. Gray D, Saggers S. Indigenous Australian alcohol and other drug issues: research from the National Drug
Institute: National Drug Research Institute, 2002.
63. Centre for Reviews and Dissemination. Parenting programmes for preventing tobacco, alcohol or drugs misuse in
children <18: a systematic review (structured abstract). Database of Abstracts of Reviews of Effects serial on the
Internet 2011;(1).
64. Toumbourou J, Gregg M. Impact of an empowerment-based parent education program on the reduction of youth
suicide risk factors. J Adolesc Health 2002;31(3):279–82.
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Ashery R, Robertson E, Kumpfer K, editors. Drug abuse prevention through family interventions. NIDA Research
Monograph 177. Rockville: US Department of Human Services, National Institute on Drug Abuse, 1998, p.103–
29.
66. Contributors to the Cochrane Collaborative and the Campbell Collaboration. Evidence from systematic reviews
of research relevant to implementing the ‘wider public health’ agenda. York: NHS Centre for Reviews and
Dissemination, 2000.
67. Kaldor J, Lapsley H, Mattick R, Weatherburn D. Six month process report on the Medically Supervised Injecting
Centre. Sydney: National Drug and Alcohol Research Centre, 2002.
68. Kaldor J, Lapsley H, Mattick R, Weatherburn D, Kimber J, MacDonald M. Twelve-month process evaluation
report on the Medically Supervised Injecting Centre. Sydney: National Drug and Alcohol Research Centre, 2002.
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Sydney: MSIC Evaluation Committee, 2003.
71. McCain MN, Mustard F. Reversing the brain drain: early study: final report. Toronto: Ontario Children’s
Secretariat, 1999.
72. Shonkoff JP, Meisels SJ, editors. Handbook of early childhood intervention, 2nd edn. Cambridge: Cambridge
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73. Shonkoff J, Phillips D, editors. From neurons to neighborhoods: the science of early childhood development.
Washington, DC: National Academy Press, 2000.
74. Faggiano F, Vigna-Taglianti F, Versino R, Zambino A, Borraccino A, Lemma P. School-based prevention for illicit
drugs’ use. Cochrane Database Syst Rev 2005;Apr 18;(2):CD003020.
75. Westerman T. Engaging Australian Aboriginal youth in mental health services. Australian Psychologist
2010;45(3):212–22.
76. Sanci L. Adolescent healthcare principles. Melbourne: The Royal Australian College of General Practitioners,
2001.
95
Chapter 4
Dental
health
Author Sandra Meihubers
Expert reviewer Kaye Roberts-Thomson
Author Penny
Expert Reviewers Rowena
Dental health
Overview
Poor dental health can affect quality of life by causing pain, infection, difficulties
with speech and eating and embarrassment about appearance. The two
main dental diseases are dental caries (tooth decay) and periodontal (gum)
disease. Dental caries is considered to be a multifactorial disease, with
some of the contributing factors being diet and nutrition (especially high and
regular consumption of black cola, sweetened fizzy drinks and sports drinks),
inadequate exposure to fluoride, poor oral hygiene practices and salivary
composition and flow.
Xerostomia or dry mouth may also contribute to dental caries development. Risk
factors for xerostomia include:
• use of common medications, particularly antidepressants, antihistamines and
antihypertensives
• radiotherapy and chemotherapy for cancers of the head and neck
• Sjögren syndrome
• HIV infection
• diabetes, particularly in people with poor glycaemic control.1,2
HIV infection can also contribute to a greater risk of periodontal disease, oral
ulceration and cancer.
Nationally, Aboriginal and Torres Strait Islander adults have greater levels of
dental caries than non-Indigenous Australians, with higher levels of untreated
caries and missing teeth and lower numbers of filled teeth.3 In children, the
number of both deciduous (first) and permanent (adult) teeth with caries (ie.
teeth that have past and/or present caries) is about twice the number than in
non-Indigenous children. The proportion of untreated dental caries is also higher
among Aboriginal and Torres Strait Islander children, which often reflects a lack
of access to dental services.4
There is little data on the prevalence of periodontal disease in Aboriginal and
Torres Strait Islander populations, however, important general risk factors for
periodontal disease include smoking, diabetes, advancing age, stress and poor
oral hygiene.5–8 Treatment of pre-existing periodontal disease has demonstrated
small but significant improvements in glycaemic control for people with type
2 diabetes, underscoring the importance of regular oral health assessments
in this population.9 There is growing evidence to suggest periodontal disease
may be associated with cardiovascular disease, stroke and pre-term low
birthweight babies, however causal links are yet to be proven, and there is
insufficient evidence to show that treatment of periodontal disease can reduce
cardiovascular events.10–12
Other major conditions of concern are oral cancer, tooth erosion (wearing away
of the hard tissues of the teeth by acids such as those found in acidic foods and
drinks, and in bulimic patients), and oral trauma (eg. through sports injuries).
Tobacco smoking and alcohol consumption are risk factors for the development
of oral cancer.
97
98
Dental health
Interventions
Recent guidelines on prevention of infective endocarditis recommend antibiotic
prophylaxis prior to dental procedures in Aboriginal and Torres Strait Islander
people with rheumatic heart disease in addition to general recommendations
for all people with prosthetic valves, previous infective endocarditis, certain
congenital heart conditions and cardiac transplantation.13,14 Maintenance of
good oral health, combined with regular checks and guidance, is more effective
in reducing the risk of infective endocarditis.
Since dental caries is considered to be a bacterial infection, the improvement
in oral health of a pregnant woman would lower the risk of transmitting harmful
oral bacteria to a newborn.15 During pregnancy there may also be a greater
risk of tooth erosion from nausea and vomiting, and progression of periodontal
disease. Standard preventive measures such as drinking fluoridated water, twice
daily use of fluoride containing toothpaste and minimising sugar consumption
are advised.16 The use of fluoride supplements is not recommended in
pregnancy as there is no evidence of its effectiveness.
Dental health
99
Recommendations: Dental health
Who is at risk?
How often?
Screening
Children aged 0–5
years
Recommend regular
review with a dental health
professional
Non-dental health
professionals are encouraged
to undertake an oral
health review including the
assessment of teeth, gums
and oral mucosa as part of
a regular health assessment
(see Table 4.1)
Opportunistic
IVC
and as part of
an annual health
assessment
17
Annually
IVC
18
Annually
IVC
18
All pregnant women
At first antenatal IVC
visit (see Chapter
9: Antenatal
care)
17
Adults with good oral
health
2 yearly
IVC
18
People aged 6–18
years
Adults with poor oral
health and/or risk
factors for dental
disease (see Table
4.2)
People with diabetes,
immunosuppression,
haematological
conditions, bleeding
disorders or
anticoagulant therapy
Chemoprophylaxis
Level/
strength of
evidence
References
Preventive
intervention type
Those with past
history of rheumatic
heart disease and
cardiovascular
abnormalities
Refer to a dental professional
and undertake an oral health
review as part of a regular
health assessment (see Table
4.1) with appropriate oral
hygiene advice to minimise
oral bacterial levels
6–12 monthly
IVC
13,19,20
Children aged 0–5
years
Recommend use of fluoride
containing toothpaste at least
once daily, from the time the
teeth start to erupt
Use a smear of paste for
children under 2 years and a
pea-size amount for children
2+ years. Toothpaste with a
fluoride concentration of 1000
ppm is recommended unless
there is a risk of fluorosis
Opportunistic
IA
17,21–23
Children aged 0–5
years where families
have evidence of
dental caries, poor
oral hygiene
Refer to dental professional for
regular application of fluoride
varnish
If resources do not permit then
continue daily use of fluoride
toothpaste and provide dietary
advice as per Table 4.1
At least every
6 months from
when the teeth
erupt, and for
a period of not
less than 24
months
IB
23,24
2–4 times
per year for
professional
application
IA
25,26
People aged >5 years
at high risk of dental
caries (see Table 4.2)
100
Dental health
Recommendations: Dental health (continued)
Environmental
People at high risk of
endocarditis
(rheumatic heart
disease, previous
infective endocarditis,
prosthetic cardiac
valves, certain forms
of congenital heart
disease, cardiac
transplantation)
Opportunistic
Recommend antibiotic
prophylaxis prior to dental
procedures. See management
guidelines for specific advice13
GPP
13,14
Communities
Advocate for fluoridation of
community water supply
1A
16
Table 4.1. Advice for good oral health practices
While review with dental professionals is recommended to comprehensively assess for caries risk and the presence of disease,
the following general principles are recommended for non-dental health professionals
Assessment
Visual inspection of teeth for evidence of caries, periodontal disease, assessment of maternal caries and/or poor oral hygiene
Assess oral hygiene practices, consumption of sucrose and sweetened drinks especially in baby bottles, ‘honey on the dummy’
or other sweet substances such as glycerine on the dummy, intake of sugared medicines
Assess access to fluoridated water supply
Advice
Brush teeth twice daily with a soft toothbrush and fluoride toothpaste and advise to spit, not rinse, excess paste
Advise about the hazards of high carbohydrate and acidic between meal snacks and drinks
Advise against high and regular consumption of black cola, sweetened fizzy drinks and sports drinks, with water being the
preferred drink
Promote breastfeeding, with weaning to a baby-cup, not a bottle
If bottles are used, advise against the use of any fluid apart from water and do not put baby to sleep with a bottle
Advise about smoking cessation and limiting alcohol consumption
Use sugar free chewing gum for saliva stimulation
Use a mouth guard when playing contact sport
Recommend regular dental check-up
Source: The RACGP 200927
Table 4.2. Risk factors for dental disease
• Poor oral hygiene practices (eg. no/irregular toothbrushing, use of hard toothbrush, no use of fluoride toothpaste, incorrect
brushing technique)
• Poor diet and nutrition (eg. high and regular consumption of sucrose and carbohydrate containing foods and drinks, especially
black cola, sweetened fizzy drinks)
• Salivary composition and flow: if poor then there is less protective effect from saliva
• Low exposure to fluoride
• Xerostomia or dry mouth can also contribute to development of dental caries. Risk factors for xerostomia include use of
common medications, particularly antidepressants, antihistamines and antihypertensives; radiotherapy and chemotherapy
for cancers of the head and neck; Sjögren syndrome; HIV infection; and diabetes, particularly in people with poor glycaemic
control
• High consumption of acidic foods and drinks such as sports drinks and juices can contribute to tooth erosion; bulimia is also
an erosion risk factor
• General risk factors for periodontal disease include smoking, diabetes, advancing age, stress and poor oral hygiene
• Tobacco smoking and alcohol consumption are risk factors for the development of oral cancer
• HIV infection can also contribute to a greater risk of periodontal disease, oral ulceration and cancer
• Other modifying risk factors can include age, socioeconomic status and access to oral health services
Dental health
Resources
Lift the lip and see my smile brochures (NSW Government)
www.health.nsw.gov.au/resources/pubs/orderform_pdf.asp
Information pamphlets for oral health and smoking, erosion, diabetes, pregnancy (Dental
Practice Education Research Unit)
www.arcpoh.adelaide.edu.au/dperu/special/
General oral health promotion information (various sources)
www.healthinfonet.ecu.edu.au/health-resources/promotion-resources
www.adaq.com.au
www.dhsv.org.au/oral-health-resources/guides-and-resources/
www.adelaide.edu.au/oral-health-promotion/
Learning modules on oral health for health professionals (Smiles for Life)
www.smilesforlifeoralhealth.com.
References
1. Rayman S, Dincer E, Almas K. Xerostomia: diagnosis and management in dental practice. New York State Dental
Journal, March 2010.
2. Walsh L. Dry mouth: a clinical problem for children and young adults. Journal of Minimum Intervention in Dentistry
2009;2(1):55–6.
3. Australia’s Dental Generations. The National Survey of Adult Oral Health 2004–06. Cat. no. DEN 165. Canberra:
Australian Institute of Health and Welfare, 2007.
4. Australian Institute of Health and Welfare. Oral health of Aboriginal and Torres Strait Islander children. AIHW cat.
no. DEN 167. Canberra: AIHW, 2007.
5. Do LG, Slade GD, Roberts-Thomson KF, Sanders AE. Smoking-attributable periodontal disease in the Australian
adult population. J Clin Periodontol 2008;35(5):398–404.
6. Mealey BL, Oates TW. Diabetes mellitus and periodontal diseases. J Periodontol 2006;77(8):1289–303.
7.
Ng SK, Keung Leung W. A community study on the relationship between stress, coping, affective dispositions and
periodontal attachment loss. Community Dent Oral Epidemiol 2006;34:252–66.
8. Taylor GW, Burt BA, Becker MP. Severe periodontitis and risk of poor glycaemic control in subjects with noninsulin dependent diabetes mellitus. J Periodontol 1996;67:1085–90.
9. Simpson TC, Needleman I, Wild SH, Moles DR, Mills EJ. Treatment of periodontal disease for glycaemic control in
people with diabetes. Cochrane Database Syst Rev 2010;May 12;(5):CD004714.
10. Genco RJ, Williams RC, editors. Periodontal disease and overall health: a clinician’s guide. Pennsylvania:
Professional Audience Communications, 2010.
11. Friedewald VE, Kornman KS, Beck JD, et al. The American Journal of Cardiology and Journal of Periodontology
Editors’ Consensus: periodontitis and atherosclerotic cardiovascular disease. Am J Cardiol 2009;104(1):59–68.
12. Helfand M, Buckley DI, Freeman M, et al. Emerging risk factors for coronary heart disease: a summary of
systematic reviews conducted for the US Preventive Services Task Force. Ann Intern Med 2009;151(7):496–507.
13. Antibiotic Expert Group. Therapeutic guidelines: antibiotic. Version 14. Melbourne: Therapeutic Guidelines Limited,
2010. Cited October 2011. Available at www.tg.org.au/?sectionid=41.
14. Farbod F, Kanaan H, Farbod J. Infective endocarditis and antibiotic prophylaxis prior to dental/oral procedures:
latest revision to the guidelines by the American Heart Association. Int J Oral Maxillofac Surg 2007;38:626–31.
15. Berkowitz RJ. Mutans Streptococci: acquisition and transmission. Pediatr Dent 2006 28(2):106–9.
16. Truman BI, Gooch BF, Sulemana I, et al. Reviews of evidence on interventions to prevent dental caries, oral and
pharyngeal cancers, and sports-related craniofacial injuries. Am J Prev Med 2002;23(Suppl 1):21–54.
17. NSW Department of Health. Early childhood oral health guidelines for child health professionals. NSW: Centre for
Oral Health Strategy, 2009.
18. National Institute for Health and Clinical Excellence. Dental recall: recall interval between routine dental
examinations. London: NICE, 2004.
19. Central Australian Rural Practitioners Association. CARPA standard treatment manual, 5th edn. Alice Springs:
CARPA, 2009.
20. Oral and Dental Expert Group. Therapeutic guidelines: antibiotic. Version 1. Melbourne: Therapeutic Guidelines
Limited, 2007.
21. Walsh T, Worthington HV, Glenny AM, Appelbe P, Marinho VCC, Shi X. Fluoride toothpastes of different
concentrations for preventing dental caries in children and adolescents. Cochrane Database Syst Rev 2010;Jan
20;(1):CD007868.
101
102
Dental health
22. Marinho VCC, Higgins JPT, Logan S, Sheiham A. Fluoride toothpastes for preventing dental caries in
children and adolescents. Cochrane Database Syst Rev 2003(1):CD002278.
23. Scottish Intercollegiate Guidelines Network. Prevention and management of decay in the preschool child.
Guideline No. 83. London: SIGN, 2005. Cited October 2011. Available at www.sign.ac.uk/pdf/sign83.pdf.
24. Marinho VCC, Higgins JPT, Logan S, Sheiham A. Fluoride varnishes for preventing dental caries in
children and adolescents. Cochrane Database Syst Rev 2002(3):CD002279.
25. Marinho VCC, Higgins JPT, Logan S, Sheiham A. Topical fluoride (toothpastes, mouthrinses, gels or
varnishes) for preventing dental caries in children and adolescents. Cochrane Database Syst Rev
2003(4):CD002782.
26. Griffin SO, Regnier E, Griffin PM, Huntley V. Effectiveness of fluoride in preventing caries in adults. J Dent
Res 2007;86(5):410-5.
practice (red book), 7th edn. Melbourne: RACGP, 2009. Cited October 2011. Available at www.racgp.org.
au/Content/NavigationMenu/ClinicalResources/RACGPGuidelines/TheRedBook/redbook_7th_edition_
May_2009.pdf.
Chapter 5
Rheumatic
heart
disease
Author Nicolette de Zoete
Expert reviewer Jonathan Carapetis
104
Rheumatic heart disease
Overview
Rheumatic heart disease (RHD) is caused by long term damage to the heart
muscle or heart valves as a result of acute rheumatic fever (ARF). Acute
rheumatic fever is a delayed autoimmune response to a throat infection caused
by Group A streptococcus (GAS) bacteria, which results in an illness that mainly
affects the heart, joints, brain and skin.1,2 An aetiologic link between GAS skin
infections and acute rheumatic fever has also been proposed, but further
research is needed to substantiate this. In 2012, Rheumatic Heart Disease
Australia published the most up-to-date prevention and management guideline
for RHD. In this guideline the Australian criteria for ARF diagnosis have been
revised and are shown in Table 5.1. The major changes from previous guidelines
include:
• the ability to diagnose a recurrence of ARF in a patient from a high risk group
who has only one major plus one minor manifestation, provided that other,
more likely diagnoses are excluded
• the inclusion of mono-arthralgia as a minor manifestation in patients from
high-risk groups
• fever can be considered a minor manifestation based on a reliable history (in
the absence of documented temperature) if anti-inflammatory medication has
already been administered
• the ability to diagnose probable ARF (level C), so as to include patients who
do not satisfy the criteria for definite ARF, but in whom the clinician feels that
ARF is the most likely diagnosis.
105
Table 5.1. Australian guideline criteria for acute rheumatic fever
Initial episode of
ARF
Recurrent
attack of ARF
in a patient with
known past ARF
or RHD
Probable ARF
(first episode or
recurrence)
Major
manifestations
Minor
manifestations
High risk groups*
All other groups
Two major or one major and two minor manifestations
Plus
Evidence of a preceding GAS infection†
2 major or 1 major and 1 minor or 3 minor manifestations
Plus
Evidence of a preceding GAS infection†
A clinical presentation that falls short by either 1 major or 1 minor manifestation, or in
the absence of streptococcal serology results, but one in which ARF is considered the
most likely diagnosis. Such cases should be further categorised according to the level of
confidence with which the diagnosis is made:
• highly suspected ARF
• uncertain ARF
Carditis (including evidence of rheumatic
valvulitis on echocardiogram)
Polyarthritis or aseptic mono-arthritis or
polyarthralgia‡
Chorea§
Erythema marginatum#
Subcutaneous nodules
Mono-arthralgia
Fever ≥38°C¶
ESR ≥30 mm/hr or CRP
≥30 mg/L
Prolonged P-R interval on ECG**
Carditis (excluding subclinical evidence
of rheumatic valve disease on
echocardiogram)
Polyarthritis‡
Chorea§
Erythema marginatum
Subcutaneous nodules
Fever ≥38°C¶
Polyarthralgia or aseptic mono-arthritis‡
ESR ≥30 mm/hr or CRP ≥30 mg/L
Prolonged P-R interval on ECG**
ARF = acute rheumatic fever, CRP = C-reactive protein, ECG = electrocardiogram, ESR = erythrocyte sedimentation
rate, GAS = group A streptococcus infection, RHD = rheumatic heart disease
* High risk groups are those living in communities with high rates of ARF (incidence >30 per 100 000 per year in
those aged 5–14 years) or RHD (all-age prevalence >2 per 1000). Aboriginal and Torres Strait Islander people living
in rural or remote settings are known to be at high risk
† Elevated or rising antistreptolysin O or other streptococcal antibody, or a positive throat culture or rapid antigen test
for GAS
‡ A history of arthritis is sufficient to satisfy this manifestation. Other causes of arthritis/arthralgia should be carefully
excluded
§ Rheumatic (Sydenham) chorea does not require other manifestations or evidence of preceding GAS infection,
provided other causes of chorea are excluded
# Erythema marginatum is a distinctive rash. Care should be taken not to label other rashes, particularly non-specific
viral exanthemas, as erythema marginatum
¶ Oral, tympanic or rectal temperature ≥38°C on admission or documented during the current illness
** Note that if carditis is present as a major manifestation, prolonged P-R interval cannot be considered an additional
minor manifestation in the same person
Source: Rheumatic Heart Disease Australia 20123
106
Individuals with ARF are generally quite unwell, in significant pain from arthritis
or arthralgia. They may require hospitalisation. Although acute episodes can be
quite dramatic, ARF is not known to cause lasting damage to the brain, joints
or skin (although there is some emerging evidence to suggest that chorea is
sometimes associated with long term cognitive or behavioural disturbances).
By contrast, damage to the heart, or more specifically the mitral and/or aortic
valves, may remain once the acute episode has resolved. RHD is the most
common cause of heart disease in children worldwide and is an important
cause of preventable premature mortality. It is also where the greatest
disparity between Aboriginal and Torres Strait Islander and non-Indigenous
cardiovascular mortality exists, with the death rates in Aboriginal and Torres
Strait Islander males and females being 15.1 and 23 times greater, respectively,
than non-Indigenous males and females.4
Both ARF and RHD are important and preventable causes of ill health and
death. They are typically associated with overcrowding, poor sanitary conditions
and other aspects of socioeconomic disadvantage.5 ARF and RHD are
rare in developed counties, but in Australia they are highly prevalent among
Aboriginal and Torres Strait Islander people living in rural and remote areas,
particularly in northern Australia. Data obtained from the Northern Territory’s
RHD control program show that [in the Northern Territory] 92% of people with
RHD are Aboriginal and/or Torres Strait Islander and of these 85% live in remote
communities and towns. Since 2000, the prevalence rate of RHD has continued
to increase, with almost 2% of the Aboriginal and Torres Strait Islander
population in the Northern Territory being affected, 3.2% of whom are aged
35–44 years. The incidence of ARF remains highest in people aged 5–14 years,
ranging from 150 to 380 per 100 000.6
GAS accounts for 15–30% of all cases of pharyngitis in children between the
ages of 5 and 15 years, and approximately 10% of adults with sore throats.7
In a small group of susceptible people (3–5% of the population), GAS throat
infections lead to ARF and acute poststreptococcal glomerulonephritis.8 Acute
poststreptococcal glomerulonephritis can also be caused by impetigo due
to GAS (‘nephritogenic strains’). While outbreaks of acute poststreptococcal
glomerulonephritis can occur warranting mass chemoprophylaxis of contacts,
rheumatic fever outbreaks have not been described in Aboriginal and Torres
Strait Islander communities, so mass chemoprophylaxis has no role in the
primary prevention of ARF at a community level.5
However, it appears that Aboriginal children in the Top End of the Northern
Territory have a low throat carriage of GAS (1–3%) and symptomatic pharyngitis
is rare in this population.9 In these children it appears that impetigo is the
most common manifestation of GAS disease and more specifically, infection
secondary to scabies infection appears to be a major contributor.
This has led to the hypothesis that pyoderma (bacterial infection of the skin),
as the major manifestation of GAS infection, has a significant role in the
development of ARF. In one Australian study, up to 50% of pyodermas were
caused by superinfected scabies. Community based programs aimed at
eradicating scabies in these endemic regions may impact on the incidence of
ARF and resulting morbidity and mortality due to RHD, although this has not
been proven.10,11
Treating pharyngitis in high risk populations with appropriate antibiotics
has been shown to reduce the rate of acute otitis media and quinsy and to
prevent individual cases of ARF that would result following symptomatic GAS
pharyngitis.12,13 The preferred recommended treatment of streptococcal throat
infection is intramuscular benzathine penicillin G (BPG). Oral phenoxymethyl
penicillin for 10 days is a second line alternative as BPG is known to be more
effective and lead to better adherence rates.
Addressing other socioeconomic factors that may contribute to the spread of
GAS in the community, such as household overcrowding, is also likely to reduce
the incidence of ARF.13
The risk of ARF after the first attack of GAS pharyngitis is approximately
0.3–3%, but with subsequent infection in someone who has already had ARF
this risk rises to 25–75%. In addition, those who suffer carditis during their initial
attack are significantly more likely to develop further carditis with subsequent
streptococcal throat infections.13 Forty percent of people newly diagnosed with
RHD in northern Australia have not been previously diagnosed with ARF,14 which
suggests that improvements in early detection are needed.
Early detection of RHD, combined with secondary prophylaxis, is the key
to minimising the severity of valvular lesions. Echocardiography has been
demonstrated to be superior to auscultation in detecting subclinical RHD in
high risk populations, however, the optimal screening strategy remains to be
confirmed.15,16 In 2011, the World Heart Federation developed a standardised
and evidence based criteria for the echocardiographic diagnosis of RHD
(Table 5.2). For people aged ≤20 years, two categories, ‘definite RHD’ and
‘borderline RHD’, are included to identify individuals in high risk populations who
may not have had time to develop the full echocardiographic manifestations of
RHD.
107
108
Table 5.2. World Heart Federation criteria for
echocardiographic diagnosis of rheumatic heart disease
1. Echocardiographic criteria for individuals ≤20 years of age
Definite RHD (either A, B, C or D)
A.Pathological MR* and at least 2 morphological features of RHD of the mitral valve†
B.MS mean gradient ≥4 mmHg (must exclude congenital mitral valve anomalies)
C.Pathological AR‡ and at least 2 morphological features of RHD of the aortic valve§
(must exclude bicuspid aortic valve and dilated aortic root)
D.Borderline disease of both aortic and mitral valve#
Borderline RHD (either A, B or C) (in high risk populations only)
A.At least two morphological features of RHD of the mitral valve† without pathological
MR or MS
B.Pathological MR*
C.Pathological AR†
Normal echocardiographic findings (all of A, B, C and D)
A.MR that does not meet all four Doppler criteria (physiological MR)*
B.AR that does not meet all four Doppler criteria (physiological AR)‡
C.An isolated morphological feature of RHD of the mitral valve (eg. valvular thickening),
without any associated pathological stenosis or regurgitation
D.Morphological features of RHD of the aortic valve§ (eg. valvular thickening), without
any associated pathological stenosis or regurgitation
2. Echocardiographic criteria for individuals >20 years of age
Definite RHD (either A, B, C or D)
A.Pathological MR* and at least 2 morphological features of RHD of the mitral valve†
B.MS mean gradient ≥4 mmHg (must exclude congenital mitral valve anomalies)
C.Pathological AR‡ and at least two morphological features of RHD of the aortic valve§
(must exclude bicuspid aortic valve and dilated aortic root)
D.Pathological AR‡ and at least two morphological features of RHD of the mitral valve†
AR = aortic regurgitation, MR = mitral regurgitation, ms = mitral stenosis, rhd = rheumatic
heart disease
* Pathological mr is defined as meeting all four of the following doppler criteria: (A) seen in 2
views; (B) in at least one view, jet length 2 cm; (C) peak velocity ≥3 m/s; (D) pan-systolic jet in
at least one envelope
† Morphological features of rhd in the mitral valve: anterior mitral valve leaflet thickening ≥3 mm
(age specific), chordal thickening, restricted leaflet motion, excessive leaflet tip motion during
systole
‡ Pathological aortic regurgitation is defined as meeting all four of the following doppler criteria:
(A) seen in 2 views; (B) in at least one view, jet length 2 cm; (C) peak velocity ≥3 m/s; (D) pansystolic jet in at least one envelope
§ Morphological features of rhd in the aortic valve: irregular or focal thickening, coaptation
defect, restricted leaflet motion, prolapse
# Combined ar and mr in high prevalence regions and in the absence of congenital heart
disease is regarded as rheumatic
Although these new, standardised criteria will greatly contribute to improved
diagnosis of RHD, questions remain about the role of echocardiography
in screening programs. Echocardiography based screening may lead to
overdiagnosis, which will require careful review to exclude RHD and avoid
unnecessary treatment. A recent study in New Zealand, using portable
echocardiograms and cardiology assessment to screen 1142 (predominately
high risk) children aged 10–13 years, found high rates of undetected RHD. It also
showed that echocardiography alone overestimated the prevalence of RHD, as it
did not distinguish underlying congenital and physiological changes from RHD.17
The 2011 World Heart Federation criteria will help to minimise this. A population
based survey in four sites across the north of Australia has been undertaken to
determine the prevalence of RHD among Aboriginal, Torres Strait Islander and
non-Indigenous children by screening children aged 5–14 years for RHD and is
due to report in 2012. This study should help to determine the most sensitive
and specific screening method for RHD and hopefully this information with help
guide future screening programs. Until these results are published, it is not
recommended that current screening programs be changed.3
The severity of, and morbidity due to, RHD can be significantly reduced by
secondary prophylaxis. Intramuscular BPG is beneficial in the prevention of
recurrent ARF. It is superior to oral penicillin in the reduction of both recurrent
ARF (87–96% reduction) and streptococcal pharyngitis (71–91% reduction).
High levels of medication adherence are associated with regression of heart
disease in approximately 50–70% of people. It is recommended that the duration
of secondary prophylaxis be based on the patient’s age and time since last
episode of ARF and that echocardiography be performed prior to stopping it. For
individuals with probable ARF that is categorised as ‘highly suspected’ (Table 5.1),
it is recommended that prophylaxis be continued for a minimum of 10 years after
the most recent suspected episode of ARF or until another diagnosis is made.
For those with ‘uncertain ARF’ it is recommended they continue prophylaxis for
12 months after diagnosis and then reassess. If there is no evidence of RHD
then consider ceasing prophylaxis, otherwise manage as per RHD severity. For
individuals with a history of ARF and no or mild RHD, prophylaxis is continued for a
minimum of 10 years since last episode of ARF or age 21 (whichever is longer). For
those with moderate RHD it is continued for a minimum of 10 years or until age 35
(whichever is longer) and for those with severe RHD it is continued for a minimum
of 10 years or until age 40 (whichever is longer).3
The fundamental goal in long term management of chronic RHD is to prevent
the need for valve surgery. Penicillin secondary prophylaxis (for prevention
of recurrent ARF) is crucial to achieving this. When adherence with penicillin
prophylaxis is low, there is greater need for surgical intervention and long term
surgical outcomes are not as good. The speciﬁc valvular lesions of RHD are
beyond the scope of this chapter, but many patients (eg. 47% of RHD patients
in the Top End of the Northern Territory) will have involvement of two or more
valves, most commonly mitral and aortic, although pathology in one is usually
dominant. The assessment of severity of each valvular lesion is made by
echocardiography as well as clinical review. Echocardiographic surveillance
in individuals with a history of ARF and RHD is an important part of ongoing
management with the frequency dependant on the severity of the RHD. It is also
recommended that high risk individuals with murmurs suggestive of RHD are
assessed with echocardiography.3
109
110
Coordinated control programs are the most effective approach to improving
BPG adherence and clinical follow up of people with RHD and for promoting
primary prevention of ARF. They enable the provision of education and training
for healthcare providers and education and health promotion for individuals,
families and the community.3 A key component of these programs is local
registers of people with RHD or a history of ARF. These can assist with routine
assessment and surveillance and recording of prophylaxis delivery and recall
of patients. Centralised registers (jurisdictional or national level) can support
the provision of prophylaxis for those who move between communities. Not
only do they help increase adherence to secondary prophylaxis, and ultimately
reduce the need for valve surgery, but registers improve case detection,
reduce recurrences of ARF and decrease hospitalisations from ARF/RHD. In
2009, Rheumatic Health Disease Australia was established as the national
coordination unit to support the control of RHD in Australia (see Resources).
There are now a number of national RHD control programs in the Top End of the
Northern Territory, central Australia, far northern Queensland and the Kimberley
in Western Australia.3
As part of coordinated control programs, the 2012 Rheumatic Heart Disease
Australia guideline recommends that a structured care plan should be used for
all individuals with a history of ARF or with established RHD and that this care
plan be based on a priority classification.3 Priority classifications 1–3 replace
the previous categories of severe, moderate and mild RHD respectively and are
outlined in Table 5.3.
As for all patients with chronic disease, routine dental care is also important in
patients with a history of ARF and/or RHD. All patients should receive education
about oral hygiene, and should be referred promptly for dental assessment and
treatment when required. This is especially important prior to valvular surgery
(indications of which are beyond the scope of this chapter), when all oral/
dental pathology should be investigated and treated accordingly. As infective
endocarditis is a dangerous complication of RHD; it is recommended in the
Australian antibiotic therapeutic guidelines that additional antibiotic prophylaxis
be given prior to dental or surgical procedures for all patients with established
RHD. Individuals with a history of ARF but no valvular damage do not require
antibiotic prophylaxis.3 Although this has not been proven, its use is supported
by animal models of endocarditis and empirical observations that have
demonstrated a reduction in bacteraemia.18
111
Recommendations: Rheumatic heart disease
Preventive
intervention type
Who is at risk?
How often?
References
Level/
strength of
evidence
Screening
All people
Recommend auscultation of the
heart to assess for previously
undiagnosed RHD
Echocardiography is not
currently recommended
to screen for previously
undiagnosed RHD*
Opportunistic
and as
part of an
annual health
assessment
GPP
3
All people with
a past history of
ARF or murmurs
suggestive of valve
disease
Referral for echocardiography
and subsequent follow
up is recommended. See
management guidelines for
specific advice3
As per
management
guidelines 3
GPP
3
Opportunistic
GPP
5
Recommend dental hygiene, and 6–12 monthly
regular review (see Chapter 4:
Dental health)
GPP
3
Behavioural
Chemoprophylaxis
People with a past Advise that the rate for
history of ARF or
recurrence of ARF is 50%
RHD
and that there is a need for
prophylactic antibiotics (see
below)
All people in high
risk communities
where GAS
infections are
common and ARF
is prevalent
Any sore throat should be
treated as if it is a GAS
pharyngitis infection with a
single intramuscular benzathine
penicillin injection (preferred)
or 10 days of oral penicillin
(see specific management
guidelines18)
Where possible this should be
based on confirmation with a
throat swab culture
Opportunistic
GPP
5
All people with
GAS pharyngitis
Treat with 10 days of
oral penicillin or a single
intramuscular benzathine
penicillin injection (see specific
management guidelines18)
There is no need to treat family
contacts of those with GAS
pharyngitis
Opportunistic
IA
13
All people with
ARF/RHD
Identify patients for secondary
antibiotic prophylaxis through
inclusion in local recall systems
and centralised rheumatic fever
register where one exists
Opportunistic
GPP
3
Categorise patients according
to their priority status (see
Table 5.3) and implement a
tailored secondary prevention
strategy (see management
guidelines for priority specific
recommendations3)
As per
individual
recall plan
IA
3
112
Recommendations: Rheumatic heart disease (continued)
Environmental
Communities
where GAS
infections are
common and ARF
is prevalent
Recommend antibiotic
prophylaxis for dental and other
high risk procedures for those
with established RHD (see
Chapter 4: Dental health, and
management guidelines18)
GPP
18
Assess for overcrowding
N/A
and refer to social support
services for housing assistance
if indicated (see Chapter 7:
Hearing loss)
If high rates of impetigo and
underlying scabies, consider
community healthy skin program
(see Chapter 2: Child health)
IIIB
19
* Echocardiography is likely to be a superior strategy to auscultation and lead to improved case detection of subclinical RHD. The
optimal echocardiography based screening strategy, however, is the subject of ongoing research and until the outcomes of this
research is known routine echocardiography screening is not recommended (see preamble for more details)
Table 5.3. Priority classifications for developing
management plans
Classification
Criteria
Priority 1 (severe)
Any of the following:
• severe valvular disease
• moderate/severe valvular lesion with symptoms
• mechanical prosthetic valves, tissue prosthetic valves and
valve repairs including balloon valvuloplasty
Priority 2 (moderate)
Any moderate valve lesion in the absence of symptoms and
with normal LV function
Priority 3 (mild)
ARF with no evidence of RHD or trivial to mild valvular
disease
Priority 4 (inactive)
Patients with a history of ARF (no RHD) for whom secondary
prophylaxis has been ceased
Resources
Updated Australian guidelines for diagnosis and management of ARF and RHD
(Rheumatic Heart Disease Australia)
www.rhdaustralia.org.au
Rheumatic heart disease: all but forgotten. A 60 minute program outlining strategies
for the treatment, control and eradication of ARF and RHD (Rural Health Education
Foundation)
www.rhef.com.au/programs/program-1/?program_id=37.
References
1. McDonald M. Acute rheumatic fever: a chink in the chain that links the heart to the throat? Lancet Infect
Dis 2004;4:240–45.
2. World Health Organization. WHO technical report series 923. Rheumatic fever and rheumatic heart
disease. Report of a WHO Expert Consultation Committee. Geneva: WHO, 2004.
3. Rheumatic Heart Disease Australia (ARF/RHD writing group), National Heart Foundation of Australia and
the Cardiac Society of Australia and New Zealand. Australian guideline for prevention, diagnosis and
management of acute rheumatic fever and rheumatic heart disease, 2nd edn. RHD Australia, 2012 (in
press).
Australia’s Aboriginal and Torres Strait Islander peoples, 2008. ABS cat no. 4704.0. Canberra: ABS,
2008. Cited October 2011. Available at www.aihw.gov.au/publications/index.cfm/title/10583.
5. Couzos S, Murray R. Aboriginal Primary healthcare: an evidence-based approach, 3rd edn. Melbourne:
6. Parnaby MG, Carapetis JR. Rheumatic fever in Indigenous Australian children. J Paediatr Child Health
2010;46(9):527–33.
7.
Bisno AL GM, Gwaltney JM Jr, Kaplan EL, Schwartz RH. Practice guidelines for the diagnosis and
management of group A streptococcal pharyngitis. Infectious Diseases Society of America. Clin Infect Dis
2002;35(2):113.
8. Lennon D. Longitudinal study of post streptococcal disease in Auckland; rheumatic fever,
glomerulonephritis, epidemiology and M typing 1981–86. NZ Med J 1988;101(Pt 2):396–8.
9. McDonald MI. Low rates of streptococcal pharyngitis and high rates of pyoderma in Australian Aboriginal
communities where acute rheumatic fever is hyperendemic. Clin Infect Dis 2006;43:683–9.
10. Carapetis JR. Success of a scabies control program in an Australian Aboriginal community. Pediatr Infect
Dis J 1997(16):494–49.
11. Wong LC. Outcome of an interventional program for scabies in an Indigenous community. Med J Aust
2001;175:367–70.
12. Del Mar CB GP, Spinks AB. Antibiotics for sore throat. Cochrane Database Syst Rev 2004(2):CD000023.
13. National Heart Foundation of New Zealand. Guidelines for rheumatic fever: diagnosis, management and
secondary prevention. Auckland: National Heart Foundation of New Zealand, 2006. Cited January 2012.
Available at www.world-heart-federation.org/fileadmin/user_upload/documents/RHD-net/AUS_NZ_
resources/Guidelines/RHDnet_NZ_RF_GL_1_diagnosis_management_and_2ary_prevention.pdf.
14. Carapetis JR. Acute rheumatic fever and rheumatic heart disease in the Top End of Australia’s Northern
Territory. Med J Aust 1996;164:146–49.
15. Carapetis JR, Hardy M, Fakakovikaetau T, et al. Evaluation of a screening protocol using auscultation and
portable echocardiography to detect asymptomatic rheumatic heart disease in Tongan schoolchildren.
Nat Clin Pract Cardiovasc Med 2008;5(7):411–7.
16. Marijon E, Ou P, Celermajer DS, et al. Prevalence of rheumatic heart disease detected by
echocardiographic screening. N Engl J Med 2007;357(5):470–6.
17. Webb RH, Wilson NJ, Lennon DR, et al. Optimising echocardiographic screening for rheumatic heart
disease in New Zealand: not all valve disease is rheumatic. Cardiol Young 2011;21(04):436–43.
19. National Heart Foundation of New Zealand. Guidelines for rheumatic fever: proposed rheumatic fever
primary prevention programme. Auckland: National Heart Foundation of New Zealand, 2009. Cited
January 2012. Available at www.toiteorapublichealth.govt.nz/vdb/document/368.
113
Chapter 6
Eye health
Author Jacki Mein
Expert reviewer Hugh Taylor
Eye health
Visual acuity
Background
Good eye health is critical to quality of life. Impaired vision, which is defined as a
visual acuity (VA) <6/12,1 often goes unrecognised and contributes significantly
to morbidity.2 Visual impairment is a risk factor for falls.3 In the elderly, untreated
cataracts increase the risk of multiple falls,4 social isolation and depression.5 The
2009 National Indigenous Eye Health Survey included a sample of Aboriginal
and Torres Strait Islander adults in urban, regional and remote settings.1 The
age adjusted prevalence of low vision was 8.6%, 2.8 times higher than rates
for non-Indigenous adults. Low vision prevalence is higher in remote and very
remote areas, ranging from 9.5–12.7%. The sampling adjusted prevalence of
blindness (VA <6/60 in the better eye, and/or combined both eyes visual field of
less than 10 degrees – in normal sighted people this is 170 degrees6) was 1.8%.
The major causes of blindness are cataract (32%), optic atrophy (14%), refractive
error (14%), diabetes (9%) and trachoma (9%).1 The rate of blindness was 6.2
times higher than in non-Indigenous Australians.
The dominant cause of low vision is refractive error (54%) with prevalence rates
around five times higher than for non-Indigenous adults. Over a third of National
Indigenous Eye Health Survey participants (39%) could not read normal size
print, and 62% reported they normally wore reading glasses for near-work (eg.
reading, sewing). Other important causes of low vision include cataract 27%
and diabetic retinopathy (12%).
Risk factors for cataract include ocular exposure to ultraviolet light,7,8 diabetes
and poor diabetic control,9 and smoking. In a recent Australian study, ‘ever
smokers’ had a 41% increased risk of developing nuclear cataract compared to
never smokers.10 Reduction of ocular sun exposure with sunglasses may assist.
Although exposure to sunlight accounts for only 10% of cataracts in an urban
non-tropical Australian population,7 this risk factor may be more important in
northern Australian populations.
The National Indigenous Eye Health Survey found 37.4% of Aboriginal and
Torres Strait Islander adults reported having diabetes with a similar prevalence
across all the regions sampled. Of these, 12% had low vision and only 20%
reported an eye examination in the past 12 months. A total of 2.5% had
proliferative retinopathy, 0.4% severe non-proliferative retinopathy, and 25%
mild/moderate non-proliferative retinopathy. Of these, only 39% had received
some laser treatment.1 Although diabetes is a risk factor for cataract there is
no robust evidence that improved diabetic treatment prevents or delays lens
opacity.11
Evidence for the effectiveness of preventive interventions
Recommendations for the school based screening of visual acuity in children
in non-trachoma endemic areas lack a research base for evidence of
effectiveness. An Australian based expert group suggests screening for age
problems on at least three occasions: birth and 3–6 months, both to pick up
serious congenital conditions; and screening at 4 years to check visual acuity
and refer if either eye is worse than 6/9, or if there is a two-line difference in
results for both eyes.12
115
116
Eye health
Visual acuity screening is advocated in older adults because refractive errors are
correctable with eyeglasses and have good outcomes with refractive surgery
if available.13 The US Preventive Services Task Force concludes that there
is insufficient evidence to assess benefits and harms of screening for visual
acuity in adults over 65 years of age.14 However, given the substantially higher
prevalence of low vision in Aboriginal and Torres Strait Islander communities,
there is a reasonable justification for visual acuity screening at younger ages.
Vision assessments are components of Medicare health assessments for all
age groups. The CARPA standard treatment manual recommends visual acuity
screening in Aboriginal and Torres Strait Islander populations aged 50 years or
more,15 while the Queensland chronic disease guidelines recommend screening
as part of Aboriginal and Torres Strait Islander health assessments from 40
years.16
The Snellen eye chart is a highly sensitive and specific recommended screening
test for visual acuity testing and is more sensitive than screening questions.17
The E-test visual acuity charts for near and distance vision are useful for people
who cannot read and were used routinely in the National Indigenous Eye
Health Survey.1 However, of even greater importance is the need to test near or
‘reading’ vision, especially in those aged over 40 years. The National Indigenous
Eye Health Survey found that 40% of Aboriginal and Torres Strait Islander adults
could not see normal sized print. Near vision test cards or any printed matter
can be used to test near vision and E-tests for near vision can also be used for
people who cannot read.
Cataract surgery has been shown to improve vision17,18 and quality of life.18 It has
also been associated with fewer vehicle accidents after cataract surgery.19 The
National Indigenous Eye Health Survey found evidence of disparities in access
to cataract surgery, with only 65% of Aboriginal and Torres Strait Islander
adults with vision loss from cataract having received surgery with more remote
people having less operations, compared with 89% of non-Indigenous adults.1
One study showed an increased risk of death in those not having cataract
surgery.20 A case record audit in the Northern Territory found cataract surgery
had a beneficial effect on visual acuity and quality of life for Aboriginal and
Torres Strait Islander people.21 While most people in this cohort were legally
blind, surgery should be performed when visual acuity is worse than 6/12 or
when patient function is impaired, although there are questions in the urban
Australian context about patient selection for cataract surgery to maximise good
outcomes.22
For people with diabetes, an annual visual acuity assessment and dilated
fundus/retinal camera examination by a trained examiner is recommended for
routine diabetic retinopathy screening.23 Early laser photocoagulation treatment
can prevent progression and save sight.24 In fact 98% of the blindness due to
diabetes can be prevented and yet only 20% of those with diabetes had had the
required annual eye examination in the National Indigenous Eye Health Survey.
Good glycaemic, lipid and blood pressure control and early treatment of any
diabetic retinopathy remain the cornerstone of primary prevention and delay of
progression of diabetic retinopathy.25,26
Eye health
117
Recommendations: Visual acuity
Preventive
intervention
type
Who is at risk?
How often?
Level/
strength of
evidence
References
Screening
Infants aged <6
months
Conduct a general eye
examination. Refer if red
eye reflex absent or other
abnormality found
As part of a
newborn and
3–6 month health
assessment
GPP
12
Children aged
4–5 years
Screen for visual acuity (VA)
(use E chart if required)
Refer if VA is less than 6/9 or
there is a two line difference
between eyes
Opportunistic
and once only
at routine health
assessment
GPP
12
All adults aged
>40 years
People with
poor near-vision
(presbyopia)
Near and far visual acuity
assessment is recommended
to detect visual loss due to
presbyopia or cataract
Annually as part
of an adult health
assessment
GPP
15–17,27
The use of near test material
and Snellen chart (and E chart
if required) is recommended for
testing visual acuity
If unable to see normal sized
print (type) refer to optometrist
or ophthalmologist for
assessment and probable
reading glasses
Snellen IC
E chart IIIC
People with
cataract
If visual acuity is worse
than 6/12 or when
function is impaired refer
to an ophthalmologist for
assessment and possible
cataract surgery
Opportunistic
GPP
22
People with
diabetes
Undertake visual acuity
and retinal assessment by
trained assessor as indicated
in diabetic management
guidelines
Annually
IA
26
GPP
26,28
Retinal photography by trained
primary care staff combined
with external review by an
ophthalmologist is a useful
strategy for comprehensive
screening
Behavioural
Current smokers
Advise smoking cessation to
reduce the risk of developing
cataracts (see Chapter 1:
Lifestyle, section on smoking)
Opportunistic
IIIC
10
All people
Recommend reduced ocular
exposure to UV-B light to
reduce risk of cataract (eg.
wearing sunglasses)
Opportunistic
IIIC
7,8
118
Eye health
Trachoma and trichiasis
Background
Trachoma is a bacterial eye disease of poor socioeconomic conditions,
including overcrowding and poor water/sewerage services.29 Active trachoma
(usually graded as TF: trachoma follicular) predominantly affects young children
and is a contagious infection of the eye by specific, non-genital strains of
the bacterium Chlamydia trachomatis. Multiple infections cause conjunctival
scarring (TS: trachomatous scarring) leading to eyelid contraction and inturned
margin (entropion) over decades (TT: trachomatous trichiasis). The resulting
inturned eyelashes rub on the eyeball causing painful corneal scarring and
opacity (CO: corneal opacity).
Trichiasis occurs when at least one eyelash rubs on the eyeball, or there is
evidence of recently removed eyelashes because of eyelash inturning.30 If not
treated with surgery to the eyelid to correct inturned eyelashes, corneal scarring
can end in blindness in later adult life, 20–40 years after the initial trachoma
infections. Australia is the only developed country in the world that still has areas
of trachoma and trichiasis.31 These occur almost exclusively in remote Aboriginal
populations in the Northern Territory, South Australia and Western Australia.
The National Indigenous Eye Health Survey1 found that the overall rate of active
trachoma (TF: trachoma follicular) in children under 5 years is 3.8%.1 There was
a steep rise in prevalence from urban and remote (0.6–1.6%) to very remote
regions (7.3%), where 50% of communities had endemic rates (>5%) of active
trachoma. Within communities trachoma is strongly clustered by households32
and within households clustered by sleeping rooms,33 suggesting continued
transmission depends on close prolonged contact.
From the National Indigenous Eye Health Survey, the community prevalence
rates of trachomatous scarring ranged from 0% to 53% (overall 15.7%), trichiasis
prevalence from 0% to 14.6% (overall 1.4%) and corneal opacity from 0% to
3.3% (overall 0.3%). These data show that blinding endemic trachoma remains
a major public health problem in very remote communities and given the long
delay in onset, scarring and blindness will persist for decades after trachoma is
eliminated.1
Evidence of the effectiveness of preventive interventions
The Communicable Disease Network of Australia Guidelines for the public
health management of trachoma in Australia, 2006, are based on the World
Health Organization (WHO) SAFE strategy.34 The acronym SAFE encompasses
an integrated approach to prevention including Surgery for trichiasis,
Antibiotics to reduce community reservoirs of trachoma infection, Facial
cleanliness in preschool children, and Environmental measures to reduce
trachoma transmission. There is good evidence to support all SAFE strategy
components.34 Chlamydia vaccine development has been flagged as a possible
complementary strategy to SAFE, but is currently many years away.35
With rapid household spread and high mobility of families in remote areas,
trachoma control and prevention is best undertaken at regional levels with
coordination of screening and mass treatment.34 Primary health practitioners
have an important role in partnering with regional population health units
to implement these programs, and they can be linked to other child health
Eye health
screening assessments (eg. anaemia and nutrition assessments). Environmental
strategies such as improved water access, access to toilets, waste and fly
control, and reduced household overcrowding also play a key role in trachoma
control.34
The diagnosis of trachoma is based on clinical grounds. Laboratory tests are
not recommended, except perhaps to exclude other bacterial infection.36 There
is no evidence that opportunistic examination and treatment for trachoma in
individual children improves community trachoma outcomes, but it may relieve
symptoms or prompt/inform discussions about the need for treatment of
households and mass treatment programs. There is evidence of effectiveness
for these larger scale community treatment programs, with a single dose of
azithromycin at 20 mg/kg orally up to 1 g repeated at least annually.37
The decision to screen and treat individuals and their contacts should, therefore,
be based on patient origin from endemic area, age and symptoms, as well as
liaison with regional trachoma control programs. Unfortunately, screening and
treatment for trichiasis have not been reported in a systematic way in most
Australian control programs,34 but with the advent of a National Trachoma
Surveillance and Reporting Unit this is improving.38 In trachoma endemic areas
(ie. where active trachoma prevalence in children under 10 years is >5%) annual
screening programs are indicated. WHO does not recommend a particular
season for screening and treatment. Even within very remote regions there may
be variation in trachoma prevalence in both place and time, due to population
mobility and environmental factors, but instability of prevalence estimates are
usually due to small survey numbers, variable screening coverage and remote
clinical staff screening skill. The Australian guidelines recommend annual
screening until reductions in prevalence to <5% are sustained for over 5 years.34
In areas where trachoma and trichiasis is endemic, adults aged 40–54 years
should be screened every 2 years, and those aged 55+ should be screened
annually for trichiasis, for example as part of an annual health assessment.34,39
The ‘3Ts’ need to be remembered for the trichiasis examination: Think to do
it, use a Thumb to lift the lid so the lashes lift away from the eye, and use a
Torch to provide enough light to see the dark lashes. Blindness due to trichiasis
is irreversible once it has occurred but progression to blindness can be
temporarily halted by surgery, because it stops eyelash rubbing and therefore
prevents corneal opacity.40 Surgery however does not alter the natural history
of trichiasis; therefore, post surgery, patients who still have vision should be
followed up annually to screen for recurrence.41 Other trichiasis complications
such as dry eyes need symptomatic treatment to prevent further complications.
119
120
Eye health
Recommendations: Eye health
Preventive
intervention type
Who is at risk?
How often?
Level/
strength of
evidence
References
Screening
People living
where trachoma
is endemic (>5%
prevalence of
active trachoma in
young children)
Implement a community
screening program in
partnership with regional
population health units to
assess the prevalence of
active trachoma
No community screening is
required where prevalence
is below 5% of children for 5
consecutive years
As per national
guideline
recommendations
(see Resources)
GPP
34
Adults aged >40
years raised
in trachoma
endemic area
Perform eye examination to
ascertain corneal scarring
and/or the presence of
trichiasis
2 yearly (age
40–54 years)
Annually (age 55+
years)
GPP
34,38,42
Those with trichiasis,* refer
to an ophthalmologist for
surgery
N/A
IIIB
40,41
Recommend to families the
importance of the following in
the prevention and control of
trachoma:
Opportunistic
IIB
and as part of an
annual child health
assessment
Behavioural
All children
from trachoma
endemic areas
• facial cleanliness of
children
• effective rubbish disposal
and other fly control
measures
• regular screening, and
treatment of infection
Chemoprophylaxis
People living
where trachoma
is endemic (>5%
prevalence of
active trachoma in
young children)
Treat case and all household As per state and
contacts using community
territory protocols
based single dose
azithromycin (A) on an annual
basis
IA
37
Environmental
All people
Assess housing situation
for overcrowding and refer
to social support services
for housing assistance if
indicated. (See Chapter 7:
Hearing loss)
N/A
GPP
34
Remote
communities
Implement joint health
promotion strategies with
state/territory government
public health units and
local shire councils for
fly control strategies and
other environmental health
standards
As per state/
territory
government plans
GPP
34
* Trichiasis is diagnosed when at least one eyelash rubs on the eyeball, or there is evidence of recently removed eyelashes because of
eyelash in-turning30
Eye health
Resources
Full report on National Indigenous Eye Health Survey
www.eyefoundation.org.au/projects/research-projects/89-minum-barrengproject
Australian guidelines for the management of diabetic retinopathy (NHMRC)
www.nhmrc.gov.au/_files_nhmrc/file/publications/synopses/di15.pdf
Patient factsheets on diabetic retinopathy (CERA)
www.cera.org.au/uploads/CERA_factsheet_DiabeticRetinopathy.pdf
Guidelines for the public health management of trachoma in Australia (Australian
Government)
www.health.gov.au/internet/main/publishing.nsf/Content/1EBA6A6D1AEB9569C
A2571570008FB93/$File/Trachoma2.pdf
At cost vision screening kits including E-test charts, which are suitable for primary care
including remote use (CERA)
www.cera.org.au/our-work/resources/vision-screening-tools.
Grading card showing the simplified trachoma grading system, which includes high
quality clinical pictures of trachoma and trichiasis (2-sided), available free (WHO)
www.who.int/blindness/publications/trachoma_english.jpg
Comprehensive practical documents including control program, surgery and
community support guides (WHO)
www.who.int/blindness/causes/trachoma_documents/en.
References
1. National Indigenous Eye Health Survey Team. Minum Barreng (tracking eyes) full report: National
Indigenous Eye Health Survey, version 2. NIEHS, 2009. Cited October 2011. Available at www.iehu.
unimelb.edu.au/publications/the_national_indigenous_eye_health_survey.
2. United States Preventive Services Task Force. Guide to clinical preventive services. Report of the
USPSTF, 2nd edn. Baltimore: Williams and Wilkins, 1996.
3. Nevitt M, Cummings SR, Hudes ES. Risk factors for injurious falls: a prospective study. J Gerontol
1991;46:M164–70.
4. Ivers R, Cumming RG, Mitchell P, Attebo K. Visual impairment and falls in older adults: The Blue
Mountains eye study. J Am Geriatr Soc 1998;46:58–64.
5. Taylor HR, Pitkin J, Cass DT. Updates in medicine: ophthalmology. Med J Aust 2002;176(29).
6. Retina Australia. Legal blindness Australian definition. Retina Australia, 2009. Cited October 2011.
Available at www.retinaaustralia.com.au/legal_blindness.htm.
7.
McCarty CA, Taylor HR. A review of the epidemiologic evidence linking ultraviolet radiation and cataracts.
Dev Ophthalmol 2002;35:21–31.
8. West S. Ocular ultraviolet B exposure and lens opacities: a review. J Epidemiol 1999;(6 Suppl):S97-101.
9. Robman L, Taylor HR. External factors in the development of cataract. Eye 2005;19(10):1074–82.
10. Tan JS, Wang JJ, Younan C, Cumming RG, Rochtchina E, Mitchell P. Smoking and the long-term
incidence of cataract: the Blue Mountains Eye Study. Ophthalmic Epidemiol 2008;15(3):155–61.
11. Congdon NG. Prevention strategies for age related cataract: present limitations and future possibilities. Br
J Ophthalmol 2001;85(5):516–20.
12. Centre for Community Child Health. National Children’s Vision Screening Project discussion paper.
Melbourne: Centre for Community Child Health, 2008.
13. Murray A, Jones L, Milne A, Fraser C, Lourenço T, Burr J. A systematic review of the safety and efficacy of
elective photorefractive surgery for the correction of refractive error. Aberdeen: Health Services Research
Unit, University of Aberdeen, 2005. Cited October 2011. Available at www.nice.org.uk/nicemedia/
live/11251/31559/31559.pdf.
14. US Preventive Services Task Force. Screening for impaired visual acuity in older adults: recommendation
statement. Ann Intern Med 2009;151:37–43.
Springs, NT: CARPA, 2009.
16. Queensland Health and the Royal Flying Doctor Service (Queensland Section). Chronic disease
guidelines, 2nd edn. Brisbane: Queensland Health, 2007.
121
122
Eye health
17. Chou R, Dana T, Bougatsos C. Screening for visual impairment in older adults: systematic review to
update the 1996 US Preventive Services Task Force Recommendation. Evidence Synthesis no. 71. AHRQ
Publication No. 09-05135-EF-1. Rockville: Agency for Healthcare Research and Quality, 2009.
18. Powe NR, Schein OD, Gieser SC, 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;112:239–52.
19. Owsley C, McGwin G Jr, Sloane M, Wells J, Stalvey BT, Gauthreaux S. Impact of cataract surgery on
motor vehicle crash involvement by older adults. JAMA 2002;288:841–9.
20. McGwin G Jr, Owsley C, Gauthreaux S. The association between cataract and mortality among older
adults. Ophthalmic Epidemiol 2003;10:107–19.
21. Hewitt A, Verman N, Gruen R. Visual outcomes for remote Australian Aboriginal people after cataract
surgery. Clin Experiment ophthalmol 2001;29(2):68–74.
22. Pager CK, McCluskey PJ, Retsas C. Cataract surgery in Australia: a profile of patient-centred outcomes.
Clin Experiment ophthalmol 2004;32(4):388–92.
23. Centre for Eye Research Australia. Diabetic retinopathy. Melbourne: CCERA, 2008. Cited October 2011.
Available at www.cera.org.au/uploads/CERA_factsheet_DiabeticRetinopathy.pdf.
24. Mohamed Q, Gillies MC, Wong TY. Management of diabetic retinopathy: a systematic review. JAMA
2007;298(8):902–16.
25. Klein R, Klein BE, Moss SE, Davis MD, DeMets DL. Glycosylated hemoglobin predicts the incidence and
progression of diabetic retinopathy. JAMA 1988;260:2864–71.
26. National Health and Medical Research Council. Guidelines for the management of diabetic retinopathy.
Canberra: Commonwealth of Australia, 2008.
27. 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):525–32.
28. Murray RB MS, Lewis PM, Mein JK, McAllister IL. Sustaining remote-area programs: retinal camera use
by Aboriginal health workers and nurses in a Kimberley partnership. Med J Aust 2005;182(10):520–3.
29. Figuiera E. Trachoma: An evidence based global and Australian perspective. Sydney: The Fred Hollows
Foundation, 2006.
30. Thylefors B, Dawson CR, Jones BR, West SK, Taylor HR. A simple system for the assessment of
trachoma and its complications. Bull World Health Organ 1987;65:477–83.
31. Mak DB, O’Neill LM, Herceg A, McFarlane H. Prevalence and control of trachoma in Australia, 1997–
2004. Comm Dis Intell 2006;30:236–47.
32. Mabey DCW, Bailey RL, Ward ME, Whittle HC. A longitudinal study of trachoma in a Gambian village.
Implications concerning the pathogenesis of chlamydial infection. Epidemiol Infect 1992;108:343–51.
33. Bailey RL, Osmond C, Mabey DC, Whittle HC, Ward ME. Analysis of the household pattern of trachoma in
a Gambian village using a Monte Carlo simulation procedure. Int J Epidemiol 1989;18:944–51.
34. Communicable Diseases Network Australia and Department of Health and Ageing. Guidelines for the
public health management of trachoma in Australia. Canberra: Commonwealth of Australia, 2011. Cited
January 2012. Available at www.health.gov.au/internet/main/publishing.nsf/Content/cda-cdna-pubstrachoma.htm.
35. World Health Organization. 10th Meeting of GET2020 Report. Making progress toward the global
elimination of blinding trachoma. Geneva: WHO, 2006.
36. Mabey DC, Solomon AW, Foster A. Trachoma. Lancet 2003;362:323–29.
37. Taylor HR, Gruen R. Global evidence mapping initiative. antibiotic treatments of trachoma: a systematic
review. Melbourne: University of Melbourne and Monash University, 2010.
38. Deapartment of Health and Ageing. Surveillance reports for active trachoma annual reports. Canberra:
DHA, 2010. Cited October 2011. Available at www.health.gov.au/internet/main/publishing.nsf/Content/
cda-trachoma-annlrpt.htm.
39. Taylor V, Ewald D, Liddle H, Warchivker I. Review of the implementation of the National Aboriginal and
Torres Strait Islander Eye Health Program. Canberra: Centre for Remote Health, 2004.
40. World Health Organization. London School of Hygiene and Tropical Medicine and the International
Trachoma Initiative. Trachoma control: a guide for program managers. Geneva: WHO, 2006.
41. Office for Aboriginal and Torres Strait Islander Health. Specialist eye health guidelines for use in
Aboriginal and Torres Strait Islander populations. Cataract, diabetic retinopathy, trachoma. Canberra:
Commonwealth of Australia, 2001.
42. Tellis B, Fotis K, Keeffe JE, Taylor HR. Trachoma surveillance annual report,2008. A report by the National
Trachoma Surveillance Reporting Unit. Commun Dis Intell 2009;33(3):275–90.
Chapter 7
Hearing
loss
Author Sophie Couzos
Expert reviewers Amanda Leach, Peter Morris
124
Hearing loss
Overview
The National Guide provides recommendations on the primary prevention of
otitis media as a cause of hearing loss, and the early detection of hearing loss
predominantly for children aged less than 15 years with some recommendations
pertaining to Aboriginal and Torres Strait Islander adults. The diagnosis and
management of otitis media and hearing loss is outside the scope of this guide, as
other sources of advice are available.1,2
Children
Ear infections are more common in Aboriginal and Torres Strait Islander children
than in non-Indigenous Australian children, and the chronic and suppurative
consequences represent a major public health problem. Chronic otitis media such
as otitis media with effusion and chronic suppurative otitis media are highly prevalent
in rural and remote Aboriginal communities. These infections occur predominantly
in Aboriginal children and cause hearing loss during the critical period of child
development, although some effects may be lifelong. Otitis media is managed at a
rate of 4 times for every 100 consultations in Aboriginal Community Controlled Health
Services. In comparison, acute otitis media is less commonly managed in private
general practice (1.2 per 100 encounters 2004–05) where over 98% of patients were
non-Indigenous.3
Other guidelines
This National Guide has cross referenced recommendations in this section with
the 2011 evidence based Recommendations for clinical care guidelines on the
management of otitis media.2
Adults
Few recent studies have examined the extent of hearing impairment in Aboriginal
and Torres Strait Islander adults. A 2006 cross sectional analysis of at least 50%
of the adult Aboriginal prisoner population in Victoria showed no difference in the
prevalence value for conductive hearing impairment between Aboriginal prisoners
and a UK age-matched cohort (6.3% compared to 6.8% adults in the age group 18–
40 years, respectively).4 Overall, self reported rates of hearing problems/ear diseases
were 12% (across all ages) in the National Aboriginal and Torres Strait Islander
Health Survey (2004–05), consistent with reporting by non-Indigenous people in the
National Health Survey (13%). However, self reported rates of Aboriginal people’s
hearing problems/ear disease were higher than the non-Aboriginal population for all
ages, except for the population aged over 55 years of age.5
Other guidelines
The 7th edition of the RACGP Guidelines for preventive activities in general practice
recommends annual questioning about hearing impairment for Australians aged 65 years
and over (B) and references the US Preventive Services Task Force (1996) and Canadian
Task Force (1995).6 In 1996, the US task force recommended ‘screening older adults
for hearing impairment by periodically questioning them about their hearing, counselling
them about the availability of hearing aid devices, and making referrals for abnormalities
when appropriate (B recommendation)’. In 2011, the US task force could not ascertain
the benefits of screening and treatment for hearing loss in older adults (>50 years) and
recommended more research. The review aimed to determine if screening for hearing
loss in asymptomatic adults (>50 years) lead to improved health outcomes. However, it
found that hearing ‘screening was not associated with any differences in hearing-related
quality of life compared with no screening’.7
Hearing loss
Preventive interventions
Immunisation
Antenatal and childhood infections
Congenital and acquired hearing loss can be prevented by immunisation (rubella,
measles, Hib, pneumococcus, meningococcus) by implementing the National
Immunisation Schedule (and variations within state and territories) from birth/infancy.
See Chapter 2 regarding recommendations to enhance immunisation coverage. In
Australia, infection rates with measles and rubella remain extremely low and no cases
of congenital rubella have been identified in the Aboriginal population for many years.
The risk of congenital rubella remains, especially in immigrants.8 Rates of congenital
syphilis in the Aboriginal population are extremely low but still occur. Fewer than
10 cases of congenital syphilis have been diagnosed annually since 2007.9 It is unclear
what proportion have congenital hearing loss as a consequence. Screening antenates
for syphilis is a key part of prevention of the disease (see Chapter 9: Antenatal care).
Pneumococcal
Pneumococcal conjugate vaccine (PCV) given to children will prevent a proportion
from developing acute otitis media, but is not the primary reason for recommending
it. The primary indication for PCV in the National Immunisation Program Schedule is
for the prevention of invasive pneumococcal disease and pneumonia.
Systematic review of randomised controlled trials for the prevention of acute otitis
media using 7-valent PCV (with CRM197-mutated diphtheria toxin carrier protein)
shows marginal (7%) reduction but may mean ‘substantial reductions from a public
health perspective’ in infant children.10 Protein D (Haemophilus influenzae derived)
conjugated pneumococcal vaccine (11-valent) has 34% efficacy in reducing acute
otitis media due to action against acute otitis media from both pneumococcus and
non-typable H. influenzae.11
Observational studies show reduced outpatient visits (20%) for acute and chronic
otitis media from PCV.12 Other studies show reduced incidence of recurrent otitis
media from PCV13,14 and reduced incidence of pressure equalising tube insertions
from conjugate pneumococcal vaccination.13–15
In contrast, 23-valent polysaccharide pneumococcal vaccine (23vPPV) has not been
shown to prevent otitis media.
13-valent PCV was approved by the US Food and Drugs Administration in 2010 for
the prevention of invasive pneumococcal disease as well as otitis media caused by
the seven serotypes also covered by 7-valent PCV, however, ‘no efficacy data for
prevention of otitis media are available for the six additional serotypes’.16
10-valent PCV (protein D conjugate: Synflorix®) was Therapeutic Goods Administration
approved in Australia in July 2009 as an alternative to 7-valent PCV for the prevention of
childhood pneumococcal infections (including invasive disease, pneumonia and acute
otitis media). 13-valent PCV was approved by the Advisory Committee on Prescription
Medicines in 2010,17 for ‘Active immunisation for the prevention of disease caused by
Streptococcus pneumoniae serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F and
23F (including invasive disease, pneumonia and acute otitis media) in infants and children
from 6 weeks up to 5 years of age’. The vaccine is not Therapeutic Goods Administration
approved for the prevention of otitis media due to non-typable H. influenzae.
This indication was approved by the Therapeutic Goods Administration in May 2010,
and announced by the Federal Minister for Health in February 2011. It took effect from
1 April 2011 on the Pharmaceutical Benefits Scheme (PBS).
125
126
Hearing loss
Influenza
Influenza vaccination in children will prevent a proportion from developing acute
otitis media, but is not the primary reason for recommending it. The efficacy of
inactivated influenza vaccine in the prevention of acute otitis media is inconclusive.
The National Immunisation Program Schedule recommends influenza vaccine for
the prevention of influenza and pneumonia. All the influenza vaccines currently
available in Australia are either split virion or subunit vaccines prepared from purified
inactivated influenza virus which has been cultivated in embryonated hens’ eggs.18
The use of influenza vaccine for the prevention of otitis media is not subsidised
under the Australian National Immunisation Program Schedule.
A 2005 systematic review showed influenza vaccination was no different from
placebo.19 A 2007 meta-analysis showed a 51% reduction in acute otitis media
overall (with 32% reduction in acute otitis media using inactivated influenza vaccine
in children).20
Recently, influenza vaccination (inactivated trivalent virosomal adjuvanted) was
effective in relative reduction of acute otitis media episodes (6 month follow up)
by 34% compared with unvaccinated controls (in children prone to recurrent otitis
media).21
Episodes of acute otitis media were reduced by 71% in a randomised controlled
trial involving children aged 18–72 months receiving inactivated trivalent influenza
vaccine. However, ‘outside of the influenza seasons, no significant effects of
vaccinations were demonstrated on the studied outcomes’.22
Pooled data from randomised controlled trials of children receiving live attenuated
influenza vaccine (aged 6–83 months) showed a 38% relative reduction in the
development of acute otitis media.23
Screening
Newborn
Because 50% of children with hearing loss have no identifiable risk factors,
universal screening (instead of targeted screening of high risk groups) has been
proposed to detect children with permanent congenital hearing loss early in life.
Neonatal hearing screening is believed to have resulted in significant cost savings
to the health system.24
Australia operates neonatal screening programs in all states/territories to varying
degree as some offer universal hearing screening and others offer targeted
screening (many other countries also have a universal newborn hearing screening
program).
In 2009, the Council of Australian Governments agreed to ensure that by the
end of 2010 every child born in Australia has access to screening for congenital
hearing impairments.25 This program is being coordinated at the federal level
with states and territories, although there is no specific federal funding for this
now national approach to newborn hearing screening. Guidelines and standards
have been endorsed by the Australian Health Ministers’ Advisory Council and
performance indicators for the monitoring of the program are in development. A
formal evaluation of cost:benefit has not been proposed (pers. comm. Department
of Health and Ageing, July 2011).
Permanent congenital hearing loss (PCHL) occurs in 1–2 infants per 1000 births.
Prevalence of PCHL is significantly higher than prevalence of other conditions for
Hearing loss
which newborn screening currently occurs (eg. phenylketonuria 1 per 10 000;
hypothyroidism 3 per 10 000; cystic fibrosis 4 per 10 000). Newborn hearing
screening leads to earlier identification and intervention, and ultimately leads to
better language development. In the absence of newborn hearing screening,
three out of 4 children with PCHL remain undiagnosed by 12 months of age
and their capacity for normal language and cognitive development is greatly
diminished.
In Western Australia, Newborn Hearing Screening (NBHS) services have
operated in selected metropolitan hospitals since 2000. From 2010, all
West Australian birthing hospitals will be required to screen all newborns
for permanent congenital hearing loss.26 In 2011, it was reported that more
than 95% of all newborns in Western Australia had received neonatal hearing
screening.27 Few data are available from other jurisdictions.
Several systematic reviews have examined universal newborn hearing
screening. The United States Preventive Services Task Force recommends
screening for hearing loss in all newborn infants before 1 month of age. Infants
who do not pass the newborn screening should undergo audiologic and
medical evaluation before 3 months of age. This is based on good quality
evidence that early detection improves language outcomes, although the net
benefit (taking account of risk of harms) is moderate. The number needed to
screen to diagnose one case is 878 and 178 for universal newborn hearing
screening and targeted screening programs, respectively.28
A Cochrane review of randomised controlled trials concluded that the long term
effectiveness of universal newborn hearing screening programs has not been
established. The review could not identify any randomised trials comparing the
long term results (psychological, language and educational related outcomes)
of either universal, targeted or opportunistic newborn hearing screening
programs.29
Another systematic review concurred that patient relevant parameters, such
as social aspects, quality of life, and educational development, have not
been adequately investigated, thereby limiting understanding of the impact of
newborn hearing screening.30
Early childhood
Specific recommendations for the Aboriginal and Torres Strait Islander
population for hearing screening from early childhood are based on the high
incidence and prevalence of otitis media in the Aboriginal population. Screening
for otitis media with effusion in non-Indigenous children is not recommended by
general guidelines (eg. the RACGP red book).
The Senate Community Affairs Reference Committee24 has recommended that
‘the Council of Australian Governments extends its commitment for universal
newborn hearing screening to include a hearing screening of all children on
commencement of their first year of compulsory schooling. Given the crisis in
ear health among Aboriginal and Torres Strait Islander people, the committee
believes urgent priority should be given to hearing screenings and follow up for
all Indigenous children from remote communities on commencement of school’.
However, according to the Darwin Otitis Guideline Group, in regions with nearuniversal conductive hearing loss due to infection (intermittent/recurrent), it is
unlikely that hearing screening at school entry will reveal information that isn’t
already known. In regions with sporadic hearing loss, monitoring for hearing
127
128
Hearing loss
loss is the preferred recommendation. School entry screening might pick up
undetected deafness (usually otitis media with effusion) warranting personal
intervention, but it is unclear if this outcome justifies school entry screening. The
Darwin Otitis Guideline Group did not recommend school entry screening for
hearing loss detection in populations with high levels (‘near universal’) of otitis
media and consequent conductive hearing loss. The group recommended that
‘regular surveillance (with appropriate testing when indicated) is preferred to
school entry screening’.
In a cross-sectional analysis over time, 19% of Aboriginal children screened at
school age screening program had unilateral/bilateral mild–moderate hearing
loss.31 There was no cohort or comparison group of non-Indigenous children,
so it is not possible to assess this significance of this level. This is the only
recent school screening report in Australia.
The US Preventive Services Task Force provides no recommendations for
hearing screening beyond those for the neonatal period. The American
Academy of Pediatrics recommends hearing screening at 4 years, and definitive
hearing testing at intervals in those children with risk factors (eg. recurrent otitis
media). No specific reference is made to school screening.
Behavioural
Parental vigilance for the detection of hearing loss in children is crucial. Around
one-quarter of hearing loss affected children had their loss identified and
initiated by parental suspicion.32,33 Other sources of identification include wellbaby checks (20%) and through risk factors (31%).32
Studies report parents are poor predictors of hearing loss from otitis media with
effusion.34,35
Breastfeeding
A meta-analysis of observational studies found that prolonged breastfeeding for
at least 3 months reduces the risk of acute otitis media by 13%.36 A cohort study
found 6 month exclusive breastfeeding protective against infectious disease.37
Smoking
Exposure to passive smoke is confirmed risk factor in cohort studies38 and
meta-analysis of those studies.39 Evidence that smoking cessation favourably
influences the progression of otitis media with effusion is lacking.
Swimming
The Norwegian Mother and Child Cohort Study conducted by the Norwegian
Institute of Public Health in children born between 1999 and 2005 followed from
birth to the age of 18 months. Children who were baby swimming (at 6 months)
were not more likely to have lower respiratory tract infections, to wheeze or to
have otitis media.40
Two meta-analyses of randomised controlled trials and cohort studies have
investigated the impact of swimming on acute otitis media occurrence (or
otorrhoea) after tympastomy tube insertion. They both found that swimming
made no difference to the occurrence of acute otitis media (or otorrhoea).41,42
Children with chronic suppurative otitis media who swim may also benefit, as
the introduction of swimming pools in two remote Aboriginal communities led
to a reduction in the prevalence of tympanic membrane perforations over 18
months,43 although this was not a controlled trial.
Hearing loss
Antibiotics
A Cochrane review of 13 randomised controlled trials found long term (>6
weeks) prophylactic antibiotics can prevent episodes of acute otitis media, but
children in the trials mostly had recurrent otitis media.44 A meta-analysis showed
that while oral antibiotics used in acute otitis media had a marginal effect in
preventing asymptomatic middle ear effusion, this benefit was outweighed by
other factors such as antibiotic resistance and treatment to prevent effusion
could not be warranted.45
There is little evidence that acute otitis media 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 otitis media, which is effective).46
Management of detected otitis media should proceed according to clinical
practice guidelines, which are distinct for the Aboriginal population.1
Prophylactic antiviral drugs
It has been reported that acute otitis media occurs in 20–50% of children under
6 years of age after influenza.47 Acute otitis media was significantly less likely in
patients with confirmed influenza infection treated with neuraminidase inhibitors
versus placebo.48
Another systematic review examined the effect of antiviral drugs on the
secondary effects of influenza (such as acute otitis media) as well as preventing
influenza in family contacts of the index case: ‘Effects of neuraminidase
inhibitors on rates of otitis media were no different in children aged 5–6 and 12
but were significantly lower in children younger than 5 years. With a household
prophylaxis strategy, 13 children would need to be treated with a 10 day course
of zanamivir or oseltamivir to prevent one additional child developing influenza
… Reductions of secondary complications could be an important factor in
the decision to treat and should be balanced with the higher rates of adverse
effects, particularly vomiting, with oseltamivir’.47
It appears therefore that in children affected with influenza, there is the option
of antiviral therapy to prevent acute otitis media (while considering the number
needed to treat to prevent one case of acute otitis media) or antibiotics when/
if acute otitis media develops. In conclusion, there is little rationale in opting for
neuraminidase inhibitors to prevent the need for antibiotic treatment for acute
otitis media as a complication of influenza.
Housing
Early and persistent otitis media could be prevented if overcrowded living
conditions of Aboriginal communities were improved.39 A strong independent
association was demonstrated between ‘reports of respiratory infection’ and
the overall ‘functional condition’ of those houses examined over 2003–04.
Statistically significant associations were found between carers’ report of
the presence of ear infections in children with the level of toilet infrastructure
and poor infrastructure overall. The study confirms ‘the potential for general
improvements in the functional state of housing infrastructure to improve
the health of children in these communities, most notably through reducing
respiratory infections’.49
Overcrowded housing has also been shown to increase the risk of
nasopharyngeal carriage of Streptococcus pneumoniae, Moraxella catarrhalis
and non-typeable H. influenzae in Aboriginal and non-Aboriginal children.
129
130
Hearing loss
Nasopharyngeal carriage of these pathogens is a well established predictor of
early onset acute otitis media and chronic otitis complications. Overcrowded
housing facilitates household transmission of otitis pathogens.50
More than a quarter of the Aboriginal population live in a house deemed to need
extra bedrooms, compared to just 5.7% of non-Indigenous people. In some
remote areas in the Northern Territory, the highest rates of overcrowding were
reported with over 70% of people living in overcrowded conditions (needing
more bedrooms).51
Handwashing
Few studies have evaluated the effects of handwashing, nose-blowing and facial
cleanliness on the prevention of acute otitis media.
A randomised controlled study examining handwashing in child day care
centres found that children in the intervention group had fewer visits to a doctor
because of an attack of acute otitis media with effusion and received 24%
fewer prescriptions for anti-microbials. There was general compliance with the
handwashing instructions.52
Regarding the prevention of the pathogens that transmit acute otitis media,
poor handwashing was a predictor of non-typable H. influenzae throat
carriage in children from child care centres.53 The risk of pneumococcal hand
contamination was eight times higher in Aboriginal children aged 3–7 years
from a remote community than in children younger than 4 years of age from
urban childcare centres (37% vs 4%), further supporting the important role of
handwashing in the prevention of otitis media.54
Noise induced hearing loss
It is likely that in many Aboriginal families, noise exposure exceeds the allowable
daily exposure of 85 decibels (dB) averaged over an 8 hour working day
(occupational standards), according to a recent survey conducted mostly in
the Northern Territory. Overcrowding is likely to contribute to excessive noise
exposure. A significant risk of noise induced hearing loss is believed to occur
in the majority of persons exposed to levels which exceed this on a long term
basis. Such exposure may create ‘a “second wave” of preventable noiseinduced sensori-neural hearing loss for those in Indigenous communities’.
Few health professionals and families are aware of the fact that excessive
exposure to loud noise over prolonged periods can damage hearing. In terms
of interventions, Aboriginal and Torres Strait Islander health workers have an
important role to play since they can best inform families about the dangers of
too much loud noise, particularly for children with a history of ear disease.55
Few studies have explored the prevalence of noise related hearing disorders
affecting Aboriginal people. The hearing status of 109 Aboriginal prisoners in
Victoria revealed that 36% had high frequency hearing loss and that this was
most consistent with a noise induced loss. Ninety-two percent had reported
exposures to loud noise.4
Hearing loss
131
Recommendations: Hearing loss
How often?
Level/
strength of
evidence
References
As per National
Immunisation
Program
Schedule
(NIPS) and
state/territory
schedules
IA
18
Age 2, 4 and
6 months, as
per NIPS and
state/territory
schedules
I–IIA
10,11
Annual influenza vaccination (inactivated As per NIPS and
virus) is recommended for any person ≥6 state/territory
months of age who wishes to reduce the schedules
likelihood of becoming ill with influenza.
Vaccination may reduce the incidence
of acute otitis media as a secondary
complication of influenza
IC
19,20,23
Offer testing for rubella immunity and
syphilis serology to prevent infections
which may lead to congenital hearing
loss
N/A
N/A
Preventive
intervention
type
Who is at
risk?
Immunisation
Children aged Vaccination is recommended to prevent
<15 years
infections that may lead to congenital or
acquired hearing loss (rubella, measles,
H. influenzae type b, meningococcus).
(See Chapter 2: Child health)
Pneumococcal conjugate vaccination
(13-valent PCV) is recommended during
infancy to prevent invasive disease,
pneumonia and acute otitis media*17
All pregnant
women
See Chapter 9:
Antenatal care
132
Hearing loss
Recommendations: Hearing loss (continued)
Screening
Newborn
infants
Ensure parents of newborn infants are
Prior to age 1
aware of the universal neonatal hearing
month
screening program being implemented
in each state/territory and have had their
newborn screened for congenital hearing
impairment
IC
28–30
Opportunistic,
antenatal and
postnatal
checks, and
as part of an
annual health
assessment
GPP
2
Opportunistic
and as part of
an annual health
assessment
GPP
2
Opportunistic
and as part of
an annual health
assessment
GPP
2
Opportunistic
and as part of
an annual health
assessment
GPP
2
School entry The routine hearing screening of all
N/A
aged children children upon commencement of their
first year of compulsory schooling may
have limited public health value and is not
encouraged
GPP
2
Adults aged
>15 years
Monitor for hearing impairment by
questioning, provide advice regarding
free hearing assessment, and make
referrals when appropriate
As part of an
annual health
assessment
GPP
6
All people
Inform patients that free hearing
assessment (and rehabilitation/hearing
aids if hearing loss is confirmed) can
be obtained as part of the Australian
Government Hearing Services Program
and the Community Services Obligation
(check eligibility criteria‡)
Opportunistic
GPP
57–60
Children aged Encourage parents to be aware of child
<15 years
developmental milestones in the early
detection of hearing loss (see Table 7.1).
Parental suspicion of hearing loss should
always be investigated (see Table 7.2).
Where relevant, provide advice regarding
free hearing assessment (see below)
Conduct ear examinations (otoscopy)
in order to detect unrecognised acute
or chronic otitis media. If detected,
refer to clinical practice guidelines for
management (see Resources)
Children aged Monitor for hearing loss
<5 years and
older children
at high risk
of hearing
Use the following audiological tools
impairment†
to monitor for hearing loss: simplified
parental questionnaires (see Table
7.1), and pneumatic otoscopy or
tympanometry (in children older than 4
months of age). These methods do not
assess hearing
Pneumatic otoscopy or tympanometry is
used to identify otitis media with effusion
(with possible conductive hearing loss).
Refer to clinical practice guidelines for
the identification and management of
otitis media with effusion (see reference
1 and 2 and Resources). Those with
suspected hearing loss (or caregiver
concerns) should be referred as shown
in Table 7.2
Hearing loss
Behavioural
Chemoprophylaxis
Environmental
133
Pregnant
women and
postnatal
period
Promote exclusive breastfeeding for
at least 4 months (and preferably to 6
months) to reduce the risk of infants
acquiring acute otitis media. Refer
women to breastfeeding support
programs if needed
Opportunistic,
antenatal and
postnatal
checks, and
as part of an
annual health
assessment
IB
36
All smokers
Promote smoking cessation and the
need to avoid children being exposed to
cigarette smoke, as passive exposure
increases the risk of acute, recurrent
and chronic otitis media. (See Chapter 1:
Lifestyle, section on smoking cessation)
Opportunistic
and as part of
an annual health
assessment
IA
39
All people
Swimming (sea, clean fresh water) should Opportunistic
be permitted including in children with a
prior history of otitis media (all forms)
IA
40–43
All people
A video otoscope may assist in helping
patients and families to understand
ear disease. This may lead to greater
engagement in its prevention and
management
Opportunistic
GPP
2
Children aged The use of prophylactic antibiotics in
<15 years
order to prevent the onset of acute otitis
media is not recommended, except in
children with recurrent otitis media§
Opportunistic
IA
42,43
The use of prophylactic antiviral drugs
in those with confirmed influenza for the
purpose of preventing the onset of acute
otitis media is not recommended
Opportunistic
IA
39,48
IIIC
39,49,50
Encourage nose-blowing, facial
Opportunistic
cleanliness and handwashing of children,
in order to prevent the transmission
of infectious disease. Frequent hand
washing in child care centres can prevent
the occurrence of childhood infections
and episodes of acute otitis media
IIC
52,53
Inform families of the danger of loud
noise (and for prolonged periods),
especially for children with a history of
ear disease (see Resources)
GPP
55
Annually
Children aged Assess children at high risk of hearing
<15 years
impairment† with regard to their housing
situation (ie. if overcrowding is likely,
functional condition of housing) and refer
to social support services for housing
assistance if indicated (see Table 7.3)61
All people
Opportunistic
* Aboriginal and Torres Strait Islander children in high risk areas are recommended to also receive 23-valent polysaccharide vaccine (PSV)
as a booster dose between 18 and 24 months of age as indicated for the prevention of invasive pneumococcal disease. High risk areas
include the Northern Territory, Queensland, South Australia and Western Australia. This vaccine is not recommended for children in New
South Wales, the Australian Capital Territory, Victoria or Tasmania18
† High risk of hearing impairment: those from socioeconomically deprived communities and from regions with a high prevalence of otitis
media
‡ Australian Government Hearing Services Program eligibility (Voucher system) includes all Australian pensioner/sickness allowance
recipients 21 years and older including a dependent of a person in that category.58 For those under 21 years, certain remote area patients,
adults with complex hearing needs, Aboriginal and Torres Strait Islander persons >50 years of age or Aboriginal participants in CDEP
programs of any age, the Community Services Obligation component also provides free hearing services59 and can be accessed by the
federally funded and sole provider of these services: ‘Australian Hearing’.57 The CSO can also be accessed by those aged 21–26 years.60
Private hearing clinics (eg. Hearing Life) provide free hearing assessments to anyone 21 years and over
§ Recurrent otitis media: the occurrence of three or more episodes of acute otitis media in a 6 month period, or occurrence of four or more
episodes in the past 12 months2
134
Hearing loss
Table 7.1. Hearing related growth milestones in children
Simplified parental questionnaires can elicit a child’s progress through the following hearing related
growth milestones:
• 3–6 months: not communicating by vocalising or eye gaze
• 9 months: poor feeding or oral coordination
• 12 months: not babbling
• 20 months: only pointing or using gestures (ie. not speaking)
• 24 months: using <20 words, not following simple requests
• 30 months: no two-word combinations
Source: Darwin Otitis Guideline Group 20102
Table 7. 2. Criteria for referral of children with suspected hearing
loss, hearing related problems elicited through simplified parental
questionnaires (Table 7. 1), and/or caregiver concerns
Age of child
Refer to
<3 years
Major regional hearing centre to determine the level of loss
<5 years and older
children at high risk of
hearing impairment*
Paediatrician and audiologist for appropriate developmental assessment and
hearing tests
<15 years
Audiologist or ENT specialist for full hearing assessment
* High risk of hearing impairment refers to people from socioeconomically deprived communities and from
regions with a high prevalence of otitis media
Source: Darwin Otitis Guideline Group 20102
Table 7.3. Definition of overcrowded housing circumstances
Households that do not meet the following requirements are deemed to be overcrowded:
• There should be no more than two persons per bedroom
• Children younger than 5 years of age of different sexes may reasonably share a bedroom
• Children 5 years of age or older of opposite sex should have separate bedrooms
• Children younger than 18 years of age and the same sex may reasonably share a bedroom
• Single household members 18 years or over should have a separate bedroom, as should parents or
couples
Source: Biddle N 200851
Hearing loss
Resources
Recommendations for clinical care guidelines on the management of otitis media
in Aboriginal and Torres Strait Islander populations (Darwin Otitis Guideline Group
in collaboration with the Office for Aboriginal and Torres Strait Islander Health Otitis
Media Technical Advisory Group)
www.health.gov.au/internet/main/publishing.nsf/Content/64B3D2636590623FC
A25722B0083428D/$File/om_pdf_version.pdf
Therapeutic Guidelines: Antibiotics
www.tg.org.au/?sectionid=41
Noise destroys your hearing (Australian Hearing)
www.hearing.com.au/upload/media-room/Noise-destroys-your-hearing.pdf.
References
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34. Lo PS, Tong MC, Wong EM, van Hasselt CA. Parental suspicion of hearing loss in children with otitis
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36. Uhari M, Mantysaari K, Niemela M. A meta-analytic review of the risk factors for acute otitis media. Clin
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38. Jacoby PA, Coates HL, Arumugaswamy A, Elsbury D, Stokes A, Monck R, et al. The effect of passive
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41. Carbonell R, Ruíz-García V. Ventilation tubes after surgery for otitis media with effusion or acute
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42. Lee D, Youk A, Goldstein NA. A meta-analysis of swimming and water precautions. Laryngoscope
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43. Lehmann D, Tennant MT, Silva DT, et al. Benefits of swimming pools in two remote Aboriginal
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137
Chapter 8
Sexual
health and
bloodborne
viruses
Author Gabrielle Hall
Expert reviewers Steven Skov, James Ward
Sexual health and bloodborne viruses
Overview
Sexually transmissible infections (STIs) and bloodborne viruses (BBVs) are
seldom diagnosed from symptomatic presentation. The majority of STIs in
Australia are diagnosed in primary care as opposed to specialised sexual health
clinics.1 In contrast to sexual health clinic settings, patients in a primary care
setting infrequently present requesting a sexual health check. In this scenario
it is necessary for the health worker to realise an opportunity for opportunistic
screening. This guide should assist in deciding which tests to include in
screening and help recognise the high risk patient and offer screening at every
appropriate opportunity. Every state and territory in Australia has a public health
department that can advise clinicians on current prevalence data and any
increased risks in their region.
The teenage pregnancy rate (women under 20 years age) in 2006 in Australia
was five times higher for Aboriginal and Torres Strait Islander women compared
to non-Indigenous women.2 The peak age group for births to Aboriginal and
Torres Strait Islander women was 20–24 years of age, compared to 30–34
years for non-Indigenous women. In the period 2001–04, 23% of Aboriginal and
Torres Strait Islander women who gave birth were younger than 20 years of age.
Only 4% of non-Indigenous women were aged under 20 years.2 This reminds
us that prevention and screening for STIs and appropriate vaccination are vital
for healthy pregnancies and need to start early for Aboriginal and Torres Strait
Islander adolescents. Counselling during the screening process should include
discussions about contraception and family planning.
There are widely varying prevalence rates for STIs within Australia and a
variation from community to community within the states and territories.3
Factors such as poverty, discrimination, substance abuse, illicit drug use
and recent incarceration all affect sexual behaviours. Table 8.1 highlights the
common risk factors for STIs and BBVs. In Aboriginal and Torres Strait Islander
populations and non-Indigenous populations, 80% of notifications occur in
the 15–29 years age group. Notification rates of STIs are generally increasing
in Australia, although disease incidence and prevalence have been difficult to
estimate reliably. The data for Aboriginal and Torres Strait Islander populations
are inconsistent, largely due to under identification of Aboriginal or Torres Strait
Islander status. There have been improvements in data collection, notification
systems and diagnostic techniques that make it difficult to compare trend data.4
The most current data are from the 2011 Australian Annual Surveillance for
Notifiable STIs.5 National STI incidence comparing Aboriginal and Torres Strait
Islander rates to that of the non-Indigenous population were:
• 1257 vs 340 per 100 000 population for chlamydia infection
• 804 vs 30 per 100 000 population for gonorrhoea
• 25 vs 6 per 100 000 population for syphilis.
Queensland defied the national trend of a decline in the rate of syphilis (notably
in the Northern Territory, South Australia and Victoria) with an increase in the
Aboriginal and Torres Strait Islander rate to 35 per 100 000. The incidence rates
for Aboriginal and Torres Strait Islander people when compared with nonIndigenous populations for newly acquired virus were:
• stable at 5 vs 1 per 100 000 population for hepatitis B virus (HBV) infection
139
140
• 141 vs 48 per 100 000 population for hepatitis C virus (HCV) infection
• 4.2 vs 4.1 per 100 000 population for human immunodeficiency virus (HIV)
infection.
The Genital Wart Surveillance Network reported a decline in diagnoses of
genital warts in female Australian women eligible for the HPV vaccine (aged
12–26 years in 2007) from 10.9% of first time uses of a sexual health service in
2004 to 4.8% in 2009.6
The 2011 Bloodborne Viral and Sexually Transmissible Infections in Aboriginal
and Torres Strait Islander people: Surveillance and Evaluation report shows
the widely varying prevalence rates from state-to-state and between major
cities, regional areas, and rural and remote regions.7 For chlamydia the rate of
diagnosis was highest in Northern Territory and Western Australia and lowest in
Tasmania and Victoria with South Australia rates falling between these regions.
Queensland and New South Wales are not included as Aboriginal and Torres
Strait Islander status is reported for less than 50% of the diagnoses. Twice as
many remote and very remote diagnoses of chlamydia were made compared
with major cities and outer regional areas. Inner regional areas have the lowest
rate of diagnosis of chlamydia for Aboriginal and Torres Strait Islander people.7
Chlamydia
Chlamydia trachomatis of immunotypes D–K is the most commonly diagnosed
STI and there has been a significant increase in notification rates since 1997.8
Asymptomatic infection is common in both sexes. In men, chlamydia commonly
causes urethritis and can also cause epidydimitis, infertility and Reiter
syndrome. In women, chlamydia can cause cervicitis with the risk of developing
salpingitis and pelvic inflammatory disease or chronic pelvic pain. Chlamydia is
efficiently transmitted vertically at birth and can cause conjunctivitis, pneumonia
and otitis media. Chlamydia is an important cause of tubal factor infertility and
ectopic pregnancy, so early testing for chlamydia prior to reproductive age
and during pregnancy is most important. Despite the need for early testing, a
2008 ecological study of chlamydia testing data (71 295 tests) and Victorian
chlamydia notification data (7006 notifications) concluded that testing in the age
groups at most risk, ie. women aged between 20 and 24 years, was low even
in those living in the most advantaged quartile.9 Early treatment of infections
can prevent complications and is effective. The immediate dose of azithromycin
currently recommended for chlamydia treatment is highly effective.10
Gonorrhoea
Gonorrhoea is a purulent infection of mucous membranes caused by
Neisseria gonorrhoeae. It causes urethral symptoms in up to 50% of men
and is largely asymptomatic in women. In men it causes urethritis, proctitis,
epididymitis and prostatitis. In women it is a major cause of cervicitis and pelvic
inflammatory disease and this can lead to chronic pelvic pain, infertility and
ectopic pregnancy. Infection during pregnancy can cause adverse outcomes
and perinatal transmission can cause gonococcal conjunctivitis. In adults,
gonococcal septic arthritis is a known presentation and in both sexes there
can be symptomatic pharyngitis. Gonococcal infection appears to increase
susceptibility to, and transmission of, HIV.
Trichomoniasis
Trichomonas is a sexually transmissible protozoal parasite that causes
vaginal discharge, however the majority of cases in high prevalence areas are
asymptomatic. The consequences of trichomoniasis are potentially important in
pregnant women in whom infection is associated with premature rupture of the
membranes and pre-term delivery however, treatment of asymptomatic infection
has not been shown to reduce these complications (see Chapter 9: Antenatal
care). It has also been associated with an increase in the acquisition of HIV. It
is associated with low economic status,11 injecting drug use and no Pap test
screening, which probably reflects lack of access to healthcare or poor health
seeking behaviours.12 It is a notifiable disease in the Northern Territory where
case notification rates are similar to those for chlamydia.13 Trichomonas is not a
notifiable disease elsewhere in Australia.
Syphilis
Syphilis is a bacterial STI caused by the spirochaete Treponema pallidum.
Syphilis is spread by direct sexual contact and most cases presents as
asymptomatic. Early syphilis is defined as the stages of syphilis (primary,
secondary and early latent syphilis) that typically occur within the first year after
acquisition of the infection. Latent syphilis is characterised by asymptomatic
infection with a normal physical examination in association with a positive
serology.14 Latent syphilis is categorised as ‘early’ or ‘late’ depending on the
established date of infection. Early latent syphilis implies infection within 1 year.
All other cases are referred to as late latent syphilis or latent syphilis of unknown
duration.14 The primary stage of syphilis is usually marked by a lesion called
a ‘chancre’, that appears 7–90 days after exposure. Weeks to a few months
later, approximately 25% of individuals with untreated infection will develop a
systemic illness that represents secondary syphilis, which commonly presents
as a maculopapular rash on the palms of the hands and the soles of the feet.
The secondary stage typically resolves spontaneously in 2–6 weeks but can
recur repeatedly during the first 2 years. Following the secondary phase there
is an asymptomatic latent stage that can be diagnosed by a positive specific
treponemal antibody test. In the early latent syphilis phase the disease is
considered contagious. In late latent syphilis it is not considered contagious.
Tertiary or late syphilis occurs in an uncertain proportion of patients infected by
T. pallidum and refers to symptomatic manifestations of the disease involving
the central nervous system, the cardiovascular system, or the skin and
subcutaneous tissues (gummas).14
Treatment of syphilis in pregnant women is important to prevent congenital
syphilis of the newborn. The rate of diagnosis of infectious syphilis was on a
decline to 25 per 100 000 in Aboriginal and Torres Strait Islander populations in
2009, whereas the rate in the non-Indigenous population rose to 6 per
100 000 in 2009.15 Despite the decline, Aboriginal and Torres Strait Islander
rates are many times higher than other Indigenous and non-Indigenous
populations in high income countries.15 In Queensland, syphilis persists in
Aboriginal and Torres Strait Islander populations at high levels of up to 52 cases
per 100 000 population compared to non-Indigenous rate of 2 cases per 100
000 population.16 The decrease in infectious syphilis has not yet been seen in
a complementary reduction of congenital syphilis where there have been 12
cases notified in Queensland since 2001. The majority of these were acquired in
remote areas.16 Syphilis in pregnancy, long recognised as a significant cause of
pregnancy loss and perinatal death in northern Queensland,17 is associated with
a high population prevalence of infection.
141
142
Human papilloma virus
Human papilloma virus (HPV) infects the cutaneous and mucosal epithelial
tissues, most commonly involving the skin or anogenital tract. Persistent
infection is the leading cause of cervical cancer and is associated with other
cancers of the vagina, vulva, penis and anus. HPV genotypes 16 and 18 are
the causative agents in 70–80% of all cervical cancers. HPV genotypes 6 and
11 are among the HPV genotypes designated as low risk (for cancer), and are
associated with 90% of genital warts. HPV infection is acquired soon after the
first sexual encounter with an infected individual. Like all STIs, peak prevalence
of HPV infection occurs within the first decade after sexual debut, typically
between 15–25 years of age in most Western countries.
In Australia, a national HPV vaccine program began in 2006 using Gardasil®.
This quadrivalent vaccine is effective against high risk HPV types 16 and 18
to prevent cervical cancer and low risk HPV types 6 and 11 for prevention of
external genital warts. HPV vaccination is currently given to girls via a school
based vaccination program in Year 7, at 12 years of age. The Australian
Immunisation Handbook recommends HPV for females aged 9–26 years.18
Population based preventive measures include dissemination of general
information about HPV.19 Health professionals should include in their sexual
health counselling discussions that cover abstinence and the importance of
using condoms ‘from start to finish’ with no unprotected genital contact. This
can also be an opportunity to discuss smoking as a risk factor, due to its
association with an increased risk of genital cancer.19
Hepatitis B and C
The rate of diagnosis of HBV infection in the Aboriginal and Torres Strait Islander
population resident in the Northern Territory, South Australia, and Tasmania was
237 cases per 100 000 in 2006 declining to 120 cases per 100 000 in 2009.
The rate of diagnosis of newly acquired HBV in the same group was 5 cases
per 100 000 in 2005–09.15 The estimated prevalence of chronic HBV in the
Aboriginal and Torres Strait Islander population ranges from 2% in some urban
communities and up to 8% in some rural communities.15 The population rate
of diagnosis of HCV infection in Aboriginal and Torres Strait Islander residents
in the Northern Territory, South Australia and Western Australia was 131 cases
per 100 000. The rate was substantially higher for Aboriginal and Torres Strait
Islander people in South Australia and Western Australia compared to the nonIndigenous population, yet it was lower for Aboriginal and Torres Strait Islander
people in the Northern Territory compared to non-Indigenous residents.15 This
may be related to different rates of injecting drug use.
Chronic HBV and HCV infections cause significant morbidity and mortality
through sequelae such as liver fibrosis, cirrhosis and hepatocellular carcinoma.
Together, they are the most common indication for adult liver transplantation in
Australia. Antiviral therapy is the standard treatment for HBV and HCV infection
in adults. It is currently not listed as approved for the treatment of children
in Australia.20 Chronic HBV causes cirrhosis in around 25% of adults over a
20-year period and is a precursor to hepatocellular carcinoma. The lifetime
risk of cirrhosis is 20–30% in perinatal and childhood infections. Studies in the
Northern Territory in the 1980s and 1990s found prevalence rates for HBsAg of
8.2% among urban and rural Aboriginal school children.21 Prevalence studies
have shown that HBsAg is highest among Aboriginal and Torres Strait Islander
prison inmates, at 12%.22 HCV transmission occurs predominately among
people with a recent history of injecting drug use. It is the underlying cause of
liver disease in 28% of liver transplants in Australia.5
Human immunodeficiency virus
The per capita rate of HIV diagnosis in the Aboriginal and Torres Strait Islander
population was similar to that in the non-Indigenous population. In the Aboriginal
and Torres Strait Islander population, the rate declined from 4.7 cases per
100 000 in 2000–04 to around 3.9 cases per 100 000 in 2005–09 but this
is based on small, localised numbers and may not reflect a national pattern.
Higher proportions of Aboriginal and Torres Strait Islander cases of HIV infection
were attributed to heterosexual contact (21% compared with 15%) and injecting
drug use (20% compared with 3%) than in non-Indigenous cases.5
HIV prevalence in Australia is lower than in most comparable high income
countries. One of the significant factors for this is the early adoption of needle
syringe programs, another was effective early education though peer groups
and community organisations. The rate of HIV notification in Aboriginal and
Torres Strait Islander people has remained relatively stable over the past 6 years
and disease incidence rates are similar in Aboriginal and Torres Strait Islander
populations and non-Indigenous populations.5 Among Aboriginal and Torres
Strait Islander people, HIV is seen more in women and heterosexual couples
and the rate is seven times greater for those who inject drugs, when compared
to subgroups of non-Indigenous people. The reason for this trend is thought
to be due to less access to appropriate health services and harm reduction
activities and increased rates of STIs.23 Co-infection with chlamydia, gonorrhoea
and/or trichomonas are significant risk factors for HIV infection, highlighting the
importance of a comprehensive and systematic management of a person’s
overall sexual health as a key strategy in reducing the risk of HIV infection.24
Interventions
Immunisation
HPV vaccine has been developed to prevent cervical cancer and the National
Immunisation Program provides vaccination for girls aged 12–13 years,
ideally before their first sexual contact. Systematic review of the efficacy of
HPV vaccination for young girls show seroconversion rates over 99.5% after
vaccination and studies are ongoing to ascertain whether a booster dose of
HPV will be required.25,26 The age standardised rate for death from cervical
cancer in Aboriginal women in Queensland, Western Australia, the Northern
Territory and South Australia from 1997 to 2000 was five times that for nonIndigenous women (11.3 vs 2.1 per 100 000 women).27,28 It is too early to see
evidence of a reduction in rates of cervical cancer after HPV vaccination, as
cancers can occur decades after infection, but there has been a decline in high
grade abnormalities on cervical lesions, particularly in women naïve to HPV
types 16 or 18.29
A systematic review of HBV vaccination in people with no previous exposure
or unknown exposure status showed that vaccination reduces the risk of
developing HBV infection by 88% for HBV surface antigen marker and 62%
for anti-core antibody marker.30 To reduce perinatal transmission of HBV in
newborn infants of HBsAg positive mothers, a systematic review concluded that
HBV immunoglobulin plus vaccine was required.31 Neonatal HBV vaccination
was introduced in the late 1980s to at risk groups in Australia. This was offered
to Aboriginal children in the Northern Territory in 1988 and in 1990, universal
infant vaccination commenced in the Northern Territory.21 The National Universal
Infant HBV Vaccination Program began in 2000. The Australian Immunisation
Handbook recommends universal neonatal HBV vaccination, ideally in the
143
144
first 24 hours of life, followed by a primary course of vaccination at 2, 4 and 6
or 12 months age.18 This includes vaccination of all adolescents aged 10–13
years who have not yet had a primary course of vaccination. Individuals
vaccinated at birth are only just reaching 23 years of age in the Northern
Territory and 11 years of age in the rest of Australia, therefore there will be a
need for prevention and management of chronic HBV among Aboriginal and
Torres Strait Islander people for decades into the future. The current Australian
Immunisation Handbook also recommends HBV vaccine for high risk individuals
who are injecting drug users, household and sexual contacts of HBV carriers,
incarcerated individuals and men who have sex with men.18 It does not
specifically recommend HBV vaccine for Aboriginal and Torres Strait Islander
people who are outside the ages eligible for the National Immunisation Program
or who are not in a high risk group. This is in contrast to the Gastroenterological
Society of Australia and New Zealand recommendations that all Aboriginal and
Torres Strait Islander people are in a higher risk group and should be screened
and vaccinated if non-immune.32 HBV vaccination for Aboriginal and Torres
Strait Islander children and young adults up to the age of 20 years are funded
through some state/territory immunisation programs. HBV vaccine for Aboriginal
and Torres Strait Islander adults over 20 years is state government funded in
New South Wales and South Australia only. In the Northern Territory, Western
Australia and Tasmania, HBV vaccines are funded for catch-up immunisation
for Aboriginal and Torres Strait Islander school-aged children only. In Victoria,
HBV vaccines are only funded for household contacts and seronegative
injecting drug users. In Queensland, HBV vaccines are only funded for school
vaccination programs.
The Australian Immunisation Handbook recommends hepatitis A vaccine for
people who have chronic HBV and/or HCV, for injecting drug users and for
men who have sex with men. There is a vaccination program for all Aboriginal
and Torres Strait children residing in the Northern Territory, Queensland, South
Australia and Western Australia.18
Screening
Screening is designed to detect disease in people without signs or symptoms
of that disease and should be followed by confirmatory testing and treatment
in the event of a positive diagnostic test. If health services do not have the
capacity to respond to a positive screening test then the test should not be
undertaken in the first place.
With the introduction of nucleic acid amplification tests (NAATs) in the 1990s,
screening for chlamydia, gonorrhoea and trichomonas is now simple. This has
had a dramatic impact on the way we screen for STIs but has resulted in a
decrease in the number of swabs sent for culture and sensitivity.33 NAATs for
chlamydia, as well as gonorrhoea and trichomonas, can be conducted on swab
specimens obtained from the endocervix (chlamydia and gonorrhoea) or high
vagina (chlamydia and trichomonas), or self administered low vaginal swabs
(SOLVS) and first void urines (FVU). Self collected samples increase ease of
screening.34 When collecting an FVU, patients should be advised that an ideal
specimen is collected 2 hours after last void; earlier specimens will lose some
sensitivity. An NAAT can be performed on a few millilitres of urine but 25 mL is
better, and refrigeration is recommended if there is a time delay beyond 24 hours
before getting the sample to the laboratory. The specimen should be frozen
if it will be longer than 4 days before processing.34 The choice of chlamydia,
gonorrhoea and trichomonas testing from FVU, SOLVS or ECS/HVS in women
should take into account patient preference. Endocervix and high vagina
swabs are the routinely collected screening tests when performing a speculum
examination.35 For men, FVU is the only screening option. The promotion of
the same method of screening (ie. FVU) for women as for men may suit some
regions. At each primary healthcare encounter that results in consideration of
STI screening, it is important to provide pretest counselling and education about
other STIs as well as safe sex advice including the use of condoms for prevention
of STIs.
NAAT is recommended for gonorrhoea screening.11 N. gonorrhoeae can be
sensitive or resistant to penicillin and resistance patterns vary. Therefore a
positive NAAT result often needs further information about the susceptibility
of the particular strain to penicillin.36 It is recommended, therefore that for
NAAT positive gonorrhoea, a swab for culture is collected within 1 week to
gather important information on sensitivities for the local population.37 While it
is recommended that women presenting with a vaginal discharge are tested
for trichomonas,11 it is not recommended as a screening test for asymptomatic
women. Local prevalence data should be used to guide the need to screen,
as the prevalence rate has been found to be high in the Northern Territory,
northern Queensland and the Kimberley region of Western Australia,38 but low in
southern urban sexual health clinic settings. A study in Sydney reported a higher
prevalence of trichomonas in an urban STI clinic population when testing using
NAATs than previously reported.17 As NAAT for trichomonas becomes more
widely available there may be updated prevalence data and recommendations
for screening.
Syphilis and HIV screening is not recommended for routine screening of
asymptomatic individuals but should be considered if the patient reports risk
factors that promote STI or BBV transmission (Table 8.1) and where local
prevalence rates are high.10 A low threshold for testing is recommended, as
some people are reluctant to disclose risk behaviours or identify their own
risk taking activities. Local prevalence data can assist in decisions to include
syphilis and HIV routinely in screening. Syphilis infection is of particular concern
during pregnancy because of the risk of transplacental infection to the fetus.
Congenital syphilis infection of the fetus is associated with several adverse
outcomes including perinatal death, pre-term birth, low birthweight, congenital
abnormalities, active congenital syphilis of the newborn and long term sequelae
such as deafness and neurological impairment.39 It is for this reason that syphilis
screening is recommended early in antenatal care. Vertical syphilis transmission
usually occurs after 4 months gestation, so early screening and treatment
should prevent most cases. Individual antenatal patients who remain at high risk
for STIs should be re-screened for relevant STIs again in the third trimester.39
Behavioural factors
Screening for STIs provides the opportunity to offer prevention and health
promotion advice. Condom use for vaginal and anal sex will significantly reduce
the risk of STIs.10 It is the most effective method of preventing HIV transmission.
When discussing safe sex practices, it is important to recommend the use of
condoms with water based lubricant for all genital contact during vaginal and
anal intercourse. It is also important to discuss the barriers to condom use
and how they might be overcome and to recommend an STI check with new
partners before couples in a monogamous relationship stop using condoms.
Discussion of issues around personal safety, self respect and respect of others
can also promote healthy and more stable relationships.40
145
146
The Queensland Sexual Health Clinical Management Guidelines has
comprehensive chapters that cover history taking and risk assessment including
a health worker’s legal obligations.41 It is important to be familiar with the
legislation in your state or territory regarding sexual activity in persons under
the age of 18 years as there are mandatory reporting requirements in some
jurisdictions.42 Pretest discussions should also include talking about what a
positive test result would mean and explaining the notification requirements for
STIs while reassuring the patient that their privacy will be respected.43
Health promotion interventions to provide information on STI transmission and
prevention as well as skill development, can have a positive effect on sexual risk
reduction for up to 3 months after intervention, measured by increased use of
condoms for vaginal intercourse.44
Contact tracing is a voluntary process where sexual contacts of index cases are
notified of their exposure to an infection. Contact tracing can be broadly used
to cover both partner notification (patient referral) and provider referral. Partner
notification involves the index case contacting his or her own sexual contacts and
the health provider advising on the information to be given to the partner. It may
also include patient delivered partner therapy (such as azithromycin for chlamydia).
Provider referral involves the healthcare worker directly advising the contact or
using their local sexual health team to perform this task. Provider referral allows
for confidential contact tracing and is the method of choice for infections such as
HIV. It is important to have access to the Australian Contact Tracing Manual (see
Resources) as this has the necessary information on how far back to trace for
individual diseases. There are very limited data to comment on the effectiveness of
contact tracing; a Cochrane review in 2001 found that health worker notification to
a contact was a more effective way to treat contacts than patient notification.45 The
strategy of contact tracing varies between states and regions. Most states have a
sexual health unit that will oversee GP notifications of HIV, syphilis and gonorrhoea,
but chlamydia partner notification is usually followed up by the GP and their clinic
health team. There is limited evidence based information regarding contact tracing
effectiveness for Aboriginal and Torres Strait Islander people. A literature review
by the Burnet Institute suggests that health worker referral or patient delivered
partner therapy is appropriate and that Aboriginal and Torres Strait Islander
health worker involvement should be offered sooner rather than later.1 It should
be noted, however, that patient delivered partner therapy is not recommended in
several Australian jurisdictions. Although the review noted that avoiding the use of
letters or the telephone to notify may be important, these strategies could still be
appropriate, depending on local circumstances and protocols.
Chemoprophylaxis
Post-exposure prophylaxis (PEP), which is the provision of a course of treatment
to someone exposed to HIV or HBV, reduces the risk of infection with the virus
and prevents disease. The exposure could be in the healthcare workplace,
exposure through sex with an infected individual or through needle sharing.
For HIV, it is recommended to start PEP within 72 hours after exposure; this
involves the prescription of antiretroviral drugs over a course of 28 days. This is
administered via a S100 prescriber for HIV drugs. It is estimated that receptive
anal intercourse and sharing injecting drug equipment with an HIV positive
individual constitutes the highest risk of transmission of HIV and concurrent
STIs are one of the cofactors that significantly increase the risk of sexual
transmission. The evidence for this secondary prevention strategy mostly comes
from observational studies on animals and mother-to-child transmission.46
Environmental influences
Harm minimisation is the principle underlying Australia’s National Drug Strategy
since 1985. It encompasses a wide range of approaches involving supply
reduction, demand reduction and harm reduction. Using clean injecting
equipment is the most effective method of preventing transmission of HIV and
HCV among injecting drug users.10 Needle and syringe exchange programs
provide sterile injecting equipment and are an effective, safe and cost effective
component of harm reduction strategies. It was found that between 1991 and
2000, needle and syringe exchange programs cost Australian governments
$130 million dollars but saved $7.8 billion by preventing 25 000 cases of HIV
and 21 000 cases of HCV.47 International research has shown that there is
a reduction of spread HIV and HCV in prisons that operate needle syringe
exchange programs and evaluation of these prison programs found that
more people access drug treatment.48 Data collected from the 2005–09
National Needle and Syringe Exchange Programs Survey show that among
those participating in their annual survey who reported recent incarceration,
approximately 1 in 3 reported injecting in prison.49 Patients in contact with
needle syringe exchanges or in primary care settings should opportunistically
be delivered brief interventions focused on motivation to assist with cessation
of drug use.50 Motivation to change behaviour can be enhanced by discussions
and feedback that explore patient perspectives and treatment options for drug
use in a non-judgemental manner. Two sessions, each lasting 10–45 minutes,
are recommended, with the primary focus on harm minimisation. In this
setting, harm minimisation involves education to reduce risky behaviours, the
consideration of abstinence, access to needle and syringe exchange programs
and opioid substitution therapy and, ideally, access to peer group educators.
There is healthy debate in Australia about current and future harm minimisation
strategies. The prohibitionist activities enacted at the level of law enforcement
include lack of access to needle and syringe exchange programs in prisons,
increasing use of drug sniffer-dogs, and lack of political support for medically
supervised injecting drug rooms versus the harm reduction approach of health
and alcohol and other drug specialists.51
Injecting drug use has been strongly linked with HIV and HCV infections and
unsafe injecting practices have led to the epidemic of HCV infections. Although
several illicit drugs can be injected (eg. opioids, methamphetamine, cocaine),
the majority of evidence on environmental interventions relates to opioid use.
Opioid dependent individuals have been found to have an annual mortality of
2–4%, or 13 times that of their peers.52 This increased mortality is primarily
due to overdoses, violence, suicide, and smoking and alcohol related causes.
Injecting drug users have a reduced quality of life due to time spent intoxicated
or seeking drugs as well as an increased rate of psychiatric comorbidity.
Opioid dependence places a significant economic burden on society through
increased healthcare costs, the criminal justice system and unemployment.
Treating opioid dependence is aimed at reducing harm and improving quality
of life. Opioid substitution therapy consists of daily administration of an opioid
agonist such as methadone or an opioid partial agonist such as buprenorphine.
The aim of opioid substitution therapy is to reduce the use of illicit opioids,
reduce injection of drugs and its risk of BBV infection, reduce criminal activity,
reduce the risk of overdose and improve psychological and physical health.52
It is a minimum standard recommendation by the World Health Organization
(WHO) that opioid agonist maintenance treatment is an option and that this
treatment is accessible to disadvantaged populations.52 WHO also recommends
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148
the availability of a range of structured psychosocial interventions such as
counselling and assistance with housing, education, employment and legal
problems. Patients with psychiatric comorbidity should have access to
psychiatric treatment. Opioid agonist maintenance treatment has been shown to
reduce the seroconversion to HIV.53 This correlates with measured reductions in
drug related and sex related risk.
General practitioners often have patients who present with requests that
hint at opioid addiction such as escalating opioid doses for chronic pain,
‘lost’ prescriptions and injection related morbidity. These are opportunities
to discuss harm minimisation strategies, including treatment options such
as opioid substitution therapy. It is important to be familiar with the opioid
pharmacotherapy prescribers in your region and referral pathways for patients
who demonstrate a willingness to change. Patients can also present in a crisis
when their level of motivation for change is high. The more readily available the
treatment program, the more likely we can take advantage of the motivational
high. Each jurisdiction in Australia has its own requirements for training of
opioid prescribers. The training is free and usually involves a half or 1 day
workshop. GPs working with Aboriginal and Torres Strait Islander people should
consider undertaking this training so that their service is able to provide fully
comprehensive primary healthcare to this vulnerable and marginalised group of
people. There are already many GP prescribers and experienced alcohol and
other drug health workers and counsellors in Aboriginal Community Controlled
Health Services in Australia who can be consulted for advice and support in this
regard.
149
Recommendations: General preventive advice
How often?
Screening
All people with
risk factors for
STIs or BBVs
(see Table 8.1)
Screen for STIs according to local
prevalence guidelines and screen for
BBVs if risk factors are present (see
specific recommendations below)
Annually and re- GPP
screen 3 months
after positive test
People
diagnosed with
an STI
Review STI risk factors and screen
On diagnosis
for other STIs according to local
and re-screen in
prevalence guidelines
3 months
Consider also screening for BBVs if
risk factors are present (see Table 8.1)
GPP
43
Sexual partners
of a person with
an STI
Ensure contact tracing is undertaken Every positive
at time of diagnosis and appropriate screen
testing and treatment is offered to
contacts, as per Australasian Contact
Tracing Manual (see Resources54)
IB
45
Behavioural
Chemoprophylaxis
Environmental
Level/
strength of
evidence
References
Preventive
intervention type
43
All sexually active Provide sexual health counselling
people
including proactive discussion of
issues of sexuality
Opportunistic
IIB
19,44
Recommend condom use with all
sexual activity
Opportunistic
IIIB
55
People at higher
risk of HBV or
HCV infection
(see Table 8.1)
Provide counselling on harm
minimisation and promote peer
education strategies around safer sex
and injecting drug use
Opportunistic
GPP
and as part of
an annual health
assessment
56
People
with opioid
dependence
Conduct brief motivational
interviewing to reduce use of illicit
drugs, harm with injecting drugs,
risky alcohol use and risk of BBV
infection and STIs, particularly for
those unlikely to attend specialist
treatment (see Resources57,58)
Opportunistic
IIIC
50
Exposure
to HIV both
occupational
and nonoccupational
Opportunistic
Assess post-exposure risk using
national guidelines (see Resources)59
and provide post-exposure
prophylaxis (PEP) within 72 hours of
the risk exposure when indicated
Refer to local jurisdictions to
source PEP starter packs and
recommendations regarding
specialist access (see Resources)60
Follow up PEP requires an authorised
prescriber (under Section 100 Special
Access Scheme)
GPP
46
People
with opioid
dependence
Opioid substitution therapy should be
made accessible to all populations,
including those in prison populations
and other closed settings
IIIB
53
Injecting drug
users
Needle and syringe programs should Opportunistic
be made available to all populations
including prison populations
IIIA
63
As early as
possible in
dependence
situation
150
Recommendations: Sexually transmissible infections
Preventive
intervention
type
Who is at risk?
How often?
Level/
strength of
evidence
References
Screening:
chlamydia
All people aged
15–29 years of age
if sexually active
All people aged
≥30 years and at
high risk (see Table
8.1)
Recommend nucleic acid
amplification tests (NAAT) via:
Annually
IA (to age 25
years)
GPP (25–29
years)
35,41
64
All pregnant
women
• endocervical swab if having a
speculum examination, or
• first void urine, or
• self administered low vaginal
swab
First visit
Pregnant women
at high risk of STI
(see Table 8.1)
First visit and
again in third
trimester
Women having
a termination of
pregnancy
Once
Men who have sex Recommend first void urine
with men
NAAT and anal swab NAAT
Annually
IA
Sexually active
people aged
15–39 years
and pregnant
women where
local prevalence
rates are high (see
reference 7)
Annually
IIB (age <25 11,41
years)
GPP (age
25–39 years
and pregnant
women)
Men who have sex Recommend throat swab
with men
NAAT and culture, plus anal
swab NAAT and culture
Annually or 3–6
monthly if high
risk (see Table
8.1)
IA
64
Screening:
Trichomonas
vaginalis
All sexually active
people aged <35
years where local
prevalence rates
are high (see
Resources)
Recommend NAAT for women
(as above) and first void urine
NAAT for men
Opportunistic if
symptomatic
IIIB
11,65
Screening:
syphilis
All pregnant
women
Recommend testing with
specific treponemal tests
(EIA or TPPA or FTA-Abs)
and non-specific treponemal
tests (RPR). Liaise with
local pathology providers to
determine which tests are
available for screening
At first visit
IIID
Repeat at 28
weeks if positive,
in a high
prevalence area
or if risk factors
for STIs are
present
66
Annually
35
Screening:
gonorrhoea
Recommend NAAT (as above)
Men who have sex Syphilis testing as above
with men
Others at high risk
of STIs
IIB
151
Recommendations: Bloodborne viruses
Preventive
intervention
type
Who is at risk?
How often?
Levels/
strength of
evidence
References
Immunisation:
HBV
Neonates
Recommend HBV vaccination
Once at birth prior
to leaving hospital
ID
30
Babies born to
mothers who are
HBsAg positive
Recommend HBV
immunoglobulin and vaccination
at birth
Complete primary course of
vaccination, followed by testing
for anti-HBs and HBsAg at
3–12 months after completing
vaccination (see Australian
Immunisation Handbook)
Immunoglobulin
IA
(HBIG) ideally
within 12 hours and
vaccination (HBV)
preferably within
24 hours (definitely
within 7 days) of
birth
18,31
Unvaccinated
people at high
risk of STI/ BBV
infection (see Table Test healthcare workers, those
at risk of severe or complicated
8.1)
disease, haemodialysis patients,
sexual partners and household
contacts of recently notified HBV
carrier for seroconversion
3 doses at 1 and
6 months*
30
Individuals exposed
to HBsAg positive
individuals or
unable to be
identified and
tested rapidly
Initiate within 72
hours (or 14 days
for sexual contact)
Offer HBV post-exposure
prophylaxis (HBIG and primary
course of vaccination) for nonimmune people
ID
4–8 weeks after the GPP
last dose
IIC
18
People with HCV
infection or chronic
liver disease not
immune to HBV
3 doses at 0, 1 and IIC
6 months*
18,67,68
Immunisation:
HPV
Girls/women prior
to first sexual
activity
Females who are
sexually active
Recommend HPV
vaccination (see Chapter 15,
recommendations for cervical
cancer prevention)
10–13 years of age: IA
school-based
14–26 years of
age at cost to the
patient
19
Immunisation:
HAV
Men who have sex
with men
Injecting drug users
People with chronic
HBV and HCV
infection
Recommend hepatitis A
Once
vaccination if serology is negative
(see Australian Immunisation
Handbook)
GPP
18,69
Screening: HBV
Non-vaccinated
or vaccine status
unknown
People at high risk
for BBVs
Healthcare workers
Offer individual HBV screening
including:
GPP
56,70,71
• HBsAg ( a marker of acute or
chronic infection)
• HBsAb (a marker of immunity)
• HBcAb (a marker of recent or
past infection)
See Resources for guidelines on
interpreting HBV tests
If serology is negative, offer HBV
vaccination as above*
Opportunistic
152
Recommendations: Bloodborne viruses (continued)
All pregnant
women
Screening: HCV
Screening: HIV
Recommend HBV screening to
At first antenatal
allow timely HBV vaccination and visit
HBIG for infant at birth
(see Chapter 9: Antenatal health)
III–3B
72,73
IIIA
69
People at high risk Offer HCV serology testing
of contracting HVC
infection (see Table
8.1)
As part of an
annual health
assessment
Infants born to HCV Offer HCV serology testing
infected mothers
18 months of age
IIA
(repeated if positive)
69,74
Pregnant women
At first antenatal
visit
75
Offer HIV serology testing
Men who have
sex with men and
others at high risk
of BBVs (see Table
8.1)
IIB
As part of an
annual health
assessment
* Not subsidised on the National Immunisation Schedule but check relevant state/territory immunisation programs
Table 8.1. Risk factors for STIs and bloodborne viruses
Risk factors for STIs
Risk factors for BBVs
• Age <30 years
• Age <35 years and sexual network
relates to a remote community
• Multiple current partners
• Engaging in group sex
• New partner
• Using condoms inconsistently
• Living in an area with a high incidence
of STIs
• Having sex while under the influence of
drugs and alcohol
• Having sex in exchange for money or
drugs
• Prison incarceration
• Victim of sexual assault
• Men who have sex with men where any
of the above risk factors are also present
• Prison incarceration: current or past
• Blood transfusion prior to 1990
• Tattoos or piercings not performed in a
sterile professional setting
• Cultural practices (ie. initiation
ceremonies)
• Current or past injecting drug use
• Household member with HBV, HCV or
HIV
• Sexual partner with HBV, HCV or HIV
• Infants of mothers infected with HCV,
HBV or HIV
Source: Bradford D, Hoy J, Matthews G 200810
Resources
Bloodborne viral and sexually transmissible infections in Aboriginal and Torres Strait
Islander people: surveillance and evaluation report 2011 (The Kirby Institute)
www.med.unsw.edu.au/NCHECRweb.nsf/resources/2011/$file/KIRBY_
ATSIP2011.pdf
Sexual health clinical management guidelines (Queensland Government)
www.health.qld.gov.au/sexhealth/documents/cm_guidelines.pdf
Clinical guidelines for the management of sexually transmissible infections among
priority populations (RACGP)
www.stipu.nsw.gov.au/pdf/STI_Rx_Priority_Populations.pdf
Guidelines for managing sexually transmissible infections
http://silverbook.health.wa.gov.au/Default.asp?PublicationID=1&SectionID=74
Management of genital Chlamydia trachomatis infection: a national clinical guideline
(Scottish Intercollegiate Guidelines Network)
www.sign.ac.uk/pdf/sign109.pdf
Sexually transmissible infections: UK national screening and testing guidelines
www.bashh.org/documents/59/59.pdf
Drug misuse: psychosocial interventions, national clinical practice guideline number 51
(National Collaborating Centre for Mental Health)
www.nice.org.uk/nicemedia/pdf/CG51FullGuideline.pdf
Australasian contact tracing manual (ASHM)
http://ctm.ashm.org.au/Default.asp?PublicationID=6&ParentSectionID=P6&Sec
tionID=733
HIV, viral hepatitis and STIs: a guide for primary care (ASHM)
www.ashm.org.au/images/publications/monographs/HIV_viral_hepatitis_and_
STIs_a_guide_for_primary_care/hiv_viral_hepatitis_and_stis_whole.pdf
Hepatitis B virus testing and interpreting results (ASHM)
www.ashm.org.au/images/publications/monographs/b%20positive/b_positivechapter_3.pdf.
Drug use resources
Counsellor’s guide to working with alcohol and drug users
www.dao.health.wa.gov.au/InformationandResources/
Publicationsandresources/Healthprofessionals.aspx
Drug and alcohol psychosocial interventions professional practice guidelines (New
South Wales Department of Health)
www.health.nsw.gov.au/policies/gl/2008/GL2008_009.html
Drug misuse: psychosocial interventions, national clinical practice guideline number 51
(National Collaborating Centre for Mental Health)
www.nice.org.uk/guidance/CG51/NICEGuidance
Guidelines for the psychosocially assisted pharmacological treatment of opioid
dependence (World Health Organization)
http://whqlibdoc.who.int/publications/2009/9789241547543_eng.pdf.
153
154
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157
Chapter 9
Antenatal
care
Author Eileen Rafter
Expert reviewers Wendy Cavilla, Vivienne Manessis
Antenatal care
Overview
Aboriginal and Torres Strait Islander mothers and babies experience an
increased risk of maternal, fetal and neonatal death, pre-term birth and low
birthweight when compared with non-Indigenous mothers and babies.1
Poor health and social disadvantage contribute to these poorer perinatal
outcomes. Aboriginal and Torres Strait Islander mothers have higher rates of
chronic disease such as diabetes and kidney disease, higher rates of sexually
transmissible infections and anaemia, higher rates of smoking and alcohol
consumption in pregnancy, higher rates of adolescent pregnancies and limited
access to affordable nutritious food and health services.2
As for all pregnant women, the antenatal care offered to Aboriginal and
Torres Strait Islander women should be woman-centred.2 This means that the
care focuses on the individual woman’s needs and preferences and that the
woman is informed and involved in decision making. Other important factors
in improving antenatal care are continuity of carer, allowing adequate time
for communication and to establish trust and rapport, and health provider
awareness of local community sociocultural factors and health needs.2,3
This chapter focuses on some key aspects of antenatal screening that are of
particular relevance to Aboriginal and Torres Strait Islander women and is not a
comprehensive guide to all antenatal screening. The first antenatal visit – which
should take place in the first trimester – is particularly important. At this visit a
comprehensive history, examination and discussion with the woman establishes
the necessary schedule of tests and visits. The majority of screening tests
are also carried out. Psychosocial assessment is also important at this stage;
screening for issues such as domestic violence, financial stress, mental health
disorders and substance use, including alcohol.
In addition to general recommendations for the first antenatal visit, specific
recommendations have been made for the following priority areas: smoking
cessation, alcohol consumption, genitourinary infection screening, mineral and
vitamin deficiency, and diabetes.
Smoking cessation
Tobacco smoking is one of the most important preventable causes of adverse
pregnancy outcomes. These adverse events include premature birth, placental
abruption (double the risk for smokers who consume more than 20 cigarettes
a day), spontaneous abortion, low birthweight,4 stillbirth5 and placenta praevia.6
Children exposed to tobacco smoke in-utero have a higher risk of SIDS, asthma
and respiratory and ear infections. In addition there is some evidence that inutero exposure is associated with psychological problems such as attention
and hyperactivity problems, disruptive and negative behaviour3 and poorer
educational performance.7 Although some studies show the harmful effect
of smoking in pregnancy is dose related,8,9 this does not obviate the need
to clearly and consistently recommend complete smoking cessation as the
safest option.2 The risk of low birthweight is greater if the woman continues to
smoke in the third trimester, with one study showing that if a woman is able to
give up smoking by her fourth month of pregnancy, her risk of delivering a low
birthweight baby decreases to nearly that of a non-smoker.10
159
160
Antenatal care
Aboriginal and Torres Strait Islander women are three times more likely to
smoke during pregnancy than non-Indigenous Australian women, with current
smoking prevalence estimated at around 50–60%.11 Higher risk groups include
teenagers and women who experience socioeconomic hardship.8,12,13 Maternal
smoking contributes to a greater proportion of the risk of prematurity and low
birthweight for Aboriginal and Torres Strait Islander babies when compared with
non-Indigenous babies.13
A higher proportion of women stop smoking during pregnancy than at
other times in their lives, leading to the hypothesis that pregnancy may be
a ‘teachable moment’ for smoking cessation.9 However, some women who
stopped smoking in pregnancy resume after birth and there is a lack of
evidence on how to prevent this.14 Some women may also take up smoking
again during pregnancy so it is important to continue enquiring about smoking
and exposure to secondhand smoke throughout pregnancy.2
The US, UK and Australia have developed guidelines recommending all
pregnant women receive brief interventions to promote smoking cessation in
pregnancy.14,15 These guidelines are currently based on the ‘5As’ (see Chapter
1: Lifestyle, introduction). There have been many studies on smoking cessation
strategies in pregnant women using a range of interventions including advice,
counselling, hypnosis, telephone support, motivational interviewing, written
and electronic resources, cognitive behavioural therapy, measurement of the
byproducts of tobacco smoking, use of nicotine replacement therapy and
assessment of readiness to quit.9 Such strategies have also been found to be
beneficial in studies involving Aboriginal and Torres Strait Islander women.16
Overall smoking cessation strategies used in early pregnancy can reduce
smoking in later pregnancy and lead to a reduction in low birthweight and
premature birth.9 Trials using cognitive behavioural therapy have the strongest
evidence and demonstrate statistically significant improvements in mean
birthweight. There is no evidence for negative psychological impacts from
behavioural interventions and indeed the psychological impact may be positive,
with women feeling that ‘somebody cared’ about their health and wellbeing.9
This suggests a caring, empathic and non-judgemental approach is more likely
to result in improved outcomes.
Addressing any underlying factors such as depression, low self esteem and
personal, social or marital disharmony are important strategies to promoting
smoking cessation. Qualitative research in Aboriginal and Torres Strait Islander
women has identified the following factors that may affect motivation or ability to
quit: smoking being perceived as reducing stress, smoothing social interactions,
providing ‘time out’, relieving boredom, controlling weight and being part of the
social norm.10,17 For some women smoking may be seen as a less immediate
problem compared with other issues. In some areas of Australia it is important
to enquire about levels of chewing tobacco as well as smoking. There is some
evidence that women with partners who smoke find it harder to quit and are
more likely to relapse if they do quit.18 However, there is a lack of evidence on
the effectiveness and cost effectiveness of interventions aimed at encouraging
partners and family members who smoke to quit and help pregnant women to
stop smoking.14
There is mixed evidence on the effectiveness of nicotine replacement therapy
(NRT) for promoting smoking cessation in pregnancy. A Cochrane review9 found
that NRT did not have a significant benefit over other types of interventions
but there have been no direct comparisons of NRT with any other strategy.
Antenatal care
The safety of NRT in terms of effect on fetal development and birth outcomes
remains unclear. If NRT is used in pregnancy there are some recommendations
that the dose of prescribed nicotine in pregnancy should be similar to a smoking
dose and that intermittent forms of NRT are preferred to continuous use
formulations as the total dose of nicotine will be less.19
Alcohol consumption
Alcohol consumption in pregnancy causes problems for both the mother and
baby. For the baby, it is associated with increased risk of severe birth defects
such as brain damage, facial deformities and growth problems, and more subtle
changes such as learning and behavioural problems. This range of problems
is known as fetal alcohol spectrum disorder. The risk to the baby is highest
in the first trimester, including the first weeks following conception when the
mother may not realise she is pregnant.3 Women who drink alcohol during
pregnancy are also more likely to have problems such as miscarriage, bleeding
during pregnancy, low birthweight babies, stillbirth, poor nutrition, anaemia
and injuries.3 It is important to ask women about their use of alcohol and
other substances at the first antenatal visit and, if appropriate, at subsequent
visits, in a sensitive, non-judgemental way. A completely safe level of alcohol
in pregnancy has not been determined.3 Not drinking alcohol in pregnancy,
particularly in the first 3 months, is the safest option.2 If women choose to drink
they should be advised to avoid getting drunk and drink no more than two
standard drinks on any 1 day and less than seven standard drinks in a week.3
Genitourinary and bloodborne virus infection screening
Several genitourinary infections are associated with adverse outcomes in
pregnancy and there is a higher prevalence of many of these infections in
Aboriginal and Torres Strait Islander women when compared with nonIndigenous women.
Sexually transmissible infections
There is considerable state and regional variation in rates of chlamydia,
gonorrhoea and trichomonas infection, with some rural and remote
communities in the Northern Territory, Queensland and Western Australia having
particularly high rates. Aboriginal and Torres Strait Islander people resident in
major cities in South Australia, Victoria and Western Australia have three times
the rate of chlamydia infection while those resident in remote and regional areas
of Australia have up to seven times the rate of chlamydia infection, compared
with the non-Indigenous population.20 One study in an urban setting showed
an approximately 20% prevalence of STIs in pregnant Aboriginal and Torres
Strait Islander women and 36% in women under 20 years of age. There was a
prevalence of 14.4% chlamydia, 6.1% gonorrhoea and 7.2% trichomonas.21 STIs
are higher in the population aged under 25 years in general (which is significant
for Aboriginal and Torres Strait Islander pregnant women given the higher
proportion of teenage pregnancies in this cohort) and in women with a recent
change in sexual partner. Besides age, other predictors for STIs identified in this
study include harmful alcohol use and unwanted pregnancy.
Some studies have found chlamydia is associated with early premature
delivery22 and intrauterine growth restriction23 and if not treated it is associated
with low birthweight and infant mortality.24 Babies born to mothers with
chlamydia also have higher rates of ophthalmia neonatorum, lower respiratory
161
162
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tract infection and pneumonia.25,26 Similarly, case reports suggest an
association between untreated gonorrhoea infection in pregnancy and preterm delivery, premature rupture of membranes, low birthweight, postpartum
endometritis and ophthalmia neonatorum.27 There is some evidence that
infection with Trichomonas vaginalis in pregnancy is associated with pre-term
birth and low birthweight28,29 but again, it is not clear whether this association is
causal.
Studies have shown that treating chlamydia infection during pregnancy reduces
the incidence of premature rupture of membranes, pre-term birth and low
birthweight babies but there is no significant evidence to show that it leads
to a decrease in the incidence of neonatal conjunctivitis or pneumonia.24,30–33
However, in the case of trichomonas, a Cochrane review looking at interventions
in pregnancy found that treatment with metronidazole, while yielding
parasitological cure rates of 90%, did not reduce pre-term birth and in one trial
might even have increased it.34
Due to its high prevalence in the under 25 years population, screening and
treatment of chlamydia is recommended in pregnant women in this age
group.2,35 In addition, screening for chlamydia and gonorrhoea in populations
with a high prevalence of STIs is recommended.2,3,35 While trichomonas
infection can be highly prevalent in some Aboriginal and Torres Strait Islander
communities there is no evidence that screening for it improves pregnancy
outcomes, and treatment of asymptomatic trichomonas in pregnancy may
cause harm.34,36
Syphilis
Syphilis infection during pregnancy can cause miscarriage, stillbirth and
congenital syphilis infection (causing permanent impairment, debilitation
and disfigurement in affected babies). Syphilis is easily and safely treated in
pregnancy with antibiotics, which can prevent these complications.37
Syphilis infection is rare in Australia but more common in the Aboriginal and
Torres Strait Islander population, particularly in more remote areas. For the
period 2005–09 the diagnosis of syphilis infection was more than four times
higher in the Aboriginal and Torres Strait Islander population than the rest of the
Australian population, with women aged 29–40 years being diagnosed at 28
times the rate for non-Indigenous women in the same age group.38
Studies have shown that universal screening significantly increases the
detection of pregnant women with syphilis compared with selective screening of
women at risk39,40 and this is cost effective even in areas of low prevalence.37,41
For this reason, and for the benefits that treatment of syphilis in pregnancy
provides to both mother and baby, universal screening for syphilis infection is
recommended in most guidelines.2,42 For women who test positive for syphilis
in early pregnancy, or for women from a population of high prevalence, a
second screening test for syphilis is recommended early in the third trimester of
pregnancy and at birth.2,3
The initial test for syphilis is usually a blood test for serum antibodies of
treponema (eg. enzyme immunoassay Treponema pallidum haemagglutination
assay: EIA-TPHA). If this is positive, a non-treponemal test (eg. VDRL or
RPR) will be performed by the laboratory to confirm diagnosis and enable a
quantitative value of disease activity. Positive results should be interpreted with
caution as past treated episodes of syphilis may still produce a low positive
result and other trepanematoses (eg. yaws, pinta) may give a false positive for
Antenatal care
syphilis. Expert advice should be sought for positive results and consideration of
testing for other STIs is advised.
HIV, hepatitis B and hepatitis C
Antenatal diagnosis of HIV and hepatitis B infection in the mother allows for
the implementation of interventions during pregnancy or at the time of birth
that can greatly reduce the risk of transmission of these infections to the child.
In the case of HIV, one study found that between 2003 and 2006, the rate of
mother-to-child transmission was 1% in women diagnosed antenatally who
used at least two interventions (antiretrovirals during pregnancy and delivery
by caesarean section) compared with a 50% rate of transmission where
there was no antenatal diagnosis or no interventions used.43 The diagnosis of
hepatitis B infection antenatally allows for the administration of vaccination and
immunoglobulin to the baby on the day of delivery to prevent mother-to-child
transmission.
Studies have shown that screening for HIV or hepatitis B based on risk factors
alone would miss a large proportion of pregnant women infected with one
or both of these viruses.44,45 For this reason, and to prevent transmission
to the baby, universal screening for hepatitis B and HIV early in pregnancy
is recommended in most guidelines.2,3,46 It is important that appropriate
counselling and consent is provided prior to testing.
The benefits of hepatitis C screening during pregnancy are doubtful as there
is no way of preventing mother-to-child transmission or of treating the virus
during pregnancy. For this reason, guidelines do not recommend universal
screening. However, some guidelines do suggest that screening of those at
risk of hepatitis C infection may be appropriate, although there is little evidence
for this.2,3 The risk factors for hepatitis C infection are a history of incarceration,
blood transfusion or invasive procedure overseas (or before 1990 in Australia),
injecting drug use, needlestick injury or tattooing (see Chapter 8: Sexual health
and bloodborne viruses).
Asymptomatic bacteriuria
Asymptomatic bacteriuria in pregnancy increases the likelihood of pyelonephritis
with an incidence of about 30% in affected women.47 There is some evidence
that untreated asymptomatic bacteriuria may be associated with low birthweight
and pre-term birth. However, other factors may be involved and there may only
be an association if the bacteriuria progresses to pyelonephritis.48 Asymptomatic
bacteriuria during pregnancy may be more common among Aboriginal and
Torres Strait Islander women than non-Indigenous women.46,49,50
A Cochrane review found that antibiotic treatment of asymptomatic bacteriuria
is effective in clearing the bacteriuria and can reduce the incidence of
pyelonephritis by 75%.51 Other evidence shows that screening for asymptomatic
bacteriuria reduces the incidence of pyelonephritis from 23.2 per 1000 women
with no screening to 16.2 with dipstick testing and 11.2 with urine culture.52
Dipstick urinalysis has high specificity but low sensitivity53 and a midstream
urine specimen for culture is recommended. There may be a role for dipstick
testing in areas where access to pathology services is limited but infection
should still be confirmed with culture.
There is no consensus in the literature about the best timing and frequency for
testing of bacteriuria in pregnancy but current Australian guidelines recommend
a single urine culture at the first antenatal visit.2
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Asymptomatic bacterial vaginosis
Bacterial vaginosis is a decrease of lactobacilli and an increase in pathogenic
bacteria (including Gardnerella vaginalis, mobiluncus, bacteroides, prevotella and
mycoplasma) in the vagina, which may cause vaginal discharge and malodour
or may be asymptomatic. Asymptomatic bacterial vaginosis in pregnancy
is associated with an increased risk of pre-term birth,54 even if the bacterial
vaginosis spontaneously resolves later in pregnancy.55 It is more common among
women of low socioeconomic status and women who had low birthweight
babies in previous pregnancies.56 Several large studies in the 1990s in the
general population found the prevalence of bacterial vaginosis to be in the range
of 9–23%,57–59 while a study in remote central Australia found a prevalence of
26–36% among non-pregnant women attending clinics for a woman’s health
assessment.60
A Cochrane review found that treatment of bacterial vaginosis with antibiotics
eradicates the infection but does not change the risk of pre-term birth, low
birthweight or premature rupture of membranes in women at low risk of preterm birth.61 However, two small studies in the review did show a decrease in
the risk of pre-term rupture of membranes and low birthweight in women with
previous pre-term birth who were treated for asymptomatic bacterial vaginosis.
Screening for asymptomatic bacterial vaginosis in women at low risk of preterm birth is not recommended.2,30,62 Women at increased risk for pre-term birth
may be offered vaginal swab testing and treatment for asymptomatic bacterial
vaginosis. Women with symptoms of bacterial vaginosis may also be offered
testing and treatment for symptom resolution.3,62 Possible adverse effects from
treatment need to be taken into account.
Mineral and vitamin deficiency screening and supplementation
Pregnancy increases nutritional demands on the body. This can exacerbate
underlying nutritional deficiencies and lead to potentially adverse effects on
the mother.63 A pregnant woman’s nutritional status influences the growth and
development of the fetus and forms the foundation for the child’s later health.64
Women from socioeconomically disadvantaged groups and those with limited
access to fresh foods may have nutritional deficiencies. Current guidelines
suggest that pregnant women with risk factors for nutritional deficiencies may
benefit from a multinutrient preparation.2 Although there are demonstrated
benefits from iron and folic acid supplementation, there is limited evidence of
improved pregnancy outcomes from multiple micronutrient supplements.63
Further, there is evidence that vitamin A, C or E supplements may in fact cause
harm and so these are not recommended for use in pregnancy.2
The following describes the micronutrients that are particularly important in
pregnancy.
Vitamin D
Ninety percent of vitamin D is obtained through synthesis in the skin from sun
exposure and the vitamin D status of a newborn is determined by the vitamin
D status of its mother. Risk factors for vitamin D deficiency include darker skin,
season, and a BMI greater than 30.65,66 A history of limited sun exposure is also
a risk factor but the association is weaker.65 Some studies have shown vitamin
D deficiency in pregnancy to be associated with an increased risk of preeclampsia and gestational diabetes, although these studies are not consistent.67
Other population based studies have shown an association between maternal
vitamin D deficiency and lower birthweights and small for gestational age
Antenatal care
babies.68 Lack of vitamin D may adversely affect fetal bone mineralisation and
tooth enamel, increase the risk of hypocalcaemic fits in babies, cause rickets in
children and osteomalacia in adults, although these consequences are rare.69
There is mounting evidence of the prevalence of vitamin D deficiency in pregnant
Australian women. A recent study showed a vitamin D deficiency (levels less
than or equal to 25 nmol/L) or insufficiency (levels between 26 and 50 nmol/L)
prevalence of 35% in Canberra and 25.7% in outer southwest Sydney.65 Other
studies have found deficiency prevalence ranging from 5.2% in Victoria66 to 15%
in Sydney.70 However, there have been few studies on the prevalence of vitamin
D deficiency in the Aboriginal and Torres Strait Islander population of Australia.
One small study in Adelaide did show some evidence of vitamin D deficiency in
Aboriginal women.71 Another more recent study, also in South Australia (n=58),
found vitamin D insufficiency to be highly prevalent among Aboriginal adults, with
low mean values in all seasons other than summer.72
Vitamin D supplementation during pregnancy improves serum levels in both
mothers and their babies and importantly no adverse effects have been
reported.73 The question remains, however, whether routine supplementation
improves pregnancy outcomes. Currently there is no evidence to suggest that
routine supplementation improves pregnancy outcomes in healthy women
without risk factors for vitamin D deficiency. There may be some benefit from
supplementation in women at risk of deficiency but the evidence is limited.2,46
Further research is required to determine the optimal timing and dosing of
vitamin D supplementation in pregnancy. Therefore decision making about
whether to offer screening for vitamin D deficiency in pregnancy should take
into consideration the individual’s risk factors, the season and climate.2 In
women with proven vitamin D deficiency, supplementation should be initiated,
depending on the level of severity and the clinical situation.
Iron
Pregnancy increases the body’s demand for iron due to the expanded red cell
volume, the demands of the developing fetus and placenta and blood loss
around the time of delivery. Iron deficiency is the most common cause of anaemia
in pregnancy in Central Australia and the Top End of the Northern Territory.3
Depending on the level of severity, anaemia can cause tiredness in the mother,
heart failure and increased chance of postpartum anaemia. Low iron stores in the
mother can cause anaemia in the baby, which is associated with developmental
delay. Risk factors for reduced iron stores early in pregnancy include poor diet,
five or more previous pregnancies, adolescent pregnancy, multiple pregnancy and
recent or current breastfeeding of another child.3 Universal screening for anaemia
in pregnancy is advised in all pregnancy guidelines.2,3,46,74
Although routine oral iron supplementation in pregnancy has been
demonstrated to reduce the incidence of anaemia there is a paucity of
evidence assessing its outcome on other clinically relevant maternal and
neonatal outcomes such as low birthweight, pre-term birth, delayed
development and infection.75 Because oral iron supplementation can cause
dose related gastrointestinal side effects and haemoconcentration75,76
routine supplementation of women with normal haemoglobin levels is
not recommended during pregnancy.2,46 Iron supplementation should be
considered in pregnant women who are anaemic, particularly if they are
symptomatic or have other health concerns.2,3 In women with proven iron
deficiency, iron supplementation should be initiated, depending on the level of
severity and the clinical situation.
165
166
Antenatal care
Folic acid
There is strong evidence that folic acid supplementation protects against
neural tube defects in pregnancy.77–79 In Australia, although there has been a
reduction in the incidence of babies born with neural tube defects in the general
population, there has not been a reduction in incidence for Aboriginal babies.80
One study found the prevalence of neural tube defects in Aboriginal and Torres
Strait Islander babies in Western Australia to be almost double that of the nonIndigenous population.81 This may, in part, be due to lower levels of folate intake
through restricted food choices. There is also evidence that knowledge about
the benefits of folic acid supplementation is at a lower level among Aboriginal
and Torres Strait Islander women, particularly adolescents.81
Daily supplementation with folic acid (400–500 mcg) is recommended
for all pregnant women, prior to conception and for the first 12 weeks of
pregnancy.2,3,46 Specific attention needs to be given to promoting folic acid
supplementation to Aboriginal and Torres Strait Islander women of childbearing
age and providing information to individual women at the first antenatal visit.2
Higher doses of folic acid (5 mg) are recommended for women at increased risk
of neural tube defects.3,74,82 These include women with a previous pregnancy
with a neural tube defect, pre-pregnancy diabetes, multiple pregnancy,
haemolytic anaemia and women on anticonvulsant medication.
Iodine
In Australia there is documented prevalence of mild to moderate iodine
deficiency in school children, healthy adults, pregnant women and people with
diabetes.83 Data are lacking on the prevalence of iodine deficiency among
Aboriginal and Torres Strait Islander communities. Iodine requirements increase
substantially in pregnancy and lactation to support the neuropsychological
development of the fetus. Mandatory fortification of bread is estimated to
increase population intakes by an average of 46 mcg per day. This will meet
the needs of most of the population but an increased intake in pregnant and
lactating women would be desirable. A recent National Health and Medical
Research Council literature review concluded that there is good evidence for the
safety and efficacy of iodine supplementation in pregnant and lactating women
and the risks of iodine deficiency significantly outweigh any potential risks during
the perinatal period.84 On this basis, iodine supplementation (up to 150 mcg per
day) is recommended for pregnant women in Australia.
Diabetes
Diabetes in pregnancy can include pre-existing known type 1 or type 2
diabetes, undiagnosed pre-existing diabetes and gestational diabetes,
which is defined as the onset of glucose intolerance in the second half of
pregnancy. All forms of diabetes in pregnancy have increased risks for both
the mother and baby, depending on the level of glycaemic control. Diabetes
in pregnancy is associated with an increased risk of induced labour, pre-term
birth, caesarean section and pre-eclampsia. Babies of mothers with diabetes in
pregnancy have higher rates of stillbirth, fetal macrosomia, low APGAR scores,
neonatal hypoglycaemia, and admission to special care baby units.85 Babies
born to mothers with pre-existing diabetes have a higher risk of congenital
malformations of the spine, heart and kidneys.86 In addition, there is evidence
that an adverse intrauterine environment is a risk factor in later life for metabolic
Antenatal care
disturbances in the babies of diabetic mothers. Raised maternal glycaemic
levels are associated with increased adiposity in childhood and other adverse
metabolic factors that may increase the risks of cardiovascular disease and
diabetes.87,88 Women with gestational diabetes also have an increased risk
of developing type 2 diabetes later in life and an increased risk of gestational
diabetes in subsequent pregnancies.
The number of women with undiagnosed pre-pregnancy type 2 diabetes and
gestational diabetes mellitus in the general population is increasing.89 Aboriginal
and Torres Strait Islander women are 10 times more likely to have pre-existing
type 2 diabetes and 1.5 times more likely to develop gestational diabetes than
non-Indigenous women.85 Therefore a large proportion of Aboriginal and Torres
Strait Islander women will have known or undiagnosed diabetes mellitus at
antenatal booking.
There is currently a lack of uniformity in the approach to diagnosing gestational
diabetes.90 The International Association of Diabetes and Pregnancy
recently published new recommendations for the diagnosis of diabetes in
pregnancy, which should provide a more consistent approach to diagnosing
both pre-existing diabetes in pregnancy and gestational diabetes.91,92 These
recommendations are based on data showing that there appears to be a linear
association between maternal plasma glucose concentration and adverse
pregnancy outcomes, including at levels below the previous criteria for a
diagnosis of gestational diabetes.91 It is likely that the International Association
of Diabetes and Pregnancy recommendations will be adopted in forthcoming
Australian guidelines (Table 9.1).
Although specific management recommendations are beyond the scope of this
guide, studies have shown that even for mild gestational diabetes, treatment
with diet and lifestyle modifications decreases the incidence of fetal macrosomia
and pre-eclampsia.93,94 Strict glycaemic control is the foundation of diabetes
management in pregnancy. Specific management guidelines are recommended
for further guidance (see Resources).
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168
Antenatal care
Recommendations: General assessment at the first antenatal visit
Level/
strength
of
evidence
References
Discuss and plan the schedule of antenatal
At first antenatal
visits with the pregnant woman based on her visit
individual needs
For an uncomplicated pregnancy review every
4 weeks until 28 weeks, then every 2 weeks
thereafter
IB
2,95
Offer an ultrasound to determine gestational
At first antenatal
age and detect multiple pregnancies (best
visit
performed between 8 and 13 weeks + 6 days
gestation)
IIIB
Measure blood pressure, height and weight
and calculate BMI
Repeated weighing during pregnancy should
be confined to circumstances where clinical
management is likely to be influenced
At first antenatal
visit
Opportunistic
IIIB
Auscultate for heart murmurs, in areas with a
high prevalence of rheumatic heart disease
At first antenatal
visit
GPP
Preventive
intervention
type
Who is at
risk?
Screening
All pregnant
women
Immunisation
How often?
GPP
Advise women to have oral health checks and At first antenatal
treatment if required (see Chapter 4: Dental
visit
health)
IIB
Offer Pap test if due
During first
trimester
GPP
Offer testing for rubella immunity
At first antenatal
visit
IIB
Check blood group and antibodies
At first antenatal
visit and 28
week visit
IB
Discuss the purpose and implications of
testing for chromosomal abnormalities to
promote an informed decision
In those wishing to proceed offer women
first trimester combined screeningβ for
chromosomal abnormalities between 11 and
13 weeks + 6 days gestation
Provide support to women in regional and
remote areas to access this screening. If
nuchal thickness ultrasound is unavailable,
offer maternal serum screening† between 15
and 17 weeks gestation
At first antenatal
visit
IB
Offer ultrasound to assess for fetal
morphology abnormalities
At 18–20 weeks
GPP
46
Pregnant
women at
risk of preeclampsia‡
Offer proteinuria testing
At first antenatal
visit and each
subsequent visit
IIB
2
All pregnant
women
Review influenza immunisation status and
offer where appropriate (see Chapter 11:
Respiratory health)
Opportunistic
GPP
96
β First trimester combined screening includes nuchal thickness ultrasound and plasma beta human chorionic gonadotropin (beta-HCG)
and pregnancy associated plasma protein A (PAPP-A)
† Maternal serum screening includes plasma maternal serum alpha fetoprotein (AFP), unconjugated oestriol and total human chorionic
gonadotropin (HCG)
‡ Risk factors for pre-eclampsia include age >40 years, first or multiple pregnancy, BMI >30, diabetes, vascular or kidney disease,
personal or family history of pre-eclampsia, raised blood pressure at first visit, pregnancy interval >10 years
Antenatal care
169
Recommendations: Smoking cessation
Preventive
intervention
type
Who is at risk?
How often?
Level/
strength of
evidence
References
Screening
All pregnant
women
Regularly assess smoking
status and remind patients
to limit/avoid exposure to
cigarette smoke
At first and
subsequent
antenatal visits
IB
2,3,9,14,15
GPP
14,15
IB
2,9
IB
2,3,9,14,15
Record in the handheld
pregnancy record (if
available) or otherwise use
local protocols to record this
information
Behavioural
Pregnant women
who smoke
Offer interventions to assist
smoking cessation ranging
from brief advice to more
intensive, multicomponent
interventions (see Chapter 1:
Lifestyle)
Chemoprophylaxis
Pregnant women
who smoke
at least 10–15
cigarettes/day
requesting
additional
assistance with
smoking cessation
Consider nicotine
At each antenatal
replacement therapy (NRT)
visit
with discretion, noting that
the safety of NRT in terms of
effect on fetal development
and birth outcomes remains
unclear
Discuss the risks and
benefits taking into account
overall clinical circumstances
If deemed necessary,
intermittent forms of NRT are
recommended rather than
continuous use formulations
to reduce the total dose of
nicotine
At first and
subsequent
antenatal visits
3,19
170
Antenatal care
Recommendations: Genitourinary and bloodborne virus infections
Preventive
intervention
type
Who is at
risk?
How often?
Level/
strength of
evidence
References
Screening
Pregnant
women aged
<25 years
Offer chlamydia testing with a
nucleic acid amplification test
(NAAT), most commonly by
PCR, using either a first void
urine, self obtained low vaginal
swab or endocervical swab
At first antenatal
visit
IIC
2,3,30
Pregnant
women from
communities
with a high
prevalence of
STIs
Offer testing for chlamydia as
above and consider testing for
gonorrhoea
At first antenatal
GPP
visit and consider
repeat testing at 36
weeks gestation
2,3
All pregnant
women
Pregnant
women from
communities
with a high
prevalence of
STIs
Offer testing for syphilis, HIV
and hepatitis B
Hepatitis C (HCV) testing is
not routinely recommended.
Screening may be discussed if
there are identifiable risk factors
for HCV infection (see Chapter
8: Sexual health, for risk factors)
Offer additional tests for syphilis
infection
At first antenatal
visit
At 28 weeks
gestation and at
birth
IA–IIB
2,3,46
All pregnant
women
Offer testing for asymptomatic
bacteriuria with a midstream
urine microscopy and culture
At first antenatal
visit
IA
2,3,30,62
GPP
2
GPP
2
GPP
2
In areas with limited access to
pathology testing, dipstick urine
tests may be used to exclude
asymptomatic bacteriuria
but positive results must be
confirmed by midstream urine
culture
Environmental
Women with
previous preterm birth
Offer vaginal swab testing and
treatment for asymptomatic
bacterial vaginosis (eg.
Gardnerella vaginalis,
Bacteroides spp.)
Women with
positive results
for an STI or
bloodborne
virus
Ensure adequate recall systems N/A
are implemented for follow up
Recommend partner treatment
and contact tracing
(See Chapter 8: Sexual health
and bloodborne viruses)
Before 20 weeks
pregnancy
Antenatal care
171
Recommendations: Alcohol consumption
Preventive
intervention
type
How often?
Level/
strength of
evidence
References
Screening
All pregnant
women
At first and
subsequent
antenatal visits
GPP
3
Behavioural
All pregnant
Advise that not drinking alcohol
women and
is the safest option in pregnancy,
women planning particularly in the first 3 months
a pregnancy
At first and
subsequent
antenatal visits
(as appropriate)
GPP
2
Pregnant
women who
drink alcohol
At first and
subsequent
antenatal visits
GPP
3,46
Ask about alcohol consumption
Advise women to avoid getting
drunk
Advise women to have no more
than two standard drinks on
any 1 day and fewer than seven
standard drinks in 1 week
Recommendations: Nutritional assessment and supplementation
Preventive
intervention
type
How often?
References
Level/
strength of
evidence
Screening
All pregnant
women
Offer a full blood examination to
assess for anaemia
At first antenatal
visit, and at 28 and
36 weeks gestation
1A
Women at
risk of vitamin
D deficiency
(limited sun
exposure, dark
skin, BMI >30)
Consider testing for vitamin D
levels, particularly in the nonsummer months
At first antenatal visit GPP
2,46,65,74,82,97,98
Behavioural
All pregnant
women
Provide information on the
benefits of a healthy diet in
pregnancy and give practical,
tailored advice on healthy eating
Early in pregnancy
3,46
Chemoprophylaxis
All pregnant
women
and those
considering
pregnancy
Recommend 500 mcg of folic
acid daily to reduce the risk of
newborn neural tube defects
At least 1 month
IA
prior to pregnancy
and for the first 12
weeks of pregnancy
2,3,46,74,82
Women with
diabetes
Recommend a higher dose of 5
mg of folic acid daily to reduce
the risk of newborn neural tube
defects
At least 1 month
IC
prior to pregnancy
and for the first 12
weeks of pregnancy
46,74,97,98
Pregnant
women with
proven vitamin D
deficiency
Advise vitamin D
supplementation – dose titrated
according to clinical situation*
(see Resources)
At diagnosis
IIB
2,46,73,82
N/A
IB
2,46,76
IB
3,74,75
Pregnant women Routine iron supplementation is
who are not iron not recommended
deficient
Pregnant women Offer iron supplementation – oral At diagnosis
with proven iron or intramuscular – dose titrated
deficiency
according to clinical situation
All pregnant
women
Offer iodine supplementation
with 150 mcg/day (see
Resources)
GPP
At first antenatal visit IIA
* Vitamin D supplementation is not subsidised under the Pharmaceutical Benefits Scheme
2,3,46
84
172
Antenatal care
Recommendations: Diabetes
Preventive
intervention
type
Who is at risk?
Screening
Pregnant women at
risk of undiagnosed
diabetes mellitus
(BMI >30 kg/m2,
family history of
diabetes, previous
gestational diabetes)
Measure fasting blood glucose At first
antenatal visit
If not feasible, alternatives
include random blood glucose
or HbA1c (see Chapter 14: Type
2 diabetes prevention and early
detection)
Pregnant women
Perform a 75 g 2 hour oral
who do not have
glucose tolerance test (OGTT)
pre-existing diabetes for diagnosis of gestational
diabetes (see Table 9.1 and
Table 9.2)
How often?
Between 24
and 28 weeks
gestation
If a 2 hour OGTT is consistently
difficult to achieve, consider
alternative tests such as a
random blood glucose or a 50
g, 1 hour glucose challenge.
If either are abnormal then
recommend a 75 g 2 hour oral
OGTT
Behavioural
Level/
strength of
evidence
References
IA
3,92
IA
92
GPP
74
GPP
3,99
Women postpartum
diagnosed with
gestational diabetes
Perform a 75 g fasting OGTT
Pregnant women
with diabetes
Offer advice and resources
At diagnosis
to promote good glycaemic
control throughout pregnancy
– encourage a healthy diet and
exercise
Consider referral to specialist
services, where available, and
consult specific management
guidelines for ongoing care (see
Resources)
IA
91,99
Non-pregnant
women who have
had gestational
diabetes in the past
Advise women of the future
risk of developing diabetes
and give advice about healthy
diet, exercise and weight (see
Chapter 1: Lifestyle)
Screen for diabetes with a
fasting blood glucose (see
Chapter 14: Type 2 diabetes
prevention and early detection)
IIB
3,99,100
At 6 weeks
postpartum
At postpartum
checks and
as part of an
annual health
assessment
Antenatal care
Table 9.1. The International Association of Diabetes and
Pregnancy Guidelines for diagnosing pre-existing diabetes
and gestational diabetes in pregnancy*
Diagnostic criteria for pre-existing diabetes
One of the following measures of glycaemia is recommended for diagnosing
pre-existing diabetes. If random plasma glucose is used, the diagnosis should be
confirmed with either a fasting plasma glucose or HbA1c
Measure of glycaemia
Consensus threshold
FPG (fasting plasma glucose)
≥7.0 mmo/L
Hb1c
≥6.5%
RPG (random plasma glucose)
≥11.1 mmol/L (confirmation with FPG/ HbA1c
recommended)
Diagnostic criteria for gestational diabetes
Using a 75 g 2 hour oral glucose tolerance test, one or more of these values is
diagnostic of gestational diabetes
Glucose measure
Glucose concentration
FPG
≥5.1 mmol/L*
1 hour plasma glucose
≥10 mmol/L
2 hour plasma glucose
≥8.5 mmol/L*
* At the time of writing these criteria had not been published by the Australian Diabetes in Pregnancy Society. Current criteria for gestational diabetes are FPG ≥5.4 mmol/L and 2 hour
plasma glucose ≥7.9 mmol/L
Source: Metzger BE, Gabbe SG, Persson B, et al 201092
Table 9.2. Current interpretive criteria for 75 g OGTT in
pregnancy in Australia
Glucose measure
Glucose concentration
Fasting
Above 5.4
2 hour
Above 7.9
Resources
Guidelines for management of diabetes in pregnancy (Australasian Diabetes in
Pregnancy Society)
www.ranzcog.edu.au/publications/statements/coll-end-statements/ADIPS-gdmmanagement-guidelines
Screening guideline for gestational diabetes (Kimberley Aboriginal Medical Services
Council)
http://resources.kamsc.org.au/downloads/cd_dip.pdf
Guidelines for treatment of vitamin D deficiency (King Edward Memorial Hospital)
www.kemh.health.wa.gov.au/development/manuals/O&G_guidelines/sectionb/1/
b1.1.9.pdf
Dietary guidelines for Australian adults (NHMRC)
www.gofor2and5.com.au/DataStore/files/pdf/n33.pdf
Iodine, public statement: iodine supplementation for pregnant and breastfeeding women
(NHMRC)
www.nhmrc.gov.au/_files_nhmrc/publications/attachments/new45_statement.pdf
173
174
Antenatal care
Clinical practice guidelines on depression and related disorders in the perinatal period
(beyond blue)
www.beyondblue.org.au/index.aspx?link_id=6.1246
Australian guidelines to reduce health risks from drinking alcohol (NHMRC)
www.nhmrc.gov.au/_files_nhmrc/publications/attachments/ds10-alcohol.pdf.
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100.Colagiuri S, Davies D, Girgis S, Colagiuri R. National evidence based guideline for case detection and diagnosis
of type 2 diabetes. Canberra: NHMRC and Diabetes Australia, 2009. Cited October 2011. Available at www.
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177
Chapter 10
Mental
health
Author Tim Senior
Expert reviewer Patricia Delaney
Mental health
Prevention of depression
Background
The National Mental Health Plan 2003–08 notes that mental health is an area
where ‘diverse views exist and ... terms are used in different ways’.1 The term
‘social and emotional wellbeing’ is often used in Aboriginal and Torres Strait
Islander communities when discussing what clinicians might consider to be
‘mental health’, as it implies a holistic, strengths-based approach rather than a
medical model.
Social and emotional wellbeing is a key component of the Aboriginal definition
of health, includes concepts of connection to country, kin and community and
is a view held across the whole lifecycle. However, much of the research in this
area is done in settings outside Indigenous communities and is grounded within
a more individualistic model of health. As such, inclusion criteria and outcomes
are determined by diagnostic categories such as those in the Diagnostic and
Statistical Manual of Mental Disorders, 4th edition (DSM-IV) (Table 10.1). In
looking at evidence to make recommendations for the prevention of depression
and suicide, this chapter recognises there can be tensions between biomedical
and Indigenous concepts of mental health and that traditional research evidence
may not be suitable in this context, particularly when assessing the suitability of
community based interventions.
Table 10.1. DSM-IV criteria for a depressive episode
• Five (or more) of the following symptoms have been present during the same
2-week period and represent a change from previous functioning; at least one of the
symptoms is either depressed mood or loss of interest or pleasure
• Depressed mood most of the day, nearly every day
• Markedly diminished interest or pleasure in all, or almost all, activities most of the day,
nearly every day
• Significant weight loss when not dieting or weight gain
• Insomnia or hypersomnia nearly every day
• Psychomotor agitation or retardation nearly every day
• Fatigue or loss of energy nearly every day
• Feelings of worthlessness or excessive or inappropriate guilt nearly every day
• Diminished ability to think or concentrate, or indecisiveness, nearly every day
• Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a
suicide attempt or a specific plan for committing suicide
• In addition the episode must interfere with the person’s daily routine or relationships,
and not have a cause such as alcohol or other drugs, a physical illness or the death of
a loved one
Source: American Psychiatric Association 200013
The extent of depression in Aboriginal and Torres Strait Islander communities
is recognised to be a large problem, though it has been difficult to measure
accurately. The National Aboriginal and Torres Strait Islander Health Survey
(NATSIHS) of 2004–05 contained questions looking at social and emotional
wellbeing (rather than depression).2 Age adjusted figures show that Aboriginal
and Torres Strait Islander people aged over 18 years are twice as likely as
non-Indigenous people to feel high or very high levels of psychological distress.
Similarly, hospitalisation rates for ‘mental and behavioural disorders’ are nearly
twice as high.
179
180
Mental health
NATSIHS also found high rates of self reported stress for Aboriginal and Torres
Strait Islander adults aged over 18 years compared to the general population
(Table 10.2).1 These stressors are interrelated, often linked to broader life
experiences, and include comorbidity associated with other medical conditions.
The high prevalence of these stressors in adults has effects on children. The
West Australian Aboriginal Child Health Survey found that 70% of children were
living in families that had experienced three or more significant life events in the
previous 12 months.3
Table 10.2. Proportions of stresses reported in the previous
12 months, by Indigenous status, year and stressor type,
Australia, 2004–05 and 2006
Type of stressor
Death of a family member or friend
Serious illness or disability
Not able to get a job
Alcohol or drug related problem
Overcrowding at home
Members of a family sent to jail/in jail
Witness to violence
Trouble with police
Discrimination/racism
Any stressor
Indigenous status/year
Indigenous
Total population
2004–06
2006
42
23
28
30
17
13
25
8.6
17
–
19
–
14
3.9
16
3.9
12
–
77
59
Source: ABS, 200640 ABS, 200731
Notes: 1. Proportions are expressed as percentages
2. The total population for ‘serous illness or disability’ data has been estimated by adding
proportions for the two sub-components, so may slightly overstate the true proportion
These figures show the levels of psychological distress and significant life
events in Aboriginal and Torres Strait Islander communities around Australia.
While there are no data that translate these into specific diagnoses within the
community, admissions for a principal diagnosis of ‘mental and behavioural
disorders’ were nearly twice as high for Aboriginal and Torres Strait Islander
people when compared with non-Indigenous people.1
The situations in which depression risk is greater and the situations in which
depression is more likely to be missed are outlined in Table 10.3.
Mental health
Table 10.3. Features of comprehensive support services
associated with improved outcomes from depression
screening
• An initial visit with a nurse specialist for assessment, education and discussion of
patient preferences and goals
• A follow up visit with a trained nurse specialist and ongoing support for adherence to
medication for those prescribed antidepressant medications
• A visit with a trained therapist for cognitive behavioural therapy
• A reduced copayment for patients referred for psychotherapy
• Professional support including the following:
– staff and clinician training (1 or 2 day workshops)
– availability of clinician manuals
– monthly training lectures
– academic detailing
– resource materials for clinicians, staff, and patients
• Institutional financial commitment
Source: O’Connor EA, Whitlock EP, Beil TL, Gaynes BN 20095
Screening for depression
A 2005 Cochrane review concluded that screening or case-finding instruments
for depression had little or no impact on the recognition, management or
outcome of depression in primary care or hospital settings.4 Evidence of
benefit from screening programs for depression has been demonstrated only
in settings where there is a substantial degree of supportive infrastructure.
Improved outcomes may be achievable where patients identified by the
screening program receive intensive support as part of a multifaceted
intervention.5 Where these intensive support services are available, sensitivity
and specificity that is comparable with other larger screening tools can be
achieved by asking the following questions:6
‘Over the past 2 weeks, have you felt down, depressed or hopeless?’
‘Over the past 2 weeks, have you felt little interest or pleasure in doing things?’
These two questions achieve 95% specificity and 66% sensitivity in general
populations. These questions have also been tested with Aboriginal people with
ischaemic heart disease attending an Aboriginal Medical Service in Darwin.7 In
this setting, a ‘Yes’ answer to either question was 100% sensitive and 12.5%
specific for depression, meaning that a negative result rules out depression but
there are many false positives. It is not clear how applicable this result is in other
Aboriginal and Torres Strait Islander communities or people without ischaemic
heart disease. Further, there is evidence to suggest that ‘probable depression’
detected with a screening tool may no longer be present 2 weeks later.8 This
suggests that repeat screening may be needed.
Although there is no evidence to suggest any harm from screening programs,
there are potential harms from treatment. Increased prescription of selective
serotonin reuptake inhibitor medications for depression is associated with an
increased risk of suicidal ideation and, in older people or those on non-steroidal
anti-inflammatory drugs, upper gastrointestinal bleeding.5 A natural desire to
use a screening tool across a population to identify and treat depression would
need to take the risk of harm into account. Given this evidence, the mainstay
of depression should continue to be the use of a careful clinical assessment in
181
182
Mental health
the context of an ongoing relationship with the patient, and the judicious use of
antidepressants as part of a management plan that includes ongoing support
from skilled healthcare professionals aware of the local culture and context.
In a systematic review commissioned by the US Preventive Health Task
Force,5 the minimum support needed to demonstrate a beneficial effect from
depression screening was availability of a nurse who screened patients,
reported the results to the physician and provided a protocol that facilitated
referral for behavioural treatment.
Interventions with the greatest beneficial effect are complex. Table 10.4
highlights the features most strongly associated with improved outcomes.
Working as part of a team, including Aboriginal and Torres Strait Islander health
workers, is considered good practice in Aboriginal and Torres Strait Islander
health. The lack of published research evidence in this area should not be
considered evidence of lack of effect.
Table 10.4. People at greater risk for depression
• Exposure to adverse psychosocial events, such as unemployment, divorce or poverty
• A previous history of depression or suicide attempts
• A history of physical or sexual abuse
• A history of substance abuse
• Presence of other chronic diseases, including chronic pain
• Multiple presentations to health services may also be an indicator of depression.
Factors that make it more likely that depression will be missed include:
– limited consultation time
– presentations of mostly physical or atypical symptoms
– health professional attitudes – eg. the belief that nothing can be done, or that
depression is a normal response to stress
– communication difficulties
Source: National Collaborating Centre for Mental Health and the Royal College of Psychiatrists
20106
Interventions to prevent depression
There is insufficient evidence to recommend behavioural programs to prevent
depression. There is weak evidence that psychosocial interventions in the
elderly may have a small effect on preventing depression.9 There is some
evidence that exercise is mildly beneficial in prevention of depression for children
and adolescents.10
There is currently limited evidence that interventions targeting children and
adolescents in other settings such as communities, schools and workplaces are
effective for children or adolescents in the long term.11 There is weak evidence
that social activities for older people can produce statistically significant
reductions in symptoms of depression, however the magnitude of effect is
unlikely to be clinically significant.9
There is no evidence to support the use of antidepressants medication for
primary prevention of depression in the general population.
Mental health
183
Recommendations: Depression prevention
Level/
strength of
evidence
References
Screening for depression is
N/A
not routinely recommended
unless comprehensive support
services are available (see
Table 10.3 )
IB
5
In the absence of services
outlined in Table 10.3, useful
support services include
those provided by social and
emotional wellbeing workers
and Aboriginal mental health
workers and psychologists with
an understanding of the local
context (see Resources)
GPP
12
If comprehensive support
services are not available then
assess for the presence of risk
factors for depression (see
Table 10.4)
GPP
6
People in whom
depression risk
is greater (see
Table 10.4)
Take a patient history to assess Opportunistic
mood and consider asking:
1B
6
All people aged
15+ years
Behavioural interventions
are not recommended for
prevention of depression
N/A
ID
9–11
Chemoprophylaxis All people aged
15+ years
Medications are not
recommended for primary
prevention of depression
N/A
GPP
N/A
IC
9,11
Preventive
intervention type
Who is at risk?
Screening
All people aged
15+ years
Behavioural
Environmental
All people aged
15+ years
How often?
• ‘Over the past 2 weeks, have
you felt down, depressed or
hopeless?’
• ‘Over the past 2 weeks,
have you felt little interest or
pleasure in doing things?’
(See Table 10.1 for diagnostic
criteria)
Community based
N/A
psychosocial programs are not
recommended for prevention of
depression
184
Mental health
Prevention of suicide
Background
Aboriginal and Torres Strait Islander people die from intentional self harm at
higher rates than non-Indigenous Australians in all states and territories. Overall,
deaths from intentional self harm in Aboriginal and Torres Strait Islander men are
2.4 times that of non-Indigenous men, and 1.7 times higher for Aboriginal and
Torres Strait Islander women. Deaths from intentional self harm occur at a much
younger age in Aboriginal and Torres Strait Islander people – around three times
higher for those aged under 25 years and for those aged 25–34 years.1 Rates of
suicide have increased over the past 3 decades.14
Research from Aboriginal communities suggests that suicide is less closely
connected with biomedical models of ‘mental health’ and has different
sociocultural meanings within those communities. Suicide may need to
be conceptualised within a broader paradigm characterised by exclusion
and disadvantage, rather than merely as part of a mental health diagnosis.
Consequently conventional suicide prevention measures based on biomedical
models of care may not meet community expectations. The method of suicide
chosen (especially by young men) and the close-knit nature of community can
impact on help seeking behaviour and have substantial impact on the family and
the community. Thus, suicide prevention measures are more likely to succeed
if they are implemented by people who are fully aware of local context. Once
again, it is important for health practitioners to work with the local Aboriginal
and Torres Strait Islander mental health workforce where available.
Screening
There is no evidence that screening for suicide risk leads to a reduction in
intentional self harm morbidity and suicide related mortality rates.15 There are
several tools available for screening for suicidal ideation, however, only one has
been validated in a primary healthcare setting: the Symptom Driven Diagnostic
System for Primary Care (SDDS-PC).16 This tool has 62 items, three of which
relate to suicidal ideation. Although individual questions in this tool are reported
to have good specificity and sensitivity, the positive predictive value is very
low. This means that many people have to be screened to prevent one suicide.
Although there is no analysis of adverse outcomes from screening tests for
suicide, the fact that large numbers may be screened without benefit suggests
there may be potential for harm. In the absence of any clear evidence on
screening, clinicians should use their clinical judgement based on knowledge
of the person and their community to assess the risk of suicide. It is worth
emphasising that this is not a recommendation not to screen for suicide risk, but
that the application of a uniform set of questions applied at a population level
has not shown any benefit. Clinicians should think of the possibility of suicide
and explore this, especially in those with:
• a past history of intentional self harm
• a history of mood disorders
• hazardous alcohol consumption or use of other recreational drugs.
Mental health
Managers of health services should note, too, that education of physicians has
also been shown to reduce suicide rates.17 Given the clustering of suicide in some
Aboriginal and Torres Strait Islander communities,18 practitioners should consider
the impact on and their response to other community members also. (See
Resources for useful information for health professionals.)
Interventions to reduce suicide risk
There is currently no evidence showing a favourable effect of behavioural
interventions on people with suicidal ideation or suicidal behaviour, though there
are some promising results for cognitive behavioural therapy or interpersonal
therapy in those at risk. However, in these studies there are a large number of
participants who have withdrawn from the study.19 There is also some evidence
that these interventions may work by ‘enhancing effective contact with those who
are suicidal’ and that other services such as telephone support or befriending
services also have some impact.20
Chemoprophylaxis in the context of suicide prevention can be thought of as
the use of pharmacological agents in mental health conditions, which prevents
suicidal behaviour or deliberate self harm. This is particularly important given that
some antidepressants have been reported to cause suicidal ideation, especially
in adolescents. At a population level there is some evidence that suicide rates are
reduced, but this is not so for individual patients with depression.21 There is no
good evidence that pharmacological treatment is effective at preventing suicide
or deliberate self harm attempts in personality disorders, bipolar disorder or
schizophrenia.22–24 As suicide is a rare event, trials are likely to be underpowered
to pick up reduced suicide rates. The goal of antidepressant treatment is
improvement in symptoms and functioning, rather than suicide prevention.
There is evidence that certain environmental measures are effective in reducing
suicide rates. Interventions that have been shown to be effective include
restricting the prescription of potentially lethal medications, restricting access to
over-the-counter medications, and legislation to restrict access to toxic chemicals
and firearms. Other broader environmental strategies, such as media policies,
school programs and education of the general public, may be effective, although
there is no clear evidence to support this at present.17 Evidence from population
studies strongly suggests that improving access to primary healthcare services in
general, and mental health services in particular, will also reduce suicide rates.25
This is particularly important for Aboriginal and Torres Strait Islander people, who
have been shown to access health services much less often than non-Indigenous
Australians prior to a suicide attempt.26
185
186
Mental health
Recommendations: Suicide prevention
Preventive
intervention type
Who is at risk?
How often?
Level/
strength of
evidence
References
Screening
All people
Screening for suicide risk is not
routinely recommended
N/A
IC
15,19
People with any one of Consider asking about past and
Opportunistic GPP
the following:
current suicidal ideation and intent
as part of a comprehensive medical
• past history of
intentional self harm history
15,17
• a history of mood
disorders
• hazardous alcohol
consumption or use
of other recreational
drugs
All people
No specific behavioural
interventions are recommended for
prevention of suicide
N/A
IC
15
People at increased
risk of suicide from
history or clinical
judgement
Consider local methods of
enhancing effective contact with
volunteer or professional agencies,
particularly access to Aboriginal
mental health workers
Ongoing
IIIC
20
Chemoprophylaxis
All people
Medication is not recommended
N/A
for the prevention of suicide
beyond a clinically indicated use
for diagnosed conditions (eg. major
mental illness)
IB
21–24,27,28
Environmental
Communities
Remove access to lethal methods
of suicide both in the community
and the household
IC
17
Communities
Advocate for community based
Ongoing
health promotion programs that
holistically address the multifactorial
nature of social and emotional
wellbeing (eg. sports events, caring
for country programs, healthy
lifestyle festivals)
GPP
N/A
Provide education for primary care
health professionals to recognise
and respond to psychosocial
distress and depression
Ongoing
IC
17
N/A
Integrating mental health services
with alcohol and other drug
services can improve service
access to youth who are at risk of
suicide
Ongoing
GPP
25
Behavioural
Ongoing
Resources
Australian Indigenous Mental Health (Royal Australian and New Zealand College of
Psychiatrists)
http://indigenous.ranzcp.org
Working together: Aboriginal and Torres Strait Islander mental health and wellbeing
principles and practice
www.ichr.uwa.edu.au/files/user5/Working_Together_book_web.pdf.
Mental health
References
1. Thomson N, MacRae A, Burns J, et al. Overview of Australian Indigenous health status. Health Infonet, April
2010 cited 2011 October 10. Available at www.healthinfonet.ecu.edu.au/health-facts/overviews.
2. Australian Bureau of Statistics. National Aboriginal and Torres Strait Islander Health Survey,2004–2005, cat. no.
4715. Canberra: ABS, 2006.
3. Zubrick SR, Silburn SR, Lawrence DM, et al. The Western Australian Aboriginal Child Health Survey: the social
and emotional wellbeing of Aboriginal children and young people. Perth: Curtin University of Technology and
Telethon Institute for Child Health Research, 2005.
4. Gilbody S, House AO, Sheldon TA. Screening and case finding instruments for depression. Cochrane Database
Syst Rev 2005 Oct 19;Oct 19;(4):CD002792.
5. O’Connor EA, Whitlock EP, Beil TL, Gaynes BN. Screening for depression in adult patients in primary care
settings: a systematic evidence review. Ann Intern Med 2009;151(11):793–803.
6. National Collaborating Centre for Mental Health and the Royal College of Psychiatrists. Depression: the
treatment and management of depression in adults. London: Royal College of Psychiatrists, 2010.
7.
Esler D, Johnston F, Thomas D, Davis B. The validity of a depression screening tool modified for use with
Aboriginal and Torres Strait Islander people. Aust N Z J Public Health 2008;32(4):317–21.
8. Gunn JM, Gilchrist GP, Chondros P, et al. Who is identified when screening for depression is undertaken in
general practice? Baseline findings from the Diagnosis, Management and Outcomes of Depression in Primary
Care (diamond) longitudinal study. Med J Aust 2008;188(Suppl 12):S119–25.
9. Forsman AK, Schierenbeck I, Wahlbeck K. Psychosocial interventions for the prevention of depression in older
adults: systematic review and meta-analysis. J Aging Health 2011;23(3):387–416.
10. Larun L, Nordheim LV, Ekeland E, Hagen KB, Heian F. Exercise in prevention and treatment of anxiety and
depression among children and young people. Cochrane Database Syst Rev 2006;Jul 19;(3):CD004691.
11. Merry S, McDowell H, Hetrick S, Bir J, Muller N. Psychological and/or educational interventions for the
prevention of depression in children and adolescents. Cochrane Database Syst Rev 2004(1):CD003380.
12. Purdie N, Dudgeon P, Walker R. Working together: Aboriginal and Torres Strait Islander mental health and
wellbeing principles and practice. Canberra: Commonwealth of Australia, 2010. Cited January 2012. Available at
www.ichr.uwa.edu.au/files/user5/Working_Together_book_web.pdf.
13. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th edn, text revision.
Washington: American Psychiatric Association, 2000.
14. Hunter E, Milroy H. Aboriginal and Torres Strait Islander suicide in context. Arch Suicide Res 2006;10(2):141–57.
15. Gaynes B, West S, Ford C, Frame P, Klein J, Lohr K. Screening for suicide risk in adults: a summary of the
evidence for the US Preventive Services Task Force. Ann Intern Med 2004;140(10):822–35.
16. Broadhead WE, Leon AC, Weissman MM, et al. Development and validation of the SDDS-PC screen for multiple
mental disorders in primary care. Arch Fam Med 1995;4(3):211–9.
17. Mann JJ, Apter A, Bertolote J, et al. Suicide prevention strategies: a systematic review. JAMA
2005;294(16):2064–74.
18. Hunter E, Harvey D. Indigenous suicide in Australia, New Zealand, Canada, and the United States. Emerg Med
(Fremantle) 2002;14(1):14–23.
19. Robinson J, Hetrick SE, Martin C. Preventing suicide in young people: systematic review. Aust N Z J Psychiatry
2011;45(1):3–26.
20. Goldney R. Suicide prevention: a pragmatic review of recent studies. Crisis 2005;26(3):128–40.
21. Schneeweiss S, Patrick A, Solomon D, et al. Variation in the risk of suicide attempts and completed suicides
by antidepressant agent in adults: a propensity score-adjusted analysis of 9 years’ data. Arch Gen Psychiatry
2010;67(5):497–506.
22. Cardish R. Psychopharmacologic management of suicidality in personality disorders. Can J Psychiatry
2007;52(6 Suppl 1):115S–27S.
23. De Hert M, Correll C, Cohen D. Do antipsychotic medications reduce or increase mortality in schizophrenia? A
critical appraisal of the FIN-11 study. Schizophr Res 2010;117(1):68–74.
24. Ernst C, Goldberg J. Antisuicide properties of psychotropic drugs: a critical review. Harv Rev Psychiatry
2004;12(1):14–41.
25. Campo J. Youth suicide prevention: does access to care matter? Curr Opin Pediatr 2009;21(5):628–34.
26. Sveticic J, Milner A, De Leo D. Contacts with mental health services before suicide: a comparison of Indigenous
with non-Indigenous Australians. Gen Hosp Psychiatry 2011;Dec 8 (Epub ahead of print).
27. Mulder R. Antidepressants and suicide: population benefit vs. individual risk. Acta Psychiatr Scand
2010;122(6):442–3.
28. Stone M, Laughren T, Jones ML, et al. Risk of suicidality in clinical trials of antidepressants in adults: analysis of
proprietary data submitted to US Food and Drug Administration. BMJ 2009 Aug 11;339:b2880.
187
Section
Chapter
11 1
Physical
Respiratory
Activity
health
Pneumococcal disease, Influenza, Asthma, COPD
Author Penny Abbott
Expert reviewer Anne Chang
Bronchiectasis
and Chronic suppurative lung disease
Author Penny
Author Anne
ExpertChang
Reviewers Rowena
Respiratory health
Pneumococcal disease prevention
Background
The pneumococcus Streptococcus pneumoniae, is a Gram positive bacterium
with more than 90 serotypes determined by the polysaccharide composition
of its capsule. It is carried by 50% of the population. It can cause noninvasive
disease such as otitis media and bronchitis and can cause serious illness
through invasive pneumococcal disease (IPD): diseases such as pneumonia,
meningitis and septicaemia. Among infectious illnesses, IPD is a leading cause
of morbidity and mortality in children and adults.1,2 Pneumococcal pneumonia
is the most common clinical presentation of IPD in adults, while bacteraemia
accounts for more than two-thirds of cases in children.2 Pneumonia commonly
occurs in people with pre-existing illnesses, such as chronic obstructive
pulmonary disease (COPD), chronic renal failure, alcoholism and diabetes, and
deaths from pneumonia are most common in people with chronic respiratory
disease or in the elderly.3 IPD in children is more common in those with immune
deficiency and chronic disease.1
Aboriginal and Torres Strait Islander children and adults have a significantly
higher incidence of all pneumococcal disease than non-Indigenous Australians,
but detailed data are available only for IPD, which has been notifiable Australia
wide since 2001.4 The risk of IPD in Aboriginal and Torres Strait Islander
children under the age of 5 years is doubled and in young adults is raised
11-fold compared to non-Indigenous people. Pneumonia is the most common
communicable disease contributor to premature death in Aboriginal adults.4
Hospitalisation for pneumonia is four times more common in Aboriginal and
Torres Strait Islander people than in non-Indigenous Australians and up to eight
times higher in younger Aboriginal and Torres Strait Islander adults.3,4
Interventions
Pneumococcal immunisation is indicated for those most at risk of initially
contracting or developing serious complications from infection. Immunisation
with the 23-valent pneumococcal polysaccharide vaccine (23vPPV) is funded
for all Aboriginal and Torres Strait Islander people aged ≥50 years and for those
aged 15–49 years who have high risk underlying conditions. These high risk
conditions include being a current smoker, suffering alcohol related disease or
having a chronic disease such as COPD, chronic renal failure or diabetes.3,5 A
single revaccination is recommended after 5 years, and a second revaccination
is recommended at either 5 years after the first revaccination or at 50 years
of age (whichever is later) for those with high risk conditions.2 Although the
Therapeutic Goods Administration issued precautionary advice early in 2011
not to administer a second dose of Pneumovax 23 due to concern regarding
increased local reactions, the most recent statement at the time of writing now
recommends to revaccinate as per previous advice.6
Despite these indications, the overall health benefits of pneumococcal
vaccination in otherwise healthy adults remain uncertain. Vaccination appears
to be most beneficial for people with chronic disease, particularly COPD and
bronchiectasis.7–9 Pneumococcal immunisation is known to be effective in
preventing invasive bacteraemic pneumococcal pneumonia, but may be less
effective in immunosuppressed patients.2,7,10,11 Population level health benefits
have been seen since pneumococcal immunisation of Aboriginal and Torres
Strait Islander adults and children became funded nationally in 1999 and
189
190
Respiratory health
2001 respectively. In 2004, the rate of IPD in children younger than 2 years
had decreased in Indigenous children (91.5 per 100 000) to become similar to
their non-Indigenous peers (93.6 per 100 000).2 The effects of pneumococcal
vaccination on adults are not as substantial and clear as in children, and may
be in part due to the indirect effects of improved herd immunity from childhood
vaccination.4,12,13 There are ongoing studies into which vaccines are likely to
be most effective in preventing pneumococcal disease in adults,14,15 and into
the changing prevalence of different pneumococcal serotypes as a result
of vaccination.13,16 Although this improvement in outcomes is encouraging,
Aboriginal and Torres Strait Islander people of all ages continue to suffer higher
rates of pneumococcal disease compared with non-Indigenous people, despite
the immunisation programs in place.4,17
Immunisation programs targeting Aboriginal and Torres Strait Islander people
demonstrate substantially lower coverage than recommended, particularly
for adults where the indications are based on presence of risk factors rather
than age.4 In many Aboriginal and Torres Strait Islander communities, overall
immunisation coverage is higher than that in non-Indigenous settings but
the timeliness of recommended immunisations lags behind, leaving children
underimmunised for their age.18 Thus, lack of apparent effect of the 23vPPV
in the prevention of IPD and pneumonia in at risk Aboriginal and Torres Strait
Islander people may be related to poor uptake rather than vaccine failure.13,19
Surveillance studies in Queensland provide ‘circumstantial evidence’ for both
indirect and direct positive effect of pneumococcal immunisation in Aboriginal
and Torres Strait Islander adults, though there has been an accompanying rise
in different serotypes of pneumococcal disease in adults.13
There is a strong evidence base for the effectiveness of recall and reminder
systems in promoting immunisation in primary care.20 Primary care, community
based strategies to improve the uptake of adult pneumococcal vaccination are
therefore recommended (see Chapter 2: Child health, for childhood vaccination
recommendations).
Respiratory health
191
Recommendations: Pneumococcal disease prevention
Preventive
intervention
type
Who is at risk?
How often?
Level/
strength of
evidence
References
Immunisation
Healthy adults aged
≥50 years
See also Chapter
2: Child health, for
childhood vaccination
recommendations
Pneumococcal vaccine
(23vPPV) is recommended
for the prevention of invasive
pneumococcal disease
Opportunistic
A second
vaccination is
recommended 5
years later
GPP
2,4,21
People aged 15–49
years who are
smokers or have
an underlying high
risk conditions (eg.
chronic cardiac,
renal or lung disease,
diabetes, alcohol
related problems,
immunosuppression)
Opportunistic
A second
vaccination is
required 5 years
later
A third vaccination
is recommended
5 years later or at
50 years of age
(whichever is later)
IIC
2,3,6,11,22–24
N/A
Promote primary care,
N/A
community based strategies
to improve pneumococcal
vaccination uptake and
timeliness, particularly the
implementation of reminder/
recall systems
IA
20,25
Communities
Promote community
awareness of benefits
and timeliness of vaccines
and enhancing access to
vaccination services
Environmental
192
Respiratory health
Influenza prevention
Background
Influenza is a common respiratory disease caused by influenza A and B viruses.
These viruses cause minor or major epidemics of seasonal influenza in most
years, usually during the winter months. In 2009, the world experienced its first
pandemic influenza since 1968 after the emergence of the novel H1N1 influenza
strain. Aboriginal and Torres Strait Islander people were disproportionately
affected by the H1N1 influenza epidemic, being four times more likely to be
admitted to hospital and accounting for 13% of the total deaths.3,26,27 There
are calls for Aboriginal and Torres Strait Islander people to be acknowledged
as a high risk group requiring specialised planning to manage future influenza
outbreaks.28
The consequences of influenza in children and healthy adults at low risk are
mainly absenteeism from school and work. However, severe disease is more
likely with advanced age, lack of previous exposure to antigenically related
influenza virus, chronic conditions such as heart or lung disease, renal failure
and diabetes, chronic neurological conditions, pregnancy and smoking.2,29
Interventions
Administration of the current influenza vaccine before winter, provides protection
against the disease and its complications in up to 70% of those who are
vaccinated.27 Immunisation should be given annually, preferably in March to April
before the Australian flu season.2
In healthy adults, influenza vaccines have only a modest effect in reducing
influenza symptoms and working days lost and no effect on hospital admission
or complication rates.30
Recommendations for vaccination of all individuals over 65 years of age and all
individuals over the age of 6 months with chronic disease is made on the basis
of the higher risk of hospitalisation and complications from influenza in these
groups.2,31–33 As yet there is limited and conflicting evidence on the effectiveness
of influenza vaccination for people aged 65 years and over and for many groups
of people with chronic disease,30,34–36 though the evidence is clearer that
influenza vaccination is effective in decreasing complications in COPD23,37 and
diabetes.38,39
Influenza vaccination has been found to be effective in reducing infection
in children.29,40–42 During the 2010 influenza season, an excess number of
cases of febrile reactions and febrile convulsions were observed in paediatric
populations following immunisation with one of the registered seasonal trivalent
influenza vaccines. This led to the suspension of the provision of this particular
vaccine to children under the age of 5 years, however the Therapeutic Goods
Administration and the Australian Technical Advisory Group on Immunisation
continued to recommend other brands of seasonal influenza vaccine for
children for whom it was indicated.31 There is as yet limited evidence that
influenza immunisation for healthy children leads to a reduction in community
transmission of influenza.29,43 Influenza vaccination during pregnancy is
recommended based on the increased morbidity and mortality of pregnant
women who contract influenza, coupled with no evidence of harm from
immunisation in pregnancy.2,44
Respiratory health
Australian guidelines recommend annual influenza vaccine should be given to
all Aboriginal and Torres Strait Islander people aged 15 years and over in view
of their substantially increased risk of hospitalisation and death from influenza
and pneumonia.2 Effective strategies to promote influenza immunisation
should be undertaken at a community level, particularly the use of recall and
reminder systems,20,25,33,45 and should be tailored to the needs of the community
concerned.
Infection control measures such as handwashing, particularly with young
children, can be effective in preventing transmission of influenza.46 Healthcare
providers can potentially transmit influenza to high risk patients and it has been
shown that vaccinating the former protects those at high risk.2,47 Implementing
barriers to transmission, such as isolation, and hygienic measures (wearing
masks, gloves and gowns) can be effective in containing respiratory virus
outbreaks or in hospital wards.46 The more expensive (but uncomfortable) N95
respirators might be superior to simple masks. It is unclear if adding virucidals
or antiseptics to normal handwashing with soap is more effective.46
Two classes of antiviral drugs are available for the treatment and prevention of
influenza: the neuraminidase inhibitors, zanamivir and oseltamivir, which are
active against both influenza A and B; and the adamantanes, amantadine and
rimantadine, which are only active against influenza A.27 The neuraminidase
inhibitors (NIs) oseltamivir (taken orally) and zanamivir (inhaled) are approved
for use in Australia for the treatment and prevention of influenza A and B.48,49
Systematic reviews on the effectiveness of NIs for influenza prophylaxis in
inter-pandemic years have come to conflicting conclusions. They generally
show limited effectiveness in preventing influenza infection, its transmission
and its complications in otherwise healthy adults.50,51 Consequently NIs are
not recommended for the prevention of influenza in healthy adults.27,48,50,51
They may, however, have a role in the prophylaxis of at risk contacts of people
with influenza, particularly during pandemics.27,50 Studies of post-exposure
prophylaxis for 10 days have enrolled patients within 36–48 hours of exposure
to a household contact, and have demonstrated a protective efficacy of 78–89%
compared with expectant treatment at the onset of symptoms.48
The decision to use NIs for prevention of influenza in at risk individuals depends
on the assessment of the likelihood of influenza, the likely benefits of treatment
based on the presence of comorbidities and the risk of developing complications.
Treatment must be initiated early in order to maximise efficacy.48,50 When initiated
promptly, antiviral therapy can shorten the duration of influenza symptoms by
1–3 days; the benefit is greatest when given within the first 24–30 hours and in
patients with fever at presentation. Little to no benefit has been demonstrated
when treatment is initiated 2 days or more after the onset of uncomplicated
influenza.
The availability of antiviral drugs, including public health policies regarding
the distribution of the national stockpile, is also taken into consideration in
a pandemic situation.48 Post-exposure prophylaxis with NIs continues to be
recommended for vulnerable Aboriginal and Torres Strait Islander household
contacts during influenza outbreaks within communities.52
193
194
Respiratory health
Recommendations: Influenza prevention
Preventive
intervention type
Who is at risk?
How often?
Level/
strength of
evidence
References
Immunisation
All people aged
≥15 years
Offer influenza vaccine in the
pre-flu season months for the
prevention of influenza (March
to April)
Annually
GPP
2
Children with
chronic illness
aged 6 months to
14 years
Annually
IIC
2,11,31
Women who
are pregnant
or planning a
pregnancy
Part of routine
antenatal care
(see Chapter 9:
Antenatal care)
IIB
2,44
Healthcare
providers
Annually
GPP
2,47
N/A
GPP
2
IIIC
46
Behavioural
Children under 6
months of age
Influenza vaccination is not
recommended
Household
contacts of a
person with
influenza
Good hygiene practice, such
Opportunistic
as frequent handwashing
and covering the mouth on
coughing or sneezing, is
recommended to decrease the
spread of influenza, particularly
to reduce transmission from
children to other household
members
Healthcare
workers
Minimise exposure risk to
N/A
patients with influenza-like
illness by adhering to current
infection control guidelines
In addition to standard
infection control procedures,
personal protective equipment
is recommended during
influenza pandemics
Chemoprophylaxis Healthy adults
Environmental
Neuraminidase inhibitors (NIs)
are generally not indicated for
the prevention of influenza
N/A
48,53
IIB
50,51
People at high
risk of influenza
complications,
where there are
high levels of
circulating virus
Consider NIs for high risk
Opportunistic
individuals in close contact
with someone with a proven
case of influenza (ideally
initiated within 48 hours),
particularly in a pandemic
situation or where there is high
levels of circulating virus
GPP
27,50,52
N/A
Primary care, community
N/A
based strategies to improve
vaccination levels, particularly
using reminder/recall systems,
should be implemented
IB
20,25,33,45
Communities
Activities should also focus
on increasing community
awareness of benefits and
timeliness of vaccines for
vaccinations and enhancing
access to vaccination services
Respiratory health
Asthma
Background
Asthma is a chronic inflammatory disease of the airways that is characterised
by variable and recurring symptoms of airway obstruction and bronchial
hyper-responsiveness, often reversible spontaneously or with treatment. The
predominant features of the clinical history are episodic difficulty in breathing
and shortness of breath often accompanied by cough.54,55 After many years, the
reversibility of airflow limitation may be incomplete in some people with asthma
due to airways remodelling.55 Asthma is commonly known as ‘short wind’ in
some Aboriginal and Torres Strait Islander communities.56
The diagnosis of asthma is a clinical one. When asthma is suspected on the
basis of symptoms, spirometry, including reversibility testing, is the preferred
initial test to determine the presence and severity of airways obstruction.57
Children over 7 years of age are usually able to perform spirometry. However,
normal spirometry, particularly when the patient is not symptomatic, does not
exclude asthma.56,57
Asthma affects 15% of Aboriginal and Torres Strait Islander people, compared
to 10% of the non-Indigenous Australian population.58,59 Compared with nonIndigenous Australians, Aboriginal and Torres Strait Islander people have twice
the rate of hospitalisation and three times the rate of death due to asthma.59,60
Surveys indicate that asthma is 1.5–4 times more prevalent in Aboriginal and
Torres Strait Islander people residing in non-remote areas compared to those in
remote areas.60,61
A long term solution to decreasing the burden of asthma may be early detection
and prevention.62,63 However at this time few measures can be recommended
for the prevention of asthma, as the underlying causes and the development of
the disease are complex and incompletely understood.54
What is meant by the prevention of asthma can be variable, with the terms
primary and secondary prevention sometimes being used when referring to
prevention of symptom exacerbations in people with an existing diagnosis
of asthma through early treatment of exacerbations or long term control of
disease.54,56 However, for the purposes of this review, the literature definitions
of prevention of asthma have been followed. Primary prevention of asthma
is defined as prevention of the onset of asthma and secondary prevention is
defined as intervention(s) for infants and children who are at high risk for the
development of asthma due to the presence of atopic disease but who have
not yet developed asthma symptoms or signs.56,57,64 An exception to this is
the primary prevention of occupational asthma through avoidance of asthmacausing agents in the work place.54,65
It is accepted that environmental and lifestyle factors interact with genetic
factors, such as an allergic tendency, to increase the risk of developing
asthma.60,66,67 There is uncertainty about how to reliably predict an increased
risk of asthma.54-56,62,67 Risk factors include a family history (particularly maternal)
of asthma and allergies, and a past history of allergies in early life.63,64 Other risk
factors for asthma that have been identified in observational studies are obesity,
environmental pollution, work related exposures and diet.55,57 For people with
high risk occupations, the presence of new onset rhinitis is associated with
increased risk for occupational asthma.56
195
196
Respiratory health
Interventions to decrease the risk of developing asthma
The most important and modifiable risk factor to reduce asthma is exposure
to environmental tobacco smoke (ETS).57,60,68–70 Interventions to reduce
ETS exposure may reduce the risk of childhood asthma and later persistent
asthma.55–57 This is of particular importance given the high rates of ETS
exposure for Aboriginal and Torres Strait Islander children both in utero and
after birth.60
There is currently little evidence to support preventive strategies to reduce the
development of asthma except for avoidance of environmental tobacco smoke
and avoidance of asthma causing agents in the workplace.60 There is conflicting
evidence on the effects of exposure to pets and other allergen sources, the
protective effects of breastfeeding and other aspects of diet and feeding in
preventing childhood asthma.60
Sensitisation to allergens, such as house dustmite and cats, is associated
with asthma, but interventions to reduce exposure to these allergens have not
been shown to prevent asthma.66,67,71 Allergen specific immunotherapy may be
effective in preventing asthma in children with seasonal allergies,67 though more
studies are needed before this can be recommended as a wider strategy for
prevention of asthma.57
The effect of breastfeeding on childhood asthma is controversial. Although
there are many other health related benefits from breastfeeding, there does not
appear to be any persistent effect of breastfeeding on asthma rates.56,70
A diet high in fruit and vegetable intake has been shown to be associated with
less asthma in children and adults in observational studies.57,72 Other dietary
interventions have not been shown to be effective in preventing asthma.
Ineffective interventions include infant feeding with soy formulae73 and the
avoidance of commonly allergenic foods during pregnancy and lactation or
in infant diets.56,70 There is insufficient evidence that dietary supplements for
mother or infant with probiotics, fish oil or antioxidants are of benefit in reducing
childhood atopy or asthma.56,57,74–76
Similarly, there is insufficient evidence that avoidance of airborne allergens in
the home and measures to reduce exposure to dustmite decrease the rates
of asthma or wheeze in young children.56,57,64 Further, there is no evidence that
house dustmite control prevents asthma exacerbations.71 Long term treatment
with antihistamines does not reduce the risk of asthma developing in children
with atopic dermatitis, including those who are sensitive to house dustmite
and/or grass pollen.56 Immunotherapy may reduce asthma risk in children with
seasonal rhinoconjunctivitis,56,67,77,78 however more studies are needed before this
can be recommended as a preventive strategy for asthma.57
Reducing exposure to potential environmental factors including allergens
in the workplace may decrease a worker’s risk of developing asthma in the
workplace. Reduction in exposure levels including the use of respiratory
protective equipment reduces but does not eliminate the risk of occupational
asthma.56,79,80
Respiratory health
197
Recommendations: Asthma
Who is at risk?
Screening
All people
Routine screening for asthma is not
N/A
recommended
Early detection strategies should be
considered (eg. clinical vigilance, detailed
history considering mimics of asthma,
and spirometry when symptoms are
suggestive)
GPP
81
Behavioural
Children
Maternal dietary restrictions during
breastfeeding or pregnancy are not
recommended for the prevention of
asthma
Opportunistic
IIIB
56,57,68
All people
A high intake of fruit and vegetables
Opportunistic
should be recommended to those with or
at risk of asthma*
IIIB
57
Chemoprophylaxis
Children with
seasonal rhinoconjunctivitis
Advise that immunotherapy is not
currently recommended as a preventive
strategy of asthma
N/A
IIB
56,57,67,77,78
Environmental
Children
Strategies to provide a smokefree
environment are recommended
Smoking cessation advice should be
given to pregnant and breastfeeding
women (see Chapter 9: Antenatal care)
Opportunistic
IIIA
54,56,57
Advise families that avoidance of
exposure to airborne allergens such as
house dustmite or pets is not shown to
be effective in preventing asthma
IIIB
56,57,64
Recommend use of respiratory protective N/A
equipment
IIIB
56,79,80
Workers in high
risk workplaces,
where exposure
to occupational
dusts and
chemicals are
likely
How often?
References
Level/
strength of
evidence
Preventive
intervention
type
* Risk factors include a family history (particularly maternal) of asthma and allergies, a past history of atopy and food allergies in early life,
obesity, low birthweight, in utero tobacco exposure, tobacco smoking, environmental tobacco smoke, environmental pollution and work
related exposures55,57,63,64,81
Resources
British Guideline on the Management of Asthma (British Thoracic Society, Scottish
Intercollegiate Guidelines Network)
www.sign.ac.uk/pdf/sign101.pdf
Multiple resources including guides to asthma management and spirometry (National
Asthma Council Australia)
www.nationalasthma.org.au
International evidence based guidelines and clinical resources (Global Initiative for Asthma)
www.ginasthma.org.
198
Respiratory health
Background
Chronic obstructive pulmonary disease (COPD) is a serious, progressive and
disabling disease and a major cause of hospital admission and premature death
in Australia.3 Some 2 million Australians are estimated to have COPD.11 The
death rate from COPD among Aboriginal and Torres Strait Islander people is
five times that of non‐Indigenous Australians.11,61 Tobacco smoking is the major
cause of COPD.3 Half of Aboriginal and Torres Strait Islander people report
that they smoke and daily smoking is twice as prevalent when compared with
non-Indigenous Australians.61,82 Further, environmental tobacco smoke (ETS)
exposure appears to be a risk factor for the development of COPD.83,84
COPD is characterised by airflow limitation that is not fully reversible and is
usually progressive. A clinical diagnosis of COPD should be considered in
any patient who has dyspnoea, chronic cough or sputum production, and a
history of tobacco smoking. The diagnosis of COPD requires demonstration
by spirometry of airflow limitation that is not fully reversible, in addition to
symptoms of dyspnoea and cough and exposure to risk factors for the disease
such as smoking. The presence of a postbronchodilator FEV1/FVC <0.70 and
FEV1 <80% predicted confirms the presence of airflow limitation that is not fully
reversible.11,22,23,85
Spirometry in association with clinical symptoms can be used to classify COPD
into:
• mild disease (Stage I: FEV1/FVC <0.70 and FEV1 >80% predicted)
• moderate disease (Stage II: FEV1/FVC <0.70 and FEV1 50–80% predicted)
• severe disease (Stage III: FEV1/FVC <0.70 and FEV1 30–50% predicted), and
• very severe disease (Stage IV: FEV1/FVC <0.70 and FEV1 <30% predicted or
FEV1 <50% predicted plus chronic respiratory failure).11,23
COPD is commonly associated with other diseases, including heart disease,
obstructive sleep apnoea, lung cancer, stroke and depression, which should be
actively identified and also carefully managed.23,86
Interventions
There is no evidence of an effective screening test for the early detection of
COPD in asymptomatic individuals. Spirometry has not been demonstrated
to improve health outcomes and there is no evidence that spirometry
screening improves smoking cessation rates.87–90 Spirometry is therefore not
recommended as a screening test but is required for diagnosis in symptomatic
individuals.11,22,87,88,91–93
The single most important intervention to prevent or reduce the progression of
COPD for most people is smoking cessation and therefore strenuous efforts
should be made to assist smokers with COPD to quit smoking.11 Similarly,
other risk factors for COPD should be reduced such as occupational dusts and
chemicals, and indoor and outdoor air pollutants.23
No medications have been shown to modify the steady decline of lung function,
which is the hallmark of COPD.11,23 For people with an established diagnosis
of COPD, much can be done, however, to improve quality of life, increase
Respiratory health
exercise capacity and reduce morbidity and mortality.11,85 The principal goals of
other therapy, aside from smoking cessation, are to optimise function through
symptom relief with medications and pulmonary rehabilitation and to prevent or
treat aggravating factors and complications.11 Mild to moderate COPD is likely
to be treated within primary care, but patients with more severe COPD require
multidisciplinary team care including consideration of pulmonary rehabilitation.91
Pulmonary rehabilitation reduces dyspnoea, fatigue, anxiety and depression,
improves exercise capacity, emotional function and health related quality of life
and enhances patients’ sense of control over their condition.11,22,23,91
There is good evidence of benefit from annual influenza vaccination in people
with COPD, with a demonstrable reduction in hospitalisations, complications
and death.11,23,37 Influenza vaccination should therefore be given in early
autumn to all patients with moderate to severe COPD.11 There is no direct
evidence of the efficacy of pneumococcal vaccine in preventing pneumococcal
exacerbations of COPD.24 There is however, evidence of benefit in elderly
populations with or without chronic disease.22 Consequently pneumococcal
vaccination (polyvalent covering 23 virulent serotypes) is recommended in this
group.11
Despite the fact that medications cannot reverse or slow the deterioration in
lung function in COPD, they have an important role in symptom control and
management of complications. Both long acting anticholinergic agents and
long acting beta agonists (LABAs) have proven effectiveness in symptom
control for COPD. Evidence is insufficient to recommend one over the other.92
Inhaled corticosteroids (ICS) should be considered in patients with moderate
to severe COPD and frequent exacerbations.11,85 While the long term adverse
effects of ICS are unknown, caution is needed if treatment is stopped as abrupt
withdrawal may be associated with worsening of symptoms.11 Combination
inhaled therapies (ICS, LABA, long acting anticholinergics) may be appropriate
in symptomatic people. The decision to use combination treatment and which
agents to use should take into account the patient’s symptomatic response,
personal preference and risk of side effects.91
Prophylactic antibiotics in chronic bronchitis/COPD have a small but statistically
significant effect in reducing the days of illness due to exacerbations of chronic
bronchitis. However, they do not have a place in routine treatment because of
concerns about the development of antibiotic resistance and the possibility of
adverse effects. Similarly, mucolytics may reduce the frequency and duration of
exacerbations but are not indicated for routine use.11,91
199
200
Respiratory health
Recommendations: Chronic obstructive pulmonary disease
Preventive
intervention type
Who is at risk?
How often?
Level/
strength of
evidence
References
Immunisation
People with
an established
diagnosis of
COPD
Offer influenza vaccine in the
pre-flu season months for the
prevention of influenza (March to
April)
Annually
IIB
11,91
See section on
pneumococcal
vaccination for
recommendations
on frequency
IIC
2,11,23,91
IIB
11
IA
11,22,87,88,
91–93
Chest X-ray is not recommended Opportunistic
for the diagnosis or screening of
COPD
Chest X-ray may be of value to
rule out other diagnoses and for
later use as a baseline
GPP
22,91
All people
Advise of the importance of not
smoking as the most effective
strategy to prevent COPD (see
Chapter 1: Lifestyle, smoking)
Opportunistic
1A
11
People with
an established
diagnosis of
COPD
Smoking cessation reduces the
rate of decline of lung function.
Counselling and treatment of
nicotine dependence should be
offered to all smokers regardless
of the presence or absence of
airflow obstruction (see Chapter
1: Lifestyle, smoking)
Opportunistic
IA
11,23,87
Pharmacotherapy (bronchodilator Opportunistic
treatment, inhaled
corticosteroids, long term
antibiotic treatment) does not
modify decline in lung function
Pharmacotherapy is useful in
decreasing symptoms and/or
complications and improving
quality of life
IA
11,23
Advise that risk factors for
COPD should be minimised (eg.
occupational exposure, ETS
and indoor/outdoor air pollution
and irritants). This may include
strategies such as adequate
ventilation when cooking with
solid fuels and avoidance
of irritants and reduction of
emissions in the workplace
IIIC
23,84
Screening
Current smokers Screen for symptoms of COPD
Opportunistic
Ex-smokers over (persistent cough/sputum
production, wheezing, dyspnoea)
35 years of age
If symptoms are present
spirometry is indicated to assess
for COPD
Spirometry is not recommended
to screen healthy adults who do
not report respiratory symptoms
Behavioural
Chemoprophylaxis People with
an established
diagnosis of
COPD
Environmental
All people
Opportunistic
N/A
Respiratory health
Resources
Screening for chronic obstructive pulmonary disease using spirometry
www.uspreventiveservicestaskforce.org/uspstf/uspscopd.htm
The COPD-X Plan. Australian and New Zealand guidelines for the management of
chronic obstructive pulmonary disease
www.copdx.org.au
Inhaler technique in adults with asthma or COPD
www.clinicalguidelines.gov.au/search.php?pageType=2&fldglrID=1564&
Chronic obstructive pulmonary disease: diagnosis and management of acute
exacerbations
www.guideline.gov/syntheses/synthesis.aspx?id=16404
Diagnosis and management of stable chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease: pulmonary rehabilitation
Management of chronic obstructive pulmonary disease in adults in primary and
secondary care (partial update)
www.guideline.gov/content.aspx?id=23860&search=asthma+and+prevention
http://guidance.nice.org.uk/CG101.
201
202
Respiratory health
Bronchiectasis and chronic suppurative
lung disease
Background
The customary diagnosis of bronchiectasis, usually defined as irreversible
airway dilatation, is based solely on high-resolution chest computed
tomography scans (HRCT). The use of a radiological definition is problematic
for several reasons, particularly clinically for Aboriginal and Torres Strait Islander
people living in remote areas.94,95 Thus, in the clinical guideline specific for
Aboriginal and Torres Strait Islander people living in remote regions94 and the
national guidelines,2,95 the preferable term is chronic suppurative lung disease
(CSLD) when symptoms and/or signs of bronchiectasis are present with or
without HRCT features. These symptoms and/or signs are: continuous, wet or
productive cough for >8 weeks ± other features such as exertional dyspnoea,
reactive airway disease, recurrent chest infections, growth failure, clubbing,
hyperinflation or chest wall deformity.95 Bronchiectasis refers to CSLD with the
presence of HRCT radiological features.95
The incidence of CSLD has declined over the past century. However, in the
past decade, it is increasingly recognised as an important contributor to chronic
respiratory morbidity in both Aboriginal and Torres Strait Islander people 94 and
other children and adults in Australia96,97 and globally.98 It is also increasingly
recognised as an alternative or concomitant diagnosis to common respiratory
conditions such as ‘difficult asthma’ and COPD.99 Two studies have described a
prevalence of bronchiectasis in COPD at 29%99 and 50%.100 In a cohort of newly
referred adults with ‘difficult asthma’, bronchiectasis was detected in 40%.101
In Aboriginal and Torres Strait Islander people, CSLD is anecdotally common
but there is little published data. In the Northern Territory, the incidence in
Aboriginal and Torres Strait Islander infants (first year of life) is 1.18 per 1000
child years102 and the prevalence is 1 in every 68 children aged <15 years.103
Hospitalisation rates for CSLD is increasing in Queensland (age standardised
rate of ~65 per 100 000 in 2005 to ~90 per 100 000 in 2009),104 with the rate
in Aboriginal and Torres Strait Islander people about 2.7 times that for nonIndigenous Queenslanders in 2009.104 There are no data for urban dwelling
Aboriginal and Torres Strait Islander people but among children newly
presenting to a respiratory service with chronic cough, Aboriginal and Torres
Strait Islander children have a significantly higher incidence of radiological
bronchiectasis compared to non-Indigenous children: 29.4% versus 6.7%
respectively.105
The morbidity of people with bronchiectasis include increased hospitalisation,
excess days off work/school, poor quality of life and complications associated
with chronic cough.106–108 Complications associated with bronchiectasis extend
beyond the respiratory system and include cardiac problems (eg. impaired left
ventricular diastolic function,199 cor pulmonale, systemic effects (eg. reduced
wellbeing and increased acute phase reactants),110 sleep disturbance96
and psychological difficulties associated with anxiety and depression.111,112
Furthermore, chronic endobronchial infection, which is present in CSLD, is
an independent risk factor for atherosclerosis, coronary heart disease and
coronary deaths.113,114
Respiratory health
The only published Australian mortality data for bronchiectasis are from a
central Australian hospital based cohort of 61 adults (97% were Aboriginal) in
which 11.5% of people had died within 12 months.115 The cohort comprised
predominantly middle aged adults (mean age 42 + SD 15 years) and most had
not received standard care: only 13 (21.3%) had lung function tests performed).115
Overseas, mortality rates vary widely from a 4 year survival of 58% (Turkey) to
75% survival at 8.8 years (Finland).116
Interventions
Despite the considerable prevalence and disease burden, services for CSLD
receive disproportionately fewer allocated resources when compared with other
chronic respiratory diseases.117–119 Effective clinical management reduces both
short103,120 and long term morbidity associated with CSLD.121,122 There is increasing
evidence that intensive treatment of children who either have bronchiectasis, or
who are at risk of developing severe bronchiectasis, prevents poor lung function
in adulthood.122–124 Cohort data have shown that approximately 80% of newly
diagnosed adults with bronchiectasis were symptomatic since childhood and that
the duration of chronic cough (the most common symptom of CSLD95) is inversely
related to lung function at diagnosis. This means that the longer the duration
of cough, the poorer the lung function at diagnosis based on forced expiratory
volume at 1 second (FEV1).125 Optimal overall management and treatment
can potentially prevent chronic respiratory disease in a substantial number of
people.126 Although robust trials are needed, primary healthcare providers can
play a crucial role in the recognition and early detection of disease as well as the
long term management to prevent complications and premature death.95
Immunisation (pneumococcal, influenza) is effective in preventing severe and
recurrent acute respiratory illnesses (ARIs),127 however data of its effectiveness
specific to the Aboriginal and Torres Strait Islander health context are lacking.128
Delayed immunisation129 is one postulate why pneumococcal conjugate-7
vaccine has not reduced ARIs in Aboriginal and Torres Strait Islander children.
This is in contrast to global data that have shown substantial ARI reduction post
pneumococcal vaccination.127
Aboriginal and Torres Strait Islander children hospitalised with pneumonia were
15 times more likely to develop bronchiectasis and for recurrent pneumonia the
risk increases further.130 In a cohort study, 25.6% of children with hospitalised
lobar pneumonia had a new diagnosed and treatable chronic respiratory illness
(18% CSLD) on follow up.131 Thus, given the link between lower ARIs and
bronchiectasis,130,131 as well as the association between duration of chronic
cough and lung function decline in adults,125 it is good clinical practice for all
children and adults with lower ARIs to be reviewed in primary care at least 3–4
weeks post episode. They should be screened for the presence of chronic
cough and persistence of other respiratory symptoms and signs (eg. wheeze and
crackles in chest auscultation).
When chronic (>4 weeks) wet cough is present, appropriate antibiotics (covering
common respiratory pathogens S. pneumoniae, Moraxella catarrhalis, H. influenzae)
are recommended. In a Cochrane meta-analysis, the cure rate in children who
received antibiotics was significantly higher than in controls and the number of
children needed to treat to demonstrate a benefit at 2 weeks was three.132 Further,
progression of illness, defined by requirement for further antibiotics, was significantly
lower in the treatment group; number needed to treat was four.132
203
204
Respiratory health
The most common symptom of CSLD is chronic cough94 and recent
unpublished data have shown that Aboriginal and Torres Strait Islander children
newly referred with chronic cough have a significantly higher likelihood of
bronchiectasis on further assessment. As chronic cough is considered ‘normal’,
it tends to be under reported by carers of Aboriginal children.133 Anecdotally,
adult Aboriginal and Torres Strait Islander people also underreport their cough.
In children, triggers for referral to a specialist include >2 episodes of chronic
(>4 weeks) wet cough per year responding to antibiotics, and chest X-ray
abnormality persisting >6 weeks following appropriate therapy.95
Frequent exacerbations, especially when hospitalisation is required, is a risk
factor for lung function decline.97,134 Thus, when exacerbations are frequent
(4–6 per year non-hospitalised episodes or 2 per year hospitalised episodes),
consider use of maintenance antibiotics in collaboration with a specialist.
Exposure to in-utero tobacco smoke is associated with lower birthweight,
increased ARI and other respiratory morbidity.135,136 Breastfeeding is protective
against development of CSLD while being born premature or small for gestation
is a risk factor.130 Primary prevention strategies to reduce these factors and
increase breastfeeding would be beneficial (see Chapter 2: Child health). The
association between poor hygiene and the excessive burden of infections
(especially respiratory and gastrointestinal) has been well demonstrated.137–139
However, data specific to Aboriginal and Torres Strait Islander people as well as
evidence based interventions are sparse138 (see Chapter 9: Hearing loss).
Respiratory health
205
Recommendations: Bronchiectasis and chronic suppurative lung disease
Preventive
intervention type
Immunisation
All children and
adults
Ensure timely immunisation As per National
IA
is provided
Immunisation
Program Schedule
(NIPS) and state/
territory schedules
Screening
People with
pneumonia and
lower acute
respiratory
infections (ARIs),
particularly
hospitalised
episodes
Ensure primary care
provider review after the
ARI episode
If wet or productive
cough* is present,
consider the diagnosis
of CSLD.† Recommence
antibiotics and undertake
investigations as per
management guidelines94
People with
recurrent lower
ARIs (particularly
if hospitalised)
Consider a diagnosis of
Opportunistic
CSLD. Repeat chest X-ray.
Refer to specialist if:
People with
persistent
chronic (>2
months) wet
cough
Behavioural
How often?
3–4 weeks post
episode then
2 weekly till
symptoms resolve
or referred
Level/strength of References
evidence
IA (antibiotics
efficacy in
treatment of wet
cough in children)
94
130–132
IIIB (screening for
CSLD post lower
ARI episode)
III (screening for
CSLD post lower
ARI episode)
94,130
Annually
Consider a diagnosis of
CSLD. Assess with a chest
X-ray and see above
If wet or productive
cough* is present,
consider the diagnosis of
chronic suppurative lung
disease.† Recommence
antibiotics and undertake
investigations as per
management guidelines94
IA (antibiotics
efficacy in
treatment of wet
cough in children)
GPP B (for
effectiveness of
screening and
antibiotics in
adults)
94,132
All infants
Promote and encourage
breastfeeding
IIIB (breastfeeding
protective)
94,130
All children
Promote good hygiene
Opportunistic
practices to reduce burden
of infections (see Chapter
7: Hearing loss)
GPP B
138
People with
CSLD or known
bronchiectasis
Assess cough severity,
quality of life, and
exacerbating factors.
Undertake regular review
to prevent and manage
complications and
comorbidities (see Table
11.1)
GPP B
94,95
• >2 episodes of chest
X-ray proven pneumonia
and/or
• chest X-ray persistently
abnormal for >6 weeks
At postnatal
checks
3 monthly clinic
review
6 monthly
specialist review
206
Respiratory health
Recommendations: Bronchiectasis and chronic suppurative lung disease (continued)
Chemoprophylaxis
Infants at risk
of exposure to
environmental
tobacco smoke
both in-utero
and in the
postnatal period
Advise and assist pregnant Opportunistic
women to avoid smoking
(See Chapter 9: Antenatal
care)
Advise parents/carers
who smoke about the
harms of environmental
tobacco smoke and the
need to limit childhood
exposure, particularly
in confined spaces (eg.
homes and motor vehicles)
(see Chapter 1: Lifestyle,
smoking)
IIIC
Mothers with or
at risk of having
babies with low
birthweights
and/or
premature
infants
Promote increased
access to comprehensive
antenatal care (see
Chapter 9: Antenatal care)
GPP
94,130
IIIC (premature and
low birthweight
infants developing
CSLD)
People with
CSLD or known
bronchiectasis
Consider maintenance
As per
antibiotics on discussion
management
with the person’s specialist guidelines94
Opportunistic
GPP C
135,136
94
*Cough is usually underreported;40 children do not usually produce sputum and hence the term wet cough (rather than productive cough)
is used94
†Bronchiectasis refers to chronic suppurative lung disease (CSLD) with the presence of high resolution chest CT (HRCT) radiological
features.95 CSLD is diagnosed when symptoms and/or signs of bronchiectasis are present with or without HRCT features.95 These
symptoms and/or signs are: continuous, wet or productive cough for >8 weeks, ± other features such as exertional dyspnoea, reactive
airway disease, recurrent chest infections, growth failure, clubbing, hyperinflation or chest wall deformity95
Table 11.1. Regular review of bronchiectasis
Regular review consists of:
• assessment of severity, which includes oximetry and spirometry
• sputum culture
• management of possible complications and comorbidities, particularly for
gastro-oesophageal reflux disease, reactive airway disease/asthma, COPD,
otorhinolaryngeal disorders and dental disease. Less commonly patients require
assessments for sleep disordered breathing, cardiac complications and referral for
lung transplantation
Source: Chang AB, Bell SC, Byrnes CA, Grimwood K, Holmes PW, King PT, et al 201095
Respiratory health
Resources
Resources for health professionals (Lung Foundation)
www.lungfoundation.com.au
Lung InfoNet
www.lunginfonet.org.au.
References
1.
Randle E, Ninis N, Inwald D. Invasive pneumococcal disease. Archives of disease in childhood.
Education and practice edition 2011;96(5):183–90.
2.
National Health and Medical Research Council. The Australian immunisation handbook, 9th edn.
3.
Australian Institute of Health and Welfare. Asthma, chronic obstructive pulmonary disease and other
respiratory diseases in Australia. Canberra: AIHW, 2010.
4.
Menzies R, Turnour C, Chiu C, McIntyre P, Department of Health and Ageing. Vaccine preventable
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Chapter 12
Cardiovascular
disease
prevention
Author David Peiris
Expert reviewers Alex Brown, Andrew Tonkin
214
Cardiovascular disease prevention
Overview
In this chapter cardiovascular disease (CVD) is used as a collective term to
include coronary heart disease (CHD), stroke and transient ischaemic attacks
(TIAs) and peripheral vascular disease (PVD).
Despite improving trends, CVD remains Australia’s biggest killer, accounting for
16% of the total disease burden and 11% of national health system expenditure.1
Aboriginal and Torres Strait Islander people experience around a five times
greater vascular disease burden than other Australians.2 This vascular disease
burden rises sharply from early adulthood. Mortality rates from CVD for
Aboriginal and Torres Strait Islander people aged 25–64 years are up to eight
times higher than for the general population,3 and CVD is the single biggest
contributor to the disease burden gap for those aged 35 years and older.2
Reductions in the prevalence of seven risk factors (tobacco smoking, high body
mass, physical inactivity, high blood cholesterol, excessive alcohol intake, high
blood pressure, and low fruit and vegetable intake) represent the most effective
prevention strategies in closing the vascular disease burden gap for Aboriginal
and Torres Strait Islander people.2 Based on the National Health Survey and the
National Aboriginal and Torres Strait Islander Health Survey, nearly all Aboriginal
and Torres Strait Islander people have at least one CVD risk factor from the age
of 18 years and 53% have three or four of these risk factors.4
Absolute risk approach to CVD prevention
Estimating the risk of CVD events requires simultaneous assessment of several
risk factors. Based on large scale epidemiological studies, there has been
a fundamental shift away from screening and managing single risk factor
abnormalities (eg. hypertension or hypercholesterolaemia, in which arbitrary
cut-points are used for defining presence or absence of a condition) towards
a global assessment of multiple risk factors to determine a person’s overall or
‘absolute’ risk of experiencing a cardiovascular event. This approach provides
greater ability to predict who is at greatest risk of a CVD event than the
traditional single risk factor approach.5
The contribution of various risk factors to a person’s overall risk is derived from
large cohort studies and several absolute CVD risk prediction equations are
now available based on these data. Importantly, however, there are currently
no Aboriginal and Torres Strait Islander population specific risk prediction
equations. The 1991 Anderson Framingham Risk Equation (FRE),6 derived from
the USA Framingham study, is the currently recommended equation for risk
estimation in Australia.7 This equation should only be applied for people without
established CVD.
There are several limitations to applying the FRE to Aboriginal and Torres Strait
Islander populations:
• it is validated for the age range 30–74 years only
• it may underestimate risk, especially for younger age groups and when
local risk factor prevalence rates and CVD incidence exceed that of nonIndigenous populations8
• in areas where there is a high prevalence of additional risk factors that are not
part of the FRE but are known to be independently associated with CVD, risk
may be underestimated.
Non-FRE risk factors of known high prevalence in Aboriginal and Torres Strait
Islander communities include family history of premature CVD, elevated body
mass index, markers of chronic kidney disease, socioeconomic hardship,
depression and psychosocial stress, and impaired fasting glucose.4 Further,
literature reviews conducted by the National Vascular Disease Prevention
Alliance have identified several clinical conditions which, if present, confer a high
degree of risk regardless of the risk estimate using the FRE.7 Table 12.1 lists the
FRE risk factors, additional risk factors for CVD that do not feature in the FRE
and a list of clinically high risk conditions in whom absolute risk calculation can
be assumed to be high. It is recommended that a comprehensive vascular risk
assessment requires assessment of all these factors.
Table 12.1. Framingham and non-Framingham CVD risk factors
Framingham risk equation
factors*†
Non-Framingham risk equation
factors‡
Clinically high risk conditions
• Age
• Gender
• Smoking status
• Systolic blood pressure
• Total cholesterol§
• HDL cholesterol§
• Diabetes status
• Left ventricular hypertrophy
(LVH)†
• Obesity (BMI >30 kg/m2 and/or waist
circumference >102 cm in men, >88 cm
in women)
• Family history of CVD before age 55
years in a mother, father or sibling
• Presence of albuminuria#
• Atrial fibrillation
• Impaired fasting glucose ≥6.1 mmol and
<7.0 mmol or glucose intolerance (2 hour
glucose ≥7.8 mmol and ≤11.0 mmol)
• Socioeconomic hardship
• Depression or other psychosocial stress
• Excessive alcohol intake
• Extreme risk factor elevations (SBP
≥180 or DBP ≥110, total cholesterol
>7.5 mmol/L)
• Type 2 diabetes and age >60 years
• Type 2 diabetes and albuminuria#
• Moderate to severe chronic kidney
disease (eGFR <45 mL/min/1.73 m2
or persistent proteinuria)
• Familial hypercholesterolaemia
*The 1991 Framingham risk equation is intended for people without CVD. The most recently recorded pre-treatment measures for
blood pressure or lipids should be used to estimate CVD risk in people already receiving treatment. Where this is not possible,
clinicians should make decisions on use of pharmacotherapy based on discussions with the patient and consideration of the
individual context
†It is preferable to assess for LVH on the basis of echocardiography criteria rather than via an electrocardiogram
‡There are many additional risk factors that are independently associated with increased CVD risk such as C-reactive protein,
coronary calcium scores, and plasma homocysteine levels. Measurement of such factors can be costly and invasive and there is
limited evidence to suggest that assessment of these risk factors substantially improves risk prediction over those listed in Table
12.1
§Fasting lipid specimens are recommended, but a reasonable estimation of risk will be obtained from a non-fasting sample in most
circumstances
#Albuminuria is defined as an albumin excretion rate >20 mcg/min or urinary albumin to creatinine Ratio >2.5 mg/mmol in males
and >3.5 mg/mmol in females
Sources: Framingham risk equation factors from Anderson K, Odell P, Wilson P, Kannel W 19916; non-Framingham risk equation
factors from National Vascular Disease Prevention Alliance 2009 and Colagiuri S, Davies D, Girgis S, Colagiuri R 20097,31 and
clinically high risk conditions from National Vascular Disease Prevention Alliance 20097
Interventions
Although there is substantial work needed to improve the evidence base for
absolute risk based screening and management for Aboriginal and Torres Strait
Islander people, the following recommendations have been made. The following
tables outline the recommendations for people without CVD and for those with
established CVD.
215
216
Recommendations: For people without an established diagnosis of CVD
Preventive
intervention type
Who is at risk?
How often?
Level/
strength of
evidence
References
Screening
Age 12–17 years
Assess smoking status, physical
activity, nutrition, BMI and waist
circumference (see Chapter 1:
Lifestyle)
Advise lifestyle risk reduction
accordingly (see Chapter 1: Lifestyle)
Opportunistic
and as part of
an annual health
assessment
GPP
4
Age 18–34 years
Assess smoking status, physical
without any vascular activity, nutrition, BMI and waist
risk factors
circumference
Also assess BP, family history of
premature CVD, diabetes risk (see
Chapter 14: Diabetes prevention),
psychosocial risk factors (see Chapter
10: Mental health) and socioeconomic
risk factors
Opportunistic
and as part of
an annual health
assessment
GPP
9
Age 18–34 years and
one or more of the
following is present:
family history of
premature CVD
or chronic kidney
disease (CKD),
overweight/obesity,
smoking, diabetes,
elevated BP
Assess risk factors as above*
Also assess serum lipids and screen
for CKD (see Chapter 13: Chronic
kidney disease prevention and
management)
Opportunistic
and as part of
an annual health
assessment
GPP
9–11
Age 35–74 years
Assess for the presence of any
Framingham, non-Framingham
risk factors and clinically high risk
conditions (see Table 12.1)
If no clinically high risk conditions
are present then calculate absolute
5 year CVD risk using the Australian
cardiovascular risk charts (Appendix
1) or the Framingham risk equation
(FRE) calculator (see Resources)
As part of an
IIB
annual health
assessment and
review according
to level of risk
(see below)
Age over 74 years
Assess for presence of any
Review
Framingham, non-Framingham
according to
risk factors and clinically high risk
clinical context
conditions (see Table 12.1) but assume
CVD risk is high
Behavioural
GPP
People with low
Advise lifestyle risk reduction as
Review risk every IA
absolute 5 year CVD needed for the following (see Chapter 2 years
risk (<10%)
1: Lifestyle):
• physical activity
• weight loss
• smoking cessation
• salt reduction to less than 4 g salt/
day (1600 mg sodium/day)
• diet rich in fruit and vegetables,
wholegrain cereals, nuts and seeds,
legumes, fish, lean meat, poultry,
low fat dairy products and limiting
saturated and trans fat intake
• limit alcohol intake to ≤2 standard
drinks/day
7,12–15
14,15
9,14,16–19
People with the
following:
217
Advise lifestyle risk reduction as above Review
Provide intensive intervention support according to
clinical context
(see Chapter 1: Lifestyle)
IB
9,11,14,15,
20–22
Consider commencing a BP lowering
medication unless contraindicated
Review
according to
clinical context
GPP
14
Review individual risk factor profile
and recommend commencing a
BP lowering medication and/or
lipid lowering medication unless
contraindicated**
Review
according to
clinical context
IB
9,11,14,15,
20–22
Recommend commencing both a BP Review
lowering medication and lipid lowering according to
clinical context
• >15% 5 year CVD medication regardless of risk factor
risk or presence of levels unless contraindicated**
any clinically high
risk conditions
(see Table 12.1)
IB
9,11,14,15,
20–22
IC
14
IA
12,24–26
• absolute 5
year CVD risk
moderate or high
(≥10%)
• presence of any
clinically high risk
conditions (see
Table 12.1)
Chemoprophylaxis People at low
absolute risk:
• <10% 5 year CVD
risk and with
BP persistently
≥160/100 mmHg
People at moderate
absolute risk:
• 10–15% 5 year
CVD risk
People at high
absolute risk:
Aspirin is not routinely recommended
Patients with atrial
fibrillation (AF)
without prior CVD
Determine the cause of AF and
manage rate and rhythm control.
Assess and manage CVD risk as
above. Consider oral anticoagulant
treatment if valvular heart disease
is present or two or more of the
following risk factors are present
(based on the CHADS2 score23):
• Congestive heart failure
• Hypertension
• Age >75 years
• Diabetes
• prior Stroke or TIA
Review
according to
clinical context
* Although absolute CVD risk assessment is currently not recommended in Aboriginal and Torres Strait Islander people aged less than 35 years,
a multifactorial assessment of CVD risk factors is still recommended to guide management decisions. Treatment on the basis of elevated single
risk factors may still be appropriate depending on the clinical context
** Specific choice of BP and lipid lowering agents and guidelines on treatment targets is beyond the scope of this guideline. See Resources for
links to specific management guidelines. If BP or lipid levels are extreme or non-responsive to treatment then further investigation for underlying
causes is recommended
218
Recommendations: For people with an established diagnosis of CVD
Who is at risk?
How often?
Screening
People with CVD
Calculation of the
absolute CVD risk using
the FRE calculator is not
recommended. Five year risk
of a subsequent CVD event is
assumed to be high
N/A
Behavioural
People with CVD
Intensive lifestyle risk factor
management as for patients
without an established
diagnosis of CVD (see Table
12.1)
Review at every
visit
1A
A tailored cardiac rehabilitation Post CVD event
program should be offered
to all people post myocardial
infarction (MI) and other acute
coronary syndromes, and to
those who have undergone
revascularisation procedures
1A
Commence BP lowering
treatment at any BP level
unless there is symptomatic
hypotension*
Lifelong
IA
9,13,27
Commence lipid lowering
treatment with a statin at
any cholesterol level unless
contraindicated*
Lifelong
IA
11,13,27
Commence low dose aspirin
Lifelong
treatment (75–150 mg) unless
contraindicated
Consider alternative antiplatelet
agents such as clopidogrel (75
mg) if aspirin hypersensitivity is
present
For people with ischaemic
stroke combination aspirin/
dipyridamole may also be
considered
IA
13,27–29
Chemoprophylaxis People with CVD
People with CHD Consider clopidogrel (75 mg) in
with stent insertion combination with aspirin
or recent acute
coronary heart
disease
People with
stroke/TIA
Level/
strength of
evidence
References
Preventive
intervention type
14
For 12 months
IIB
post stent insertion
depending on
stent type and
circumstances of
implantation
Oral anticoagulant treatment
Lifelong
is recommended if AF or
cardio-embolic stroke is
present unless contraindicated.
Consultation of specific
management guidelines is
recommended (see Resources)
IA
9,13,14,16–19
27,29
13,26,30
* Specific choice of BP and lipid lowering agents and guidelines on treatment targets is beyond the scope of this guideline. See
Resources for links to specific management guidelines. If BP or lipid levels are extreme or non-responsive to treatment then further
investigation for underlying causes is recommended
Resources
For absolute risk calculation consult:
The Australian cardiovascular risk charts (see Appendix 1) and
www.heartfoundation.org.au/SiteCollectionDocuments/aust-cardiovascularrisk-charts.pdf
Calculators embedded in clinical software programs
Framingham Risk Equation calculator
www.cvdcheck.org.au
For blood pressure and lipid management guidelines consult:
Guidelines for the management of absolute cardiovascular disease risk:
www.heartfoundation.org.au/SiteCollectionDocuments/Guidelinesmanagement-absolute-cardiovascular-disease-risk.pdf
For oral anticoagulant management recommendations consult:
Therapeutic Guidelines: Cardiovascular.
References
1. Australian Institute of Health and Welfare. Australia’s health 2010. Australia’s health series no. 12. Cat. no.
AUS 122. Canberra: AIHW, 2010. Cited October 2011. Available at www.aihw.gov.au/publications/index.
cfm/title/11374.
3. Couzos S, Murray R. Aboriginal Primary healthcare: an evidence-based approach, 3rd edn. Melbourne:
4. Australian Institute of Health and Welfare. Cardiovascular disease and its associated risk factors in
Aboriginal and Torres Strait Islander peoples 2004–05. Cardiovascular disease series no. 29. Cat. no.
CVD 41. Canberra: AIHW, 2008.
5. Jackson R, Lawes C, Bennet D, Milne R, Rodgers A. Treatment with drugs to lower blood pressure and
blood cholesterol based on an individual’s absolute cardiovascular risk. Lancet 2005;365:434–41.
6. Anderson K, Odell P, Wilson P, Kannel W. Cardiovascular disease risk profiles. Am Heart J
1991;121(1):293–8.
7.
National Vascular Disease Prevention Alliance. Guidelines for the assessment of absolute cardiovascular
risk. National Vascular Disease Prevention Alliance, 2009.
8. Wang Z, Hoy W. Is the Framingham coronary heart disease absolute risk function applicable to Aboriginal
people? Med J Aust 2005;182(2):66–9.
9. National Heart Foundation of Australia. Guide to management of hypertension 2008. Sydney: National
Heart Foundation of Australia, updated December 2010. Cited January 2012. Available at www.
heartfoundation.org.au/SiteCollectionDocuments/HypertensionGuidelines2008to2010Update.pdf.
10. Caring for Australasians with Renal Impairment. Screening for chronic kidney disease – draft guideline.
Sydney: CARI, 2011.
11. National Heart Foundation of Australia, Cardiac Society of Australia and New Zealand. Position Statement
on Lipid Management. Heart Lung Circ 2005;14:275–91.
12. Goldstein LB, Adams R, Alberts MJ, et al. Primary prevention of ischemic stroke: a guideline from the
American Heart Association/American Stroke Association Stroke Council. Stroke 2006;37(6):1583.
13. National Stroke Foundation. Clinical guidelines for stroke management. Melbourne: National Stroke
Foundation, 2010.
14. National Vascular Disease Prevention Alliance. Guidelines for the management of absolute cardiovascular
disease risk. National Vascular Disease Prevention Alliance, 2012.
15. New Zealand Guidelines Group. New Zealand cardiovascular guidelines handbook: a summary resource
for primary care practitioners. Wellington: New Zealand Guidelines Group, 2009. Cited October 2011.
Available at www.nzgg.org.nz/search?resource_type=Guideline+summary.
16. Wolff T, Miller T. Evidence for the reaffirmation of the US Preventive Services Task Force recommendation
on screening for high blood pressure. Ann Intern Med 2007;147(11):787.
17. Dickinson HO, Mason JM, Nicolson DJ, et al. Lifestyle interventions to reduce raised blood pressure: a
systematic review of randomized controlled trials. J Hypertens 2006;24:215–33.
18. McFadden CB, Brensinger CM, Berlin JA, Townsend RR. Systematic review of the effect of daily alcohol
intake on blood pressure. Am J Hypertens 2005;18(2):276–86.
219
220
19. Xin X, He J, Frontini MG, Ogden LG, Motsamai OI, Whelton PK. Effects of alcohol reduction on blood
pressure: a meta-analysis of randomized controlled trials. Hypertension 2001;38(5):1112.
20. Mancia G, De Backer G, Dominiczak A, et al. 2007 Guidelines for the management of arterial
hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of
Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2007;25(6):1105.
21. National Institute for Health and Clinical Excellence. Management of hypertension in adults in primary
care. London: National Institute for Health and Clinical Excellence, 2006. Cited October 2011. Available at
www.nice.org.uk/nicemedia/pdf/CG034NICEguideline.pdf.
22. National Institute for Health and Clinical Excellence. Lipid modification: cardiovascular risk assessment
and the modification of blood lipids for the primary and secondary prevention of cardiovascular disease.
London: National Institute for Clinical Excellence, 2008. Cited October 2011. Available at www.nice.org.
uk/nicemedia/pdf/CG67NICEGuideline.pdf.
23. Gage BF, van Walraven C, Pearce L, et al. Selecting patients with atrial fibrillation for anticoagulation.
Circulation 2004 October 19,2004;110(16):2287–92.
24. Aguilar MI, Hart R. Oral anticoagulants for preventing stroke in patients with non-valvular atrial fibrillation
and no previous history of stroke or transient ischemic attacks. Cochrane Database Syst Rev 2005;July
20;(3):CD001927.
25. Singer DE, Albers GW, Dalen JE, et al. Antithrombotic therapy in atrial fibrillation. Chest 2008;133(Suppl
6):546S.
26. National Institute for Health and Clinical Excellence. The management of atrial fibrillation. London:
National Institute for Health and Clinical Excellence, 2006. Cited October 2011. Available at http://
guidance.nice.org.uk/CG36/Guidance/pdf/English.
27. National Heart Foundation of Australia, Cardiac Society of Australia and New Zealand. Reducing risk
in heart disease (updated 2008). Melbourne: National Heart Foundation, 2007. Cited January 2012.
Available at www.heartfoundation.org.au/SiteCollectionDocuments/Reduce-risk-in-heart-diseaseguideline.pdf.
28. Graham I, Atar D, Borch-Johnsen K, et al. European guidelines on cardiovascular disease prevention in
clinical practice. Fourth Joint Task Force of the European Society of Cardiology and other societies on
cardiovascular disease prevention in clinical practice. Eur J Cardiovasc Prev Rehabil 2007;14:S1.
29. Acute Coronary Syndrome Guidelines Working Group. Guidelines for the management of acute coronary
syndromes. Med J Aust 2006;184(8 Suppl):S9–29.
30. Furie KL, Kasner SE, Adams RJ, et al. Guidelines for the prevention of stroke in patients with stroke or
transient ischemic attack: a guideline for healthcare professionals from the american heart association/
american stroke association. Stroke 2011 Jan;42(1):227–76.
31. Colagiuri S, Davies D, Girgis S, Colagiuri R. National evidence based guideline for case detection and
diagnosis of type 2 diabetes. Canberra: NHMRC and Diabetes Australia, 2009. Cited October 2011.
Available at www.nhmrc.gov.au/_files_nhmrc/publications/attachments/di17-diabetes-detectiondiagnosis.pdf.
Section 13
Chronic
kidney
disease
prevention
and
management
Author Tim Usherwood
Expert reviewer Mark Thomas
222
Chronic kidney disease prevention and management
Overview
Chronic kidney disease (CKD) is defined as either kidney damage or glomerular
filtration rate (GFR) less than 60 mL/min/1.73 m2, or both, persisting for at least
3 months. Kidney damage in this definition includes pathological abnormality or
a marker of damage such as abnormalities in blood tests, urine tests or imaging
studies.1 CKD is classified into six stages depending on GFR as outlined in Table
13.1.1,2 Note that Stage 2 CKD requires evidence of kidney damage in addition
to reduced GFR, whereas Stages 3A–5 are defined entirely on the basis of
measured GFR.
Table 13.1. Stages of chronic kidney disease
Stage
Description
GFR
(mL/min/1.73 m2)
1
Kidney damage* with normal or increased GFR
>89
2
Kidney damage* with mild reduced GFR
60–89
3A
Moderately reduced GFR
45–59
3B
Moderately reduced GFR
30–44
4
Severely reduced GFR
15–29
5
Kidney failure
<15 or dialysis
* Kidney damage includes pathological abnormality or a marker of damage such as
abnormalities in blood tests, urine tests or imaging studies1
Aboriginal and Torres Strait Islander people have a greatly increased prevalence
of CKD,3 and are approximately 10 times more likely than non-Indigenous
Australians to develop end stage kidney failure.4 However, there is great variation
in prevalence between Aboriginal and Torres Strait Islander communities; rates
are highest in remote areas and lowest in urban areas.5 Rates also correlate
strongly with socioeconomic disadvantage.6 The reasons are multifactorial7 but
important modifiable risk factors in Aboriginal and Torres Strait Islander people
are thought to be the same as those in non-Indigenous people: overweight and
obesity, diabetes, hypertension and smoking.3,4
Reduced GFR and raised albumin excretion are independent risk factors for
mortality.8 The bulk of this mortality is due to cardiovascular disease, and people
with CKD are at higher risk of dying from coronary heart disease or stroke than
they are of progressing to end stage kidney disease.9,10 Even mild reduction
in GFR is associated with excess cardiovascular and stroke risk,11,12 while at
any given level of kidney function, microalbuminuria or macroalbuminuria is
associated with increased cardiovascular and stroke morbidity and mortality.13,14
Interventions
GFR testing
In clinical practice, GFR is often estimated [as eGFR] from serum creatinine
and other parameters including gender and age using a formula such as the
CKD-EPI.2 Care should be taken in accepting an eGFR value. Factors such
as intercurrent illness, diet, underweight, overweight or obesity can bias the
estimate. Furthermore, no formula has yet been validated for Aboriginal or
Torres Strait Islander people.15
Proteinuria and albuminuria testing
Abnormal proteinuria is an important marker of kidney damage. Urinary protein
usually includes albumin, and the proportion of total protein that is albumin is
typically increased at higher levels of proteinuria.16 In diabetes and under most
other circumstances, measurement of urinary albumin is a more sensitive test
for CKD than testing for proteinuria; in the AusDiab study, only 8% of adults
with proteinuria tested negative for albuminuria.16 The majority of international
guidelines recommend screening for albuminuria rather than proteinuria for
the detection of CKD.17 However, it is important to note that not all individuals
with CKD exhibit abnormal albumin or protein excretion, and also that a
small proportion of patients with abnormal proteinuria, such as those with
tubulointerstitial disease or myeloma, may excrete abnormal amounts of nonalbumin protein only.
Abnormal albumin excretion is classified as microalbuminuria (30–300 mg/24
hr) or macroalbuminuria (>300 mg/24 hr).17 A properly performed dipstick test, if
negative, rules out macroalbuminuria but not microalbuminuria; a positive result
required confirmation by laboratory methods.18 It is often convenient to measure
albumin-creatinine ratio (ACR) or if indicated, protein-creatinine ratio (PCR), on
a spot specimen preferably taken during first morning void. Table 13.2 provides
definitions for microalbuminuria and macroalbuminuria based on ACR estimation.
However, the relationship between this ratio and the albumin excretion rate is
influenced by many factors so that estimation of 24 hour excretion from the ACR
value is not recommended.17
Table 13.2. Definitions of normal albumin excretion, microalbuminuria
and macroalbuminuria
Urinary ACR
Urinary albumin
excretion per 24
hours
Gender
Normal albumin
excretion
Microalbuminuria
Macroalbuminuria
Male
<2.5 mg/mmol
2.5–25 mg/mmol
>25 mg/mmol
Female
<3.5 mg/mmol
3.5–35 mg/mmol
>35 mg/mmol
Either
<30 mg/24 hr
30–300 mg/24 hr
> 300 mg/24 hr
Albumin excretion may be increased by urinary tract infection, acute febrile
illness, high dietary protein, heart failure, recent heavy exercise or some
drugs. Menstruation or vaginal discharge may also increase urinary albumin
measurement. Definition of abnormal albuminuria requires at least two elevated
ACR measurements in a 3 month period, therefore a single abnormal test should
be repeated.17
Primary prevention
Evidence supports the efficacy and cost effectiveness of screening for CKD risk
factors, and for albuminuria and reduced GFR, in Aboriginal and Torres Strait
Islander people.19,20 The optimal age to start screening is, however, less clear. In
a cohort of urban and rural Aboriginal children followed up for 4 years from 10
years of age, more than 70% potential markers of CKD (haematuria, albuminuria,
systolic and diastolic hypertension) found at baseline did not persist on follow
up.21 On the other hand, in a study of the prevalence of proteinuria, hypertension
and diabetes in Aboriginal adults above the age of 25 years living in remote
223
224
communities, the probability of an individual aged 25–34 years having at least one of
these abnormalities was approximately three times higher than for a participant in the
national AusDiab study; this differential increased further in older age groups.22 Based
on this evidence, screening for CKD risk factors from age 18 years is recommended. If
any risk factors are present then CKD screening for albuminuria and reduced eGFR is
recommended.
The robust epidemiological evidence and plausible biological explanations for the
association of overweight and obesity, diabetes, hypertension and smoking with CKD
suggest that interventions to prevent diabetes,23,24 to promote exercise, healthy diet
and normal weight, to limit salt intake and to discourage smoking have the potential
also to reduce the incidence of CKD.25–28 Programs that promote maternal health
during pregnancy and prevent streptococcal infection in childhood may also reduce
future risk of CKD.29
Secondary prevention
Active treatment of CKD, once detected, can slow progression to end stage disease,
and reduce cardiovascular endpoints. Patients should be assisted to quit smoking,27
reduce excess weight30 and take regular exercise.28 Limiting dietary sodium intake
to 100 mmol (6 g salt) per day may reduce both blood pressure (BP) and albumin
excretion.30
An ACE inhibitor or ARB is generally the firstline treatment for lowering BP and protein
excretion. These two classes of drug should not normally be prescribed together;
although the combination may reduce both BP and proteinuria to a greater extent than
monotherapy with either, it may worsen kidney outcomes.31
Statins reduce lipid concentrations and cardiovascular endpoints in patients with CKD,
irrespective of stage, but no benefit on all cause mortality has been established.32,33
The reno-protective effects of statins are uncertain because of relatively sparse data
and possible outcomes reporting bias.
Reasons for referral
The interventions tabulated in this chapter are concerned with preventing kidney
disease, detecting and slowing the progression of established CKD, and reducing the
associated risks of cardiovascular disease and stroke. While they are all amenable to
delivery in the primary care setting, patients with more advanced disease or significant
comorbidities, or at risk in other ways, are likely to benefit from referral to a secondary
care nephrology service.34 The Caring for Australians with Renal Impairment guidelines35
recommend referral of patients with:
• Stage 4 or 5 CKD of any cause
• persisting albuminuria (ACR >30 mg/mmol)
• Declining eGFR >5 mL/min/1.73 m2 in 6 months (average of at least three
measurements)
• CKD and elevated BP that is not at target despite at least three BP lowering
medications
• unexplained anaemia (<100 g/L) with eGFR <60 mL/min/1.73 m2.
225
Recommendations: Chronic kidney disease detection and management
Preventive
intervention type
How often?
Level/
strength of
evidence
References
Screening
All adults aged
18–29 years
without any CKD
risk factors
Screen for CKD risk factors
(overweight or obesity, diabetes,
elevated BP and smoking, family
history of kidney disease)
As part of an
annual health
assessment
IIIB
20
People aged
18–29 years
with one of the
following CKD
risk factors:
Screen for CKD with eGFR and
urinary albumin-creatinine ratio
(ACR)
A first void specimen is preferred
If urine ACR is raised then repeat
once or twice over 3 months. For
further quantification consider
collecting a timed specimen
Every 2 years (or IIIC
more frequently
if CVD risk is
elevated – see
Chapter 12:
Cardiovascular
disease
prevention)
20
Annually
IIIB
36
Offer smoking cessation support
on smoking)
Advise avoidance of exposure to
environmental tobacco smoke
Opportunistic
IIIB
27,30,37
Encourage regular physical
exercise appropriate to their
physical ability and medical history
on physical activity)
Opportunistic
IIB
28,30
If overweight or obese encourage
weight loss
Offer group diet and exercise
sessions if available, especially for
patients with type 2 diabetes (see
Chapter 1: Lifestyle, section on
overweight/obesity)
Opportunistic
IB
30,38
Advise to limit dietary sodium
intake to 100 mmol/day (6 g salt
per day) or less
Opportunistic
IIIB
30
Opportunistic
As above
for each risk
factor
27,28,30,37–39
• family history
of CKD or
premature
CVD
• overweight/
obesity
• smoking
• diabetes
• elevated BP
All people ≥30
years
Behavioural
Adults with any
Offer individualised, structured
risk factors for
education about risk factor
CKD (see above) avoidance and management
Adults with CKD Lifestyle risk factor management
stages 1–3 (see as above
Table 13.1)
Patients with CKD should be
advised not to use salt substitutes
that contain high amounts of
potassium salts
226
Recommendations: Chronic kidney disease detection and management (continued)
Advise consuming the
recommended daily intake of
protein for adults (0.75 g/kg/day)
Chemoprophylaxis All people with
CKD
Opportunistic
IIC
30,39
A daily fluid intake of 2–2.5 L
Opportunistic
(including the fluid content of foods)
is generally sufficient, although this
might need to be varied according
to individual circumstances
IIIC
30
Regularly review medications
to identify and avoid those with
potential nephrotoxicity
Advise patients taking an
angiotensin converting enzyme
(ACE) inhibitor or angiotensin
II receptor blocker (ARB) plus
diuretic to avoid non-steroidal antiinflammatory drugs (other than low
dose aspirin if indicated)
GPP
40,41
IA
42–45
IIB
31
IA
37,45,46
Opportunistic
IA
37
Opportunistic
BP check at
every visit
IIIB
43,44
IB
45,47
IB
32
IIIB
29,48
Opportunistic
at every
medication
change
Adults with CKD Commence treatment with an ACE At diagnosis
and albuminuria inhibitor or ARB, regardless of BP
(see Table 13.2) level. The goal is >50% reduction
in albumin excretion without
symptomatic hypotension
Alternative agents include calcium
channel blockers
An ACE inhibitor and an ARB
should not normally be prescribed
together
Adults with CKD Commence treatment with an ACE At diagnosis
and diabetes
inhibitor or ARB regardless of BP
level
Blood glucose control in patients
with CKD and diabetes should be
optimised, generally aiming for an
HbA1c target of 7%
Adults with CKD Consider use of more than one
and elevated BP drug to achieve adequate BP
control. (The number of drugs
required tends to increase with
declining GFR)
If prescribed a BP lowering
medication aim for a target of
<140/90 mmHg, or <130/80
mmHg in the presence of micro- or
macro-albuminuria (with or without
diabetes)
Adults with CKD Statins should be prescribed
according to level of overall
cardiovascular risk (see Chapter
12: Cardiovascular disease
prevention)
Environmental
Communities
with high
prevalence of
scabies and
pyoderma
At diagnosis
Support the implementation of
N/A
population based strategies for
reduction of scabies and pyoderma
among children (see Chapter
2: Child health and Chapter 5:
Rheumatic heart disease)
Resources
Chronic kidney disease management in general practice, 2nd edn (Kidney Health
Australia)
Caring for Australians with Renal Impairment guidelines
www.cari.org.au.
References
1. Levey AS, de Jong PE, Coresh J, et al. The definition, classification and prognosis of chronic kidney
disease: a KDIGO Controversies Conference report. Kidney Int 2010 Dec 8;80(1):17–28.
2. Australian Creatinine Consensus Working Group. Chronic kidney disease and automatic reporting of
estimated glomerular filtration rate: new developments and revised recommendations (draft). Australian
Creatinine Consensus Working Group, 2011.
3. Australian Institute Health and Welfare. Chronic kidney disease in Australia 2005. Canberra: AIHW, 2005.
4. Jose M, McDonald S, Excell L, editors. End-stage kidney disease among Indigenous peoples of Australia
and New Zealand. Australia and New Zealand Dialysis and Transplant Registry. Adelaide: ANZDATA
Registry, 2009.
5. Preston-Thomas A, Cass A, O’Rourke P. Trends in the incidence of treated end-stage kidney disease
among Indigenous Australians and access to treatment. Aust N Z J Public Health 2007;31(5):419–21.
6. Cass A, Cunningham J, Snelling P, Wang Z, Hoy W. End-stage renal disease in indigenous Australians: a
disease of disadvantage. Ethn Dis 2002 Summer;12(3):373–8.
7.
Cass A, Cunningham J, Snelling P, Wang Z, Hoy W. Exploring the pathways leading from disadvantage to
end-stage renal disease for indigenous Australians. Soc Sci Med 2004 Feb;58(4):767–85.
8. Matsushita K, van der Velde M, Astor BC, et al. Association of estimated glomerular filtration rate and
albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative
meta-analysis. Lancet 2010 Jun 12;375(9731):2073–81.
9. Weiner DE, Tighiouart H, Amin MG, et al. Chronic kidney disease as a risk factor for cardiovascular
disease and all-cause mortality: a pooled analysis of community-based studies. J Am Soc Nephrol
2004;15(5):1307–15.
10. National Vascular Disease Prevention Alliance. Guidelines for the assessment of absolute cardiovascular
risk. National Vascular Disease Prevention Alliance, 2009.
11. Di Angelantonio E, Chowdhury R, Sarwar N, Aspelund T, Danesh J, Gudnason V. Chronic kidney disease
and risk of major cardiovascular disease and non-vascular mortality: prospective population based
cohort study. BMJ 2010;341:c4986.
12. Lee M, Saver JL, Chang KH, Liao HW, Chang SC, Ovbiagele B. Low glomerular filtration rate and risk of
stroke: meta-analysis. BMJ 2010;341:c4249.
13. Schmieder RE, Schrader J, Zidek W, et al. Low-grade albuminuria and cardiovascular risk: what is the
evidence? Clin Res Cardiol 2007;96(5):247–57.
14. Lee M, Saver JL, Chang KH, Liao HW, Chang SC, Ovbiagele B. Impact of microalbuminuria on incident
stroke: a meta-analysis. Stroke 2010 Nov;41(11):2625–31.
15. Maple-Brown LJ, Lawton PD, Hughes JT, et al. Study protocol: accurate assessment of kidney function in
Indigenous Australians: aims and methods of the eGFR study. BMC Public Health 2010;10:80.
16. Atkins RC, Briganti EM, Zimmet PZ, Chadban SJ. Association between albuminuria and proteinuria in the
general population: the AusDiab Study. Nephrol Dial Transplant 2003 Oct;18(10):2170–4.
17. Australasian Proteinuria Consensus Working Group. Chronic kidney disease and measurement of
albuminuria/proteinuria: a position statement (draft). Australasian Proteinuria Consensus Working Group,
2011.
18. White SL, Yu R, Craig JC, Polkinghorne KR, Atkins RC, Chadban SJ. Diagnostic accuracy of urine
dipsticks for detection of albuminuria in the general community. Am J Kidney Dis 2011 Mar 14.
19. Mathew T, Corso O. Review article: Early detection of chronic kidney disease in Australia: which way to
go? Nephrology 2009 Jun;14(4):367–73.
20. Caring for Australasians with Renal Impairment. Screening for chronic kidney disease: draft guideline.
Sydney: CARI, 2011.
21. Haysom L, Williams R, Hodson EM, et al. Natural history of chronic kidney disease in Australian
Indigenous and non-Indigenous children: a 4-year population-based follow-up study. Med J Aust
2009;190(6):303–6.
22. Hoy WE, Kondalsamy-Chennakesavan S, Wang Z, et al. Quantifying the excess risk for proteinuria,
hypertension and diabetes in Australian Aborigines: comparison of profiles in three remote communities
in the Northern Territory with those in the AusDiab study. Aust N Z J Public Health 2007;31(2):177–83.
23. Lindstrom J, Ilanne-Parikka P, Peltonen M, et al. Sustained reduction in the incidence of type 2
diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study. Lancet 2006 Nov
11;368(9548):1673–9.
227
228
24. Paulweber B, Valensi P, Lindstrom J, et al. A European evidence-based guideline for the prevention of type 2
diabetes. Horm Metab Res 2010;42(Suppl 1):S3–36.
25. Forman JP, Stampfer MJ, Curhan GC. Diet and lifestyle risk factors associated with incident hypertension in
women. JAMA 2009;302(4):401–11.
26. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary
Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med
2001;344(1):3–10.
27. Jones-Burton C, Seliger SL, Scherer RW, et al. Cigarette smoking and incident chronic kidney disease: a
systematic review. Am J Nephrol 2007;27(4):342–51.
28. White SL, Dunstan DW, Polkinghorne KR, Atkins RC, Cass A, Chadban SJ. Physical inactivity and chronic
kidney disease in Australian adults: the AusDiab study. Nutr Metab Cardiovasc Dis 2011;21(2):104–12.
29. Hoy WE, Kincaid-Smith P, Hughson MD, et al. CKD in Aboriginal Australians. Am J Kidney Dis 2010;56(5):983–
93.
30. Caring for Australasians with Renal Impairment. Lifestyle modification, including nutrition interventions in
patients with stages 1–3 CKD – draft guideline. Sydney: CARI, 2011.
31. Mann JF, Schmieder RE, McQueen M, et al. Renal outcomes with telmisartan, ramipril, or both, in people at
high vascular risk (the ONTARGET study): a multicentre, randomised, double-blind, controlled trial. Lancet
2008 Aug 16;372(9638):547–53.
32. Strippoli GF, Navaneethan SD, Johnson DW, et al. Effects of statins in patients with chronic kidney disease:
meta-analysis and meta-regression of randomised controlled trials. BMJ 2008;336(7645):645–51.
33. Baigent C, Landray MJ, Reith C, et al. The effects of lowering LDL cholesterol with simvastatin plus ezetimibe
in patients with chronic kidney disease (Study of Heart and Renal Protection): a randomised placebocontrolled trial. Lancet 2011;377(9784):2181–92.
34. Black C, Sharma P, Scotland G, et al. Early referral strategies for management of people with markers of
renal disease: a systematic review of the evidence of clinical effectiveness, cost-effectiveness and economic
analysis. Health Technol Assess 2010;14(21):1–184.
35. Caring for Australasians with Renal Impairment. When to refer for specialist renal care: draft guideline. Sydney:
CARI, 2011.
36. Caring for Australasians with Renal Impairment. Education strategies: draft guideline. Sydney: CARI, 2011.
37. Chadban S, Howell M, Twigg S, et al. Prevention and management of chronic kidney disease in type 2
diabetes. Nephrology 2010;15:S162–S94.
38. Deakin T, McShane CE, Cade JE, Williams RD. Group based training for self-management strategies in people
with type 2 diabetes mellitus. Cochrane Database Syst Rev 2005;Apr 18;(2):CD003417.
39. Robertson L, Waugh N, Robertson A. Protein restriction for diabetic renal disease. Cochrane Database Syst
Rev 2007;Oct 17;(4):CD002181.
40. Thomas MC. Diuretics, ACE inhibitors and NSAIDs: the triple whammy. Med J Aust 2000;172:184–5.
41. Kidney Health Australia. Chronic kidney disease management in general practice, 2nd edn. Melbourne: Kidney
Health Australia, 2011.
42. James MT, Hemmelgarn BR, Tonelli M. Early recognition and prevention of chronic kidney disease. Lancet
2010;375(9722):1296–309.
43. Crowe E, Halpin D, Stevens P. Early identification and management of chronic kidney disease: summary of
NICE guidance. BMJ 2008;337:a1530.
44. Levin A, Hemmelgarn B, Culleton B, et al. Guidelines for the management of chronic kidney disease. CMAJ
2008;179(11):1154–62.
45. Caring for Australasians with Renal Impairment. Medical therapies to reduce chronic kidney disease
progression and cardiovascular risk: draft guideline. Sydney: CARI, 2011.
46. Strippoli GF, Bonifati C, Craig M, Navaneethan SD, Craig JC. Angiotensin converting enzyme inhibitors and
angiotensin II receptor antagonists for preventing the progression of diabetic kidney disease. Cochrane
Database Syst Rev 2006;Oct 18;(4):CD006257.
47. National Heart Foundation of Australia. Guide to management of hypertension 2008. Sydney: National Heart
Foundation of Australia. Updated December 2010. Cited January 2012. Available at www.heartfoundation.org.
au/SiteCollectionDocuments/HypertensionGuidelines2008to2010Update.pdf.
48. Andrews RM, Kearns T, Connors C, et al. A regional initiative to reduce skin infections among aboriginal
children living in remote communities of the Northern Territory, Australia. PLoS Negl Trop Dis 2009;3(11):e554.
Chapter 14
Type 2
diabetes
prevention
and early
detection
Author Justin Coleman
Expert reviewers David Atkinson, Stephen Colagiuri
230
Type 2 diabetes prevention and early detection
Overview
Type 2 diabetes is most commonly found in obese adults who develop
increasing insulin resistance over months or years. For these patients there
is a substantial ‘prediabetic’ window period of opportunity to offer preventive
interventions. Screening for diabetes is safe, accurate and cost effective, and
detects a substantial proportion of people who may not otherwise have received
early intervention.1 This chapter discusses type 2 diabetes in adults who are not
pregnant.
The prevalence of type 2 diabetes in Aboriginal and Torres Strait Islander
populations is 3–4 times higher at any age than the general population, with
an earlier age of onset.2 The precise prevalence is hard to pinpoint; a 2011
systematic review of 24 studies showed prevalence estimates ranged from
3.5–31%, with most lying between 10% and 20%. Diabetes prevalence in
remote populations is approximately twice that of urban populations and is
higher among Aboriginal and Torres Strait Islander people.3
Aboriginal and Torres Strait Islander men and women die from diabetes
at 23 and 37 times the rate of non-Indigenous Australian men and women
respectively, in the 35–54 years age group.4 Large scale clinical trials have
demonstrated that appropriate management of diabetes can prevent the
development or delay the progression of complications such as myocardial
infarction, eye disease and renal failure.5
Obesity is a very strong predictor for diabetes; a body mass index (BMI) ≥30 kg/
m2 increases the absolute risk of type 2 diabetes by 1.8–19-fold, depending on
the population studied. A cohort study of non-diabetic Aboriginal adults aged
15–77 years in central Australia found that those with a BMI of ≥25 kg/m2 had 3.3
times the risk of developing diabetes over 8 years of follow up compared to those
with a BMI <25 kg/m2.1 The AusDiab study found that three measures of obesity:
BMI, waist circumference and waist-to-hip ratio, all had similar correlations with
diabetes and CVD risk.6 Waist circumference performed slightly better than BMI
at predicting diabetes in a remote Aboriginal community.7
Interventions
Screening
Type 2 diabetes is generally underdiagnosed. Australia’s largest diabetes
population study, which screened over 11 000 randomly selected people
using an oral glucose tolerance test, found that, of the 7.4% who had diabetes,
half (3.7%) had not been diagnosed previously, in an even spread across all
age groups.8 A smaller study of Aboriginal and Torres Strait Islander people
in Darwin found an overall diabetes prevalence of 17%, of which a third were
previously undiagnosed. When those undiagnosed were assessed for diabetes
complications, 19% had albuminuria, 14% had peripheral vascular disease, 6%
had neuropathy and none had retinopathy.9
Screening for undetected diabetes is an efficient method of preventing
complications from this disease.1 Screening for diabetes will also detect
pre-diabetes – impaired glucose tolerance (IGT) and/or impaired fasting
glucose (IFG) – which cannot be detected clinically, but which is associated
with an increased risk of developing diabetes and cardiovascular and other
macrovascular disease.10
Screening for diabetes in adults who are not pregnant should be done on an
opportunistic basis, in the primary care setting, rather than in mass screening
programs.1 Aboriginal and Torres Strait Islander people should be screened for
diabetes from age 18 years, rather than from 40 years in the general Australian
population.1 Although historically a fasting glucose was recommended as
the sole initial test,11 the 2009 National Health and Medical Research Council
(NHMRC) guideline recommends a three-step process:1 First, perform a formal
assessment of risk factors, this then determines who requires a fasting glucose
sample, and finally, those with equivocal glucose results require an oral glucose
tolerance test (OGTT).
The recommended risk assessment tool is AUSDRISK, which contains
information on age, gender, ethnicity, family history, hypertension, smoking,
diet, physical activity and obesity. AUSDRISK has been validated12 in the
general Australian population and is available as an interactive online page or
a paper printout. Those whose AUSDRISK score is ≥12 proceed to a fasting
plasma glucose test (FPG), or a random blood glucose test (RBG) if this is more
practical.
The use of the AUSDRISK tool in assessing whether Aboriginal and Torres
Strait Islander people should have blood glucose testing is controversial. The
tool incorporates lower cutoff points for waist circumference measurements
that are considered specific for Aboriginal and Torres Strait Islander
people; this does not necessarily take into consideration the considerable
heterogeneity of this population in Australia. Some clinics may decide the time
spent on the tool adds an obstacle that results in fewer patients having any
diabetes assessment at all. Other clinics may find the AUSDRISK screening
questions a useful prompt for discussing diabetic risk factors.
In diagnosing diabetes, if FPG or RBG indicates diabetes, unless the patient
has diabetic symptoms this should be confirmed by retesting on a separate
day, because intra-individual variation occurs.
A laboratory venous glucose test is more reliable than a capillary point-of-care
test (finger prick), but the latter may sometimes be more practical and has the
important advantage of being able to take further action on the same visit. An
opportunistic random blood glucose sample is a reasonable alternative to a
231
232
fasting sample in situations where the patient is unlikely to return for a fasting
test, but the ‘equivocal’ range is altered to 5.5–11 mmol/L.1
Glycated haemoglobin (HbA1c), long used as a measure for assessing
glycaemic control in people with diabetes, is not currently recommended
for diagnosing diabetes in Australia, according to the NHMRC guidelines,1
although the 2010 USA guidelines for the first time included this indication, at a
threshold of ≥6.5%.13 The recommendations may well soon change in Australia.
The National Vascular Disease Prevention Alliance 2011 Australian guidelines
state: ‘When a fasting sample is not possible, non-fasting glucose can be
measured with further testing required if the result is ≥5.5 mmol/L. HbA1c can
be used to diagnose diabetes with a level ≥6.5% being diagnostic’.14
This recommendation has also been adopted by the World Health Organization
as a diagnostic option.15 Currently, there is no Medicare rebate payable for
measuring HbA1c in order to diagnose diabetes.
HbA1c results are affected by inter-laboratory variability (steadily improving),
haemoglobin variants and alterations in red blood cell turnover (including
pregnancy).16 Point-of-care capillary HbA1c testing has been shown to be an
accurate alternative to laboratory testing in a remote Aboriginal community.17
Behavioural interventions
People with established type 2 diabetes can have their mortality halved by
intensive treatment of multiple cardiovascular risk factors.18 For those with IGT,
the Finnish Diabetes Prevention Study showed that interventions aimed at
modifying weight, diet and exercise not only halved the incidence of diabetes
at 4 years compared to a control group (NNT=8), but maintained most of this
benefit for at least 3 years after the initial intervention was ceased.19 There is
strong evidence that lifestyle modifications that focus on weight loss, dietary
change and increased physical activity should be offered to all individuals at
high risk of developing type 2 diabetes.1 However, the recent large ADDITION
randomised trial showed that early, intensive risk factor management in newly
diagnosed type 2 diabetics resulted in only a small reduction in the incidence
of cardiovascular events and death.18 This outcome in European patients aged
40–69 years has uncertain applicability in the Aboriginal and Torres Strait
Islander context.
Dietary intervention can effectively delay or prevent diabetes. Two high quality
studies have randomised people without diabetes into individual dietary
counselling versus routine treatment.20 The Da Qing IGT and Diabetes Study
found that, after 6 years, the group given specific dietary advice had a 33%
reduction in the incidence of diabetes compared to the control group. The Oslo
Diet and Exercise Study found significant reductions in fasting blood glucose,
insulin resistance and body mass index compared to the control group at 1
year.20 However, an 8-year follow up study in a remote Aboriginal community
found that interventions targeting the community store and community
nutritional education did not alter trends towards increasing prevalence
of obesity and diabetes, possibly due to the limited healthy food choices
available.21
Dietary recommendations are found in the Australian dietary guidelines
(see Chapter 1: Lifestyle, section on overweight/obesity).
Physical activity improves insulin sensitivity and promotes peripheral glucose
uptake. The diabetic related benefits of regular exercise are not limited to
subjects who are successful in losing weight. In the Finnish Diabetes Prevention
Study, subjects who exercised for at least 4 hours per week but did not lose
weight still had a markedly decreased incidence of diabetes compared to those
who were sedentary.19 A systematic review found good evidence of reduced
diabetes for walking briskly for ≥2.5 hours per week.22 Ideally, a diabetes
prevention strategy involves the combined interventions of diet modification
and increased exercise. A systematic review of eight trials that combined these
two interventions found the relative risk of diabetes was 0.63 compared to the
control groups.23 A 7-year follow up study in a remote Aboriginal community
involving diet and physical activity interventions found that, despite an increase
in average BMI, the prevalence of IGT decreased and diabetes prevalence did
not increase, possibly due to improved physical activity.24 Watching television
is associated with diabetes; in Australia, those who watch TV for more than 14
hours per week are 2.3 times as likely to develop new diabetes as those who
watch less than 14 hours.8
The national physical activity guidelines recommend a gradual increase in
activity intensity to a goal of at least 30 minutes of moderate physical activity on
most, preferably all, days (see Chapter 1: Lifestyle, section on physical activity).
Chemoprophylaxis and surgery
Current NHMRC guidelines state that, as many of the medications used in
diabetes prevention studies have established side effects, potential benefits and
harms should be taken into account before considering pharmacotherapy.1
Oral hypoglycaemic medication at the prediabetic stage can delay or prevent
progression to diabetes, but is less effective than lifestyle changes. A large
USA trial randomised subjects with prediabetes into an intensive lifestyle
modification program, metformin or placebo.25 At 3 years, the metformin group
had a 31% less progression to diabetes compared to placebo (NNT=13.9).
However, the lifestyle changes group showed a significantly larger relative risk
reduction of 58% (NNT=6.9) across all ages and ethnic groups, so the trial was
prematurely discontinued. A meta-analysis of 31 randomised trials in people at
risk of diabetes showed metformin improves weight, lipid profiles and insulin
resistance, and reduces new onset diabetes by 40%.26
Rosiglitazone and pioglitazone have consistently shown a potent beneficial
effect in diabetes prevention but are associated with significant adverse effects,
particularly new onset of congestive heart failure.27
A Cochrane review showed that acarbose reduces the incidence of type 2
diabetes by 25% (NNT=10) in patients with IGT.28 A study randomising obese
subjects into receiving lifestyle advice plus either orlistat (a weight loss agent)
or placebo found that, in the subgroup who had IGT at baseline, orlistat gave
a 45% risk reduction of progression to diabetes at 4 years.29 A high number
discontinued therapy: 48% of the orlistat group and 66% of the control group.
Surgical weight loss interventions for severe obesity can result in a dramatic
reduction in diabetes. The Swedish Obese Subjects Study compared subjects
who had bariatric surgery with matched controls. At 2 years, the 1845 surgery
cases had a 32-fold reduction in incidence of newly diagnosed diabetes.27 At
8 years, the prevalence of diabetes in the surgery group remained unchanged
from baseline, but had tripled (from 7.8% to 24.9%) in the matched controls.30
233
234
All people at risk for diabetes should be offered lifestyle advice encouraging
increased physical activity and improved dietary intake, and advised as to the
benefits of weight loss. People who are morbidly obese and potentially suitable
for bariatric surgery should be encouraged to consider surgical referral, if
available.
Environmental
In remote and rural areas, poor food supply undermines efforts to address
the poor nutritional status of Aboriginal and Torres Strait Islander people.
Community stores are frequently the only food source outside traditional bush
food.31 Various programs to influence the quality and cost of high nutritional
foods in community stores have had some success; a retail co-operative
in Arnhem land provided 100% freight-subsidised fruit and vegetables and
doubled the intake of these foods per person at 3 years.32 However, the only
study of a remote Aboriginal community store intervention that directly reported
on diabetes prevalence did not show any improvement.21 More studies are
needed.
Surveys in many remote and rural Aboriginal communities have shown
facilities for sporting and recreational activities are lacking, yet these are a high
priority for community members.33 Further studies are required to assess the
association between sport uptake and diabetes in Aboriginal and Torres Strait
Islander communities.
235
Recommendations: Type 2 diabetes prevention and early detection
Preventive
intervention type
Who is at risk?
Screening
Adults ≥18 years
from regions with a
high prevalence of
diabetes (≥5%)
AND/OR
Adults with any of the
following high risk
conditions:
Behavioural
How often?
References
Level/
strength of
evidence
Measure fasting plasma glucose or
Annually as part IIB
random venous blood glucose
of an adult health
assessment
A laboratory test is preferable, but
finger prick testing is an alternative.
HbA1c may also be used as a
screening test for the diagnosis of
diabetes*
Perform oral glucose tolerance test
• previous IGT or IFG in those with equivocal results as
above
• history of
gestational diabetes The 2006 WHO/International
Diabetes Federation criteria should
mellitus
be used to diagnose type 2 diabetes,
• history of polycystic IGT and IFG (see Table 14.1)
ovary syndrome
• history of
cardiovascular
disease
• current
antipsychotic
medication use
1
All adults ≥18 years
from regions with
a low population
prevalence for
diabetes (<5%)
1
Consider screening using AUSDRISK Annually as part IIIB
tool to determine if blood testing is
of an adult health
required (see Resource)
assessment
If AUSDRISK score is ≥12 then
proceed as above for high risk
populations
People <18 years with Consider the potential for early
overweight/obesity
onset type 2 diabetes and consider
testing according to clinical context
(see Chapter 1: Lifestyle, section on
overweight/obesity)
Opportunistic
GPP
34
All people
Opportunistic
and as part of
an annual health
assessment
IA
1,8
Measure BMI and waist
circumference
Advise minimum of 30 minutes
moderate activity on most days
Encourage diet rich in vegetables,
fruits, legumes, high fibre cereals,
fish, and lean meats. Limit fats, salt,
sugar, alcohol
For people overweight or obese
(see recommendations in Chapter
1: Lifestyle, section on overweight/
obesity)
Mothers of young
babies
Encourage infant breastfeeding (see
Chapter 2: Child health)
236
Recommendations: Type 2 diabetes prevention and early detection (continued)
People with BMI ≥35
kg/m2
Advise intensive lifestyle modification Opportunistic
as above
Discuss risks and benefits of bariatric
surgery and consider referral if
services are available (see Chapter
1: Lifestyle, section on overweight/
obesity)
IIIC
1
Chemoprophylaxis People with a high
risk condition (see
above) or at high risk
of diabetes based on
an AUSDRISK score
≥15
Advise intensive lifestyle modification Opportunistic
as above
If lifestyle modification is unable to
be achieved, the use of metformin,
acarbose, rosiglitazone or orlistat
has been shown to delay or prevent
the onset of diabetes
These medications all have potential
risks (in particular rosiglitazone).
None is PBS funded for people
without diagnosed diabetes, so their
use is not recommended at present
1B
1
Advocate for multifactorial and
coordinated community based
interventions to increase access
to healthy and nutritious food and
promotion of increased physical
activity (see Chapter 1: Lifestyle,
section on physical activity)
GPP
35–38
Environmental
Communities
N/A
* HbA1c testing for the purpose of diagnosing diabetes cannot currently be claimed from Medicare
Table 14.1. Diagnostic criteria for type 2 diabetes and
intermediate hyperglycaemia
Type 2 diabetes
Fasting plasma glucose*
≥7.0 mmol/L or
Random venous glucose (point of care)*
≥11.1 mmol/L or
2-hr plasma glucose†
≥11.1 mmol/L or
Glycated haemoglobin (HbA1c)‡
≥6.5%
Impaired glucose tolerance (IGT)
Fasting plasma glucose
<7.0 mmol/L and
≥7.8 and <11.1 mmol/L
Impaired fasting glucose (IFG)
6.1–6.9 mmol/L and if measured
<7.8 mmol/L
Non-diabetes
≤6.0 mmol/L or
Random venous glucose (point-of-care)
≤6.0 mmol/L
*The diagnosis of type 2 diabetes requires two positive blood tests on separate days unless the
plasma glucose is unequivocally elevated in the presence of acute metabolic decompensation or
obvious symptoms such as excessive thirst and polyuria
†Venous plasma glucose 2-hr after ingestion of 75 g oral glucose load. If 2-hr plasma glucose is
not measured, status is uncertain as type 2 diabetes or IGT cannot be excluded
‡Currently recommended in some, but not all guidelines. HbA1c is not funded by Medicare for the
initial diagnosis of diabetes
Source: Colagiuri S, Davies D, Girgis S, Colagiuri R 20091
Resource
AUSDRISK tool:
www.ausdrisk.com.au
www.ausdrisk.org.au/Portals/O/Risk-test.pdf.
References
1. Colagiuri S, Davies D, Girgis S, Colagiuri R. National evidence based guideline for case detection and
diagnosis of type 2 diabetes. Canberra: NHMRC and Diabetes Australia, 2009. Cited October 2011.
Available at www.nhmrc.gov.au/_files_nhmrc/publications/attachments/di17-diabetes-detectiondiagnosis.pdf.
2. De Courten M. Review of the epidemiology, aetiology, pathogenesis and preventability of diabetes
in Aboriginal and Torres Strait Islander population. Canberra: International Diabetes Institute and
Commonwealth Department of Health and Family Services, 1998.
3. Minges K, Zimmet P, Magliano D, Dunstan D, Brown A, Shaw J. Diabetes prevalence and determinants in
Indigenous Australian populations: a systematic review. Diabetes Res Clin Pract 2011;93:139–49.
Cited Oct 2011. Available at www.aihw.gov.au/publications/index.cfm/title/10583.
6. Daniel M, Rowley K, 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):1993–8.
7.
Dalton M, Cameron A, Zimmet P, et al. Waist circumference, waist–hip ratio and body mass index and
their correlation with cardiovascular disease risk factors in Australian adults. J Intern Med 2003;254:555–
63.
8. Dunstan D, Zimmet P, Welborn T, et al. The rising prevalence of diabetes and impaired glucose tolerance:
the Australian Diabetes, Obesity and Lifestyle Study. Diabetes Care 2002;25(5):829–34.
9. Cunningham J, O’Dea K, Dunbar T, Weeramanthri T, Shaw J, Zimmet P. Socioeconomic status and
diabetes among urban Indigenous Australians aged 15–64 years in the DRUID study. Ethn Health
2008;13(1):23–7.
10. Twigg SM, Kamp MC, Davis TM, Neylon EK, Flack JR. Prediabetes: a position statement from the
Australian Diabetes Society and Australian Diabetes Educators Association. Med J Aust 2007;186:461–5.
11. National Health and Medical Research Council. National evidence based guidelines for the management
of type 2 diabetes mellitus: primary prevention, case detection and diagnosis. Canberra: Commonwealth
of Australia, 2001.
12. Chen L, Magliano DJ, Balkau B, et al. AUSDRISK: an Australian type 2 diabetes risk assessment tool
based on demographic, lifestyle and simple anthropometric measures. Med J Aust 2010;192(4):197–202.
13. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care
2010;33(Suppl 1):S62–9.
14. National Vascular Disease Prevention Alliance. Guidelines for the management of absolute cardiovascular
disease risk 2011.
15. World Health Organization. Use of glycated haemoglobin (HbA1c) in the diagnosis of diabetes mellitus.
Geneva: WHO, 2011. Cited October 2011. Available at www.who.int/diabetes/publications/reporthba1c_2011.pdf.
16. Shaw JE, d’Emden MC, Goodall I. Is Australia ready to use glycated haemoglobin for the diagnosis of
diabetes? Med J Aust 2011;195:7–8.
17. Martin DD, Shephard MDS, Freeman H, et al. Point-of-care testing of HbA1c and blood glucose in a
remote Aboriginal Australian community. Med J Aust 2005;182:524–7.
18. Griffin S, Borch-Johnsen K, Daviese MJ, Khuntif K, Rutten GE. Effect of early intensive multifactorial
therapy on 5-year cardiovascular outcomes in individuals with type 2 diabetes detected by screening
(ADDITION-Europe): a cluster-randomised trial. Lancet 2011;378(9786):156–67.
19. Tuomilehto J, Lindstrom J, Eriksson J, Valle T, Hamalainen H. Prevention of type 2 diabetes mellitus by
changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001;344(18):1343–
50.
20. Nield L, Summerbell C, Hooper L, Whittaker V, Moore H. Dietary advice for the prevention of type 2
diabetes mellitus in adults. Cochrane Database Syst Rev 2008;Jul 16;(3):CD005012.
21. McDermott R, Rowley KG, Lee AJ, Knight S, O’Dea K. Increase in prevalence of obesity and diabetes and
decrease in plasma cholesterol in a central Australian Aboriginal community. Med J Aust 2000;172:480–
4.
22. Jeon C, Lokken P, Hu F, Van Dam R. Physical activity of moderate intensity and risk of type 2 diabetes.
Diabetes Care 2007;30:744–52.
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23. Orozco L, Buchleitner A, Gimenez-Perez G, Roqué i Figuls M, Richter B, Mauricio D. Exercise or exercise
and diet for preventing type 2 diabetes mellitus. Cochrane Database Syst Rev 2008;Jul 16;(3):CD003054.
24. Rowley KG, Gault A, McDermott R, Knight S, McLeay T, O’Dea K. 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;23:898–904.
25. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, et al. Reduction in the
incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393–403.
26. Salpeter SR, Buckley MS, Kahn JA, Salpeter EE. Meta-analysis: metformin treatment in persons at risk for
diabetes mellitus. Am J Med 2008;121:149–57.
27. Karam JG, McFarlane SI. Update on the prevention of type 2 diabetes. Curr Diab Rep 2011;11:56–63.
28. Van de Laar F, Lucassen P, Akkermans R, Van de Lisdonk E, De Grauw W. Alpha-glucosidase inhibitors
for people with impaired glucose tolerance or impaired fasting blood glucose. Cochrane Database Syst
Rev 2006;Oct 18;(4):CD005061.
29. Torgerson J, Hauptman J, Boldrin M, Sjostrom L. Xenical in the prevention of diabetes in obese subjects
(XENDOS) study. Diabetes Care 2004;27:155–61.
30. Sjöström CD, Peltonen M, Wedel H, Sjöström L. Differentiated long-term effects of intentional weight loss
on diabetes and hypertension. Hypertension 2000;36:20–5.
31. National Health and Medical Research Council. Nutrition in Aboriginal and Torres Strait Islander Peoples:
an information paper. Canberra: NHMRC, 2000. Cited October 2011. Available at www.nhmrc.gov.
au/_files_nhmrc/publications/attachments/n26.pdf.
32. Lee A, Hobson V, Katarski L. Review of the nutrition policy of the Arnhem Land Progress Association.
Aust NZ J Public Health 1995;20(5):538–44.
33. National Aboriginal Community Controlled Health Organisation. Evidence base to a preventive health
assessment in Aboriginal and Torres Strait Islander peoples. South Melbourne: The Royal Australian
College of General Practitioners, 2005.
34. Rosenbloom AL, Silverstein JH, Amemiya S, Zeitler P, Klingensmith GJ. Type 2 diabetes mellitus in the
child and adolescent. Pediatr Diabetes 2008;9(5):512–26.
35. Black A. Evidence of effective interventions to improve the social and environmental factors impacting on
health: informing the developments of Indigenous community agreements. Canberra: Office for Aboriginal
and Torres Strait Islander Health, 2007.
36. Browne J, Laurence S, Thorpe S. Acting on food insecurity in urban Aboriginal and Torres Strait Islander
communities: policy and practice interventions to improve local access and supply of nutritious food,
2009. Cited October 2011. Available at www.healthinfonet.ecu.edu.au/health-risks/nutrition/otherreviews.
37. Bravata DM, Smith-Spangler C, Sundaram V, et al. Using pedometers to increase physical activity and
improve health. JAMA 2007;298(19):2296–304.
38. Bauman A, Bellew B, Vita P, Brown W, Owen N. Getting Australia active: towards better practice for the
promotion of physical activity. Melbourne: National Public Health Partnership, 2002.
Chapter 15
Prevention
and early
detection of
cancer
Author Nadia Lusis
Expert reviewers Bruce Armstrong (prostate and bowel),
Vijenti Chandra (breast and cervical), Greg Dore (liver)
240
Prevention and early detection of cancer
Overview
Cancer is estimated to account for 6% of the health gap between Aboriginal
and Torres Strait Islander people and the total population. Aboriginal men have
a 1.7 times higher burden of disease and Aboriginal women a 1.9 times higher
burden of disease due to cancer when compared to the total Australian male
and female population respectively.1
Inadequate identification of Indigenous status on cancer registries and in
death registers in many jurisdictions means that reported statistics on cancer
incidence and mortality are likely to underestimate true rates of cancer. Available
statistics on cancer in Aboriginal and Torres Strait Islander people show that
while overall cancer incidence may be lower, Aboriginal and Torres Strait
Islander people have a higher incidence of preventable cancers, such as lung,
cervical and liver cancer. In addition, due to later diagnosis and poorer access
to adequate treatment, Aboriginal and Torres Strait Islander people have higher
case fatality rates for many cancers compared to the rest of the population.2
Prevention of cervical cancer
Background
The incidence of cervical cancer in Aboriginal and Torres Strait Islander women
is about 2.4–3 times greater than in non-Indigenous women.3,4 Cervical cancer
is the third most common cause of death due to cancer in Aboriginal and Torres
Strait Islander women, with the years of life lost due to cervical cancer being
5.7 times greater and the mortality rate being 5.6 times higher in Aboriginal and
Torres Strait Islander women compared to non-Indigenous women.1,5 One study
suggested that Aboriginal women in remote areas appeared to be at higher risk of
cervical cancer than those in urban areas.6
Interventions
Vaccination against human papillomavirus (HPV) is recommended due to
the link between cervical HPV infection and the development of cervical dysplasia.
As the efficacy of vaccination in preventing HPV infection and cervical dysplasia
decreases with the increasing number of previous sexual partners, vaccination
should preferably be given prior to onset of sexual activity, or otherwise as early
as possible. Studies in the 14–26 years age group have provided evidence for
immunogenicity and prevention of high grade squamous cervical lesions, while
studies in other age groups at this stage provide evidence for immunogenicity
only. See the Australian Immunisation Handbook for more details.7–12
Pap tests have been shown to reduce the risk of developing cervical cancer. In
2008–09 in Australia, 61.2% of the target population participated in screening,
with the lowest participation rates in the lowest (53.3%) compared to the highest
(64.3%) socioeconomic quintile.5 Cervical screening state registries do not
systematically collect information on the Aboriginal and Torres Strait Islander
status of women screened.5 Aboriginal and Torres Strait Islander women tend to
have lower participation rates in screening programs, with studies using indirect
methods to calculate their participation rates are 30–50% lower than for nonIndigenous women.13,14
Factors that may increase participation of Aboriginal and Torres Strait Islander
women in cervical cancer screening are inclusion of cervical screening programs
within primary healthcare services, culturally appropriate care, appropriate staff
including female staff and involvement of Aboriginal and Torres Strait Islander
health workers, community participation and linkages between services.13,15–17
The Practice Incentives Program (PIP) provides financial incentives for accredited
health services to provide Pap screening.
Pap testing recommendations apply to asymptomatic women. Women with
symptoms, abnormalities of the cervix on examination or glandular abnormalities
on smears should be referred for specialist review and treatment.
A review of the National Cervical Screening Program is planned, and once
this is complete the National Health and Medical Research Council (NHMRC)
guidelines18 are likely to be reviewed, which may result in changes to these
recommendations. The National Cervical Screening Program recommends
Pap tests be used as the primary method for population screening until there
is sufficient evidence indicating the effectiveness of newer cervical screening
technologies such as Thinprep and HPV tests.19 Women vaccinated against HPV
should follow the same cervical screening recommendations as unvaccinated
women.20
241
242
Recommendations: Cervical cancer prevention and detection
Who is at risk?
How often?
Immunisation
Girls aged 10–13
years
Promote human papilloma virus
(HPV) vaccination for the prevention
of cervical cancer ideally prior to the
onset of sexual activity
Recommend HPV vaccination as
part of school based vaccination
programs. If not accessed in a
school program then offer through
clinic/community services
As per National
IIB
Immunisation Program
Schedule (NIPS)
(varies between states
and territories)
10,21
Girls aged 14–18
years
Promote HPV vaccination for the
prevention of cervical cancer ideally
prior to the onset of sexual activity*
As per Australian
Immunisation
Handbook
IIB
10,21
Women aged
19–26 years
Promote HPV vaccination for the
prevention of cervical cancer for
health benefit, but likely to be less
effective*
Women aged
27–45 years
HPV vaccination may be of some
benefit depending on sexual history†
Women aged
18–69 years who
have ever been
sexually active
Offer Pap test screening from
18–20 years or 1–2 years after first
sexual intercourse (whichever is
later) regardless of whether HPV
vaccination has been given
Every 2 years
IIA
22,23
Women aged 70+ Offer Pap test screening to women
years who have
who have never had a Pap test or
ever been sexually who request a Pap test
active
Pap test screening
IIA
may cease for women
aged 70 years who
have had two normal
Pap smears within the
past 5 years
22,23
Women at
higher risk (eg.
previous cervical
abnormalities,
immune
suppression, in
utero exposure to
diethylstilboestrol)
Offer Pap test screening
Management regimen GPP
is complex: see
NHMRC guidelines
18
Women who have
been previously
treated for high
grade squamous
intraepithelial
lesion
Offer annual Pap test screening
combined with cervical HPV testing
for 2 or more consecutive years, if
not already done following specialist
treatment
If both tests are
negative in 2
consecutive years,
screening for average
risk population can
recommence
IIIC
18,24
All women
Assess smoking status and advise
on increased risks of cervical
dysplasia and cervical cancer (see
Chapter 1: Lifestyle, section on
smoking)
As part of an annual
health assessment
IIIB
25,26
Offer a sexual health review (see
Chapter 8: Sexual health and
bloodborne viruses)
health assessment
Screening
Behavioural
Level/
strength
of
evidence
References
Preventive
intervention
type
* Currently not subsidised through the NIPS
† 4-valent HPV vaccine (Gardasil®) is not registered by the Therapeutic Goods Administration for use in this age group due to lack of safety
and efficacy data at the time of writing this guideline
Resources
Screening to prevent cervical cancer: guidelines for the management of asymptomatic
women with screen detected abnormalities (NHMRC)
www.nhmrc.gov.au/publications/synopses/wh39syn.htm
The Australian Immunisation Handbook (NHMRC): HPV chapter
www.immunise.health.gov.au/internet/immunise/publishing.nsf/Content/
Handbook-hpv.
243
244
Prevention and early detection of liver
(hepatocellular) cancer
Background
Limited data are available on the incidence and mortality from liver cancer in
Aboriginal and Torres Strait Islander people, and different jurisdictions report
different results. Northern Territory data showed the age standardised incidence
rates were 6.6 times higher in Aboriginal men and 4.5 in Aboriginal women,
and the mortality rate ratio was 8.7 for men and 7.0 for women.3 However, in
Queensland, based on cancer registry data, no difference was shown in liver
cancer incidence or mortality between Aboriginal and non-Aboriginal people.27
Hepatocellular carcinoma (HCC) is almost always preceded by cirrhosis. Major
risk factors for cirrhosis (and therefore HCC) in Australia are chronic hepatitis B
and C infection, alcoholic liver disease and fatty liver disease. Notification rates
for hepatitis B and C are higher for Aboriginal and Torres Strait Islander people.
The prevalence of hepatitis B infection in Aboriginal and Torres Strait Islander
populations has been estimated to be 2% in the urban areas and 8% in rural
areas, compared to less than 1% for the total Australian population.2 Despite
2.5% of the Australian population identifying as Aboriginal or Torres Strait
Islander, Aboriginal and Torres Strait Islander people are estimated to account
for 16% of the population with chronic hepatitis B infection.28
Low rates of identification of Indigenous status on infectious disease
notifications makes data difficult to interpret. It is estimated that 4% of Aboriginal
and Torres Strait Islander people have chronic hepatitis C compared to 1%
of non-Indigenous people, however, data quality is poor, with identification of
Aboriginal and Torres Strait Islander status for those newly diagnosed with
hepatitis C in 2009 occurring in only 39% of reports.28
Some people are at higher risk of being infected with hepatitis B or C
(Table 15.1).
Table 15.1. Risk factors for hepatitis B and C infection
Those at higher risk of hepatitis B infection include non-immune household or sexual
contacts of people with acute or chronic hepatitis B; people aged 15–30 years; babies
born to mothers with hepatitis B infection; people with multiple sexual partners; men
who have sex with men; people who inject drugs; people at occupational risk or in
prison/detention; and people with chronic liver disease, hepatitis C infection, HIV or
impaired immunity
Those at higher risk of hepatitis C infection include people who have ever injected drugs
for recreational purposes; people who have ever been incarcerated; those with tattoos
and body piercings; recipients of blood products, tissues or organs prior to February
1990 in Australia or anytime overseas; and sexual partners of those with hepatitis C
infection if blood has been associated with sexual activity
See also Chapter 8: Table 8.1: Risk factors for sexually transmissible infections and bloodborne
viruses
Sources: National Health and Medical Research Council 2008 and Department of Health and
Ageing 201010,29
245
Interventions
Hepatitis B vaccination reduces the risk of chronic hepatitis B infection, which is
a risk factor for the development of HCC. Aboriginal people are considered by
the World Health Organization to be a priority group for hepatitis B vaccination
due to intermediate to high endemicity of hepatitis B infection.30 The US Centres
for Disease Control recommends screening and hepatitis B vaccination for
all people from geographic areas with a prevalence of hepatitis B of >2%.31
Universal infant vaccination and catch-up adolescent vaccination is currently
available through the National Immunisation Program. Vaccination for other
groups may be funded through state and territory health department programs.
Hepatitis B antiviral therapy for those with chronic hepatitis B reduces liver
disease progression and risk of HCC. Licensed therapies provided through the
S100 scheme include tenofovir, entecavir and pegylated interferon.
Hepatitis C antiviral therapy for those with chronic hepatitis C reduces liver
disease progression and risk of HCC. Licensed therapy provided through the
S100 scheme is pegylated interferon and ribavirin.
Recommendations: Liver cancer prevention and detection
Preventive
intervention type
Who is at risk?
How often?
Level/
strength of
evidence
References
Immunisation
All people
Review if hepatitis B
vaccination is indicated
(see recommendations in
Chapter 8: Sexual health
and bloodborne viruses
and Chapter 2: Child
health)
See Chapter 8
See Chapter
8
32
Screening
All people
Review if hepatitis B and
C screening is indicated
(see recommendations in
See Chapter 8
See Chapter
8
32,33
People with
chronic liver
disease or
chronic hepatitis
infection
Recommend specialist
review to consider
if screening for
hepatocellular carcinoma
using alpha fetoprotein
(AFP) and ultrasound is
warranted
6–12 monthly as
part of specialist
management plan
IIIC
34–37
Adolescents and
adults
Assess levels of alcohol
consumption and advise
about safer levels of
alcohol consumption to
reduce long terms risk
of alcohol related harm
section on alcohol and
Chapter 3: The health of
young people)
health assessment
IIIB
38
People with
overweight/
obesity
Advise of the risks of liver
Opportunistic
disease and promote
weight reduction strategies
section on overweight/
obesity)
GPP
39
Behavioural
246
Recommendations: Liver cancer prevention and detection (continued)
People at higher
risk of hepatitis B
or C infection (see
Table 15.1)
Provide counselling on
harm minimisation and
promote peer education
strategies around safer
sex and injecting drug
use where relevant (see
Opportunistic and
health assessment
GPP
29
People with
chronic liver
disease or
chronic hepatitis
infection
Provide counselling
regarding risks of alcohol
consumption
6–12 monthly as
required
GPP
36
Assess disease severity
and suitability for antiviral
treatment
Regular monitoring for
disease progression is
recommended
Refer to national or local
guidelines for management
recommendations (see
Resources)
See management
guidelines and/or
contact local services
for advice
IIIC
36,40
Chemoprophylaxis People with
chronic hepatitis
B† or hepatitis C
infection
* The World Health Organization recommends screening and hepatitis B vaccination for all people from geographic areas with a
prevalence of hepatitis B of >2%.30,31 The prevalence of hepatitis B infection in the Aboriginal population has been estimated to be 2%
in the urban areas and 8% in rural areas2
†Hepatitis B surface antigen positive >6 months
Resources
The Australian immunisation handbook (NHMRC): hepatitis B chapter
www.immunise.health.gov.au/internet/immunise/publishing.nsf/Content/
Handbook-hepatitisb
Australia and New Zealand chronic hepatitis B recommendations (Gastroenterological
Society of Australia and Digestive Health Foundation)
www.gesa.org.au/files/editor_upload/File/Professional/CHB.pdf
HIV, viral hepatitis and STIs: a guide for primary care (Australasian Society for HIV
Medicine: further resources will be available through ASHM in 2012, including
information on access to new treatment options for some people with chronic hepatitis
C infection)
www.ashm.org.au/default2.asp?active_page_id=133.
247
Prevention and early detection of
breast cancer
Background
Breast cancer is the most common cancer diagnosed in Aboriginal and Torres
Strait Islander women, despite an under-reporting rate of at least 10%.41 Despite
the age standardised incidence of breast cancer being estimated at around 30%
lower for Aboriginal compared to non-Aboriginal women,3,4 it is estimated that
there is a similar burden of disease, that the years of life lost may be 1.5 times
higher and mortality rates may be up to 1.5 times greater for Aboriginal women.1,4,41
Aboriginal and Torres Strait Islander women have lower participation rates in
mammographic screening programs. The estimated participation of Aboriginal
and Torres Strait Islander women in the BreastScreen program for the target
age range of 50–69 years, using self identification, has remained constant from
2002–03 to 2007–08 at 36%, while participation of non-Indigenous women rose
from 50.0% to 54.8% over the same timeframe.42
Estimating risk based on family history
Estimations of the risk of breast cancer based on family history are available
(see Resources). Table 15.2 highlights risk categories based on the National
Breast and Ovarian Cancer Centre recommendations.43 The risk calculation may
differ from the more up-to-date online resource but is provided for situations
where the online resource may not be available.44
Table 15.2. Risk categories for breast cancer based on family history
Category 1
At or slightly above average
risk (no more than 1.5 times the
population average risk)
Category 2
Moderately increased risk
(1.5–3 times the population
average risk)
Category 3
Potentially high risk (may be more than 3
times the population average risk)
No confirmed family history of
breast cancer
One first degree relative diagnosed
with breast cancer at age 50 years
or older
One second degree relative
diagnosed with breast cancer at
any age
Two second degree relatives on the
same side of the family diagnosed
with breast cancer at age 50 years
or older
Two first degree or second degree
relatives diagnosed with breast
cancer, at age 50 years or older, but
on different sides of the family (ie.
one on each side of the family)
One first degree relative diagnosed
with breast cancer before the age
of 50 years (without the additional
features of the potentially high risk
group – see category 3)
Two first degree relatives, on the
same side of the family, diagnosed
with breast cancer (without
the additional features of the
potentially high risk group – see
category 3 )
Two second degree relatives,
on the same side of the family,
diagnosed with breast cancer,
at least one before the age of
50 years, (without the additional
features of the potentially high risk
group – see category 3)
Two first degree or second degree relatives on
one side of the family diagnosed with breast or
ovarian cancer plus one or more of the following
on the same side of the family:
Source: National Breast and Ovarian Cancer Centre 201043
• additional relative(s) with breast or ovarian
cancer
• breast cancer diagnosed before the age of 40
years
• bilateral breast cancer
• breast and ovarian cancer in the same
woman
• Jewish ancestry
• breast cancer in a male relative
One first degree or second degree relative
diagnosed with breast cancer at age 45 years
or younger plus another first degree or second
degree relative on the same side of the family
with sarcoma (bone/soft tissue) at age 45 years
or younger
Member of a family in which the presence of a
high risk breast cancer or ovarian cancer gene
mutation has been established
248
Interventions
Mammographic screening for women at average or slightly above average risk is
currently recommended at 50–69 years, and is available but not recommended
as routine for women in this risk group aged 40–49 years. For both of these age
groups, mammographic screening has been shown to reduce breast cancer
mortality.
There are some concerns about an increased risk of overdiagnosis and
overtreatment of breast cancers that may never become clinically significant
and the psychological effects of increased investigation for false positive results;
this warrants more definitive research to quantify the magnitude of these effects.
It should be noted that the risk of breast cancer increases from age 40–69
years, and thus there may possibly be more benefit for older women in each
age group. Women should be provided with information to allow an informed
decision based on their individual risk and preferences. Routine mammographic
screening is not recommended for women younger than 40 years. Routine
mammographic screening is not recommended for women aged 70 years
or older. The risk of breast cancer increases with age, but decisions about
mammographic screening need to take into account general health and other
patient factors to decide on potential benefits of screening.45–50
Participation in mammographic screening may be improved by organised
patient reminder and recall systems.51 Strategies to increase participation of
Aboriginal and Torres Strait Islander women need to be tailored to suit the local
circumstances, including provision of appropriate information on prevention
and early detection of breast cancer, female health staff, collaboration between
Aboriginal health services and BreastScreen Australia, use of mobile screening
units and coordination of screening with health assessment recalls.15–18
Magnetic resonance imaging (MRI) screening combined with mammography
has been shown to be more sensitive than mammography alone in women
younger than 50 years at high risk of breast cancer. This option may be
considered as part of specialist review. A Medicare rebate is available when
referred by a specialist.52
Population screening by regular clinical breast examination cannot be
recommended due to lack of evidence that it reduces mortality from breast
cancer.48,50,53
Regular breast self examination cannot be recommended due to lack of
evidence that it reduces mortality from breast cancer.50,53–55
Hormone replacement therapy (HRT), ie. combined (oestrogen-progesterone)
at or around the time of menopause increases the risk of breast cancer. The
risk increases with duration of use, especially after 5 years. Women should be
informed of the risks and benefits of HRT use to allow an informed decision to
be made. For women who have had a hysterectomy, oestrogen-only HRT may
be a better choice.56 Current evidence suggests that use of combined HRT
does not have an additive effect when combined with a family history risk of
breast cancer.57
Chemoprophylaxis (ie. tamoxifen and raloxifene) have shown some benefit in
preventing breast cancers, though with a risk of adverse effects. At December
2010, neither had Pharmaceutical Benefits Scheme approval for primary
prevention of breast cancer in Australia. Trials of aromatase inhibitors are also
being conducted.54,58–60
249
Recommendations: Breast cancer prevention and detection
Preventive
intervention type
Who is at risk?
How often?
of evidence
Screening
All women
Ask about family history of breast
cancer to ascertain the individual
risk of developing breast cancer
(see Table 15.2)
As part of an
annual health
assessment
GPP
43
IIC
50,53–55
Discuss ‘breast awareness’ rather
than promoting regular breast
self examination (ie. ‘get to know
what your breasts normally look
and feel like’) and ask women
to promptly report persistent or
unusual changes
Women aged
40–49 years at
or slightly above
average risk (see
Table 15.2)
Routine mammographic
screening is not recommended
If requested, provide information
about mammographic screening
to allow an informed decision
based on individual risk and
preferences
N/A
IB
46,49,50,61
Women aged
40–49 years
at moderately
increased risk
(see Table 15.2)
Consider annual mammography
starting at age 40 years
Consider referral to family
cancer clinic or specialist cancer
clinic where available for initial
assessment of risk of developing
cancer. This includes advice
on the role of genetic testing,
strategies to reduce risk of
cancer, and information about
early detection (see Resources)
Annually
GPP
43
Women aged
50–69 years at
or slightly above
average risk (see
Table 15.2)
Recommend mammography
Every 2 years
screening and provide information
to allow an informed decision
based on individual risk and
preferences
IB
45–50,62
Women aged
50–69 years
at moderately
increased risk
(see Table 15.2)
Recommend routine
mammography screening
Consider referral to family cancer
clinic* or specialist cancer clinic
for initial assessment
Every 2 years
GPP
43
Consider
annually
GPP
43
Offer referral to a family cancer
clinic* for risk assessment,
possible genetic testing and
development of a management
plan
When calculated GPP
to be at
potentially high
risk, and as
needed
43
Consider MRI breast screening in
addition to mammography if aged
<50 years. (Specialist referral
is required to claim a Medicare
rebate)
Consider annual IIIB
screening
depending on
specialist advice
52
Consider clinical breast
examination
As part of a well
women’s check
43
Women at
Recommend mammographic
potentially high
screening regardless of age
risk of breast
cancer (see Table
15.2)
GPP
250
Recommendations: Breast cancer prevention and detection (continued)
Behavioural
All women
Promote physical activity as
physical inactivity increases the
risk of breast cancer (see Chapter
1: Lifestyle, section on physical
activity)
As part of an
annual health
assessment
(see Chapter 1:
Lifestyle)
IIIB
1,63,64
Advise that alcohol consumption
increases the risk of breast
cancer, and that if alcohol is
consumed it should be done
at safe levels (see Chapter 1:
Lifestyle, section on alcohol)
IIIB
38,64–66
Advise that cigarette smoking
increases the risk of breast
cancer, and support people who
smoke to quit (see Chapter 1:
Lifestyle, section on smoking)
IIIC
67,68
Advise that maintaining a healthy
weight lowers the risk of breast
cancer (see Chapter 1: Lifestyle,
section on overweight/obesity)
IIIB
64
Pregnant and
breastfeeding
women
Advise that breastfeeding has
been shown to reduce the risk
of breast cancer, and support
women to breastfeed their infants
(see Chapter 2: Child health,
section on anaemia)
During and
following
pregnancy
IIIB
64,69
Women on
combined
hormone
replacement
therapy (HRT)
Advise about risks and benefits
of combined HRT; in particular
advise about increased risk of
breast cancer with continuous
use for more than 5 years
When
considering
commencing
HRT and every
6 months for
women on
combined HRT
I-IIIA
56,70,71
IIID
54,58–60
Chemoprophylaxis Women at
potentially high
risk, and women
aged >35 years
at moderate risk
Consider specialist referral to
discuss preventive treatment with
tamoxifen or raloxifene
Use is not currently approved for
subsidy under the Pharmaceutical
Benefits Scheme for the primary
prevention of breast cancer
(See Resources)
*Family cancer clinics provide counselling and information for families with a history of cancer on inheriting cancer, individual risk, screening,
cancer risk reduction strategies, and genetic testing where appropriate. Clinics are conducted through the public hospital system and there
is no direct cost to the patient for consultation or genetic testing. Location of family cancer clinics in Australia can be found at
www.cancer.org.au/File/Aboutcancer/Family_Cancer_Clinics_31OCT06.pdf
Resources
Family cancer clinics (Cancer Australia)
http://canceraustralia.nbocc.org.au/fraboc/clinic.html
Online calculator, familial risk assessment – breast and ovarian cancer (National Breast
and Ovarian Cancer Centre)
www.nbocc.org.au/fraboc/ or http://canceraustralia.nbocc.org.au/fraboc
Advice about familial aspects of breast cancer and epithelial ovarian cancer (National
Breast and Ovarian Cancer Centre
www.nbocc.org.au/view-document-details/bog-advice-about-familial-aspectsof-breast-cancer-and-epithelial-ovarian-cancer
Advice for women seeking advice about risk reducing medication (Cancer Australia)
http://canceraustralia.nbocc.org.au/view-document-details/rrm-risk-reducingmedication-for-women-at-increased-risk-of-breast-cancer-due-to-familyhistory.
251
252
Prevention and early detection of
colorectal (bowel) cancer
Background
Colorectal cancer is the third most common cancer diagnosed in both
Aboriginal men and women.3 The aged standardised incidence of colorectal
cancer from available data showed a 41% lower relative risk in Aboriginal and
Torres Strait Islander people compared to non-Indigenous people.4 Despite the
lower incidence of bowel cancer, due to later stage at diagnosis,2 the burden
of disease (measured in disability adjusted life years [DALYs]) for colorectal
cancer in Aboriginal people was 1.1 times higher than that of the total Australian
population.1 One review of participation in the National Bowel Cancer Screening
Program estimated that the participation rate for non-Indigenous Australians
was 2.1 times greater than that for Aboriginal and Torres Strait Islander people.72
The lower participation of Aboriginal and Torres Strait Islander people in
the bowel cancer screening program may be due to lack of awareness,
inappropriateness of educational material in testing packs, cultural reasons,
beliefs about bowel cancer, a higher risk of not having a fixed address, and
underidentification of Aboriginal or Torres Strait Islander origin when returning
forms. Culturally appropriate population and localised health promotion
campaigns and information, recommendations for testing by a person’s health
service, alternative methods of distributing test kits, and specific strategies to
promote screening through Aboriginal and Torres Strait Islander health services
may increase participation in screening.73–75
Estimating risk based on family history
The 2005 National Health and Medical Research Council endorsed Guidelines
for the prevention, early detection and management of colorectal cancer76 are
used to determine an asymptomatic person’s risk of colorectal cancer based on
family history. Table 15.3 highlights the risk factors for each risk category. Also
see Resources.
253
Table 15.3. Risk categories for colorectal cancer based on family history
Category 1
Those at or slightly above
average risk based on
family history
Category 2
Those at moderately
increased risk based on
family history
Category 3
Those at potentially high risk based on
family history
No personal history of
colorectal cancer, colorectal
adenomas or chronic
inflammatory bowel disease
and no confirmed close family
history of colorectal cancer
or
One first degree (parent,
sibling, child) or second degree
(aunt, uncle, niece, nephew,
grandparent, grandchild)
relative with colorectal cancer
diagnosed at age 55 years or
older
or
Two relatives diagnosed with
colorectal cancer at age 55 or
older but on different sides of
the family
One first degree relative with
colorectal cancer diagnosed
before the age of 55 years
(without potentially high risk
features as in category 3)
or
Two first or one first and one
second degree relative/s
on the same side of the
family with colorectal cancer
diagnosed at any age
(without potentially high risk
features as in category 3)
Three or more first degree relatives or a
combination of first and second degree
relatives on the same side of the family
diagnosed with colorectal cancer
or
Two or more first or second degree relatives
on the same side of the family diagnosed with
colorectal cancer plus any of the following high
risk features:
• multiple colorectal cancers in a family
member
• colorectal cancer before the age of 50 years
• a hereditary non-polyposis colorectal cancer
(HNPCC) related cancer (endometrial,
ovarian, stomach, small bowel, renal pelvis
or ureter, biliary tract, brain cancer)
or
• at least one first degree or second degree
relative with a large number of adenomas
throughout the large bowel (suspected
familial adenomatous polyposis (FAP)
or
• member of a family in which a gene mutation
that confers a high risk of colorectal cancer
has been identified
Interventions
The evidence for faecal occult blood testing (FOBT) screening is that it is
most appropriate for those aged 50–75 years. Screening could be considered
for those aged 76–85 years depending on patient circumstances. Evidence
is lacking for benefit of screening for those aged >85 years.76–79 A limited
National Bowel Cancer Screening Program concluded in 2010, and plans for
further government funding remain uncertain. FOBT kits (for a fee) may be
obtained through The Cancer Council and some GPs and pharmacies.80,81
Sigmoidoscopy (preferably flexible) every 5 years from the age of 50 years76 or
colonoscopy every 10 years79 may be alternatives to second yearly FOBT. GPs
can also refer patients for examination of faecal specimens for occult blood
under Medicare Benefits Schedule (Items 66764, 66767 and 66770).
There is ongoing debate about the benefits of using aspirin for prevention of
adenomas and colorectal cancers.76,82–87 For people with previous adenomas
who are at higher risk of colorectal cancer, benefits of reduction in recurrent
adenoma and colorectal cancer may outweigh the risks of harm.76,84,88
254
Recommendations: Colorectal cancer prevention and detection
Preventive
intervention type
How often?
of evidence
Screening
All people
Ask about family history of
colorectal cancer (see Table
15.3) in order to estimate the
individual risk of developing
colorectal cancer
health assessment
GPP
76
People at or
slightly above
average risk
age 50+ years
(category 1:
Table 15.3)
Consider faecal occult
blood test (FOBT)* and
refer all abnormal results
for appropriate diagnostic
evaluation
Every 2 years from
age 50–75 years, and
could be continued
beyond 75 years
depending on individual
circumstances*
IA
76–79
People at
moderate risk
(category 2:
Table 15.3)
Consider referral for
colonoscopy
(Flexible sigmoidoscopy
and double contrast barium
enema or CT colonography
may be offered if colonoscopy
is contraindicated)
Every 5 years starting at IIIC
age 50 years, or at an
age 10 years younger
than the age of first
diagnosis of bowel
cancer in the family,
whichever comes first
76
Those at
potentially high
risk (category 3:
Table 15.3)
Consider referral to a
specialist service for further
risk assessment and possible
genetic testing, and to a
bowel cancer specialist to
plan appropriate surveillance
(See Resources for specific
recommendations for
screening for those with FAP
or HNPCC)**
At the time of
determining the
individual is at high risk
Offer referral later
if not done at initial
assessment
IIIC
IIIC
Past history of
adenoma
Undertake surveillance
colonoscopy
Timeframe for
surveillance
colonoscopy varies
(see Resources)
IA
76
All people
Provide lifestyle risk factor
counselling on the benefits
health assessment
of regular physical activity,
maintaining healthy weight,
alcohol intake in the low risk
range, avoidance of tobacco
smoking, restricting energy
intake and dietary fat (see
Chapter 1: Lifestyle)
Also recommend consuming
only moderate amounts of red
meat, minimising consumption
of charred and processed
meats, and consuming
vegetables and dietary fibre as
these foods may be protective
IIIC
1,38,65,66,76
Behavioural
Chemoprophylaxis Following
complete
removal of
adenoma at
colonoscopy
Consider prophylactic aspirin
use (in consultation with a
specialist)
At time of diagnosis with IIC
colorectal adenoma
76,84,88
*Free, one-off FOBTs are offered to people turning 50, 55 or 65 years between January 2011 and December 2014. GPs can also refer patients
for examination of faecal specimens for occult blood under Medicare Benefits Schedule (Items 66764, 66767 and 66770)
**Familial adenomatous polyosis (FAP); hereditary non-polyosis colorectal cancer (HNPCC)
Resources
Guidelines for the prevention, early detection and management of colorectal cancer
used to determine a person’s risk of colorectal cancer based on family history
www.nhmrc.gov.au/publications/synopses/cp106/cp106syn.htm or summary at
www.cancer.org.au/file/HealthProfessionals/ClinicalpracticeguidelinesJuly2008.
pdf
Familial aspects of bowel cancer: a guide for health professionals
www.health.gov.au/internet/screening/publishing.nsf/Content/1F35A75DC194E5
9CCA2574EB007F7532/$File/familial-guide.pdf.
255
256
Early detection of prostate cancer
Background
After lung cancer, prostate cancer is the second most common cancer
diagnosed in Aboriginal men.3 The age standardised incidence of
prostate cancer in Aboriginal men was estimated to be 55% less than
for non-Aboriginal men, with a corresponding mortality rate that was
26% lower. Missing data on Indigenous status was estimated to be
18%.4
Factors that may increase the relative risk of prostate cancer are:
• two or more relatives affected
• lower age at diagnosis of relative(s)
• one first degree relative with prostate cancer (brother higher risk then
father)
• one second degree relative with prostate cancer (smaller increase in
risk than first degree relative).
Being a carrier of BRAC1 or BRCA2 mutations also increases risk.89,90
Screening for prostate cancer
Neither the blood prostate specific antigen (PSA) test nor digital rectal
examination (DRE) is currently recommended for population screening
for prostate cancer in Australia. Men who are concerned about their
risk of prostate cancer, should discuss screening with their doctor.
Doctors should help such men to make a fully informed decision
whether or not to commence regular PSA screening. If a decision is
made to commence an individual screening program, starting from
50 years of age is generally considered appropriate, with an interval
of 1–2 years between PSA tests. The balance of benefits of early
detection of prostate cancer and its harms (particularly the side effects
of investigation of an elevated PSA and treatment, and the possibility
of unnecessary treatment for cancers that would never have been
diagnosed except for PSA screening) remain a subject of debate.91–100
Recommendations: Prostate cancer prevention and detection
Preventive
Who is at risk?
intervention type
Screening
Men at average
risk
The decision to conduct
prostate specific antigen
(PSA) testing and digital
rectal examination (DRE)
Men at potentially should be individualised as
higher risk due to population based screening
is not recommended
family history
How often?
Level/
strength of
evidence
References
Opportunistic
IIID
91–100
Opportunistic
IID
89,90
Resources
The early detection of prostate cancer in general practice: GP/patient show card
www.cancerqld.org.au/content/Document/The%20Early%20Detection%20
of%20Prostate%20Cancer.pdf
Let sleeping dogs lie? What men should know before getting tested for prostate
cancer
http://ses.library.usyd.edu.au/bitstream/2123/6835/3/Let-sleeping-dogs-lie.pdf.
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74. Christou A, Katzenellenbogen JM, Thompson SC. Australia’s national bowel cancer screening program:
does it work for indigenous Australians? BMC Public Health 2010;10:373.
75. Christou A, Thompson SC. How could the National Bowel Cancer Screening Program for Aboriginal
people in Western Australia be improved? Report to the WA Bowel Cancer Screening Implementation
Committee, Department of Health, Western Australia, 2010. Cited October 2011. Available at www.
healthnetworks.health.wa.gov.au/cancer/docs/Aboriginal_Bowel_Cancer_Final_Report.pdf.
76. Australian Cancer Network Colorectal Cancer Guidelines Revision Committee. Guidelines for the
prevention, early detection and management of colorectal cancer, 2005. Cited October 2011. Available at
www.nhmrc.gov.au/publications/synopses/cp106/cp106syn.htm.
77. Hewitson P, Glasziou P, Irwig L, Towler B, Watson E. Screening for colorectal cancer using the faecal
occult blood test, Hemoccult. Cochrane Database Syst Rev 2007;Jan 24;(1):CD001216.
78. Zauber AG, Lansdorp-Vogelaar I, Knudsen AB, Wilschut J, Ballegooijen Mv, Kuntz KM. Evaluating test
strategies for colorectal cancer screening: a decision analysis for the US preventive services task force.
Ann Intern Med 2008;149:659–69.
79. US Preventive Services Task Force. Screening for colorectal cancer: US Preventive Services Task Force
recommendation statement. Ann Intern Med 2008;149(9):627–37.
80. Department of Health and Ageing. National Bowel Cancer Screening Program: about the program.
Canberra: Commonwealth of Australia, 2009. Cited October 2011. Available at www.cancerscreening.
gov.au/internet/screening/publishing.nsf/Content/bowel-about.
81. Cancer Council Victoria. Faecal occult blood tests. Melbourne: Cancer Council Victoria, 2010. Cited
October 2011. Available at www.cancervic.org.au/preventing-cancer/attend-screening/bowel_cancer_
screening/faecal_occult_blood_tests.
82. US Preventive Services Task Force. Routine aspirin or nonsteroidal anti-inflammatory drugs for the
primary prevention of colorectal cancer: US Preventive Services Task Force Recommendation Statement.
Ann Intern Med 2007;146:361-4.
83. Rostom A, Dubé C, Lewin G, et al. Nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors
for primary prevention of colorectal cancer: a systematic review prepared for the US Preventive Services
Task Force. Ann Intern Med 2007;146(5):376–89.
84. Dubé C, Rostom A, Lewin G, et al. The use of aspirin for primary prevention of colorectal cancer: a
systematic review prepared for the US Preventive Services Task Force. Ann Intern Med 2007;146(5):365–
75.
85. Asano TK, McLeod RS. Non steroidal anti-inflammatory drugs (NSAID) and aspirin for preventing
colorectal adenomas and carcinomas. Cochrane Database Syst Rev 2004(2):CD004079.
86. Rothwell PM, Wilson M, Elwin C-E, et al. Long-term effect of aspirin on colorectal cancer incidence and
mortality: 20-year follow-up of five randomised trials. Lancet 2010;376(9754):1741–50.
87. Cuzick J, Otto F, Baron JA, et al. Aspirin and non-steroidal anti-inflammatory drugs for cancer prevention:
an international consensus statement. Lancet Oncology 2009;10(5):501–7.
88. Cole BF, Logan RF, Halabi S, Benamouzig R, Sandler RS, Grainge MJ, et al. Aspirin for the
chemoprevention of colorectal adenomas: meta-analysis of the randomized trials. J Natl Cancer Inst
2009 February 18,2009;101(4):256–66.
89. Zeegers MPA, Jellema A, Ostrer H. Empiric risk of prostate carcinoma for relatives of patients with
prostate carcinoma: a meta-analysis. Cancer 2003;97(8):1894–903.
90. Liede A, Karlan BY, Narod SA. Cancer risks for male carriers of germline mutations in BRCA1 or BRCA2:
a review of the literature. J Cancer Res Clin Oncol 2004;22(4):735–42.
91. Djulbegovic M, Beyth RJ, Neuberger MM, et al. Screening for prostate cancer: systematic review and
meta-analysis of randomised controlled trials. BMJ 341:c4543.
92. Ilic D, O’Connor D, Green S, Wilt T. Screening for prostate cancer. Cochrane Database Syst Rev 2006;Jul
19;(3):CD004720.
93. US Preventive Services Task Force. Screening for prostate cancer: US Preventive Services Task Force
recommendation statement. Ann Intern Med 2008;149:185–91.
94. Schröder FH, Hugosson J, Roobol MJ, et al. Screening and prostate-cancer mortality in a randomized
European study. N Engl J Med 2009;360(13):1320–8.
95. Andriole GL, Grubb RL, Buys SS, et al. Mortality results from a randomized prostate-cancer screening
trial. N Engl J Med 2009;360(13):1310–9.
96. Cancer Council Australia. Position statement: Prostate cancer screening. Sydney: Cancer Council
Australia, 2008. Cited October 2011. Available at www.cancer.org.au/File/PolicyPublications/Position_
statements/PS-Prostate_cancer_screening_Apr08.pdf.
May_2009.pdf.
98. Andrology Australia. Andrology Australia statement on PSA testing for prostate cancer. Andrology
Australia, 2009. Cited October 2011. Available at www.andrologyaustralia.org/docs/AndrologyAustralia_
PSAposition_webversion_140509.pdf.
99. NHS Cancer Screening Programmes. About the Prostate Cancer Risk Management Programme.
London: NHS Cancer Screening Programmes, 2010. Cited October 2011. Available at www.
cancerscreening.nhs.uk/prostate/about-pcrm.html.
100.New Zealand Guidelines Group. Update of evidence for prostate-specific antigen (PSA) testing
in asymptomatic men. NZGG, 2009. Cited October 2011. Available at www.nzgg.org.nz/library_
resources/57_psa_testing.
101.Cancer Council Queensland. The early detection of prostate cancer in general practice: GP/Patient show
card. Brisbane: Cancer Council Queensland, 2007. Cited October 2011. Available at www.cancerqld.org.
au/content/Document/The%20Early%20Detection%20of%20Prostate%20Cancer.pdf.
102.Chapman S, Barratt A, Stockler M. Let sleeping dogs lie? What men should know before getting tested
for prostate cancer. Sydney: Sydney University Library, 2010. Cited October 2011. Available at http://ses.
library.usyd.edu.au/bitstream/2123/6835/3/Let-sleeping-dogs-lie.pdf.
261
Chapter 16
Preventive
health for
the elderly
Author Emma Fitzsimons
Expert reviewer Dina LoGiudice
Preventive health for the elderly
Overview
Aboriginal and Torres Strait Islander communities have different age structures
from the non-Indigenous population, due to high fertility and increased mortality
at all ages, giving a much lower median age (20.2 years vs 36.3 years). The
aged population is therefore smaller as a proportion, with 7% of Aboriginal and
Torres Strait Islander people being over 55 years and only 3% over 65 years.
The corresponding figures for non-Indigenous Australians are 22% and 13%
respectively.1 In 2006 this amounted to 40 297 Aboriginal and Torres Strait
Islander people over 55 years, or 0.8% of the over 55 years total Australian
population. This contrasts with almost 5 million non-Indigenous people in the
same age group. Of the total Australian population aged 75 years and older,
only 0.4% (5000 people) identify as Aboriginal and/or Torres Strait Islander.
However, demographic shifts are occurring, and the number of Aboriginal and
Torres Strait Islander people over 55 years is projected to double between
2006 and 2021.2 The care of the elderly is becoming more important as the
population ages. In addition, many of the disorders which affect elderly people
occur at younger ages for Aboriginal and Torres Strait Islander people.
Many areas of preventive care for the elderly are covered in other chapters
of the National Guide, in particular vision (Chapter 6), hearing (Chapter 7),
respiratory disease (Chapter 11) and cardiovascular health (Chapter 12). This
chapter will cover three important issues relating to the elderly not covered
elsewhere in the guide: osteoporosis, falls and dementia.
263
264
Osteoporosis
Background
Osteoporosis is defined as a condition in which there is low bone mass and
deterioration of the microarchitecture of the bones, causing bone fragility and
an increased risk of fracture. It is usually diagnosed by a bone mineral density
(BMD) test, dual energy X-ray absorptiometry (DXA), which measures BMD at
the hip and spine. BMD is expressed as a T-score, defined by the World Health
Organization (WHO) as a measure of standard deviation from the reference
values of bone density for a person aged 30 years of the same sex.3 A T-score
of –2.5 or lower is diagnostic of osteoporosis, and a T-score between –1.0 and
–2.5 is diagnostic of osteopaenia.
Osteoporosis is common in the general population, with 27% of women and
11% of men over 60 years of age meeting the WHO criteria for osteoporosis.4
The lifetime risk of a minimal trauma fracture is approximately 56% for women
aged over 60 years and 29% for men aged over 60 years.5 These fractures can
occur at sites other that the classic osteoporotic sites of wrist, hip and vertebra.
Little is known, however, about the prevalence of osteoporosis in Aboriginal
and Torres Strait Islander people. One study from Cairns found that the age
standardised rate of hip fracture among Aboriginal and Torres Strait Islander
people was similar to non-Indigenous people, though in that study the fractures
in Aboriginal and Torres Strait Islander women tended to occur at a somewhat
older age.6
A number of factors increase the risk of osteoporotic fractures. Women have
approximately double the lifetime risk of men. Fracture incidence increases
exponentially with age in both men and women, approximately doubling with
each decade.7,8 A previous fracture doubles the risk of subsequent fracture,
and a previous vertebral fracture increases the risk of a further vertebral fracture
4–5 times.9,10 Low bone density as measured by DXA approximately doubles
the fracture risk for each unit of standard deviation from the mean (each –1.0 of
T-score).11 A history of falls at least doubles the risk of an osteoporotic fracture
compared to non-fallers.12
A family history of fragility fractures after age 50 years, kyphosis or diagnosed
osteoporosis in a father, mother and sister increase the risk of osteoporotic
fractures.13 A meta-analysis found smoking increases the risk of osteoporosis
after the menopause with an average of 2% greater bone density loss per
decade for smokers compared with non-smokers.14 Smokers had a 17%
increased risk of hip fracture at age 60 and a 108% increased risk at age 90
compared with non-smokers after adjusting for other risk factors.14 There was
also a dose-response relationship between the number of cigarettes smoked
per day and the risk of hip fracture.14 Low body mass index has also been shown
to be associated with lower bone density after menopause, and more rapid
bone loss than in heavier women.15 Other risk factors include immobility, vitamin
D deficiency and certain medications, especially corticosteroids, excessive
thyroxine, anti-androgen and anti-oestrogen treatments, selective serotonin reuptake inhibitors, thiazolidenediones and certain anti-epileptic drugs.5
A fracture risk calculator has been developed based on data from the Dubbo
Osteoporosis Epidemiology Study (see Resources). An individual’s age, gender,
fracture and fall history and BMD are used to calculate an estimated 5 and 10
year absolute fracture risk for both hip fracture and any fragility fracture.
Interventions
Calcium intake
The recommended daily intake of calcium varies according to age. The best
dietary sources of calcium are milk, hard cheeses and yoghurt. Other sources
with moderate calcium content include white bread, sardines and calcium
enriched soy milk. Adequate dietary intake has been shown to be as effective as
supplements. For people unable to achieve adequate intake through diet alone,
supplementation is necessary.5 Dietary intake should especially be assessed in
people who are commencing specific anti-osteoporosis therapies.
Vitamin D
Vitamin D is primarily formed in the skin from sunlight exposure although small
amounts are found in the diet. It has been estimated that fair-skinned people in
Australia can produce adequate vitamin D with sun exposure to their face, arms
and hands for a few minutes either before 10 am or after 3 pm on most days of
the week.16 In winter in southern parts of Australia this exposure may need to
be longer. People with darker skin require more sun exposure. The evidence for
the use of vitamin D supplementation in preventing bone loss and osteoporotic
fractures is mixed. A benefit has been shown for treating those at high risk of
vitamin D deficiency (residents of aged care facilities and housebound people)
and for these groups, vitamin D supplementation is considered standard care.5
For those in the community, the results are less clear and supplementation
should be reserved for those at high risk. In addition, the benefits of specific
anti-osteoporotic therapies have been demonstrated in the context of adequate
vitamin D levels. Patients who are to be commenced on specific antiosteoporotic medication should have their vitamin D levels checked and should
commence supplementation if their level is less than 60 nmol/L.5
Exercise
Regular, high intensity weightbearing exercise has been shown to slow bone
density loss in postmenopausal women and older men.5 For bone health, short,
intense exercise sessions are better than prolonged, less intense exercise.
People without osteoporosis should be encouraged to exercise at least three
times weekly for 1 year to improve BMD, and ideally they should participate
in 30–40 minute sessions 4–6 times per week.5 Walking, jogging, dancing,
tennis and strength and resistance training are recommended.17 There is some
evidence that regular exercise throughout the lifespan increases bone density.
Children and adolescents who are more active achieve higher bone density, and
this is maintained into middle age.17
People diagnosed with osteoporosis need to have these recommendations
modified because of their increased risk of fracture. They should undergo
high intensity strength training and low impact weightbearing exercise.13 High
intensity strength training is the use of moderate to high overload resistance
to increase muscle strength and BMD. Low impact weightbearing exercise is
defined as exercise performed while standing but with one foot always on the
floor. High impact activities such as jumping are not appropriate for people with
established osteoporosis. In addition, people with osteoporosis may benefit
from flexibility and balance training to reduce the risk of falls.5 A physiotherapist,
exercise physiologist or other appropriately trained professional should
supervise the introduction of an exercise program for people with osteoporosis.
265
266
Smoking cessation
The increased risk of fracture significantly declines from around 10 years after
giving up smoking.18
Pharmacological treatment
Bisphosphonates may be used in both primary prevention and after
osteoporosis is established. Note that they have been shown to be effective in
primary prevention (in postmenopausal women at risk of osteoporosis) but are
not listed on the Pharmaceutical Benefits Scheme (PBS) for this indication.
Hormone replacement therapy
Oestrogen +/– progestogens are effective in improving BMD and reducing
the risk of fractures in postmenopausal women. They have been shown to
be effective in primary prevention and in treating established osteoporosis.
However there are a number of adverse effects including an increased risk
of invasive breast cancer, stroke and thromboembolic events. The potential
benefits and harms must be carefully considered. Long term use is not
recommended by existing guidelines.5
Strontium
Strontium ranelate has been shown to decrease BMD loss in early
postmenopausal women. It is not approved on the PBS for primary prevention
but is approved for the treatment of established osteoporosis.
Table 16.1. Risk levels for osteoporosis
Average risk
Moderate risk
High risk
All postmenopausal women
and men over 50 years of
age
Age 60–70 years and any of the following:
• Previous fracture due to
minimal trauma
• Vertebral fractures
• family history of osteoporotic fractures
• hypogonadism
• prolonged glucocorticoid use (>3 months)
• inflammatory conditions
• malabsorption, eg. coeliac disease
• hyperparathyroidism
• hyperthyroidism
• smoking
• history of a fall
• age over 70 years
267
Recommendations: Osteoporosis
Level/
strength of
evidence
References
Assess risk factors for
As part of an
osteoporosis (see Table 16.1) annual health
assessment
IIB
5
People at moderate
and high risk (see
Table 16.1)
Recommend dual energy
X-ray absorptiometry (DXA)
to determine bone mineral
density (BMD)
If DXA confirms
osteoporosis then manage
as high risk
At baseline,
then 2 yearly if
needed
IA
5
All postmenopausal
women and men over
50 at all levels of risk
Advise adequate dietary
calcium intake: 1300 mg/day
for women over 50 and men
over 70; 1000 mg/day for
men 50–70 years
Opportunistic
IA
and as part of
an annual health
assessment
5
Preventive
intervention type
Who is at risk?
Screening
All postmenopausal
women and men over
50 years of age
Behavioural
How often?
Recommend smoking
cessation (see Chapter
1: Lifestyle, section on
smoking)
Recommend maintenance
of a healthy weight and
body mass index (see
Chapter 1: Lifestyle, section
on overweight/obesity)
IA
Advise adequate but safe
sunlight exposure as a
source of vitamin D*
GPP
People at average and Advise regular high intensity
moderate risk (see
weightbearing exercise for
Table 16.1)
postmenopausal women
and older men aiming
to achieve a target of 30
minutes/day on most days
of the week (see Chapter 1:
Lifestyle, section on physical
activity)
Opportunistic
1A
and as part of
an annual health
assessment
5
People at high risk
(see Table 16.1)
Advise regular low impact
weightbearing exercise as
part of a tailored program
emphasising improved
balance and flexibility
Opportunistic
GPP
and as part of
an annual health
assessment
5
Consider calcium
supplementation for those
with inadequate dietary
intake
Also consider vitamin D
supplementation for those
with inadequate sunlight
exposure, particularly those
in residential care
Opportunistic
ID
and as part of
an annual health
assessment
5
Consider bisphosphonates†
in conjunction with
calcium and vitamin D
supplementation
At diagnosis
5
Chemoprophylaxis All postmenopausal
women and men over
50 at all levels of risk
People at moderate
and high risk (see
Table 16.1)
IA
268
Recommendations: Osteoporosis (continued)
Environmental
Consider hormone
replacement therapy to
increase BMD and reduce
fracture risk. Long term use
is not recommended due to
increased potential for harm,
particularly increased breast
cancer and cardiovascular
disease risk
IA
Consider strontium ranelate‡
See management guidelines
for further information§
IIC
People at high risk
(see Table 16.1)
If the above medications are At diagnosis
ineffective or contraindicated
consider selective oestrogen
receptor modulators
(raloxifene) or parathyroid
hormone (teriparatide)‖
See management guidelines
for further information§
IIC
5
People at moderate
and high risk
Consider a multifactorial falls At diagnosis
reduction program (see Falls
recommendations below)
ID
5)
*Fair-skinned people in Australia can produce adequate vitamin D with sun exposure to their face, arms and hands for a few minutes
either before 10 am or after 3 pm on most days of the week. In winter in southern parts of Australia this exposure may need to be longer.
People with darker skin generally require more sun exposure16
†Bisphosphonates are subsidised under the PBS for the following conditions: concurrent use of oral corticosteroids (>7.5 mg/day) for
3 months or more and a BMD T-score of –1.5 or less, women aged ≥70 years with a BMD T-score of –2.5 or less, any person with a
radiologically confirmed fracture due to minimal trauma
‡ Strontium is subsidised under the PBS for the following conditions: women aged >70 years with a BMD T-score of –3.0 or less, all
people with a radiologically confirmed fracture due to minimal trauma
§ Refer to clinical practice guidelines for specific treatment recommendations19
‖ Selective oestrogen receptor modulators and teriparatide are not subsidised under the PBS in the absence of a fracture due to minimal
trauma. Recommend review the PBS for specific criteria
Resources
Fracture risk calculator
www.fractureriskcalculator.com
RACGP guidelines
www.racgp.org.au/Content/NavigationMenu/ClinicalResources/
RACGPGuidelines/osteoporosis1/RACGP_Osteo_guideline.pdf
RACGP algorithm for the detection, prevention and treatment of osteoporosis
www.racgp.org.au/Content/NavigationMenu/ClinicalResources/
RACGPGuidelines/osteoporosis1/OP_Algorithm.pdf
Guidelines for exercise in preventing and treating osteoporosis
www.osteoporosis.org.au/health-professionals/research-positionpapers/#makebreak
Risks and benefits of sun exposure
www.osteoporosis.org.au/images/stories/documents/research/Sunexposure_
OA_2007.pdf.
Falls
Background
A fall is defined as ‘an event which results in a person coming to rest
inadvertently on the ground or floor or other level’.20 Studies in Australia and
similar countries have demonstrated that 30–40% of people over the age of
65 years fall each year, and a proportion of these will have serious injuries and
require hospitalisation.21 Half of all falls occur in the home, mostly during the
day, and mostly due to ‘slipping, tripping and stumbling’.22 Ten to fifteen percent
of those who fall will sustain serious injuries, with 2–6% sustaining fractures
and 0.2–1.5% sustaining a hip fracture.21 In Australia, falls account for 3.8% of
hospital separations and 9.3% of all hospital bed days for people aged 65 years
and over.22 A fall (whether or not it results in serious injury) may also result in a
fear of falling, and consequent decreased mobility and independence, which in
turn may increase the chance of the person subsequently requiring residential
care.
Aboriginal and Torres Strait Islander people have increased rates of
hospitalisation for falls when compared with other Australians, especially in
the 25–65 years age group, but the average length of stay is shorter.23 This
suggests that the increased risk for falling due to age is occurring at a younger
age in Aboriginal and Torres Strait Islander people, but that the average severity
of injury may be less. However, the number of Aboriginal and Torres Strait
Islander people in the over 55 years age group is increasing rapidly,2 and the
number of falls in the elderly may increase proportionally.
269
270
Recommendations: Falls prevention
Preventive
intervention type
How often?
Level/
strength of
evidence
References
Screening
All people aged
≥50 years at all
risk levels
Annually
IA
24,25
Residents of
RACF staff should screen for risk
aged care
factors for falls to allow for an
facilities (RACFs) individualised fall prevention plan
6 monthly
IIB
26
People with a
past history of
falls
Recommend a detailed assessment
including the following:
Opportunistic
IA
25
Those with
falls due to
carotid sinus
hypersensitivity
Consider referral for pacemaker
insertion
As needed
IIC
27
Those with vision Referral for cataract surgery
threatening
cataract disease
As needed
IIC
27
All people aged
≥50 years
As part of an
annual health
assessment
IA
25
As part of an
annual health
assessment
IIC
26
Consider vitamin D supplementation As part of an
(see also osteoporosis section)
annual health
assessment
IC
27,28
Review medications
IIB
21
Behavioural
Assess for risk factors for falls (see
Table 16.2)
• cardiac and neurological disease
assessment
• medication review
• assessment of vision, gait and
balance
• home environment assessment
Recommend exercise which may
include the following modalities:
• multicomponent group exercise
(defined as targeting at least two
of the following: strength, balance,
endurance and flexibility)
• tai chi as a group exercise
• individually prescribed exercise
to be carried out at home as
per Australian physical activity
guidelines (see Chapter 1:
Lifestyle, section on physical
activity)
People at high
risk
Chemoprophylaxis People aged
≥50 years with
known vitamin
D deficiency
or inadequate
exposure to
sunlight
People at high
risk taking
medications
Recommend gait, balance and
functional coordination exercises as
part of a multifactorial intervention
At least
annually and
recommend
6 monthly for
people taking
four or more
medications
If taking psychotropic medications
review the indications and consider
gradual withdrawal if clinically
appropriate
Opportunistic
and as
part of an
annual health
assessment
IIC
29
Consider home medication review
by a pharmacist
Annually or
IIB
when there is a
clinical need
30
Annually
IIA
31
Consider vitamin D supplementation Ongoing
IA
27
All people aged
>50 years not at
high risk
Home assessment and intervention
is not recommended
N/A
IA
25
People at high
risk
Arrange for home assessment
and intervention involving a
multidisciplinary team
One-off for
those with
poor vision;
opportunistic
for all others
IIC
25,27
People in RACFs Consider use of hip protectors
who are at high
risk of falls
Opportunistic
IIB
5
People in RACFs Arrange medication review by a
pharmacist
Environmental
Table 16.2. Risk factors for falls
• Increasing age
• Past history of falls
• Neurological conditions: stroke, Parkinson disease, peripheral neuropathy
• Multiple medications
• Psychotropic medications
• Impaired balance, gait and mobility
• Reduced muscle mass
• Visual impairment
• Cognitive impairment
• Depression
• Fear of falling
• Low levels of physical activity
Source: The RACGP 200924
271
272
Dementia
Background
Dementia is a syndrome of impairment of brain functions, which may include
changes in language, memory, perception, personality and cognitive skills,
caused by a range of disease processes.32 In general, consciousness is not
impaired but thinking is disordered. Impairment in activities of daily living or in
social or occupational functioning are required to meet diagnostic criteria for the
International Classification of Diseases, Version 10 (ICD-10) and the Diagnostic
and Statistical Manual of Mental Disorders, 4th edition, Text Revision (DSM-IVTR) respectively.32
In Australia, Alzheimer disease accounts for approximately 50% of cases of
dementia. Vascular dementia accounts for another 20%. Some people have
features of both and may be described as having ‘mixed’ dementia. Dementia
with Lewy bodies causes about 15% of cases and has some distinguishing
features such as prominent visual hallucinations and parkinsonian motor signs.
Frontotemporal dementia is responsible for 5% of cases but proportionately
more cases of early onset dementia, and is distinguished by prominent
behavioural symptoms, personality change and impaired executive function.
There are also many less common causes of dementia.
A number of medical conditions need to be excluded in people presenting with
symptoms or signs or dementia, as treatment may fully or partially reverse the
cognitive impairment. Delirium, if present, must be detected and the cause
treated. Other conditions that may mimic or exacerbate dementia include
thyroid disorders (hypothyroidism or thyrotoxicosis), vitamin deficiencies (most
commonly B12 and folate), depression, electrolyte disturbances and normal
pressure hydrocephalus. Medications frequently cause or exacerbate cognitive
problems.33
People with dementia are at an increased risk of falls (2-fold increase), fracture
(3-fold increase), delirium (5-fold increase), depression and epilepsy (6-fold
increase). They are also at increased risk of oral disease, malnutrition and
weight loss and urinary incontinence. Few studies have been undertaken into
the prevalence of dementia in Aboriginal and Torres Strait Islander populations.
Zann’s 1987 study reported a prevalence of 20% for dementia or suspected
dementia in Aboriginal and Torres Strait Islander people aged over 65 years in
northern Queensland.34 Following the development of the Kimberley Indigenous
Cognitive Assessment tool, a prevalence study in the Kimberley documented a
dementia prevalence of 12.4% in those over aged 45 years and 26.8% in those
aged over 65 years, or five times the rate in the overall Australian population.35
In that population, factors associated with dementia included older age, male
gender and no formal education. After adjusting for age, gender and education,
dementia was associated with current smoking, previous stroke, epilepsy, head
injury, poor mobility, incontinence and falls.36 This suggests that population
based interventions to reduce the incidence of dementia should include
smoking cessation and better control of vascular disease risk factors. Better
education for Aboriginal and Torres Strait Islander children may provide some
protection from dementia in the longer term, as may interventions to prevent
head injury.37
Interventions
Screening for dementia has not been recommended in guidelines published
to date.33,38–40 However, there are increasing calls to consider introducing
screening because there is some evidence that early non-pharmacological
intervention may improve cognitive outcomes for people with early cognitive
impairment. Screening may allow the early detection of reversible causes
or exacerbating factors for cognitive decline. Early diagnosis also allows the
person with dementia to make plans for the future, including for issues such
as enduring power of attorney, while they are still able to do so.41 However,
there may be significant stigma associated with a diagnosis of dementia, and
by definition, screening involves detecting cases while they are asymptomatic.
Older Aboriginal and Torres Strait Islander people have important roles in culture
and community and these may be able to continue to be performed adequately
when a person has mild cognitive impairment.34 Thus, current guidelines
recommend case finding (asking about those with symptoms who may need
further evaluation) rather than screening.24,42 Opportunistic case finding should
be pursued in Aboriginal and Torres Strait Islander people over the age of 50
years.
Case finding involves being alert for concerns raised by the individual or family
members. Cognition is evaluated using a screening tool. The Mini Mental State
Examination and the General Practitioner Assessment of Cognition (GPCOG)
require English skills and results will be dependent on the level of schooling
attained. The Kimberley Indigenous Cognitive Assessment has been developed
for use with people living in rural and remote areas, and those who may have
had little formal schooling. Interpreters may be required for the assessment.
There is evidence of benefit from cholinesterase inhibitors (donepezil,
rivastigmine, galantamine) for the management of mild to moderate dementia.
However, there is no evidence that these medications are effective in reducing
the risk of dementia in people with mild cognitive impairment and there is no
medication intervention that has been shown to be effective in preventing the
onset of dementia.43
273
274
Recommendations: Dementia
Preventive
intervention type
Who is at risk?
How often?
Level/
strength of
evidence
References
Screening
Asymptomatic
people
Dementia screening is not
routinely recommended
N/A
IIIC
38–40,44
People with
symptoms such
as memory loss
or behaviour
change, or
if there are
concerned family
members
Consider administration of one of Opportunistic
the following cognitive screening
tests:
GPP
24,33,42,45,46
People with
risk factors
for dementia
including
excessive
alcohol intake,
tobacco smoking
hypertension,
diabetes,
depression
Management of dementia risk
Opportunistic
factors is recommended for
multiple health benefits, however,
there is limited evidence that this
leads to a reduction in dementia
incidence
GPP
36,39,47
Anti-dementia drugs are not
recommended
1B
43
Behavioural
Chemoprophylaxis People without
a confirmed
diagnosis of
dementia
• Mini Mental State Examination
• General Practitioner
Assessment of Cognition
• Kimberley Indigenous
Cognitive Assessment
(see Resources)
N/A
Resources
Care of patients with dementia in general practice (The Royal Australian College of
General Practioners and NSW Health)
www.racgp.org.au/Content/NavigationMenu/RemovedArchived/CareofPatients
withDementia/20060413dementiaguidelines.pdf
Kimberley Indigenous Cognitive Assessment
www.wacha.org.au/kica.html
General Practice Assessment of Cognition
www.gpcog.com.au.
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7.
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10. Ross PD, Davis JW, Epstein RS, Wasnich RD. Pre-existing fractures and bone mass predict fracture
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IOF_2006.pdf.
18. Cornuz J, Feskanich D, Willett WC, Colditz GA. Smoking, smoking cessation, and risk of hip fracture in
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mediacentre/factsheets/fs344/en.
21. Australian Commission on Safety and Quality in Healthcare. Guidebook for preventing falls and harm from
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22. Bradley C, Pointer S. Hospitalisations due to falls by older people, Australia 2005–06. Adelaide: AIHW,
2009.
23. Helps YL, Harrison JE. Hospitalised injury of Australia’s Aboriginal and Torres Strait Islander people
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25. Gillespie L, Robertson M, Gillespie W, et al. Interventions for preventing falls in older people living in the
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29. Campbell A, Robertson M, Gardner M, Norton R, Buchner D. Psychotropic medication withdrawal
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30. Pit SW, Byles JE, Henry DA, Holt L, Hansen V, Bowman DA. A Quality Use of Medicines program for
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33. Bridges-Webb C, Wold J. Care of patients with dementia in general practice. Sydney: The Royal
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35. Smith K, Flicker L, Lutenschlager N, et al. High prevalence of dementia and cognitive impairment in
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36. Smith K, Flicker L, Dwyer A, et al. Factors associated with dementia in Aboriginal Australians. Aust N Z J
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Appendix 1
277
Appendix 1
Australian cardiovascular risk charts
Figure 1. Australian cardiovascular risk charts (continued)
People with diabetes
Non-smoker
6
7
Systolic blood pressure (mmHg)
120
120
179 *
179 *
160
160
140
140
120
120
179 *
179 *
160
160
140
140
120
120
Age
35–44
160
140
120
8
179 *
160
4
5
6
7
8
4
140
120
4 5 6 7 8
5 6 7 8
Age
55–64
Age
45–54
Charts in this age
Age
bracket are for use in
35–44
Aboriginal and Torres
Strait Islander
only 4 5 6 7 8
4 5 6 populations
7 8
Total cholesterol:HDL ratio*
sterol:HDL ratio*
Women
Smoker
140
179 *
harts in this age
cket are for use in
riginal and Torres
Strait Islander
opulations only.
Non-smoker
Age
65–74
160
140
Age
45–54
Men
Smoker
179 *
160
Age
55–64
5
Non-smoker
Smoker
179 *
Age
65–74
4
Women
Men
Smoker
omen
4
5
6
7
179 *
179 *
160
160
140
140
120
120
179 *
179 *
160
160
140
140
120
120
179 *
179 *
160
160
140
140
120
120
Men
Non-smoker
Smoker
Adults over the age of
60 with diabetes are
equivalent to high risk
(>15%), regardless
of their calculated risk
level. Nevertheless,
reductions in risk
factors in this age
group can still lower
overall absolute risk
People without diabetes
Systolic blood pressure (mm Hg)
diovascular risk charts
179 *
179 *
160
160
140
140
120
120
8
4 5
Non-smoker
Smoker
Age
65–74
Age
55–64
Age
45–54
Charts in this age
Strait Islander
populations only
6
7
8
4
5
6
7
Age
35–44
8
4
5
6
7
8
4
5
6
7
* In accordance with Australian guidelines, patients with systolic blood pressure ≥180 mmHg,
ralian guidelines, patients with systolic blood pressure ≥180 mmHg,
* In accordance with Australian guidelines, patients with systolic blood pressure ≥ 180
or a total cholesterol of >7.5 mmol/L, should be considered at increased absolute risk of CVD.
>7.5 mmol/L, should be considered at increased absolute risk of CVD.
or a total cholesterol of > 7.5 mmol/L, should be considered at increased absolute ris
Risk level for 5 year cardiovascular (CVD) risk
rdiovascular (CVD) risk
Moderate risk
10–15%
High risk
Low risk
5–9%
<5%
≥30%
Moderate risk
Risk level for 5-year cardiovascular (CVD) risk
Low risk
10–15 %
25–29%
High risk
5–9%
≥ 30%
<5%
25–29%
20–24%
20–24%
16–19%
16–19%
Notes: The risk charts include values for SBP alone, as this is the most
informative of conventionally measured blood pressure parameters for
cardiovascular risk.
risk charts
ting to the person’s diabetes status,
and age. ‘Smoker’ is defined as
garette smoker or former smoker
he previous 12 months. The charts
adults aged 45–74 years (and
res Strait Islander adults aged
ithout known history of CVD or
at high risk.
oose the cell nearest to the
blood pressure (SBP) and total
L ratio. For example, the lower left
smokers without diabetes who
have a TC:HDL ratio of less than
than 130 mm Hg.
3.refers
Thecollectively
colourtoof
the cell
the
person
falls
into
CVD
coronary
heart that
disease
(CHD),
stroke and
other
vascular
diseaseprovides
including peripheral
disease
and renovascular
disease.
their arterial
5-year
absolute
cardiovascular
risk
(see
legend
for
category).
For people
Charts level
are based
on the
NVDPA’sabove
Guidelines
for risk
the assessment
of absolute
cardiovascular
disease
risk and adapted
with permission
from New Zealand
who fall
exactly
on a threshold
between
cells,
Guidelines Group. New Zealand Cardiovascular Guidelines Handbook: A Summary
use the cell corresponding to higher risk. The risk
Resource for Primary Care Practitioners. Second edition. Wellington, NZ: 2009.
calculator may underestimate cardiovascular risk in
www.nzgg.org.nz.
these groups:
• Aboriginal and Torres Strait Islander adults
• adults with diabetes aged 60 years or less
• adults who are overweight or obese
• socioeconomically deprived groups.
readings on two occasions).
igh-density lipoprotein cholesterol
ure correct ratio is used).
16
Heart Foundation Guide to management of hypertension 2008
© Heart Foundation Guide to management of hypertension 2008
15
Moderate risk
10–15 %
Low risk
5–9%
< 5%
278
Appendix 1
Figure 1. Australian cardiovascular risk charts
diovascular risk charts
179 *
160
Age
55–64
Age
45–54
160
120
120
160
179 *
140
160
120
140
120
179 *
160
179 *
140
160
120
140
120
179 *
140
160
120
4
5
6
7
8
4
5
6
7
8
160
179 *
140
160
120
140
140
179 *
160
4
Smoker
Age
65–74
179 *
179 *
Age
35–44
Non-smoker
179 *
140
Age
65–74
Smoker
Smoker
5
6
7
140
8
120
Non-smoker
Age
55–64
Age
45–54
Age
Charts in35–44
this age
4 5 6 7Strait
8 Islander 4 5 6 7 8
populations only
ratio*
4 5 Total
6 7cholesterol:HDL
8
4
5
6
120179 *
160
179 *
140
160
120
140
120179 *
160
179 *
140
160
120
140
Women
Non-smoker
4
Age
45–54
6
7
8
4
5
6
7
160
120
179 *
160
140
120
179 *
160
140
120
179 *
Charts in this age
Strait Islander
populations only
5
Smoker
140
Age
55–64
160
179 *
140
160
120
140
7 8
120
179 *
Non-smoker
Age
65–74
120
179 *
Non-smo
Men
Smoker
Non-smoker
Men
Smoker
Men
omen
Women
160
140
Age
35–44
120
4
8
4
5
6
7
8
5
6
4 5 Total
6 7ch
sterol:HDL ratio*
* In accordance with Australian guidelines, patients with systolic blood pressure ≥180 mmHg,
* In accordance with
or a total cholesterol of >7.5 mmol/L, should be considered at increased absolute risk of CVD.
or a total cholestero
ralian guidelines, patients with systolic blood pressure ≥180 mmHg,
* In accordance with Australian guidelines, patients with systolic blood pressure ≥ 180
>7.5 mmol/L, should be considered at increased absolute risk of CVD.
or a total cholesterol of > 7.5 mmol/L, should be considered at increased absolute ris
Risk level for 5 year cardiovascular (CVD) risk
Risk level for 5-yea
High risk
rdiovascular (CVD) risk
Moderate risk
10–15%
Low risk
5–9%
<5%
≥30%
Moderate risk
10–15%
25–29%
Low risk
High risk
Risk level for 5-year cardiovascular (CVD) risk
High risk
5–9%
<5%
≥ 30%
20–24%
Moderate risk
Low risk
10–15 %
25–29%
16–19%
5–9%
< 5%
20–24%
16–19%
How to use the risk charts
risk charts
1. Identify the table relating to the person’s diabetes status,
sex, smoking history and age. ‘Smoker’ is defined as
3. The colour of the cell that the person falls into
ting to the person’s diabetes status,
either current daily cigarette smoker or former smoker
provides their 5-year absolute cardiovascular risk
and age. ‘Smoker’ is defined as
who has quit within the previous 12 months. The charts
level (see legend above for risk category). For people
garette smoker or former smoker
should be used for all adults aged 45–74 years (and
who fall exactly on a threshold between cells,
he previous 12 months. The charts
all Aboriginal and Torres Strait Islander adults aged
adults aged 45–74 years (and
35 years and older) without known history of CVD or
res Strait Islander adults aged
already known to be at high risk.
these groups:
ithout known history of CVD or
2. Within the chart, choose the cell nearest to the
at high risk.
person’s age, systolic blood pressure (SBP) and total
oose the cell nearest to the
• adults with
diabetes
aged
years orthe
less
cholesterol
(TC):HDL
ratio.
For 60
example,
lower left
blood pressure (SBP) and total
cell contains all non-smokers without diabetes who
L ratio. For example, the lower left
are 35–44 years and have a TC:HDL ratio of less than
smokers without diabetes who
socioeconomically
deprived
4.5•and
a SBP of less than
130 mmgroups.
Hg.
have a TC:HDL ratio of less than
• SBP (mean of two readings on two occasions).
than 130 mm Hg.
readings on two occasions).
igh-density lipoprotein cholesterol
ure correct ratio is used).
3. The colour of the cell that the person falls into
provides their 5-year absolute cardiovascular risk
level (see legend above for risk category). For people
who fall exactly on a threshold between cells,
these groups:
• adults with diabetes aged 60 years or less
• socioeconomically deprived groups.
• Total cholesterol/high-density lipoprotein cholesterol
(HDL-C) ratio (ensure correct ratio is used).
Heart Foundation Guide to management of hypertension 2008
© Heart Foundation Guide to management of hypertension 2008
15
15
≥ 30%
25–29%
20–24%
16–19%
Appendix 2
279
Appendix 2
Abbreviations used in this guide
13vPCV
13-valent pneumococcal conjugate vaccine
23vPPV23-valent pneumococcal polysaccharide
vaccine
7vPCV
7-valent pneumococcal conjugate vaccine
AAP
American Academy of Pediatrics
ABS
Australian Bureau of Statistics
ACCHSAboriginal Community Controlled Health
Services
CHB
chronic hepatitis B
CHD
coronary heart disease
CI
confidence interval
CKD
chronic kidney disease
CKD-EPIChronic Kidney Disease Epidemiology
Collaboration
COAG
Council of Australian Governments
COPD
chronic obstructive pulmonary disease
ACE
angiotensin converting enzyme
ACIR
Australian Childhood Immunisation Register
CRAFFTCar, Relax, Alone, Forget, Friends, Trouble
[screening tool]
ACR
albumin-creatinine ratio
CRP
c-reactive protein
AF
atrial fibrillation
CSLD
chronic suppurative lung disease
CSO
Community Services Obligation
AFPalpha-fetoprotein
AHMACAustralian Health Ministers' Advisory
Council
AHWAboriginal and Torres Strait Islander health
worker
AIDS
acquired immunodeficiency syndrome
Anti-HBs
anti-hepatitis B surface antigen (antibody)
AOM
acute otitis media
APGARAppearance, Pulse, Grimace, Activity,
Respiration [newborn assessment tool]
CSOM
chronic suppurative otitis media
CT
computed tomography
CVD
cardiovascular disease
DALY
disability adjusted life years
dBdecibel
dBHL
decibel hearing level
DBP
diastolic blood pressure
DESdiethylstilbestrol
APSGN
acute post-streptococcal glomerulonephritis
DMSA
dimercaptosuccinic acid (scan)
ARB
angiotensin receptor blocker
DRE
digital rectal examination
ARF
acute rheumatic fever
ARI
acute respiratory illness
DSM-IVDiagnostic and Statistical Manual of Mental
Disorders, 4th edition
ASHM
Australasian Society for HIV Medicine
AUDIT
Alcohol Use Disorders Identification Test
AUDIT-CAlcohol Use Disorders Identification Test –
Consumption
AusDiab
Diabetes Australia
AUSDRISKAustralian Type 2 Diabetes Risk
Assessment tool
DSM-IV-TRDiagnostic and Statistical Manual of Mental
Disorders 4th edition – Text Revision
DXA
dual energy X-ray absorptiometry
ECGelectrocardiogram
ECHOechocardiogram
ECS
endocervical swab
eGFR
estimated glomerular filtration rate
BBV
bloodborne virus
EIA enzyme immunoassay
BHCG
beta human chorionic gonadotropin
BMD
bone mineral density
EIA-TPHAenzyme immunoassay Treponema pallidum
haemagglutination assay
BMI
body mass index
BP
blood pressure
BPG
benzathine penicillin G
BRCA
breast cancer susceptibility gene
CABG
coronary artery bypass graft
CAR
Children at Risk [program]
CARPACentral Australian Rural Practitioners
Association
CDC
Centers for Disease Control
ENT
ear nose and throat
ESR
erythrocyte sedimentation rate
ESRD
end stage renal disease
ETS
environmental tobacco smoke
FAP
familial adenomatous polyposis
FDA
Food and Drug Administration
FEV1
forced expiratory capacity in 1 second
FOBT
faecal occult blood test
FPG
fasting plasma glucose
280
Appendix 2
FRA-BOCfamilial risk assessment – breast and
ovarian cancer
FRE
Framingham Risk Equation
FTA-Absfluorescent treponemal antibody –
absorption
FTT
failure to thrive
FVC
forced vital capacity
FVU
first void urine
GAS
Group A Streptococcus (bacteria)
GDM
gestational diabetes mellitus
GFR
glomerular filtration rate
GIgastrointestinal
GP
general practitioner
GTT
glucose tolerance test
Hbhaemoglobin
HbA1c
glycosylated haemoglobin
HBcAb
hepatitis B core antibody
HBIG
hepatitis B immunoglobulin
HBsAb
hepatitis B surface antibody
HBsAg
hepatitis B surface antigen
HBV
hepatitis B virus
HCC
hepatocellular carcinoma
HCG
human chorionic gonadotropin
HCV
hepatitis C virus
HDL
high density lipoprotein
HEEADSSS Home, Education, Eating, Activities, Drugs,
Sexuality, Suicidality, Safety [screening tool]
IRIS
Indigenous Risk Impact Screen
IUD
intrauterine device
KICAKimberley Indigenous Cognitive
Assessment
LABA
long acting beta agonist
LARC
long acting reversible contraception
LRTI
lower respiratory tract infection
LVH
left ventricular hypertrophy
MCUG
micturating cystourethogram
MHR
maximum heart rate
MI
myocardial infarction
MMN
multiple micronutrients
MNmicronutrient
MoBa
Norwegian Mother and Child Cohort Study
MRI
magnetic resonance imaging
MSM
men who have sex with men
MSS
maternal serum screening
MST
Multisystemic Treatment [program]
NAAT
nucleic acid amplification test
NATSIHSNational Aboriginal and Torres Strait
Islander Health Survey
NATSIHSNational Aboriginal and Torres Strait
Islander Household Survey
NHMRC National Health and Medical Research
Council
NI
neuraminidase inhibitor
NICENational Institute for Health and Clinical
Excellence (UK)
Hib
Haemophilus influenzae type B
HIV human immunodeficiency virus
HNPCC
hereditary non-polyposis colorectal cancer
HPV
human papillomavirus
HRCT
high resolution computed tomography
HRT
hormone replacement therapy
HSIL
high grade squamous intraepithelial lesion
NVDPANational Vascular Disease Prevention
Alliance
HSV
herpes simplex virus
OR
odds ratio
HVS
high vaginal swab
OCP
oral contraceptive pill
IADPInternational Association of Diabetes and
Pregnancy
OGTT
oral glucose tolerance test
ICD-10 International Classification of Disease 10th
edition
OM
otitis media
OME
otitis media with effusion
OST
opioid substitution therapy
PAPP-A
pregnancy-associated plasma protein A
PBS
Pharmaceutical Benefits Scheme
PCHL
permanent congenital hearing loss
PCI
percutaneous coronary intervention
PCR
polymerase chain reaction
PCR
protein-creatinine ratio
PCV
pneumococcal conjugate vaccine
ICS
inhaled corticosteroids
ID
iron deficiency
IDA
iron deficiency anaemia
IDF
International Diabetes Federation
IFG
impaired fasting glucose
IGT
impaired glucose tolerance
IMintramuscular
IPD
invasive pneumococcal disease
NIEHS
National Indigenous Eye Health Survey
NIPS
National Immunisation Program Schedule
NNT
number needed to treat
NRT
nicotine replacement therapy
NSP
needle syringe program
Appendix 2
PEDSParents’ Evaluation of Developmental
Status [screening tool
PEP
post exposure prophylaxis
PID
pelvic inflammatory disease
PIP
Practice Incentives Program
ppm
parts per million
PSA
prostate-specific antigen
PSV
polysaccharide vaccine
PVD
peripheral vascular disease
RACF
residential aged care facility
RACGP [The] Royal Australian College of General
Practitioners
RCT
randomised controlled trial
RHD rheumatic heart disease
RPG
random plasma glucose
RPR
rapid plasma reagin
RR
relative risk
SAFESurgery, Antibiotics, Facial (cleanliness),
Environmental measures
SBP
systolic blood pressure
SD
standard deviation
SDDS-PCSymptom Driven Diagnostic System for
Primary Care
SIDS
sudden infant death syndrome
SMS
short message service
SOLVS
self-administered low vaginal swab
SR
systematic review
SSRI
selective serotonin reuptake inhibitor
STI
sexually transmissible infection
TF
trachoma follicular
TGA
Therapeutic Goods Administration
TIA
transient ischaemic attack
TPPA Treponema pallidum particle agglutination
assay
TS
trachomatous scarring
TT
Trachomatous trichiasis
UNHS
Universal Newborn Hearing Screening
USPSTF
United States Preventive Services Taskforce
UTI
urinary tract infection
UV-B
ultraviolet B
VA
visual acuity
VUR
vesico-ureteric reflux
WHO World Health Organization
281

Evidence base to a preventive health assessment in

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