Red Book 8th Edition PDF

Guidelines for preventive
activities in general practice

8th edition
Guidelines for preventive
activities in general practice
8th edition
Guidelines for preventive activities in general practice
8th edition
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.
Whilst 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.
Recommended citation
Guidelines for preventive activities in general practice, 8th edn.
East Melbourne: Royal Australian College of General Practitioners, 2012.
Published by
The Royal Australian College of General Practitioners
RACGP House
100 Wellington Parade
East Melbourne VIC 3002 Australia
T 03 8699 0414
F 03 8699 0400
www.racgp.org.au
ISBN 978-0-86906-344-6
First edition published 1989

Second edition published 1993
Third edition published 1994
Fourth edition published 1996
Fifth edition published 2001
Fifth edition (updated) published 2002
Sixth edition published 2005
Seventh edition published 2009
This eighth edition published 2012, reprinted September 2013
Cover image © istockphoto/skodonnell
© 2012 The Royal Australian College of General Practitioners
8th edition iii
Acknowledgements
The Royal Australian College of General Practitioners (RACGP) gratefully acknowledges the generous
contribution of the following authors and reviewers of the Guidelines for preventive activities in general
practice (the ‘red book’) 8th edition.
Red book taskforce members

Dr Evan Ackermann
Chair, Red Book Taskforce, Chair, National Standing Committee for Quality Care, RACGP
Professor Mark Harris
Centre for Primary Health Care and Equity, University of New South Wales, National Standing Committee
for Quality Care, RACGP
Dr Karyn Alexander
General practitioner, Victoria
Dr Meredith Arcus
General practitioner, Western Australia
Linda Bailey
Project manager, Red Book Taskforce
Dr John Bennett
Chair, National Standing Committee for e-Health, RACGP
Associate Professor Pauline Chiarelli
School of Health Sciences, University of Newcastle, New South Wales
Professor Chris Del Mar
Faculty of Health Sciences and Medicine, Bond University, Queensland
Professor Jon Emery
School of Primary, Aboriginal and Rural Health Care, The University of Western Australia, National Standing
Committee for Research, RACGP
Dr Ben Ewald
School of Medicine and Public Health, University of Newcastle, New South Wales
Dr Dan Ewald
General practitioner, New South Wales; Adjunct Associate Professor, Northern Rivers University Centre for
Rural Health; and Clinical Advisor North Coast NSW Medicare Local
Professor Michael Fasher
Adjunct Associate Professor, University of Sydney; and Conjoint Associate Professor, University of Western
Sydney, New South Wales
Dr John Furler
Department of General Practice, The University of Melbourne, Victoria
Dr Faline Howes
General practitioner, Tasmania
Dr Caroline Johnson
Department of General Practice, The University of Melbourne, Victoria, National Standing Committee
for Quality Care, RACGP
Dr Beres Joyner
General practitioner, Queensland
Associate Professor John Litt
Department of General Practice, Flinders University, South Australia, Deputy Chair, National Standing
Committee for Quality Care, RACGP
iv Guidelines for preventive activities in general practice
8th edition
Professor Danielle Mazza

Department of General Practice, School of Primary Care, Monash University, Victoria, National Standing
Committee for Quality Care, RACGP
Professor Dimity Pond
School of Medicine and Public Health, University of Newcastle, New South Wales
Associate Professor Lena Sanci
Associate Professor Jane Smith
Faculty of Health Sciences and Medicine, Bond University, Queensland
Dr Tania Winzenberg
Deputy Chair, National Standing Committee for Research, RACGP
Reviewers
Dr Stuart Aitken
Gold Coast Sexual Health Clinic, Queensland
Professor Adrian Bauman
School of Public Health, The University of Sydney, New South Wales
Dr Glenise Berry
Australian & New Zealand Society for Geriatric Medicine
Dr Mark Bolland
School of Medicine, The University of Auckland, New Zealand
Dr Chris Bourne
Sydney Sexual Health Centre, Sydney Hospital, New South Wales
Robert Boyd-Boland
Australian Dental Association
Professor Henry Brodaty
Dementia Collaborative Research Centre, University of New South Wales and Prince of Wales Hospital
Kate Broun
Cancer Council Victoria
Leanne Burton
NSW STI Programs Unit, Sydney Sexual Health Centre, Sydney Hospital, New South Wales
Professor Ian Caterson
Centre for Overweight and Obesity, The University of Sydney, New South Wales
Samantha Chakraborty
beyondblue
Professor Stephen Colagiuri
Institute of Obesity, Nutrition and Exercise, The University of Sydney, New South Wales
Dr Michael Crampton
National Immunisation Committee
Dr Michael D’Emden
Diabetes Australia
Dr Joanne Dixon
Human Genetics Society of Australasia
Professor Peter Ebeling
Osteoporosis Australia
Associate Professor Matt Edwards
Department of Paediatrics, University of Western Sydney, New South Wales
Professor John Eisman
Garvan Institute of Medical Research, New South Wales
8th edition v
Shelley Evans
Osteoporosis Australia
Dr Linda Foreman
General practitioner, Adelaide, South Australia
Professor Robert Goldney
Discipline of Psychiatry, The University of Adelaide, South Australia
Associate Professor Jane Halliday
Public Health Genetics, Murdoch Childrens Research Institute, Victoria
Associate Professor Kelsey Hegarty
Kelvin Hill
National Stroke Foundation
Dr Elizabeth Hindmarsh
General practitioner, Sydney, New South Wales
Barbara Hocking
Sane Australia
Dr Cathy Hutton
National Immunisation Committee
Professor Henry Krum
Centre of Cardiovascular Research and Education in Therapeutics, Monash University, Victoria
Professor Stephen Lord
Neuroscience Research Australia
Professor Finlay Macrae
Colorectal Medicine and Genetics, The Royal Melbourne Hospital, Victoria
Professor Rebecca Mason
Australian & New Zealand Bone and Mineral Society
Associate Professor Tim Mathew
Kidney Health Australia
Associate Professor Sylvia Metcalfe
Genetics Education & Health Research, Murdoch Childrens Research Institute, Victoria
Dr Viviene Milch
National Breast and Ovarian Cancer Centre, New South Wales
Carolyn Murray
NSW STI Programs Unit, Sydney Sexual Health Centre, Sydney Hospital, New South Wales
Professor Mark Nelson
Menzies Research Institute, University of Tasmania
Professor Ian Olver
Cancer Council Australia
Dr Rod Pearce
Australian Technical Advisory Group on Immunisation
Dr Carole Pinnock
Repatriation General Hospital, Flinders University, South Australia
Professor Ian Reid
Faculty of Medical and Health Sciences, The University of Auckland, New Zealand
Ann Robertson
The Royal Australian and New Zealand College of Obstetricians and Gynaecologists
Professor Ann Roche
National Centre for Education and Training on Addiction, Flinders University, South Australia
vi Guidelines for preventive activities in general practice
8th edition
Dr Jeff Rowland
Australian & New Zealand Society for Geriatric Medicine
Professor John Saunders
Consultant Physician in Internal Medicine and Addiction Medicine, Sydney, New South Wales
Associate Professor Jonathan Shaw
Baker IDI Heart & Diabetes Institute, Victoria
Professor James St John
Dr Graeme Suthers
South Australia Clinical Genetics Service, South Australia
Shanthi Thuraisingam
National Heart Foundation of Australia
Professor Stephen Twigg
Central Clinical School, The University of Sydney, New South Wales
Dr Angela Taft
Mother and Child Health Research, La Trobe University, Victoria
Jinty Wilson
Heart Foundation and National Vascular Prevention Disease Alliance
Dr Brendan White
Australian Dental Association (NSW Branch), New South Wales
Dr Clive Wright
Chief Dental Officer, NSW Health, New South Wales
Professor Nicholas Zwar
School of Public Health and Community Medicine, University of New South Wales, New South Wales
Members of the Australian & New Zealand Society for Geriatric Medicine Council
Members of the Australian Dental Association Oral Health Committee
Members of the Paediatrics & Child Health Division, Royal Australasian College of Physicians
Representatives from Cancer Council Victoria
Organisational representatives
Lisa Dive
Royal Australasian College of Physicians
Chris Enright
Engy Henein
Royal Australasian College of Physicians
Ruth Hertan
National Stroke Foundation and National Vascular Disease Prevention Alliance
Diana Reddan
National Stroke Foundation
Jared Slater
Optometrists Association Australia
We gratefully acknowledge the expert reviewers and representatives from the above organisations
who contributed scholarly feedback.
8th edition vii
Abbreviations and acronyms
13vPCV 13-valent pneumococcal conjugate vaccine dTPa Diphtheria,tetanus, acellular pertussis (adolescent/
adult version)
23vPPV Pneumococcal polysaccharide vaccine
DXA Dual-energy X-ray absorptiometry
ABCD Asymmetry, border, colour, diameter
ECG Electrocardiograph
ABI Ankle:brachial index
EFG Elevated, firm, growing for more than 1 month
ACE Angiotensin converting enzyme
eGFR Estimated glomerular filtration rate
ACR Albumin-creatinine ratio
ESRD End stage renal disease
AF Atrial fibrillation
ALA Alpha-linolenic acid FAP Familial adenomatous polyposis
AMD Aged-related macular degeneration FH Familial hypercholesterolaemia
APC Adenomatous polyposis coli FOBT Faecal occult blood test
ASCIA The Australasian Society of Clinical Immunology GFR Glomerular filtration rate
and Allergy GP General practitioner
AUSDRISK Australian Type 2 Diabetes Risk Assessment Tool HbA1c Glycated haemoglobin
BCG Bacillus Calmette-Guérin HCG Human chorionic gonadotrophin
BMD Bone mineral density
HDL High density lipoprotein
BMI Body mass index
HDL-C High density lipoprotein-cholesterol
BNP B-type natriuretic peptide
hepA Hepatitis A
BP Blood pressure
hepB Hepatitis B
BRCA1 Breast cancer susceptibility gene 1
HFE (gene) Haemochromatosis
BRCA2 Breast cancer susceptibility gene 2
Hib Haemophilus influenzae type b
CA Cancer antigen
HIV Human immunodeficiency virus
CA125 Cancer antigen 125
HNPCC Hereditary non-polyposis colon cancer
CF Cystic fibrosis
HPV Human papillomavirus
CHD Coronary heart disease
HSIL High grade squamous intraepithelial lesion
CKD Chronic kidney disease
IADL Instrumental activities of daily living
COPD Chronic obstructive pulmonary disease
IFG Impaired fasting glucose
CRC Colorectal cancer
IGT Impaired glucose tolerance test
CRP High sensitivity C-Reactive Protein
IPV Inactivated poliomyelitis
CT Computerised tomography
IS Intussuseption
CVD Cardiovascular disease
LDL Low density lipoprotein
DBP Diastolic blood pressure
LDL-C Low density lipoprotein-cholesterol
DNA Deoxyribonucleic acid
LSIL Low grade squamous intraepithelial lesion
DLCN Dutch Lipid Clinic Network (criteria)
LUTS Lower urinary tract symptoms
DPA Docosapentaenoic acid
LVH Left ventricular hypertrophy
DRE Digital rectal examination
MBS Medicare Benefits Schedule
DT Diphtheria,tetanus
MMR Measles, mumps and rubella
DTpa Diphtheria,tetanus, acellular pertussis
(child version) MMRV Measles, mumps, rubella and varicella
viii Guidelines for preventive activities in general practice
8th edition
MMSE Mini-Mental State Examination
MRI Magnetic resonance imaging
MSM Men who have sex with men
MSU Midstream urine
MUKSB Modified UK Simon Broome criteria
NAAT Nucleic acid amplification test
NHMRC National Health and Medical Research Council
NIP National Immunisation Program
NIPS National Immunisation Program Schedule
NMSC Non-melanoma skin cancer
NTD Neural tube defect
PCR Polymerase chain reaction
PEDS Parents’ evaluation of developmental status

PET-CT Positron Emission Tomography – Computed
Tomography
PND Postnatal depression

RACGP The Royal Australian College of General Practitioners
RCT Randomised controlled trial
SBP Systolic blood pressure
SES Socioeconomic status
SIDS Sudden infant death syndrome
SNAP Smoking, nutrition, alcohol, physical activity
SPF Sun protection factor
STIs Sexually transmitted infections
TG Triglyceride
TIA Transient ischaemic attack
TUGT Timed up and go test
UACR Urine Albumin-to-Creatinine Ratio
VV Varicella Vaccination
VZV Varicella Zoster Virus
WHO World Health Organization

8th edition ix
Contents
I. Introduction 1
The Australian experience 1
Preventive health activities 2
Screening versus case finding 2
Screening principles 3
II. Patient education and health literacy 4
Impact of patient education 4
Approaches to patient education 4
The complex needs and health problems of disadvantaged groups 5
III. Development of the red book 6
Sources of recommendations 6
Scope and limitations of the red book 6
IV. How to use the red book 7
Organisational detail 7
V. What’s new in this 8th edition? 9
1. Preventive activities prior to pregnancy 11
What does pre-conception care include? 11
2. Genetic counselling and testing 14
3. Preventive activities in children and young people 17
Early intervention 17
4. Preventive activities in middle age 26
5. Preventive activities in older age 28
5.1 Immunisation 28
5.2 Falls and physical activity 29
5.3 Visual and hearing impairment 31
5.4 Dementia 32
6. Communicable diseases 34
6.1 Immunisation 34
6.2 STIs 37
7. Prevention of chronic disease 40
7.1 Smoking 42
7.2 Overweight 43
7.3 Nutrition 45
7.4 Early detection of problem drinking 47
7.5 Physical activity 49
x Guidelines for preventive activities in general practice
8th edition
8. Prevention of vascular and metabolic disease 50

8.1 Assessment of absolute cardiovascular risk 50
8.2 BP 51
8.3 Cholesterol and other lipids 53
8.4 Type 2 diabetes 55
8.5 Stroke 57
8.6 Kidney disease 58
9. Early detection of cancers 60
9.1 Skin cancer 60
9.2 Cervical cancer 63
9.3 Breast cancer 65
9.4 Ovarian cancer 67
9.5 Oral cancer 68
9.6 CRC(bowel cancer) 68
9.7 Testicular cancer 71
9.8 Prostate cancer 71
10. Psychosocial 73
10.1 Depression 73
10.2 Suicide 75
10.3 Identification of intimate partner violence 76
11. Oral hygiene 78
12. Glaucoma 79
13. Urinary incontinence 80
14. Osteoporosis 82
15. Screening tests of unproven benefit 85
References 87
Appendix 1: Dutch Lipid Clinic Network Criteria for making a diagnosis 115
of Familial Hypercholesteroloemia (FH) in adults
Appendix 2: ‘Red flag’ early intervention referral guide 117
Appendix 3: Audit-C (available for use in the public domain) 118
Appendix 4:The Australian Type 2 Diabetes Risk Assessment tool – AUSDRISK 120
Appendix 5: Australian cardiovascular risk charts 122
Appendix 6:The three incontinence questions 124
Glossary 125
8th edition 1
I. Introduction
General practice is at the forefront of healthcare in Australia and in a pivotal position to deliver preventive healthcare.
More than 125 million general practice consultations take place annually in Australia and 83% of the Australian
population consult a general practitioner (GP) at least once a year.1 Preventive healthcare is an important activity in
general practice. Preventive healthcare includes the prevention of illness, the early detection of specific disease, and the
promotion and maintenance of health. Preventive care is based on a partnership between a GP and a patient, designed
to help each patient reach their goals of maintaining or improving health.
Prevention is the key to Australia’s future health – both individually and collectively. It is estimated that 80% of premature
heart disease, stroke and type 2 diabetes and 40% of cancer could be prevented through interventions that lead to
healthy diet, regular physical activity and avoidance of tobacco products.2 Preventive care is also critical in addressing
the health disparities faced by disadvantaged and vulnerable population groups.
To facilitate evidence-based preventive activities in primary care, The RACGP has published the Guidelines for preventive
activities in general practice (the ‘red book’) since 1989. The red book is now widely accepted as the main guide to the
provision of preventive care in Australian general practice.
The red book provides a comprehensive and concise set of recommendations for patients in general practice with
additional information about tailoring risk and need. It provides the evidence base for which primary healthcare
resources can be used efficiently and effectively while providing a rational basis to ensure the best use of time and
resources in general practice.
The red book’s companion publication, National guide to a preventive health assessment for Aboriginal and Torres
Strait Islander peoples (2nd edition), is intended for all health professionals delivering primary healthcare to the
Aboriginal and Torres Strait Islander population.
The Australian experience

Health reform in Australia has led to a renewed focus on preventive healthcare. The role of general practice in
prevention has been recognised by the Council of Australian Governments3 and by the Australian Government’s
Preventative Health Taskforce and Primary Health Care Strategy.4,5
Deaths and hospitalisations from preventable illness have continued to decline within Australia. Still, the leading causes of
death and disability in Australia are preventable or able to be delayed by early treatment and intervention (Figure 1).6
Figure 1. Potentially avoidable deaths
Reproduced with permission from the Australian Institute of Health and Welfare. Australia’s health 2012.
Australia’s health series no. 13, cat. no. AUS 156. Canberra: AIHW, 2012.6
2 Guidelines for preventive activities in general practice
8th edition
A recent Australian review7 concluded that lifestyle interventions could have a large impact on population health. The
cardiovascular absolute risk approach and screening for diabetes and chronic kidney disease (CKD) were also given
high priority for action.
Despite this evidence and wide acceptance of its importance, real and perceived barriers have meant preventive
interventions in general practice remain underutilised, being the primary reason for the consultation in only seven of every
hundred clinical encounters.8 This is small when it is considered that preventable chronic diseases, along with biomedical
risk factors, account for approximately one-fifth of all problems currently managed in Australian general practice.9
Each preventive activity uses up some of the available time that GPs have to spend with their patients. It may also
involve direct or indirect costs to the patient. Much more needs to be done to support and improve proper evidence-
based preventive strategies, and to minimise practices that are not beneficial or have been proven to be harmful. The
RACGP has been championing this cause since foundation, and encourages all general practices, GPs and their
teams to prioritise appropriate preventive health activities within their practices.
Preventive health activities

‘Prevention is better than cure’ is an instinctive concept and its appeal is embedded in the medical and political
culture. Yet we now know from the evidence that some preventive activities are not always effective or appropriate;
indeed, some are quite harmful.
Many preventive activities have the potential to be associated with harm. For example, screening may lead to
overdiagnosis, causing needless anxiety, appointments, tests, drugs and even operations. Therefore, it is crucial that
evidence clearly demonstrates that benefits outweigh those harms for each preventive activity.
While greater societal awareness and attention on preventive activities is important, challenges are presented by
the involvement of single-disease health groups, special interest societies and specialist groups that only visualise a
refined subset of patients. These groups often utilise marketing strategies to promote their cause, and this often results
in confusing messages for GPs and their patients. Determining whether a preventive activity is beneficial, harmful or
of indeterminate effect (there is not enough evidence on which to base a decision) requires a consistent, unbiased,
evidence-based approach.
No area typifies this more clearly than the area of cancer screening. The even-handed interpretation of evidence,
balancing harms and benefits, managing overdiagnosis and overtreatment, has been a goal of those drafting the
prostate and breast cancer sections of the red book since the early editions. These screening activities have polarised
different sectors of the health professions.
The RACGP looks forward to resolving the controversies surrounding contentious areas of screening to assist GPs in
caring for their patients. In these guidelines, only those screening activities where evidence demonstrates that benefits
outweigh harms have been included. Section 15 of the red book provides some guidance on common tests where this
is not the case.
Screening versus case finding

Screening has been defined as ‘the examination of asymptomatic people in order to classify them as likely or unlikely
to have a disease’.10 The primary purpose of screening tests is to detect early disease in apparently healthy individuals.
In these guidelines screening usually refers to early detection using questions or a test, which GPs perform either
when patients present for preventive care or opportunistically when patients present for other reasons. Proactive recall
of patients for screening is warranted for high-risk groups, or for conditions where population coverage has been
identified by the government as a public health priority. These include immunisation and screening for cervical, breast
and colorectal cancers (CRC) and diabetes.
Screening tests are not ‘case finding’ or ‘diagnostic’ tests. The purpose of a diagnostic test is to establish the
presence (or absence) of disease as a basis for treatment decisions in symptomatic or screen-positive individuals
(confirmatory test), for example, taking a midstream urine (MSU) sample for evaluation of a urinary tract infection, or
performing mammography for a suspicious breast lump.
8th edition 3
Screening and case finding carry different ethical obligations. If the practitioner initiates the screening, there needs
to be conclusive evidence that the procedure can positively affect the natural history of the disorder. Moreover, the
risks of screening in asymptomatic individuals must be carefully considered as the patient has not asked the health
professional for assistance. This situation is somewhat different from case finding, where the patient has presented
with a particular problem or has asked for some level of assistance. In this situation, there is no guarantee of benefit
of the tests undertaken and, it could be argued, there is at least some implied exposure to risk (as in performing
colonoscopy to investigate abdominal pain). Many health practitioners confuse the difference between screening
and case-finding tests. This often obscures the arguments surrounding the benefits and harms of screening tests.
Screening principles
The World Health Organization (WHO) has produced guidelines11,12 for the effectiveness of screening programs.
We have kept these and the United Kingdom National Health Service’s guidelines13 in mind in the development of
recommendations about screening and preventive care.
The condition
• It should be an important health problem.
• It should have a recognisable latent or early symptomatic stage.
• The natural history of the condition, including development from latent to declared disease, should be adequately
understood.
The test
• It should be simple, safe, precise and validated.
• It should be acceptable to the target population.
• The distribution of test values in the target population should be known and a suitable cut-off level defined and
agreed.
Treatment
• There should be an effective treatment for patients identified with evidence that early treatment leads to better
outcomes.
• There should be an agreed policy on who should be treated and how.
Outcome
• There should be evidence of improved mortality, morbidity or quality of life as a result of screening and that the
benefits of screening outweigh the harm.
• The cost of case finding (including diagnosis and treatment of patients diagnosed) should be economically
balanced in relation to possible expenditure on medical care as a whole.
Consumers
• Consumers should be informed of the evidence so that they can make an informed choice about participation.
Screening activities in general practice are complex; they involve patients accessing care as well as general
practices adopting systematic approaches to registering and recalling patients, and organising their efforts
to maximise the effectiveness of each consultation in providing preventive care.14 Effective screening requires
consideration of subgroups in the population who may have a higher prevalence of a disease or risk factor, or who
may have difficulty accessing services.15
In Australia, there is an increasing number of Medicare items for health assessments in particular population
groups: preschool children, Aboriginal children and adults, refugees, people with an intellectual disability, those
aged 45–49 years (with a risk factor), and those aged 75 years or over. There is evidence that these assessments
improve the likelihood of preventive care being received.16 However, it is important that such ‘health checks’ involve
preventive interventions for which there is clear evidence of their effectiveness.
8th edition
II. Patient education and health literacy

Impact of patient education
Patient education and counselling contribute to behaviour change for primary prevention of disease17. More broadly,
they may also help create greater ‘health literacy’ – the knowledge and skills patients require to maintain their
own health, including use of health services. The use of behavioural techniques, especially for self-monitoring, is
recommended, as is the use of personal communication and written or other audiovisual materials.17
Patients view the GP as a key first contact and credible source of preventive advice.
Factors that increase the effectiveness of patient education delivered by GPs include:
• assessing the patient’s health literacy18
• the patient’s sense of trust in their GP19
• face-to-face delivery20
• patient involvement in decision-making21–23
• highlighting the benefits and the costs24, 25
• strategies to help the patient remember what they have been told26
• tailoring the information to the patient’s interest in change27
• strategies that address the difficulty in adherence23, 28
• the use of decision aids.29
Many prevention activities involve a change in health-related behaviour. As the patient plays a large role in making this
happen, it is useful to facilitate more active inclusion of patients in their care. This process is an essential component
of self-management strategies30, 31 and has the potential to increase the patient’s responsibility for their health. In
addition, it:
• enhances the quality of communication32, 33
• enhances the patient-doctor consultation21
• can reduce the cost of aspects of care through better informed patients22
• increases the demand and use of appropriate referral to other health professionals and agencies32
• increases adherence to recommended prevention activities and therapeutic regimens.32, 34
For those whose first language is not English, a professional interpreter should be considered.
Approaches to patient education

Patients need to develop their own understanding of the problem and what can be done about it. For simple
behavioural changes, such as having a Pap test, patients weigh up the perceived benefits and costs.35 These benefits
and costs may include answers to the following questions.
• How big is the problem to the individual?
• What are the consequences of not doing the test?
• What are the benefits?
• What are the barriers?
Some health education may require more complex actions over a period of time such as changing diet, stopping
smoking or increasing physical activity. The ‘stages of change model’36 identifies five basic stages of change, which
are viewed as a cyclical, ongoing process during which the person has differing levels of motivation or readiness
to change, and the ability to relapse or repeat a stage. Each time a stage is repeated, the person learns from the
experience and gains skills to help them move to the next stage.
8th edition 5
Table II.1 Stages of change model

Pre-contemplation The person does not consider the need to change
(Not thinking about change) • Has not had sufficient experience with negative consequences.
Contemplation The person considers changing a specific behaviour

(Thinking of change) • Begins to seek relevant information.
• Re-evaluates behaviour.
• Obtains help from others to support future attempts.
• Still weighs up options and isn’t ready to take action.
Determination The person makes a serious commitment to change

(Ready for change) • Is ready to take action in the next 30 days.
• Needs to set goals and develop priorities in order to manage their illness.
Action Change begins (these can be large or small changes)

(Changing behaviour) • Makes efforts to modify habits and environment.
• Increasingly uses behavioural processes of change (e.g. stimulus control and
counter-conditioning).
Maintenance Change is sustained over a period of time

(Maintaining change) • Counter-conditioning and self-liberation peak.
• Takes responsibility for actions.
• Is susceptible to relapse so remain aware of environmental and internal stimuli that
may trigger problem behaviours.
Motivational interviewing is dealt with in more detail in the RACGP green book.
The complex needs and health problems of disadvantaged groups

The complex needs and health problems of disadvantaged groups and the interactions between social,
psychological, environmental and physical determinants of health mean that special effort is required for patient
education to be effective. In particular, GPs need to employ a range of strategies and work in collaboration with
other services.37 To be effective in patient education for Indigenous communities, GPs need an understanding of
the Aboriginal and Torres Strait Islander view of health, culture and history and an ability to provide services within a
culturally appropriate framework. This also requires GPs to collaborate with other agencies and providers to ensure
the provision of high-quality preventive healthcare for Indigenous Australians.38
8th edition
III. Development of the red book
These Guidelines for preventive activities in general practice, 8th edition, have been developed by a taskforce of
GPs and experts to ensure that the content is the most valuable and useful for GPs and their teams. The guidelines
provide an easy, practical and succinct resource. The content broadly conforms to the highest evidence-based
standards according to the principles underlying the Appraisal of Guidelines Research and Evaluation.39, 40
The dimensions addressed are:
• scope and purpose
• clarity of presentation
• rigour of development
• stakeholder involvement
• applicability
• editorial independence.
The red book maintains developmental rigour, editorial independence, relevance and applicability to general practice.
The Red Book Taskforce also welcomes its companion document, the National guide to a preventive health
assessment for Aboriginal and Torres Strait Islander peoples, 2nd edition (the National guide). This publication is a
collaborative effort with the National Aboriginal Community Controlled Health Organisation and the RACGP National
Faculty of Aboriginal and Torres Strait Islander Health, and is intended for all health professionals delivering primary
healthcare to the Aboriginal and Torres Strait Islander population. For preventive care to be most effective, it needs
to be planned, implemented and evaluated. Planning and engaging in preventive health is increasingly expected by
patients. The RACGP thus provides the red book and National guide to inform evidence-based guidelines, and the
green book to assist in development of programs of implementation. The RACGP is planning to introduce a small set
of voluntary clinical indicators to enable practices to monitor their preventive activities.
Sources of recommendations
The recommendations in these guidelines are based on current, evidence-based guidelines for preventive activities. We
focused on those most relevant to Australian general practice. Usually this means that the recommendations are based
on Australian guidelines such as those endorsed by the National Health and Medical Research Council (NHMRC).
In cases where these are not available or recent, other Australian sources have been used, such as guidelines
from the Heart Foundation, Canadian or United States preventive guidelines, or the results of systematic reviews.
References to support these recommendations are listed. However, particular references may relate to only part of
the recommendation (e.g. only relating to one of the high-risk groups listed) and other references in the section may
have been considered in formulating the overall recommendation.
Scope and limitations of the red book

These guidelines have not included detailed information on the management of risk factors or early disease (e.g.
what medications to use in treating hypertension). Similarly, they have not made recommendations about tertiary
prevention (preventing complications in those with established disease). Also, information about prevention of
infectious diseases has been limited largely to immunisation and some sexually transmitted infections (STIs).
There is limited advice about travel medicine. Information on travel medicine can be obtained from the Centres for Disease
Control and Prevention at www.cdc.gov/travel/index.htm or WHO International Travel and Health at www.who.int/ith/
These recommendations are based on the best available information at the time of writing. On past experience this
means that the guidelines will remain current for no longer than 2 years. Any update information will be posted on
the RACGP website. More information and guidelines can be found on the NHMRC website www.nhmrc.gov.au/
guidelines; the Australian Government clinical guidelines portal www.clinicalguidelines.gov.au; and the Cochrane
Collaboration website www.cochrane.org/
8th edition 7
IV. How to use the red book

These guidelines are designed to be used in a number of ways, all of which can be useful in day-to-day general
practice. The red book can be used as a:
• guide to who is most at risk and for whom screening or preventive care is most appropriate
• refresher to check the latest recommendations
• reminder to check at a glance what preventive activities are to be performed in various age groups and how often
• checklist of preventive activities used according to an individual patient’s health profile
• patient education tool, to demonstrate to patients the evidence that exists for preventive activities
• study guide – a comprehensive list of references is provided (links to further original sources are provided in the
electronic version where appropriate). This allows more in-depth information on a particular topic.
Organisational detail
The information in these guidelines is organised into three levels.
The first level is the lifecycle chart, which highlights when preventive activities should be performed and the
optimum frequency for each activity. The lifecycle chart is organised by age and clinical topic. Simply check the
column under a particular age group to see what activities should be considered for the patient. The preventive
activities that are recommended for everyone within a particular age range, and for which there is sound research
evidence, are shaded in red while activities to be performed only in patients with risk factors or where the evidence
is not as strong are shaded in light red.
A copy of this chart can be downloaded from the RACGP website and attached to the patient record as a
systematic reminder for preventive activities. You can also use it as a wall chart, or keep it handy on your desk.
The second level is more detailed and presents a summary of recommendations in addition to tables that identify
what preventive care should be provided for particular groups in the population.
This edition of the red book adopts the most recent NHMRC levels of evidence and grades of recommendations.41
Recommendations in the tables are graded according to levels of evidence and the strength of recommendation.
The levels of evidence are coded by the roman numerals I–IV while the strength of recommendation is coded by the
letters A–D. Practice Points are employed where no good evidence is available. In most cases a Practice Point will
replace what has been classed in previous red book editions as level V evidence.
8th edition
Table IV.1 Coding scheme used for levels of evidence and grades of recommendation
Levels of evidence
Level Explanation
I Evidence obtained from a systematic review of level II studies
II Evidence obtained from a randomised controlled trial (RCT)
III–1 Evidence obtained from a pseudo-randomised controlled trial (i.e. alternate allocation or some
other method)
III–2 Evidence obtained from a comparative study with concurrent controls:

• non-randomised, experimental trial
• cohort study
• case-control study
• interrupted time series with a control group.
III–3 Evidence obtained from a 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
Practice Point Opinions of respected authorities, based on clinical experience, descriptive studies or reports of
expert committees
Grades of recommendations
Grade Explanation
A Body of evidence can be trusted to guide practice
B Body of evidence can be trusted to guide practice in most situations
C Body of evidence provides some support for recommendation(s) but care should be taken in its
application
D Body of evidence is weak and recommendation must be applied with caution
Only key references used to formulate the recommendations are included in the tables. Where the evidence is
available on the internet, the web link is given to enable easy access to original materials.
There is also information on how the preventive care should be implemented, for example, a brief outline of the
method of screening.
Finally, there is a third level of information, which is included in implementation tables, on particular disadvantaged
population groups that may be at risk of not receiving preventive care and what should be done to increase their
chance of preventive care.
8th edition 9
V. What’s new in this 8th edition?
The format of this 8th edition of the red book is similar to the 7th edition and is designed to be used together with
the other preventive resources such as the RACGP publications, the green book and SNAP (smoking, nutrition,
alcohol and physical activity) guidelines. There is increased information about what should be covered in health
assessments or health checks for particular groups. Levels of evidence and recommendations are now presented
alongside ‘What should be done?’ and ‘How often?’. References are listed in a separate column. We have increased
the amount of guidance, while trying to maintain brevity to improve clarity.
Table V.1 Key changes in the 8th edition

Section Change
Genetic counselling and testing (Section 2) Guidance on familial hypercholesterolaemia (FH) has been
added.
Preventive activities in children and young people The Australian Government has announced a Universal
(Section 3) Child Health Check at age 3 years. This will be introduced
in 2013 and will replace the health check at age 4 years.
The contents of the new check were not available prior
to publication of this edition. It is expected that the new
check will easily fit into the system of prevention and
promotion outlined in this section.
New information that describes evidence-based
interventions for babies of depressed mothers (as distinct
from interventions targeting the mother’s depression) has
been added.
As this edition was finalised, the RACGP adopted a
document outlining ‘the role of general practice in the
provision of healthcare to children and young adults’. It
may be useful to read this document as a companion
piece to Section 3: Preventive activities in children and
young people.
Reference to new United States Preventive Services Task
Force (USPSTF) recommendations for obesity screening
and screening for depression in adolescents have been
included.
Preventive activities in older age (Section 5) New information about possible prevention of dementia
by attention to cardiovascular risk factors has been
added.
Information about influenza vaccination has been
included.
New and more detailed information about falls
assessment and prevention has been included.
Communicable diseases (Section 6) Chlamydia screening for both sexes up to age 29 years
has been added.
Human papilomavirus (HPV) vaccine for both sexes
commencing in 2013 has been added.
Information about combined measles, mumps, rubella,
varicella (MMRV) at 18 months to be both the second
dose of measles, mumps, rubella (MMR) and the first
dose of varicella vaccine has been added.
8th edition
Section Change
Prevention of chronic disease (Section 7) New recommendations about weight management (in
line with the new NHMRC guidelines) including diet and
physical activity strategies have been included.
Prevention of vascular and metabolic disease (Section 8) There is greater emphasis on assessment and
management of cardiovascular risk for patients aged
45–74 years (in line with the new NHMRC guidelines). This
includes treatment targets for blood pressure (BP) and
lipids and new recommendations for screening as well as
management of high-risk patients for renal disease.
Early detection of cancers (Section 9) This section has been updated with new evidence;
however, little has changed in the recommendations for
screening for most cancers.
Attention is drawn to possible changes in
recommendations for cervical cancer (Pap) screening
as new national guidelines are being prepared by the
National Cervical Screening Program.
CRC guidelines have been updated and provide more
information, which may help GPs decide if a patient is at
high risk.
Prostate cancer screening remains controversial. New
trial data do not provide unequivocal directions to screen
or not screen for prostate cancer using the PSA test,
with or without digital rectal examination (DRE). The
medical community remains divided on the issues. From
a general practice viewpoint, it is unclear whether the
advantages of screening (still very uncertain) outweigh
the harms (becoming more clearly defined). The updated
recommendation is to not raise the issue with every
eligible man, but wait until you are asked about screening.
In light of many other proven preventive activities that
could be more usefully addressed in men, we believe that
prostate cancer screening remains low on the priority list.
Oral hygiene (Section 11) Additional advice on oral health messages is included
from an Australian National Consensus workshop
conducted in 2011.
The ‘Lift the lip’ dental check for early identification of oral
problems has been added.
Glaucoma (Section 12) Updated recommendations in line with new NHMRC

guidelines from 2010 have been added.
Osteoporosis (Section 14) Details of risk factors have been refined.

Changes to criteria for recommending bone mineral
density (BMD) measurement have been included.
Guidance on frequency of BMD measurement have been
added.
Recommendation to use absolute risk estimation to aid
decision-making has been included.
Cautionary notes on use of calcium supplementation have
been included.
Evidence levels have been clarified.
8th edition 11
1. Preventive activities prior to pregnancy
Age <2 2–3 4–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 ≥65
Every woman aged 15–49 years should be considered for pre-conception care (C). Pre-conception care is a set
of interventions that aim to identify and modify biomedical, behavioural and social risks to a woman’s health or
pregnancy outcome through prevention and management.42 This should include smoking cessation (A)43 and
advice to consider abstinence from alcohol (especially in the early stages of pregnancy),44 folic acid and iodine
supplementation (A),45, 46 review of immunisation status (C),47 medications (B)48 and chronic medical conditions,
especially glucose control in patients with diabetes (B).49
There is evidence to demonstrate improved birth outcomes with pre-conception healthcare in women with
diabetes, phenylketonuria and nutritional deficiency50 as well as benefit from the use of folate supplementation
and a reduction in maternal anxiety.51 The information below lists all the potential interventions that have been
recommended by expert groups in pre-conception care (C).
What does pre-conception care include?

Medical issues
Reproductive life plan
Assist your patient in developing a reproductive life plan that includes whether they want to have children. If they do,
discuss the number, spacing and timing of intended children.
Reproductive history
Ask if there have been any problems with previous pregnancies such as infant death, foetal loss, birth defects
particularly neural tube defects (NTD), low birthweight, pre-term birth, or gestational diabetes. Are there any ongoing
risks that could lead to a recurrence in a future pregnancy?
Medical history
Ask if there are any medical conditions that may affect future pregnancies. Are chronic conditions such as diabetes,
thyroid disease, hypertension, epilepsy and thrombophilia well managed?
Medication use
Review all current medications including over-the-counter medications, vitamins and supplements.
Genetic/family history
Assess risk of chromosomal or genetic disorders, (e.g. cystic fibrosis (CF), fragile X, Tay–Sachs disease,
thalassaemia, sickle cell anaemia and spinal muscular atrophy), by collection of data on family history and ethnic
background. Provide opportunity for carrier screening for these and other more common genetic conditions.
General physical assessment

Conduct Pap test and breast examinations before pregnancy if indicated or due. Also assess body mass index
(BMI), and BP and ask about periodontal disease.
Substance use
Ask about tobacco, alcohol and illegal drug use.
8th edition
Vaccinations
Vaccinations can prevent some infections that may be contracted during pregnancy. If previous vaccination history
or infection is uncertain, testing should be undertaken to determine immunity to varicella and rubella. Women
receiving live viral vaccines such as MMR and varicella should be advised against becoming pregnant within 28
days of vaccination. Recommended vaccinations are:
• MMR
• varicella (in those without a clear history of chickenpox or who are non-immune on testing)
• influenza (recommended during pregnancy to protect against infection if in second or third trimester during
influenza season)
• diphtheria, tetanus, pertussis (DTpa) (to protect newborn from pertussis).
Lifestyle issues
Family planning
Based on the patient’s reproductive life plan (see above), discuss fertility awareness and how fertility reduces
with age, chance of conception, and risk of infertility and foetal abnormality. For patients not planning to become
pregnant, discuss effective contraception and emergency contraceptive options.
Folic acid supplementation

Women should take a 0.4–0.5 mg supplement of folic acid per day for at least 1 month prior to pregnancy, and for
the first 3 months after conception. In women at high risk (i.e. with a reproductive or family history of NTD, women
who have had a previous pregnancy affected by NTD, women on anti-epileptics, and women who have diabetes)
the dose should be increased to 5 mg per day.
Healthy weight, nutrition and exercise

Discuss weight management and caution against being overweight or underweight. Recommend regular,
moderate-intensity exercise and assess risk of nutritional deficiencies (e.g. vegan diet, lactose intolerance, calcium
or iron and vitamin D deficiency due to lack of sun exposure).
Psychosocial health
Provide support and identify coping strategies to improve your patient’s emotional health and wellbeing.
Smoking, alcohol and illegal drug cessation (as indicated)

Smoking, illegal drug and excessive alcohol use during pregnancy can have serious consequences for an unborn
child and should be stopped prior to conception.
Healthy environments
Repeated exposure to hazardous toxins in the household and workplace environment can affect fertility and
increase the risk of miscarriage and birth defects. Discuss the avoidance of TORCH infections: Toxoplasmosis,
Other – such as syphilis, varicella, mumps, parvovirus and human immunodeficiency virus (HIV) – Rubella,
Cytomegalovirus, Herpes simplex.
• Toxoplasmosis: avoid cat litter, garden soil, raw/undercooked meat and unpasteurised milk products, and wash
all fruit and vegetables.
• Cytomegalovirus, parvovirus B19 (fifth disease): discuss importance of frequent handwashing, and child and
healthcare workers further reducing risk by using gloves when changing nappies.
• Listeriosis: avoid paté, soft cheeses (feta, brie, blue vein), pre-packaged salads, deli meats and chilled/smoked
seafood. Wash all fruit and vegetables before eating. Refer to Australian food standards at www.foodstandards.
gov.au/foodmatters/pregnancyandfood.cfm regarding folate, listeria and mercury.
• Fish: limit fish containing high levels of mercury.
8th edition 13
Table 1.1 Pre-conception: preventive interventions

Intervention Technique References
Folate High-risk women: 5 mg/day supplementation ideally beginning at least 1 month prior 45, 52–54
supplementation to conception and for first trimester.
Most women: 0.5 mg/day supplementation ideally beginning at least 1 month prior to
conception and for first trimester.
Iodine All women who are pregnant, breastfeeding or considering pregnancy should take an 46
supplementation iodine supplement of 150 micrograms (μg) each day.
Smoking Women should be informed that tobacco affects foetal growth and all women should 55
cessation be advised to stop smoking. Evidence exists to suggest improved cognitive ability
in children of mothers who quit smoking during gestation (III,A). Pharmacotherapy
should be considered when a pregnant woman is otherwise unable to quit, and when
the likelihood and benefits of cessation outweigh the risks of pharmacotherapy and
potential continued smoking.
Alcohol and illicit For women who are pregnant or planning a pregnancy, not drinking is the safest 44
drug use option. The risk of harm to the foetus is highest when there is high, frequent, maternal
alcohol intake. The risk of harm to the foetus is likely to be low if a woman has
consumed only small amounts of alcohol before she knew she was pregnant. Women
should be informed that illicit drugs may harm foetuses and advised to avoid use.
Interpregnancy There are worse perinatal outcomes with interpregnancy intervals <18 months or 56
interval >59 months, namely preterm birth, low birth weight and small for gestational age.
Chronic diseases Optimise control of existing chronic diseases (e.g. diabetes, hypertension, epilepsy). 54
Avoid teratogenic medications.
Pre-conception Address risk factors using Pregnancy Lifescripts

care resources for (resources are in process of being updated in 2012).
GPs and patients
Health inequity
About half of women in Victoria, New South Wales and South Australia supplement their diet with folate peri-
conceptionally. This figure is lower in: 57
• women in lower socioeconomic groups
• Indigenous women
• rural women
• younger women
• multiparous women.
Strategy
As per general principles as discussed in Section I: Introduction and as outlined in the RACGP green book.
Population health surveys in three states (New South Wales 2007–08, Australian Capital Territory 2007–08 and
Tasmania 2009) showed that about half of all Australian mothers took folic acid supplements just prior to and
during their first trimester of pregnancy, as recommended. Supplement use was lower in mothers without tertiary
qualifications and in those living in more disadvantaged and remote areas.
8th edition
2. Genetic counselling and testing
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
There is evidence to recommend offering specific genetic tests to pregnant women, couples planning a pregnancy,
and neonates (as part of the newborn screening program) (C). Other genetic tests are appropriate for certain
conditions where the individual is considered to be at increased risk (A).
In order to identify patients who may potentially benefit from genetic testing, the GP must ensure that a
comprehensive family history is taken from all patients including first-degree or second-degree relatives (A) and
regularly updated. A family history should ideally extend to three generations, covering both sides of the family and
ethnic background. Age of onset of disease and age of death should be recorded where available.
The presence of genetically determined disease may be suggested by increased frequency and early onset of
cancers in families, premature ischaemic heart disease or sudden cardiac death, intellectual disability, multiple
pregnancy losses, stillbirth or early death, and children with multiple congenital abnormalities. Also, patients of
particular ethnic backgrounds may be at increased risk and benefit from genetic testing for specific conditions.
Possible consanguinity (cousins married to each other) should be explored, for example, by asking, ‘Is there any
chance that a relative of yours might be related to someone in your partner’s family?’. GPs should consider referral
to or consultation with a genetic service (general or cancer genetics) for testing because test results, (which rely on
sensitivity, specificity and positive predictive value) are not straightforward. Testing often involves complex ethical,
social and legal issues. Waiting lists for genetic services are usually more than 1 month, so direct consultation and
liaison by telephone are necessary when the genetic advice could affect a current pregnancy.
Table 2.1 Genetic testing: identifying risks

Who is at risk? What should be done? How often? References
Breast and ovarian cancer
See Section 9.3: Breast cancer
Colon cancer
See Section 9.6: CRC (bowel cancer)
FH
Increased risk Assess their probability of At first 58–60

• Premature ischaemic heart disease (men aged <55 having FH using the Dutch presentation
years, women aged <60 years) Lipid Clinic Network (DLCN)
criteria or Modified UK
• First-degree relative with premature ischaemic heart
Simon Broome (MUKSB)
disease (men aged <55 years, women aged <60 years)
criteria (III,B) (Appendix 1)
• Total cholesterol >7.5 or LDL-C >4.9
Offer referral to a lipid
• First-degree relative with a total cholesterol >7.5 or disorders clinic if DLCN
LDL-C >4.9 score >3 or the MUKSB
• Tendon xanthomata or arcus cornealis at age <45 years suggests possible FH
8th edition 15

Cystic fibrosis
Increased risk
• Northern European or Ashkenazi Jewish ancestry Offer referral for genetic Test couple 61–63
• Family history of CF, or a relative with a known CF counselling and testing (III,B) prior to
mutation If patient is pregnant, contact pregnancy or
genetic services to organise in first trimester
• Where partner is affected or is a known carrier of CF
screening in first trimester
• Partners from Northern European, Ashkenazi Jewish
backgrounds who are consanguineous (cousins married
to each other)
• Men with infertility suspected or due to congenital
absence of the vas deferens
Down syndrome
At risk Combined maternal serum In first or 63–67
• All pregnant women and ultrasound screening in second
first trimester trimester
Maternal serum screening in
second trimester* (C)
Significantly increased risk Foetal diagnostic genetic In first or 64
• Women who have had a previous Down syndrome testing (C) second
pregnancy Offer referral for genetic trimester
• Women with positive maternal serum screening/nuchal counselling
translucency ultrasound in first trimester or maternal
serum screening in second trimester
• Parent with a chromosomal rearrangement (e.g.
balanced translocation of chromosome 21)
Hereditary haemochromatosis (HFE)
Increased risk
• Patients with liver disease of unknown cause, including Test for transferrin At first 63, 68–70
those with suspected alcoholic liver disease saturation and serum ferritin presentation
• All first-degree relatives of patients with concentration. If fasting
haemochromatosis, known mutation in HFE gene transferrin saturation >45%
or fasting ferritin >250 µg/L
• Patients with conditions that could be a complication
on more than one occasion,
of HFE (diabetes mellitus, atypical arthritis,
test for HFE mutations (II,A).
cardiomyopathy, erectile dysfunction or chronic fatigue)
If HFE mutation identified,
discuss options for genetic
testing and referral for
genetic counselling of at-risk
family.
Children of C282Y
heterozygotes should only
be tested if the other parent
has the C282Y mutation.
Testing children in affected
families is generally not
recommended until age
18 years unless symptomatic.
Other first-degree relatives of
C282Y heterozygotes should
be tested with iron studies.
If these are positive, discuss
genetic testing and referral
for genetic counselling.
8th edition

Haemoglobinopathies and thalassaemias
Increased risk
• People from any of the following ethnic backgrounds: Mean corpuscular Test couple 70, 71
Southern European, African (including Americas volume, mean corpuscular prior to
and Caribbean), Middle Eastern, Chinese, Indian haemoglobin, ferritin pregnancy or
subcontinent, Central and South East Asian, Pacific Haemoglobin in first trimester
Islander, New Zealand Maori, South American and electrophoresis
some northern Western Australian and Northern (III,B)
Territory Indigenous communities
Seek advice from
haematology or
genetic services about
deoxyribonucleic acid (DNA)
testing especially for alpha-
thalassaemia carriers
Fragile X syndrome
Increased risk Karyotype/comparative Any age for

Children or adults of either sex with one or more of the genomic hybridisation by diagnosis 73, 74
following features: microarray and DNA test for Prior to
fragile X pregnancy
• developmental delay including intellectual disability of
unknown cause Refer to genetic services to ascertain
for genetic counselling and reproductive
• autistic-like features
testing at-risk family (I,A) risk
• attention deficit hyperactivity disorder
• speech and language problems
• social and emotional problems, such as aggression or
shyness
• a female with a history of primary ovarian insufficiency (IV,B) 72, 75
or premature menopause (age <40 years)
• adults with ataxia, balance problems and Parkinsonism (IV,A) 76
• relative with a fragile X mutation
* First trimester Down syndrome screening:
• free beta human chorionic gonadotrophin (HCG), pregnancy associated plasma protein at 10–12 weeks
(this also provides risk for trisomy 18, Edwards syndrome)
• nuchal translucency screen at 11 weeks 3 days–13 weeks 6 days.
Second trimester serum screening:
• beta HCG, unconjugated oestriol, alpha-fetoprotein and inhibin A ideally at 15–17 weeks; also gives risk
for Edward syndrome and NTDs.
8th edition 17
3. Preventive activities in children and young people
Early intervention
Prevention and promotion in the early years, from conception to age 5 years, is important for an individual’s lifelong
health and wellbeing.77 It may also be an opportunity to redress health inequalities.78, 79 In adolescence, neuro-
developmental studies support the value of early intervention to prevent ongoing harm.80
Many infants and children visit their GP frequently and adolescents visit at least once a year.81 This frequent contact
provides opportunities for disease prevention and health promotion.
Evidence provides moderate support for the hypothesis that ‘accessible, family-centred, continuous,
comprehensive, coordinated, compassionate and culturally effective care improves health outcomes for children
with special healthcare needs’.82 There is also evidence that supports the beneficial impact of similar care for
children without special healthcare needs.83
There is little Australian research investigating interventions based in general practice. Recommendations in this
section are largely drawn from expert consensus and parental values.
Health inequity
Compared with non-Indigenous Australians, Aboriginal and Torres Strait Islander children are three times more likely to
die before their first birthday, five times more likely to succumb to sudden infant death syndrome (SIDS), twice as likely
to be born premature or with low birthweight, and nearly four times as likely to be hospitalised with respiratory infection.
Indigenous Australian mothers are eight times more likely than non-Indigenous mothers to receive inadequate antenatal
care and rates of breastfeeding are lower in Indigenous than non-Indigenous communities.84
There is a socioeconomic gradient in the health of Australian children and young people, both Indigenous and non-
Indigenous, which has an impact that is both immediate and lifelong. There are large numbers of vulnerable children in
the mid-socioeconomic range of the population and it is the size of this group that justifies universal intervention. On the
other hand, the magnitude of the ill-health experienced by the smaller number at the bottom of the spectrum justifies
targeted intervention. Michael Marmot has attempted to resolve this tension by arguing for ‘proportionate universalism’.78
Maternal smoking during pregnancy is more prevalent among women of lower socioeconomic status (SES) and single
mothers, and is strongly associated with low birthweight. Mothers from lower socioeconomic backgrounds have
fewer and less regular antenatal visits. Lower rates of breastfeeding and shorter duration of breastfeeding have been
reported for mothers in a variety of disadvantaged backgrounds including single, low income, migrant, unemployed
families, poorly educated parents and disadvantaged communities. Higher mortality rates in infancy and childhood
including deaths from neonatal hypoxia, SIDS, prematurity-related disorders, and accidental and non-accidental injury
are reported for lower socioeconomic children and children living in disadvantaged neighbourhoods.84 Health inequity
present at school entry gets worse thereafter. The Australian data was summarised in Alan Hayes in 2011.79
8th edition
Table 3.1 Age-related health checks in children and young people

Age What should be done? References
Neonatal • Vitamin K and immunisation as per the Australian Government Department of Health and Ageing
Australian Immunisation Handbook at www.immunise.health.gov.au (A)
Assessment
• Metabolic screen (IV,B) 85
• Nutrition assessment: review feeding method. Support and appropriately promote breastfeeding 86
(C) (see Table 3.3 comment a). New NHMRC guidelines expected in 2012
• Universal hearing assessment see www.health.nsw.gov.au/initiatives/swish/index.asp and
www.aussiedeafkids.org.au/newborn-hearing-screening.html
• Physical exam as outlined in the Child Health Record (C) (see Table 3.3 comment b) 87
• Identify family strengths, elicit concerns and promote parental confidence, competence and mental 88
health (C)
Preventive counselling and advice
• Injury prevention: promote safety from accidental and non-accidental injury. This includes the risks 87
to baby of passive smoking, SIDS and UV exposure (III,B)
• Settling (Practice Point)
• Maternal health (Practice Point)
2, 4, 6 • Immunisation as per the Australian Government Department of Health and Ageing Australian
months Immunisation Handbook at www.immunise.health.gov.au (A)
Assessment
• Physical exam as outlined in the Child Health Record (C) (see Table 3.3 comment b) 87
• Nutrition assessment: promote breastfeeding appropriately. Introduction of solids: be aware of 86, 89
conflicting expert advice concerning the best age at which to introduce solids (B) (see Table 3.3
comment a) New NHMRC guidelines expected in 2012
• Developmental progress including vision and hearing (see Table 3.3 comment c) 88
• Quality of child–parent relationship (C) 88, 90
• When the baby is presented as a ‘problem’ assess parental mental health, family functioning 91
(including the possibility of domestic violence) and social support (C) (see Table 3.3 comment d)
• Encourage discussion related to physical activity recommendations (B) (see Table 3.3 comment e)
• Injury prevention – promote safety from accidental and non-accidental injury, includes the risks to 87, 92, 93
baby of passive smoking, SIDS, UV exposure, water, home environment (III,B)
• Settling (Practice Point)
• Maternal health (Practice Point)
• Teething (Practice Point)
• Play (Practice Point)
12 & 18 Assessment
months • ‘Lift the lip’ dental check (C) (see Table 3.3 comment f)
• Nutrition and physical activity (B) (see Table 3.3 comment e). New NHMRC guidelines expected in 2012 94, 95
• Risk of iron depletion and vitamin D deficiency (C) 86, 91
• Developmental progress including vision and hearing (see Table 3.3 comment c) 96, 97
• Family functioning, dysfunction (including domestic violence) and the social environment (C) 88, 90
(see Table 3.3 comments h and i)
• Social and emotional wellbeing (Practice Point) 88, 90
• Toilet training (Practice Point)
• Behaviour and behaviour management techniques (Practice Point)
8th edition 19
2 years • Immunisation as per the Australian Government Department of Health and Ageing Australian
Immunisation Handbook at www.immunise.health.gov.au (A)
Assessment
• Physical exam as outlined in the Child Health Record (C) (see Table 3.3 comments b and g) 87
• Developmental progress including vision and hearing (see Table 3.3 comment c)
• ‘Lift the lip’ dental check (C) (see Table 3.3 comment f) 94, 95
• Emerging behavioural or emotional problems (C)
• When the child presents with behavioural or emotional problems consider family functioning 88, 90
(including the possibility of domestic violence) and the family environment more generally (C)
(Practice Point explanatory comments h and i)
• Injury prevention (III,B)
• Sun protection (Practice Point) 87, 92, 93
• Social and emotional wellbeing (C) 88, 90
3 years Assessment
• Check vision (B) (see Table 3.3 comment j) 98
The Universal Child Health Check at age 3 years will replace the current Healthy Kids check at age
4 years. To be introduced by the Australian Government in 2013. Details not available at the time of
publication.
4 years • Immunisation as per the Australian Government Department of Health and Ageing Australian
Immunisation Handbook at www.immunise.health.gov.au (A)
Healthy Kids Check see Table 3.3 comment k 99–102
Assessment
• Physical assessment (B) (see Table 3.3 comment k)
Also recommended
• Developmental and emotional progress (see Table 3.3 comment c)
• ‘Lift the lip’ dental check (C) (see Table 3.3 comment f) 94, 95
• Assess the quality of family functioning when there are emotional or behavioural problems (C) 88, 90
(see Table 3.3 comments h and i)
• Injury prevention (III,B) 92, 93
• Sun protection (Practice Point)
8th edition
Age What should be done? References

6–13 Assessment
years • Growth velocities including BMI opportunistically (B) 103
• Discussion relating to progress at school (C) 88
• ‘Lift the lip’ dental check (C) (see Table 3.3 comment f). Encourage regular dental reviews 94, 95
• Family functioning and family environment (C) (see Table 3.3 comments h and i) 88, 90
• Anticipate and look for emerging behavioural or emotional problems (C) 88, 90
• Injury prevention (II) 92, 93
• Sun protection
14–19 • Immunisation as per the Australian Government Department of Health and Ageing Australian
years Immunisation Handbook at www.immunise.health.gov.au (A)
Assessment
• Growth velocities including BMI opportunistically (B) (see Table 3.3 comment l) 103, 104
• Screen sexually active young people for chlamydia (Section 6.2.1: Chlamydia and other STIs)
• Screening of adolescents (age 12–18 years) for major depressive disorder when systems are in 105
place to ensure accurate diagnosis, psychotherapy (cognitive–behavioural or interpersonal), and
follow-up (B) (see Table 3.3 comment m)
• Injury prevention – harm minimisation (C) (see Table 3.3 comment n) 88, 92, 93
• Sun protection
• Social and emotional wellbeing (II,C) 88, 90
• Oral health 94, 95
• Advocate for models of care that facilitate the transition of young people with chronic disease or
disability from tertiary paediatric care to effective primary care with access to adult specialist care
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Table 3.2 Age-related physical assessment in children and young people

Age Required physical assessment
Neonatal • Weight
• Length
• Head circumference
• Head shape, including fontanelle
• Mouth/palate, facies and ears
• Eyes: observation, appearance and red reflexes
• Neurological and developmental status, including responsiveness and tone
• Cardiovascular status
• Umbilicus
• Skin
• Femoral pulse (for radio-femoral delay)
• Hips (Barlow and Ortolani), limbs, joints, hands (palmar creases), feet (for talipes)
• Genitalia, testes, anal region
• Any parental concerns?
2, 4 & 6 months • Weight

• Length
• Head circumference
• Eyes: observation, fixation and following
• Cardiovascular status
• Umbilicus
• Skin
• Femoral pulse
• Hips, limbs, joints
• Genitalia, testes, anal region
• Oral health, ‘lift the lip’ from age 6 months
• Developmental progress
12 & 18 months • Weight velocity

• Height velocity
• Head circumference velocity
• Eyes and vision: observation, fixation and following, corneal light reflex
• Testes
• Oral health, ‘lift the lip’
• Developmental progress
2 years • Weight velocity

• Length velocity
• Head circumference velocity
• Evaluate gait
• Oral health, ‘lift the lip’
• Assess development and behaviour
8th edition
Age Required physical assessment

3 years • Vision screening
• The Universal Child Health Check at age 3 years will replace the current Healthy Kids check at age 4 years.
To be introduced by the Australian Government in 2013. Details not available at the time of publication.
4 years • As outlined by the Health Kids Check:
–– height and weight (plot and interpret growth curve/calculate BMI)
–– eyesight
–– hearing
–– oral health (teeth and gums)
–– toileting
–– allergies.
6–13 years • Weight and height (plot and interpret growth curve and calculate BMI)
14–19 years • Weight and height (plot and interpret growth curve and calculate BMI)
Table 3.3 Explanatory notes for Practice Points
Practice Comment
Point
a The Australasian Society of Clinical Immunology and Allergy (ASCIA) issued a position paper (2008) that supports
‘the introduction of solids that the family usually eats after 4 months regardless of whether the food is thought
to be highly allergenic’89 The ASCIA position is in conflict with the current policy of the RACGP on breastfeeding,
based on the NHMRC guideline,86 which recommends exclusive breastfeeding until age 6 months. This
uncertainty merits frank discussion.
b Physical exam:
• complete the Child Health Record (also known as the Parent Held Record), which is given at birth87
• see outline in Table 3.2 Age-related physical assessment in children and young people.
Note: Parents value reviewing completed growth charts. Velocities are more important than the centile position of
single measurements. Multiple measurements have the further advantage of allowing inaccurate measurements to
become evident as outliers.
c Developmental progress
Evidence continues to build that early intervention can counteract biological and environmental disadvantage and
set children on a more positive developmental trajectory.106
Early intervention presupposes early detection. Prior to age 3 years the rate of attaining developmental milestones
varies so much that the simple application of screening ‘tools’ would excessively detect developmental delay
(false positive). This risk is reduced after age 3 years.
In the earliest years, guides to developmental progress can be used to initiate an ongoing conversation with
parents to elicit their concerns about their child’s progress. ‘Asking repeatedly should help reluctant parents gain
confidence in their observations and facilitate their willingness to share concerns. The value of such discussions is
clear; children with disabilities are 11 times more likely to be enrolled in needed interventions.’107
There is little evidence available; however, early detection is known to help reduce disability in some instances,
and also allows for referral to community services, which can potentially decrease family stress.
Developmental milestone assessments are outlined in the Child Health Record, which is provided at birth.
Acknowledging that parents are the best source of information about their own children, a parent-completed
screening tool, such as the Parent Evaluation of Developmental Status (PEDS), can be used to identify any
concerns about their child’s development. The information gathered helps the GP gain a better understanding of
the progress of each child. Further information on the PEDS questionnaire can be accessed at www.rch.org.au/
ccch/resources_and_publications/Monitoring_Child_Development/
Prompts to assist assessment of development include:
• Learn the Signs – Act Early at www.cdc.gov/ncbddd/actearly/index.html
• Red Flags Early Intervention Guide at www.health.qld.gov.au/rch/professionals/brochures/red-flag.pdf
See also Appendix 2. Further information on the Ages and Stages Questionnaire is at http://agesandstages.com
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d • At present there is insufficient evidence for either benefit or harm in screening for postnatal depression (PND).
However, PND is known to have an unfavourable impact on the quality of attachment and family functioning.
Further, there are evidence-based interventions for both PND108 and for improving the quality of mother–infant
interaction adversely affected by PND.109, 110
e Physical activity recommendations for children aged 0–5 years

• Being physically active every day is important for the healthy growth and development of infants, toddlers and
preschoolers.
• For infants (birth to 1 year) physical activity – particularly supervised floor-based play in safe environments –
should be encouraged from birth.
• Before infants begin to crawl, encourage them to be physically active by reaching and grasping; pulling and
pushing; moving their head, body and limbs during daily routines and during supervised floor play, including
tummy time. Once infants are mobile, encourage them to be as active as possible in a safe, supervised and
nurturing play environment.
• Toddlers (age 1–3 years) and preschoolers (age 3–5 years) should be physically active every day for at least
3 hours, spread throughout the day.
• Young children don’t need to do their 3 hours of physical activity all at once. It can be accumulated throughout
the day and can include light activity such as standing up, moving around and playing, as well as more vigorous
activity like running and jumping. Active play is the best way for young children to be physically active.
• Children aged younger than 2 years should not spend any time watching television or using other electronic
media (DVDs, computer and other electronic games) and for children aged 2–5 years these activities should be
limited to less than 1 hour per day.
• Watching television and DVDs and playing computer games usually involve sitting for long periods – time that
could be spent playing active games or interacting with others.
• Infants, toddlers and preschoolers should not be sedentary, restrained or kept inactive for more than 1 hour at a
time, with the exception of sleeping.
Physical activity recommendations for children aged 5–12 years
• A combination of moderate and vigorous activities for at least 60 minutes a day is recommended. Examples of
moderate activities are a brisk walk, a bike ride or any sort of active play.
• More vigorous activities will make kids ‘huff and puff’.
Physical activity recommendations for young people aged 12–18 years
• At least 60 minutes of physical activity every day is recommended. This can be built up throughout the day with
a variety of activities.
• Physical activity should be done at moderate to vigorous intensity.
f ‘Lift the lip’ screening tool for the prevention and early detection of tooth decay in children:
• complete and also teach parents to simply lift the top lip of child, looking for signs of tooth decay (e.g. white
lines on top of teeth below gumline or discolouration of the teeth that cannot be brushed off). Encourage
parents to complete once a month
• encourage dental hygiene twice a day: no toothpaste under 17 months and low fluoride toothpaste up to age 5
years
• encourage dental visits annually after age 12 months.
See also NHMRC research at www.nhmrc.gov.au/national_register_public_health_research/29331 and
Section 11: Oral hygiene.
g The American Academy of Paediatrics has recommended the annual plotting of BMI for all patients aged 2 years
and older, and parent-held records produced by Australian jurisdictions follow this recommendation. This is not
supported by the United States Preventive Services Task Force (USPSTF). There is potential for causing harm
by either inappropriate diagnosis of ‘overweight’ or inappropriate reassurance of ‘healthy weight’. The risk will
be minimised if clinicians remember that in the preschool years, small errors in measuring either height/length or
weight cause large errors in the position of the calculated BMI on the BMI centile chart. This is because centile
lines are crowded together in the preschool ages.
h An Australian RCT demonstrated that a coordinated cross agency system of parenting support, which included
general practice, produced meaningful effects at the population level.90
8th edition
Practice Comment
Point
i ‘For pre-school children, family support and parenting programs continue to be the most effective method of
preventing the onset of emotional and behavioural problems, which predispose to mental illness in later childhood
and adolescence’.88, 106
j The USPSTF concludes with moderate certainty that vision screening for all children at least once between
the ages of 3–5 years to detect the presence of amblyopia or its risk factors has a moderate net benefit.98 The
USPSTF concludes that the benefits of vision screening for children aged <3 years are uncertain and that the
balance of benefits and harms cannot be determined for this age group.
Various screening tests that are feasible in primary care are used to identify visual impairment among children.
These include visual acuity tests, stereoacuity tests, the cover–uncover test, and the Hirschberg light reflex test
(for ocular alignment/strabismus), as well as the use of autorefractors (automated optical instruments that detect
refractive errors) and photoscreeners (instruments that detect amblyogenic risk factors and refractive errors).
The Universal Child Health Check at age 3 years will replace the current Healthy Kids Check at age 4 years – this
is to be introduced by the Australian Government in 2013 (details not available at the time of publication).
k Australian Government Department of Health and Ageing Medicare Benefits Schedule (MBS) Primary Care Items:
• Healthy Kids Check for children aged at least 3 years and less than 5 years, who have received or who are
receiving their age 4-year immunisation
• once only to an eligible patient
• the Healthy Kids Check is an assessment of a patient’s physical health, general wellbeing and development
with the purpose of initiating medical interventions as appropriate.
The Healthy Kids Check must include the following basic physical examinations and assessments:
a. height and weight (plot and interpret growth curve/calculate BMI)
b. eyesight
c. hearing
d. oral health (teeth and gums)
e. toileting
f. allergies.
The medical practitioner is required to note if a copy of the department’s publication Get Set 4 Life – habits for
healthy kids has been provided to the patient’s parent(s)/guardian at www.health.gov.au/internet/main/publishing.
nsf/content/47B8A7F882590379CA25759B001EE259/$File/GetSet4LifeBrochure.pdf
The medical practitioner is also required to note that the age 4-year immunisation has been given (including
evidence provided).
See also www.health.gov.au/internet/main/publishing.nsf/Content/Health_Kids_Check_Factsheet
l The USPSTF recommends that clinicians screen children aged 6 years and older for obesity and offer them or
refer them to comprehensive, intensive behavioural interventions to promote improvement in weight status (B).103
• There is a moderate net benefit for screening children aged 6–18 years.
• As a screening tool, BMI is an ‘acceptable measure for identifying children and adolescents with excess
weight’.103
• The definitions used by the USPSTF have changed since the 2005 report. Overweight is now defined as having
a BMI between the 85th and 94th percentiles for the individual’s age and gender, and obesity is defined as
having a BMI at ≥95th percentile for age and gender. BMI-for-age percentile is not a direct measure of adiposity,
but it correlates fairly well with percentile rankings of directly measured per cent body fat (with correlations
generally between 0.78 and 0.88) in children. Because BMI changes with age, percentile scores based on age-
specific and gender-specific norms are used to monitor growth.
National Institute of Clinical Excellence (also known as NICE)104
• BMI (adjusted for age and gender) is recommended as a practical estimate of overweight in children and young
people, but needs to be interpreted with caution because it is not a direct measure of adiposity.
• Waist circumference is not recommended as a routine measure, but may be used to give additional information
on the risk of developing other long-term health problems.
• Bio-impedance is not recommended as a substitute for BMI as a measure of general adiposity.
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m Mental, emotional, behavioural disorder in Australian young people

• Fifty per cent of adult disorders have onset by age 14 years.
• Fourteen per cent to 18% of children and young people experience mental health problems of clinical
significance.
• Depression and coping with stress are priorities for:
–– 16% of those aged 11–14 years
–– 21% of those aged 15–19 years.111
• The USPSTF recommends screening of adolescents (aged 12–18 years) for major depressive disorder when
systems are in place to ensure accurate diagnosis, psychotherapy (cognitive–behavioural or interpersonal), and
follow-up105 (B).
• Risk factors for major depressive disorder include parental depression, having comorbid mental health or
chronic medical conditions, and having experienced a major negative life event.105
n • Promoting health and minimising harm is a whole-of-community opportunity and responsibility. Celebrating
strengths, explaining confidentiality (including its limits) and using the HEADSS framework (below) to explore
with young people the context in which they live are strategies likely to improve the clinician’s capacity to
promote health and minimise morbidity112 (C).
–– Home
–– Education/Employment
–– Activities
–– Drugs
–– Sexuality
–– Suicide
• Young people who present frequently are at higher risk of having a mental health problem.113
• Provide messages that encourage delay in initiation of potentially risky behaviours, and, at the same time,
promote risk-reduction strategies if adolescents choose to engage or are already engaging in the behaviour.
• Use principles of motivational interviewing in the assessment and discussion of risky health behaviours with
adolescent patients (including safe practice for the sexually active).
• Be familiar with the resources in the community that provide harm reduction programs for substance abuse,
pregnancy prevention and injury prevention.
• Be familiar with resources in the community that provide parenting skills training for parents of young people.
• Advocate for the introduction, further development and evaluation of evidence-based prevention and treatment
programs that use a harm reduction philosophy in schools and communities (C).
8th edition
4. Preventive activities in middle age
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
The recommended specific activities for low-risk patients in the 45–64 years age group are listed below. Patients
should be offered these opportunistically, or at 2–5-year intervals.
Planned health checks in middle-aged adults have been demonstrated to improve the frequency of management
of smoking, nutrition, alcohol and physical activity (SNAP) behavioural risk factors; screening for cervical and CRC
and hyperlipidaemia, in general practice.16, 114, 115 There is also evidence that Indigenous health checks improve early
detection of diabetes and provision of preventive care.116 However, there is mixed evidence for the effectiveness
of interventions to address multiple risk factors.117 These checks may be facilitated by involvement of practice
nurses.118–120 Interventions should be tailored to level of risk and use of the 5As framework (Ask, Assess, Advise,
Assist and Agree, Arrange follow-up) is recommended as a guide to their delivery in primary healthcare.121
Table 4.1 Age-related health checks in middle age

Age What should be done? Pages
45–49 Ask about:
years • SNAP and readiness to change 40–49
• risk of diabetes using Australian Type 2 Diabetes Risk Assessment Tool (AUSDRISK) 55–57 Appendix 4
• depression in increased risk groups (past history, physical illness, other mental problems, etc.) 73–74
• risk factors for osteoporosis 82–83
• skin cancer. 60–62
Measure:
• weight, height (calculate BMI) and waist circumference 43–44
• BP 51–53
• fasting lipids 53–55
• fasting blood glucose in patients at high risk of diabetes. 55–57
Perform:
• Pap test every 2 years 63–65
• mammography if family history indicates high risk. 65–67
Calculate:
• absolute cardiovascular risk. Appendix 5
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Age What should be done? Pages

50–64 Ask about:
years • SNAP and readiness to change 40–49
• risk of diabetes using AUSDRISK 55–57 Appendix 4
• depression in increased risk groups (past history, physical illness, other mental problems, etc.) 73–74
• risk factors for osteoporosis 82–83
• skin cancer. 60–62
Measure:
• weight, height (calculate BMI) and waist circumference 43–44
• BP 51–53
• fasting lipids 53–55
• fasting blood glucose in patients at high risk of diabetes 55–57
• urinalysis for protein. 58–59
Perform:
• Pap test every 2 years 63–65
• CRC screening with faecal occult blood testing (FOBT) at least every 2 years 68–70
• mammography every 2 years 65–67
• vaccination for dTpa. Consider influenza and pneumococcal vaccination if high risk. 35–36
Calculate:
• absolute cardiovascular risk. Appendix 5
Table 4.2 Preventive interventions in middle age

Health education Tailor health advice or education to the patient’s risk, stage of change and health 36
literacy (see Section II Patient education and health literacy).
Practice Use clinical audit to identify patients who have not had preventive activity. Recall to 122
organisation practice or opportunistically arrange a health check.
Implementation
Health inequity
Individual behavioural counselling is most likely to be effective for patients from disadvantaged backgrounds if linked
to community resources and if financial and access barriers are addressed. Provider attitudes are also important in
building self-efficacy among patients from these groups. Aboriginal and Torres Strait Islander and low SES patients
have higher risk of disease, but are less likely to be offered preventive interventions.
Strategies
Strategies to increase screening and effective motivational and behavioural interventions in this group are discussed
in the RACGP green book.
8th edition
5. Preventive activities in older age
Older people are at increased risk of multiple chronic conditions that may impair their function and quality of life.
Those living alone are particularly vulnerable. Their health problems may be exacerbated by poor nutrition, lack of
physical activity and lack of sun exposure.
Older people may rely on the help and support of family and carers. Carers, particularly carers for people with
dementia or depression, are at risk of depression, anxiety, emotional distress, loneliness and isolation but their
healthcare needs are often overlooked.123–127 Their need for support should be assessed when possible128 (C).
Carer support resources are helpful for carer wellbeing and may delay the need for the older person to be relocated
to a residential facility.123, 129–131 People should be advised to plan for their care as they get older. This includes
organising wills, power of attorney and an advance care plan.
Medication-related problems may cause unnecessary hospital admission, adverse drug reactions and other
adverse outcomes for people living in the community.132 GPs should review medications in older people, particularly
for vulnerable groups. Vulnerability factors include:
• recent discharge from hospital
• high-risk drug groups (e.g. anticoagulants)
• confusion/cognitive impairment or dementia
• history of falls
• currently taking five or more regular medications
• target disease states where medication management is an important process of care (CKD, congestive cardiac
failure)133
• multiple chronic medical problems
• regular use of alcohol
• previous adverse drug reaction.
GPs may consider a pharmacist medication review. The most successful interventions have been delivered by
small numbers of pharmacists working in close liaison with primary care doctors (III,C).134 The review should include
consideration of the need for each medication; issues around patient compliance and understanding of the medication;
screening for side effects, particularly falls and cognitive impairment; and consideration of the use of aids such as dosette
boxes and Webster packaging. A review of the combined anticholinergic load and sedative load of the medications may
also be done, as anticholinergic and sedative loads increase the rate of confusion and other adverse side effects.
5.1 Immunisation
Immunisation is recommended for adults aged 65 years and over, according to the Australian Government Department
of Health and Ageing Australian Immunisation Handbook.
Table 5.1 Immunisation: preventive interventions in older age
Vaccination: Annual influenza vaccination in the pre-flu season months (III,C). 135
influenza
Vaccination: Pneumococcal polysaccharide vaccination (23vPPV) is recommended for the 136
pneumococcal prevention of invasive pneumococcal disease (II,B).
Vaccination should be done opportunistically. One dose is currently recommended
except for those who have a condition that predisposes them to an increased risk of
invasive pneumococcal disease.
See http://immunise.health.gov.au/internet/immunise/publishing.nsf/Content/
pneumo23-atagi-statement-cnt.htm
Vaccination: A single dose of zoster vaccine is recommended for adults aged 60 years and over (II,B) 137
herpes zoster See also Section 6.1: Immunisation.
8th edition 29
5.2 Falls and physical activity

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Advice about moderate physical activity is recommended for all older people138, 139 (A).
Approximately 30% of people aged 65 years or older report one or more falls in the last 12 months.140 For the
older person, physical activity provides many benefits, as well as minimising some of the limitations of later life (e.g.
reduced mobility, tendency to fall and reduced interaction with the environment).141
Table 5.2.1 Falls: identifying risks

Who is at risk of falls? What should be done? How often? References
Average risk Screen for falls and risk factors Every 12 months 139, 142, 143
• All people aged 65 years or more for falls* (I,A)
Moderately high risk Screen for risk factors and Every 6 months 140, 142
• Older people presenting with one or more involve in preventive activities*
falls, who report recurrent falls or with (I,A)
multiple risk factors (see Table 5.2.2)
* If the person has inadequate sun exposure, Vitamin D supplement should be recommended to reduce the risk of fracture.144
8th edition
Table 5.2.2 Falls: preventive interventions

Screening for falls Ask the following three screening questions: 140, 142,
risk 1. Have you had two or more falls in the past 12 months? 145–150
2. Are you presenting following a fall?
3. Are you having difficulty with walking or balance?
If the answers to any of these are positive:
• obtain relevant medical history, complete a physical examination, and perform
cognitive and functional assessments
• determine multifactorial fall risk: 151
–– history of falls
–– multiple medications, and specific medications (e.g. psychotropic medications
and opiate-containing analgesic agents)
–– impaired gait, balance and mobility
–– impaired visual acuity, including cataracts
–– issues with bifocal or multifocal spectacle use
–– reduced visual fields
–– other neurological impairment
–– muscle weakness
–– cardiac dysrhythmias
–– postural hypotension
–– foot pain and deformities and unsafe footwear
–– home hazards
–– vitamin D deficiency.
There are many fall risk-assessment tools. However, reports from researchers are 152
variable, so no single tool can be recommended for implementation in all settings
or for all subpopulations within each setting. A quick screening tool is the ‘timed up
and go test’ (TUGT), which involves looking for unsteadiness as the older person
gets up from a chair without using his or her arms, walks 3 metres and returns. The
usefulness of timing this test as a predictor of falls has been questioned.
Simple alternatives to the TUGT are the repeated chair standing test and the 153
alternate step test. The repeated chair standing test measures how quickly an older
person can rise from a chair five times without using the arms. A time of >12 seconds
indicates an increased fall risk. The alternate step test measures how quickly an
older person can alternate steps (left, right, left, etc.) onto an 18 cm high step a total
of eight times. A time >10 seconds indicates an increased fall risk. The Quickscreen
assessment tool, developed and validated for use in an Australian population, 154
includes these tests as well as simple assessments of medication use, vision,
sensation and balance.
See also Section 13: Urinary incontinence
8th edition 31
Falls risk reduction • Prescribe or refer for a home-based exercise program and/or encourage 155–161
participation in a community-based exercise program. In either case, exercise
for preventing falls needs to include medium-intensity to high-intensity balance
training (i.e. exercises must be undertaken while standing and challenge balance),
and be of long duration, preferably ongoing. Exercise programs targeting non- 162
English speaking patients may need to address cultural norms about appropriate
levels of physical activity.
• Physical activity recommendations for older adults from the American College of 163
Sports Medicine and American Heart Association are:
–– do moderately intense aerobic exercise 30 min/day, 5 days/week or vigorous
aerobic exercise 20 min/day, 3 days/week and
–– do 8–10 muscle strength training exercises, 10–15 repetitions of each exercise
2–3 times/week and
–– if at risk of falling, perform balance exercises and have a physical activity plan.
• Review medications and discontinue centrally acting medications where clinically
appropriate.
• Consider prescribing vitamin D for people with vitamin D levels <50 nmol/L for 164
older people living in the community (III,C) and consider routinely prescribing
vitamin D (unless contraindicated) for all older people living in residential aged care
(I,B), as routine sun exposure in residential aged care may not be feasible.
• See also Section 14: Osteoporosis.
• Refer people with painful feet or foot deformities to podiatry for intervention.
• Provide advice on the dangers of bifocal and multifocal glasses when walking
outdoors (as these blur ground-level obstacles) and recommend the wearing of
single lens glasses when outdoors.
• Identify cataracts and refer for cataract extraction.
• Refer people with a history of recent falls for an occupational therapy home
assessment.
5.3 Visual and hearing impairment

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Visual acuity should be assessed from age 65 years using the Snellen chart (B) in those with symptoms or who
request it. There is no evidence that screening of asymptomatic older people results in improved vision.165
Hearing loss is a common problem among older individuals and is associated with significant physical, functional
and mental health consequences. Annual questioning about hearing impairment is recommended with people aged
65 years and over (B).
In some states and territories, there are legal requirements for annual assessment (e.g. driving over age 70 years).166
Eye disease and visual impairment increase threefold with each decade of life after age 40 years. They are often
accompanied by isolation, depression and poorer social relationships, and are strongly associated with falls and hip
fractures.167 It should be determined whether the patient is wearing an up-to-date prescription, and whether there
is a possibility of falls because they are no longer capable of managing a bifocal, trifocal or multifocal prescription.
People at greater risk of visual loss are older people and those with diabetes and a family history of vision
impairment. Cataracts are the most common eye disease (42% of cases of visual impairment), followed by age-
related macular degeneration (AMD) (30%), diabetic retinopathy and glaucoma. The leading causes of blindness in
those aged >65 years are AMD (55%), glaucoma (16%) and diabetic retinopathy (16%).168
8th edition
Table 5.3.1 Visual and hearing impairment: identifying risks

Who is at higher risk of hearing loss? What should be done? How often? References
People ≥65 years Screen for hearing impairment Every 12 months 169
(II,B)
Table 5.3.2 Visual and hearing impairment: preventive interventions

Visual • Use a Snellen chart to screen for visual impairment in the elderly if requested or if 165, 170
impairment: case indicated by symptoms. There is no evidence that screening asymptomatic older
finding people results in improvements in vision.
• See also Section 12: Glaucoma.
Hearing • A whispered voice out of field of vision (at 0.5 metre) or finger rub at 5 cm has a high 169, 171
impairment sensitivity for hearing loss, as does a single question about hearing difficulty.
screening
5.4 Dementia
With people aged over 65 years, clinicians should be alert to the symptoms and signs of dementia. These may
be detected opportunistically and assessed using questions addressed to the person and/or their carer (C).
Depression and dementia may co-exist. When a person has dementia, adequate support is required for the person,
carer and family. Counselling and education are important. Management priorities will vary from patient to patient,
but there may be a need to consider medical management of dementia, behaviour and comorbidity, legal and
financial planning, driving and advance care planning.172
Table 5.4.1 Dementia: identifying risks

Average risk No evidence of benefit from n/a 173, 174
• Those without symptoms screening (II,C)
Moderate risk
• Risk increases with increasing age Case finding and early n/a 175–177
• A family history of Alzheimer disease intervention (III,C)
• People with history of repeated head trauma 178
• People with Down syndrome
• Those with elevated cardiovascular risk (heart 179–184
disease, stroke, hypertension, obesity, diabetes,
elevated homocysteine, elevated cholesterol)
177
• Those with depression or a history of depression
• Those with symptoms (see Table 5.4.2)
8th edition 33
Table 5.4.2 Dementia: preventive interventions

Case finding and • Ask ‘How is your memory?’ and obtain information from others who know the 185
confirmation person (e.g. repeating questions, forgetting conversations, double buying, unpaid
bills, social withdrawal).
186, 187
• Other symptoms may include a decline in thinking, planning and organising and
reduced emotional control or change in social behaviour affecting daily activities.
Not everyone with dementia has memory problems as an initial symptom (C). Other
clues are missed appointments (receptionist often knows), change in compliance
with medications and observable deterioration in grooming, dressing.
• Over several consultations, obtain the history from the person and family/carer, and
perform a comprehensive physical examination. Undertake cognitive assessment
using:
– Mini-Mental State Examination (MMSE) at www.minimental.com
– General Practitioner Assessment of Cognition at www.gpcog.com.au 186
– clock drawing test 188
– R
owland Universal Dementia Assessment Scale at www.fightdementia.org.au/ 189
understanding-dementia/rowland-universal-dementia-assessment-scale.aspx is
a multicultural cognitive assessment scale that has been used to detect dementia
across cultures.
• The MMSE is the most widely used and evaluated scale.
• Assess functional status. The Instrumental Activities of Daily Living at
www.abramsoncenter.org/PRI/documents/IADL.pdf assessment tool may be used.
All screening instruments used to assess dementia in general practice have high
rates of overdiagnosis (false positives) and underdiagnosis (false negatives), so the
full clinical presentation needs to be taken into account.
Early intervention • Evidence is growing that attention to cardiovascular risk factors may improve 179–184
and prevention cognitive function and/or reduce dementia risk. A 2012 review has suggested that
there is sufficient evidence now for clinicians to recommend the following strategies
for early intervention and prevention of dementia: increased physical activity
(e.g. 150 minutes per week of moderate-intensity walking or equivalent), social 190
engagement (increased number of social activities per week) and cognitive training
and rehabilitation.
See also Section 7: Prevention of chronic disease, Section 8: Prevention of vascular
and metabolic disease and Section 10: Psychosocial
8th edition
6. Communicable diseases
GPs have an important role in the prevention and management of communicable diseases. This includes advice on
prevention, immunisation, early detection and treatment.
Updates on communicable diseases and notification requirements are available from the Australian Department of
Health and Ageing at www.health.gov.au/internet/main/publishing.nsf/Content/cda-surveil-nndss-casedefs-distype.htm
GP’s laboratories and hospitals are required by law to notify particular infectious diseases to their local or state
public health units (this law overrides all privacy regulations). A list of state-specific notifiable infectious diseases
is also available from state health department websites. This role has become almost completely automated
by pathology laboratories as a result of advances in information technology. The GP may still need to ensure
notification has occurred on occasions where a clinical diagnosis is made, or where clinical information is required.
Please note that varicella and zoster are notifiable diseases with or without the need for pathology testing.
6.1 Immunisation
Age <2 2–3 4–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 ≥65
Immunisation is recommended for all children and adults at particular ages, according to the Australian
Immunisation Handbook (A). GPs should advocate immunisation and counter the common misunderstandings and
antivaccine campaigns.
The National Immunisation Program Schedule (NIPS) lists the recommended funded vaccines. There may be
other vaccines that are not funded but are recommended in the Australian Immunisation Handbook. There may be
variability in vaccines recommended/funded, for example, hepatitis A vaccine (hep A).
Vaccination for special high-risk groups

Adults or children who develop asplenia, HIV infection or a haematological malignancy, or who receive a bone
marrow or other transplant (following recovery), may not be fit for some vaccinations, or may require additional
vaccinations, including the need for repeat vaccinations at http://immunise.health.gov.au
Health inequity
For immunisation to be effective there needs to be high coverage. Thus GPs need to be aware of groups with lower
levels of age-appropriate immunisation including:191
• families with young parents under age 25 years192, 193
• single-parent families and families with more than one child194
• migrant families, particularly in the first years of their arrival in Australia, or if a language other than English is spoken at
home192–196
• families where the parents are unemployed,191, 195 on low incomes192, 195 or have very high or very low education
levels193, 194, 197
• families who move frequently196
• Aboriginal children in rural and urban areas.198, 199
For young people with a chronic illness, cost may be a barrier to achieving appropriate immunisation against influenza
and pneumococcal infection.200
8th edition 35
Table 6.1.1 The National Immunisation Program Schedule

Sequence Age Vaccine
1 Birth* • Hepatitis B (hep B)
2 6–8 weeks • hep B
1 • DTPa
1 • Haemophilus influenzae type b (Hib)
1 • Inactivated poliomyelitis (IPV)
1 • 13-valent pneumococcal (13vPCV)
1 • Rotavirus†
3 4 months • hep B
2 • DTPa
2 • Hib
2 • IPV
2 • 13vPCV
2 • Rotavirus†
4 6 months • hep B
3 • DTPa
3 • Hib
3 • IPV
3 • 13vPCV
(3) • Rotavirus† (Rotateq only)
6 months to <5 years • Influenza (for all Aboriginal and Torres Strait Islander peoples) annually
5 12 months • hep B (fifth dose for those born <32 weeks or <2000 g birthweight)
4 • Hib
1 • MMR first dose
1 • Meningococcal C (MenCCV)
4 • 13vPCV booster for high-risk groups
1 12–18 months • hep A (for Aboriginal and Torres Strait Islander peoples in the Northern Territory,
Queensland, South Australia and Western Australia only)
2 18 months‡ • MMR and varicella, or MMRV instead of separate varicella at 18 months and MMR
at age 4 years (when available)
2 18–24 months • hep A (for Aboriginal and Torres Strait Islander peoples in the Northern Territory,
Queensland, South Australia and Western Australia only)
4 24 months • 13vPCV booster (for Aboriginal and Torres Strait Islander children)
4 4 years • DTPa
4 • IPV
2 • MMR (to be superseded by combined MMRV at 18 months by 2016)
1 • 23vPPV (only for high-risk groups )
1&2 12–13 years • hep B (2 adult doses for those not vaccinated against hepatitis B)
1 • Varicella (catch up until all immunised)
1, 2 & 3 • HPV (three doses over 6 months, for both sexes – catch-up 2013–15)
5 15 years • dTpa is the adult/adolescent vaccine
15–49 years • Influenza (for all Aboriginal and Torres Strait Islander peoples) annually
• 23vPPV (only at-risk Aboriginal and Torres Strait Islander peoples)
8th edition
Sequence Age Vaccine

50 years and over§ • Influenza (Aboriginal and Torres Strait Islander peoples)
• 23vPPV (Aboriginal and Torres Strait Islander peoples)
65 years and over • Influenza
• 23vPPV
* hep B vaccine (dose 1 or 0) should be given to all infants within 24 hours of birth ideally, but at most within 7 days of birth. Infants
whose mothers are hepatitis B surface antigen positive should be given hepatitis B immunoglobulin within 12 hours of birth.
† Rotavirus vaccines are contraindicated in infants with a history of intussusception (IS), or predisposing abnormality to IS, or severe
combined immunodeficiency. Rotavirus vaccines are time limited and differ in number of doses and timing:
• Dose 1 must be given before age 12 weeks (Rotateq) or 14 weeks (Rotarix) or not at all.
• Dose 2 must be given before age 24 weeks (Rotarix) or before 28 weeks (Rotateq) or not at all.
• Dose 3 ONLY for Rotateq must be given before age 32 weeks or not at all.
‡ MMR dose 2, previously at age 4 years, and separate varicella at 18 months, is to be replaced by combined MMRV at 18 months
and predicted to be available by July 2013.
§ It is recommended that all people aged 50 years should be given DT. dTpa is preferred instead of DT to protect from pertussis. This
is funded for parents and ‘carers of infants’ under age 6 months in some states. It can be given regardless of timing of previous DT.
Table 6.1.2 Recommended vaccines in the Australian Immunisation Handbook not in the NIPS
Age Vaccine
Soon after birth Bacillus Calmette–Guérin (or BCG) (for Aboriginal and Torres Strait Islander peoples in the Northern
Territory, Queensland, and parts of Northern South Australia).
From 6 months Annual influenza vaccination is recommended for any person aged ≥6 months where there is a wish to
reduce the likelihood of becoming ill with influenza. Only Influvac or Vaxigrip influenza vaccines are suitable
for use from the age of 6 months.
Under 14 years Varicella: a second dose improves protection from varicella from 94% to 98%
Parents and DTpa is recommended to protect the infant from pertussis. To maximise the protection of infants, the
carers of infants options are to give before, immediately after, or in the third trimester of pregenancy. The dTpa vaccine can
under age 6 be given at any time after DT and dTpa may be given again 10 years after previous dTpa. Please refer to
months the Australian Immunisation Handbook for details.
50 years dTpa is preferred to DT

(This booster dose is recommended if no tetanus immunisation was received in the previous 10 years)*
From 60 years Zoster virus live vaccine (e.g. Zostavax) for prevention of shingles
All healthcare hep B (and hep A in some jurisdictions)

workers Annual influenza
dTpa
MMR (if not immune)
Varicella (if not immune)
Men who have hep B and hep A

sex with men
Injecting drug
users
* It is recommended that all 50-year-olds should be given DT. dTpa is preferred instead of DT to protect from pertussis. This is
funded for parents and ‘carers of infants’ under age 6 months in some states. It can be given regardless of timing of previous DT.
8th edition 37
Immunisation information resources include:

• the Australian Government Immunisation Handbook is online at http://immunise.health.gov.au
• the Australian Childhood Immunisation Register enquiry line is available on telephone 1800 653 809. This phone
number can be used to obtain information on the vaccination history of individuals from birth–7 years of age given
since 1 January 1996
• the National Centre for Immunisation Research & Surveillance is at www.ncirs.usyd.edu.au
Notification of adverse events

The reporting of adverse events following vaccinations varies geographically. It is possible to report direct to the
Therapeutic Goods Administration from anywhere in Australia by telephoning 1800 044 114, or visiting its website at
www.tga.gov.au/hp/problem-medicine-reporting-reactions.htm
6.2 STIs
STIs are frequently seen in general practice, especially chlamydia, which is typically asymptomatic. It is important to
detect it early in order to minimise potential complications, such as infertility, and to prevent transmission to others.
It may also be appropriate to screen for other STIs. The individual’s age and sexual behaviour and community STI
prevalence all influence the level of risk, and should influence the choice of STI screening tests.
Sexual health consultation

Many patients and doctors do not like discussing sexual histories even when the patient is requesting STI testing,
or it is indicated. While taking a sexual history is an important part of the assessment and management of STIs, it
should not be a barrier to offering STI testing. The patient may not disclose the truth to avoid embarrassment.201
A non-judgemental attitude and environment will maximise patient disclosures on sexual matters.202 It is important
to ask open questions and to avoid terms that make assumptions about sexual behaviour or orientation
(e.g. by using the term ‘partner’). Issues to cover include current sexual activity, gender and number of partners,
contraception (including use of condoms), immunisation status and other risk factors for blood-borne viruses (such
as injecting drug use, tattooing and piercing). Investigations should be explained, and patients should be counselled
and asked for consent before ordering tests such as HIV or hepatitis C.
Contact tracing is an important part of the management of most STIs, and it is the responsibility of the diagnosing
clinician to facilitate the process of notifying current and past partners. This may be by a direct approach from the
patient or their treating health professional, or by using online partner notification services such as:
• www.letthemknow.org.au
• www.thedramadownunder.info/notify (for males with male partners)
• www.bettertoknow.org.au (for Aboriginal youth).
For more information and to determine ‘how far back to trace’ see the contact tracing manual at http://ctm.ashm.
org.au/ or contact tracing tool at http://www.stipu.nsw.gov.au/content/Document/GP%20Contact%20Tracing%20
Tool.pdf
In the case of a notifiable condition, the patient should be informed that case notification to public health authorities
will occur. Notification should be made as prescribed by the department of health in your state or territory.
8th edition
6.2.1 Chlamydia and other STIs

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Screening for chlamydia infection in all sexually active people aged 15–29 years is recommended because of
increased prevalence and risk of complications.203
Younger sexually active youth should not be excluded from case finding, or identifying any safety or abuse issues.
Women with untreated chlamydia infections have a 2–8% risk of infertility.204 Other STIs to consider screening for
in higher risk individuals are gonorrhoea, HIV and syphilis.205 The risk for gonorrhoea, HIV and syphilis is low for
heterosexuals in all major cities in Australia and New Zealand206 but rates of gonorrhoea and syphilis may be higher in
remote community settings. The individual’s age and sexual behaviour and community STI prevalence influence the
level of risk and should guide STI testing recommendations for patients. (Please refer to tables for guidance.)
Men who have sex with men (MSM) should be screened for gonorrhoea, chlamydia, syphilis and HIV every 12 months.
Men who have multiple sexual contacts should be screened more often. Most MSM with STIs have no symptoms.207
Screening for hepatitis C should be provided if the patient is HIV positive or there is a history of injecting drug use.
There is good evidence that all pregnant women at risk should be screened for hepatitis B, HIV and syphilis;205
screen for chlamydia and possibly gonorrhoea if the patient is considered to be particularly at risk.208, 209
Table 6.2.1.1 STIs: identifying risks
Who is at higher risk of infection and What should be done? How often? References
complications?
High-risk asymptomatic
• All sexually active young people aged Urine or genital swab for Every 12 months 203, 210–215
15–29 years, particularly if: chlamydia (II, A) A good opportunity
– under age 20 years Consider other infections based is at same time 216
– Aboriginal or Torres Strait Islander on risk assessment such as as Pap test or
gonorrhoea, hepatitis B, syphilis presentation for
– inconsistent or no condom usage
and HIV other reasons
– recent change in sexual partner
Consider trichomonas in remote
communities (III)
Asymptomatic men who have sex with men
• Higher risk in those who:217 Urine and rectal swab for Every 12 months 217, 218, 219
–– have unprotected anal sex chlamydia polymerase chain and 3–6 monthly in
reaction (PCR) higher risk men
–– have had >10 partners in past 6 months
Throat and rectal swab for
–– participate in group sex or use recreational
gonorrhoea PCR (III, B)
drugs during sex
Serology for HIV, syphilis and
hepatitis A and B serology if not
vaccinated or immune
Also offer hepatitis A and B
vaccination (III,B)
Sexual contacts from the last 6 months of Test and treat contacts If chlamydia infection 220–223
infected women and men presumptively (II,A) found (and treated),
For how far back to trace, see www.stipu.nsw. Consider other infections based repeating testing
gov.au/content/Document/GP%20Contact%20 on risk assessment such as to check for re-
Tracing%20Tool.pdf gonorrhoea, hepatitis B (if not infection after 3–12
vaccinated), syphilis and HIV (III,B) months may be
appropriate
Low risk heterosexual asymptomatic Urine PCR or genital swab for 219
requesting ‘STI check-up’ chlamydia, serology for hepatitis
B (if not vaccinated or immune),
syphilis and HIV (III, B)
8th edition 39
Table 6.2.1.2 Tests to detect STIs

Test Technique Site References
Nucleic acid • Should be (20 mL) first void urine (passed at least 1 hour after last having Urine, 206, 222, 224
amplification urinated (i.e. not midstream) (I,B) endocervix 219
test (NAAT) • PCR endocervical or vaginal swab (patient can self-collect) also possible or vagina
most in females (I,B)
commonly by
• This technique has also been validated for anal or throat swabs:
PCR
– r ectal swab should be inserted ~3 cm into anus and rotated
(asymptomatic men who have sex with men can be taught to perform
this test themselves, with the aid of a visual diagram. See www.stipu.
nsw.gov.au/icms_docs/117569_Self_Collected_Specimen_Chart.pdf
– throat swab should sample the posterior pharyngeal wall and tonsillar
crypts
• NAATs are highly sensitive and specific for chlamydia and gonorrhoea
from all specimens. False positive gonorrhoea results can occur,
especially if testing low-risk individuals. However, laboratories usually
perform supplemental assays to confirm results for gonorrhoea.
Gonorrhoea • Rectal swab should be inserted 3 cm into anus and rotated 225
microscopy, • MCS is of use to guide treatment where resistance to antibiotics is a
culture and problem
sensitivity
(MCS)
Implementation
Chlamydia is the most common and curable STI in Australia. Notification rates per 100 000 have increased from
35.4 in 1993 to 319 in 2010, mostly in those aged 15–29 years.226 Estimated infection rates of the sexually active
population in this age group vary from 4–12%. Young Aboriginal and Torres Strait Islander peoples have the highest
infection rates, which are 12–34% in some locations. There is also an increased risk of gonorrhoea and syphilis
among Aboriginal and Torres Strait Islander peoples.
Screening of sexually active women under age 25 years for chlamydia on an annual basis has been shown to halve
the infection and complication rates204, 227 All partners of those infected should be tested and treated presumptively.
A systematic review has shown that providing patient-delivered partner therapy to index cases is more effective in
reducing infection rates than paper-based methods of contact tracing.228 It is important to ensure current sexual
partners are treated simultaneously. Referral to a sexual health clinic may provide improved contact tracing and
should be considered for problematic repeated infections.229
Untreated pregnant women infected with chlamydia have a 20–50% chance of infecting their infant at delivery.230
8th edition
7. Prevention of chronic disease
The SNAP risk factors are common among patients attending general practice.231 They contribute significantly to the
burden of disease, largely due to their effect on the incidence and complications of chronic diseases such as diabetes,
cardiovascular disease (CVD), chronic respiratory disease and some cancers.2, 232 While there is some debate about the
impact and effectiveness of GPs and practice nurses on a patient’s lifestyle,233–235 most accept that GPs and their teams
have a role and can be effective in each of the SNAP lifestyle areas. including smoking,55, 236, 237 hazardous drinking,44, 238
physical activity239–241 and dietary change.239, 242
Each of these risk factors may interact with each other throughout the lifecycle and need to be considered together rather
than separately. Behavioural counselling approaches such as motivational interviewing243 may be tailored to the patient’s
readiness to change their behaviour (see the RACGP green book for more details)244 and should consider the patient’s
literacy and health literacy.243 The 5As121, 245–249 is an internationally accepted framework for organising the assessment and
management of all the behavioural risk factors in primary healthcare. It consists of:
• Ask – a systematic approach to all patients regarding their smoking, nutrition, alcohol or physical activity, which may occur
opportunistically as they present for other conditions and/or by recall for health checks
• Assess – assess readiness to change, and dependence (for smoking and alcohol)
• Advise – provide brief, non-judgemental advice with patient education materials (such as Lifescripts) and work with the
patient to set agreed goals
• Assist – provide motivational interviewing; refer to telephone support services, group lifestyle programs or individual
providers (e.g. dietitian or exercise physiologist); and consider pharmacotherapy
• Arrange – regular follow-up visits to monitor maintenance and prevent relapse.
A systematic approach to identifying chronic disease can be more effective as a larger number of eligible subjects are
identified and assisted.244, 250, 251
8th edition 41
Health inequity
Disadvantaged people (low incomes and/or education) have higher rates of smoking and alcohol use, poorer diets and
lower levels of physical activity. These higher rates are a product of social, environmental factors and individual factors,
which interact. Individual behavioural counselling is most likely to be effective for patients from disadvantaged backgrounds
if linked to community resources and if financial and access barriers are addressed.
Smoking is one of the preventable risk factors to show the greatest inequities across groups. Most disadvantaged groups
have significantly higher smoking rates. Smoking status varies by education level, employment status, SES, geographic
location and Indigenous status.252 While the proportion of people smoking across all of these groups either declined
significantly or remained relatively stable between 2007 and 2010, significant inequities remain. In 2010, 24.6% of people
aged over 14 years in the lowest SES areas smoked, compared with 12.5% in people from the highest SES areas. People
living in remote and very remote areas are about 1.7 times as likely to smoke as those living in major cities. While the
proportion of Aboriginal and Torres Strait Islander current daily smokers aged 15 years and over fell from 49% to 45%
between 2002 and 2008, Aboriginal and Torres Strait Islander peoples are still nearly twice as likely as non-Indigenous
people to be current daily smokers.253, 254 The Centre for Excellence in Indigenous Tobacco Control provides resources
and strategies at www.ceitc.org.au Smoking is also more prevalent in patients with long-term mental illness, who are more
prone to nicotine addiction.255
Overweight and obesity rates are higher in socioeconomically disadvantaged people and the gap between these and other
socioeconomic groups is widening.256 Aboriginal and Torres Strait Islander peoples and those from the Pacific Islands have
higher rates of overweight and obesity as well as a higher incidence of vascular disease.257 Aboriginal and Torres Strait
Islander communities in remote regions face significant access barriers to nutritious and affordable food.258, 259 Nutritious
food tends to cost more in rural and remote areas, and cost may also be an issue in low socioeconomic groups.260
Low income groups are less likely to be offered interventions to prevent being overweight261 (see Section 1: Introduction.)
Interventions to improve physical activity among socially disadvantaged patients need to be linked to community programs
that improve the physical environment and opportunities to exercise and to programs that remove cost barriers.262 Provider
attitudes are also important in building self-efficacy among patients from these groups.262, 263 Improvements in physical
activity for Aboriginal and Torres Strait Islander patients may be achieved by linking health advice with locally available and
appropriate community sport and recreation programs as well as social support programs (such as group activities).264
Risky alcohol use is also frequently associated with mental health issues.265, 266 Having both risk factors may not be readily
recognised and may reduce access to and receipt of treatment services.267 Alcohol has tended to produce a greater
burden of harm in more socially disadvantaged groups268, 269 partly through the more hazardous pattern of drinking270 and
partly through the associated poverty associated with lower SES.271 Recognition and treatment is also impeded by the
social stigma associated with problematic use of alcohol.271, 272
8th edition
7.1 Smoking
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Smoking status and interest in quitting should be assessed for every patient over age 10 years.55, 237, 273–275 All patients
who smoke, regardless of the amount they smoke, should be offered smoking cessation advice. This should include:
• asking about their interest in quitting (B)
• advising to stop smoking (A), agreeing on quit goals and offering pharmacotherapy if appropriate275, 276 (A)
• offering referral to a proactive telephone callback cessation service (e.g. the Quitline 13 7848)277 (A)
• following up to support maintenance and prevent relapse using self-help or pharmacotherapy278(A).
To assess nicotine dependence:
• ask about the time to first cigarette and the number of cigarettes smoked a day. There is a high likelihood of nicotine
dependence if the person smokes within 30 minutes of waking and smokes more than 10–15 cigarettes a day
• explore whether the patient had withdrawal symptoms when they previously attempted to quit.
Table 7.1.1 Smoking: identifying risks

Average risk Ask about quantity and frequency Opportunistically* (III,C) 55, 237, 274,
• Everyone over age 10 years of smoking (I,A). Offer smoking 279–282
cessation advice, set quit goals, offer
pharmacotherapy, referral and follow-up
as appropriate (II,A).
High risk (people who smoke and who have the following characteristics)
• Aboriginal and Torres Strait Offer smoking cessation advice. Agree Opportunistically, ideally at 280
Islander peoples on quit goals, offer pharmacotherapy every visit* (III,C)
and culturally appropriate referral and
support (II,A).
• People with mental illness Offer smoking cessation advice and Opportunistically, ideally 55, 273, 279,
make careful use of pharmacotherapy every visit* (III,C) 281, 282
given significant impact of nicotine
and nicotine withdrawal on drug
metabolism† (I,A).
• Pregnant women Offer smoking cessation advice, agree At each antenatal visit (III,C) 273, 283–285
on quit goals, offer referral to a quit
program (I,A).
• People with other drug-related Offer smoking cessation advice and Opportunistically, ideally 55, 279, 282,
dependencies make careful use of pharmacotherapy every visit* (III,C) 286, 287
given significant impact of nicotine
and nicotine withdrawal on drug
metabolism† (I,A).
• People with smoking-related Offer smoking cessation advice Opportunistically, ideally 55, 274, 282,
disease highlighting specific disease-related every visit* (III,C) 283
benefits of quitting; refer to smoking
programs (I,A).
• Parents of young babies and Offer smoking cessation advice. If the Opportunistically, ideally 55, 198, 274,
children parent is unable to quit advise to: every visit* (III,C) 284, 288
• smoke away from children
• not smoke in confined spaces with
children (e.g. when driving) (I,A).
* See Effect of smoking abstinence on medications, Appendix 9, New Zealand smoking cessation guidelines 2007 at www.treatobacco.
net/en/uploads/documents/Treatment%20Guidelines/New%20Zealand%20treatment%20guidelines%20in%20English%202007.pdf
† While enquiry about smoking should occur at every opportunity, be aware of patient sensitivity. Non-judgemental enquiry about
smoking is associated with greater patient satisfaction.283, 286, 289
8th edition 43
Implementation
At an individual patient level, GPs and their teams can influence smoking rates by systematically providing
opportunistic advice and offering support to all attending patients who smoke.44, 168, 259, 290, 291 GPs tend to underutilise
effective treatment strategies for example, referral to the Quitline,292–294 pharmacotherapy,284, 288, 295, 296 and
motivational interviewing.284, 288, 297
There is a lack of evidence for greater effectiveness of stage-based approaches,298 and interest in quitting fluctuates over
time.299 The stages of change model provides a useful framework to help clinicians identify smokers and provide tailored
support for a smoker’s level of interest in quitting in a way that is time efficient and likely to be well received.300–302
Pregnant women find it especially difficult to quit: pregnancy alters nicotine metabolism and heightens withdrawal
symptoms and the support from partners is an important element in quitting.240, 241 Higher smoking rates in disadvantaged
individuals reflect greater neighbourhood disadvantage, less social support, greater negative affect and lower self-
efficacy.303 Removing access barriers and providing incentives to motivate patients to quit may improve quit rates.304, 305
A whole-of-practice approach that includes a supportive infrastructure has a big impact on GP effectiveness in
smoking cessation.236, 237, 244, 306, 307 The RACGP green book outlines a range of effective implementation strategies in
smoking cessation.244
7.2 Overweight
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
BMI and waist circumference should be measured every 2 years (A). BMI on its own may be misleading, especially
in older people and muscular individuals, and classifications may need to be adjusted for some ethnic groups.308
Waist circumference is a strong predictor of health problems.309, 310
Patients who are overweight or obese should be offered individual lifestyle education (A).121, 311, 312 Restrictive dieting
is not recommended for children and adolescents. A modest loss of 5% of starting body weight in adults who are
overweight is sufficient to achieve some health benefits.312–315
Table 7.2.1 Obesity-related complications: identifying risks
Average risk Assess BMI and waist circumference in all adults aged Every 2 years 311, 313
• All patients over 18 years (I,A). (IV,D)
In children and adolescents use age-specific BMI
charts (see Section 3: Preventive activities in children
and young people) (III,C).
Offer education on nutrition* and physical activity† (I,A).
Increased risk Assess BMI and waist circumference in all adults over Every 12 months 264, 311
• Aboriginal and Torres Strait age 18 years (I,B). (IV,D)
Islander peoples and those Offer individual or group-based education on nutrition 313, 316
from Pacific Islands and physical activity (II,A).
• Patients with existing diabetes
or CVD, stroke, gout or liver
disease
Identified risk Assess weight and waist circumference (I,B). Every 6 months§ 311
• Patients who are overweight Develop weight management plan‡ (II,B). (III,C) 317, 318
or obese Consider referral for self-management support or
coaching in an individual or group-based diet or
physical activity program or allied health provider (e.g.
dietitian, exercise physiologist, psychologist).
* For more information see the NHMRC Dietary guidelines for Australian adults.
† For more information see the NHMRC Physical activity guidelines.
‡ See Obesity management guidelines: the plan should include frequent contact (not necessarily in general practice), realistic
targets, and monitoring for at least 12 months.
§ Review impact on changes in behaviour in 2 weeks.
8th edition
Table 7.2.2 Overweight and obesity: assessment and preventive interventions

Assessment Technique References
BMI BMI = body weight in kilograms divided by the square of height in metres. BMI of 25 or 311, 319
greater conveys increased risk
Waist An adult’s waist circumference is measured halfway between the inferior margin 311, 319
circumference of the last rib and the crest of the ilium in the mid-axillary plane over bare skin. The
measurement is taken at the end of normal expiration.
• ≥94 cm in males and ≥80 cm in females conveys increased risk.
• ≥102 cm in males and ≥ 88 cm in females conveys high risk.
Weight 1. Advise that weight loss can have health benefits, including reduced BP and prevention
reduction of diabetes in high-risk patients.
2. Start a lifestyle program that includes reduced caloric intake (aiming for 600 Kcal or 320, 321
2500 KJ energy deficit) and increased physical activity (increasing to 60 minutes of
moderate-intensity 5 days per week) supported by behavioural counselling.
3. Agree on goals, including a realistic initial target of 5% weight loss. Make contact 322, 323
(visits, phone, etc.) 2 weeks after commencing the program to determine adherence
and if goals are being met.
4. If no response (<1 kg weight or 1 cm waist) after 3 months, consider alternative 324
approaches, including the addition of medication such as Orlistat.
5. After achieving initial weight loss, advise that patients may regain weight after 2 325–329
years without a maintenance program that includes support, monitoring and relapse
prevention.
Bariatric surgery may be considered in patients who fail lifestyle interventions and who
have a BMI of 35+ with comorbidities, such as poorly controlled diabetes, who are
expected to improve with weight reduction.
Table 7.2.3 Obesity and risk of CVD and type 2 diabetes in Australian adults
Classification BMI (kg/m2) Disease risk (relative to normal measures)
Underweight <18.5 –
Healthy weight 18.5–24.9 –
Overweight 25.0–29.9 Increased
Obesity 30.0–39.9 High to very high
Severe obesity >40 Extremely high
Reproduced from National Health and Medical Research Council. Overweight and obesity in adults – a guide for general
practitioners. Canberra: NHMRC, 2003311
Implementation
Strategy
Body weight is associated with the balance between levels of dietary intake and physical activity. Environmental,
cultural, genetic and lifestyle factors all contribute to overweight and obesity. Changes in the balance between energy
intake (increasing) and energy expenditure (decreasing) have been identified as major contributors to rising obesity.
There is little consensus on the relative importance of dietary intake compared with physical activity.319, 330 Regular
physical activity is protective against unhealthy weight gain and reduces CVD risk as well as CVD risk factors such as
overweight, high BP, levels of high density lipoprotein (HDL) and total blood cholesterol, and type 2 diabetes.331–333
Dietary behaviour influences the risk of coronary heart disease (CHD) and stroke due to the combined effects of
individual dietary factors and total energy intake – if this leads to excess weight.331
Strategies to increase screening in this group are discussed in the RACGP green book and the National guide to a
preventive health assessment in Aboriginal and Torres Strait Islander people, 2nd edition.
8th edition 45
7.3 Nutrition
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Ask adults how many portions of fruits or vegetables are eaten in a day and advise to follow the Dietary guidelines
for Australian adults.334 (B). Brief lifestyle advice should be given to reduce saturated fat and sodium and increase
fruit and vegetable portions (2 + 5 portions) as these are associated with a lower risk of CVD and diabetes.335
Breastfeeding should be promoted as the most appropriate method for feeding infants and one that offers
protection against infection and some chronic diseases.336 See Section 3: Preventive activities in children and young
people for nutrition-related recommendations.
Table 7.3.1 Nutrition-related complications: identifying risk

Average risk Ask about number of portions of fruits Every 2 years 292, 337, 338
• All patients and vegetables eaten per day, amount of (IV,D)
sodium, and amount of saturated fat eaten
(II,B).
All patients should be advised to follow the
NHMRC Dietary guidelines for Australian
adults and the Heart Foundation guidelines
(see Table 7.3.2).
High risk Provide lifestyle advice to reduce dietary Every 6 months 338–341
• Overweight or obese saturated fat, sodium and increase fruit and (III,C)
vegetables. (See Section 7.2: Overweight
• High cardiovascular absolute risk
for dietary recommendations for overweight
(>15%)
and obesity) (II,B).
• A past or first-degree family history of
Provide self-help nutrition education
CVD (including stroke) before age 60
materials and refer to a dietitian or group
years. For personal history the age
diet program (II,B).
doesn’t matter.
• Type 2 diabetes or high risk for diabetes
8th edition
Table 7.3.2 Nutrition-related complications: preventive interventions

Vitamin Vitamin supplementation is not of established value in asymptomatic individuals* 342
supplements (with the exception of folate and iodine in pregnancy). Routine screening for vitamin D
deficiency is not recommended in low-risk populations.
Dietary Enjoy a wide variety of foods each day: 334

recommendations • five portions of vegetables and two portions of fruit343, 344
• three portions of cereals (including breads, rice, pasta and noodles)
• one to two portions of lean meat, fish, poultry and/or alternatives
• at least 2 g per day alpha-linolenic acid by including foods such as canola-based
or soybean-based oils and margarine spreads, seeds (especially linseeds),
nuts (particularly walnuts), legumes (including soybeans), eggs and green leafy
vegetables
• drink plenty of water.
Take care to:
• limit saturated fat and moderate total fat intake338 but consume about 500 mg
per day of combined docosahexaenoic acid and eicosapentaenoic acid through
a combination of the following:345 two or three serves (150 g serve) of oily fish per
week, fish oil capsules or liquid, food and drinks enriched with marine omega-3
polyunsaturated fatty acids346
• limit salt intake347 to less than 6 g of salt a day (approximately 2300 mg of sodium a
day), which is approximately 1½ teaspoons of salt
• limit alcohol intake
• consume only moderate amounts of sugars and foods containing added sugars.
• prevent weight gain: be physically active and eat according to energy needs
• care for food: prepare and store it safely
• encourage and support breastfeeding.
Note: There are also dietary guidelines for children and adolescents: Dietary
guidelines for children and adolescents in Australia, incorporating the infant feeding
guidelines for health workers.86
For specific advice, especially patients with specific conditions, refer to a
dietitian.
The Heart Foundation has a number of nutrition position statements at
www.heartfoundation.org.au/information-for-professionals/food-professionals/Pages/
guides-policies-position-statement.aspx
Encourage Encourage and support exclusive breastfeeding for 4–6 months, then the introduction 334
breastfeeding of complementary foods and continued breastfeeding thereafter. It is recommended
that breastfeeding continue until age 12 months and thereafter as long as mutually
desired.
* Prevalence of nutritional deficiency is high in certain groups such as people with alcohol dependence and elderly living alone
or in institutions.
8th edition 47
Implementation
Strategy
Refer to general principles as discussed in Section 1: Introduction and Section 7: Prevention of chronic disease and
as outlined in the RACGP green book. Lifescripts provide guidance on portions and what foods to eat at www.health.
gov.au/internet/main/publishing.nsf/Content/lifescripts-clinical
It is important to consider cultural and religious beliefs in recommending dietary changes. A full range of Lifescripts
resources have been produced for use with Aboriginal and Torres Strait Islander peoples at www.healthinfonet.ecu.
edu.au/key-resources/promotion-resources?lid=16071
7.4 Early detection of problem drinking

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
All patients should be asked about the quantity and frequency of alcohol intake from age 15 years (A). Those
with at-risk patterns of alcohol consumption should be offered brief advice to reduce their intake348 (A). Provide
interventions using brief motivational interviewing targeted at high-risk use (I,B).349–351
The lifetime risk of harm from drinking alcohol increases with the amount consumed. 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. Short-term risks stem from the risks of accidents and injuries occurring immediately after drinking.
Table 7.4.1 Alcohol-related complications: identifying risk

Low risk Ask about the quantity and frequency of Every 2–4 years (III,C) 44
• All patients aged 15 years alcohol intake (II,B).
and over Advise if drinking alcohol to drink two
drinks per day or less and no more than
four drinks on any one occasion (II,B).
Increased risk Advise children aged under 15 years not to Opportunistically (III,C) 44
• Children and adolescents drink (III,B).
Advise young people aged 15–17 years to
delay drinking as long as possible (III,B).
• Older people* Inform that there is an increased risk of Opportunistically (III,C) 352–354
potential harm from drinking (III,B).
• Young adults, who have a 355
higher risk of accidents and
injuries
• People with a family history of 356–358

alcohol dependence
• Individuals who are Advise that non-drinking is the safest Opportunistically (III,C) Driving 359,
participating or supervising option: driving (I,A), other areas (III,C). 360
risky activities (e.g. driving, 361–364
boating, extreme sports,
diving, using illicit drugs)
• Women who are pregnant or Advise that non-drinking is the safest Opportunistically or at 44, 365, 366
planning a pregnancy option (I,A). each antenatal visit (III,C)
8th edition

• People with a physical Advise that non-drinking is the safest Opportunistically (III,C) 44, 367
condition made worse by option but weigh up pros and cons for
alcohol: each individual (I,A).
–p
ancreatitis Advise those with hypertension, or taking
– diabetes antihypertensive medication, to limit
alcohol intake to no more than two (for
– hepatitis/chronic liver
men) or one (for women) standard drinks
disease
per day (II,B).
– peptic ulcer
– hypertension
– sleep disorders
– sexual dysfunction
– other major organ disease
• People with a mental health Assess whether there are possible harmful Opportunistically (III,C) 368–370
problem made worse by interactions between their medications and
alcohol (e.g. anxiety and alcohol (II,A).
depression)
• People taking medications Opportunistically (III,C) 371, 372

* Older people who have a higher risk of falls and are more likely to be taking medication.354
Table 7.4.2 Alcohol-related complications: preventive interventions

Brief intervention • Brief interventions for problem drinkers halve the mortality rate in this group. 44, 373
• Brief advice in general practice has been demonstrated to have resulted in a 238, 348, 356,
reduction in drinking of about six standard drinks per week for men. 374, 375
• The impact of brief advice on reduction in consumption for women is less clear. 356–358, 374,
• While there is no clear dose–response curve for spending more time counselling 375
subjects who are drinking at risky levels, the minimum time to achieve some impact 358, 375, 376
is between 5 and 15 minutes. 238
• While some have argued that screening of itself constitutes a brief intervention, the 377
impact of interventions of less than 5 minutes is less clear. 356, 376, 378
Implementation
Strategy
In the Australian setting, fewer than one in three females and one in six males with documented alcohol dependence
seek any form of treatment.379 The barriers to identifying and treating patients with risky or problematic drinking are
numerous380–385 and include: stigma associated with diagnosis, gender (females less likely to receive treatment),
shorter consultations, self-perceived skills and scepticism about the benefit of treatment. Nevertheless, the number
needed to treat (return on effort) using brief interventions is one in eight: eight hazardous drinkers need to be treated
to produce one who will reduce drinking to low risk levels.238, 356, 358, 374, 375, 386
Implementation is improved through:
• screening/routine enquiry of all patients in the target group, especially using non-confrontational tools
(e.g. computerised screening).387–389 Alternatively, embed enquiry about drinking in opportunistic assessment
of lifestyle or use a structured questionnaire, for example the AUDIT-C (Appendix 3).390, 391 (Note that the risk
assessment should use the NHMRC guidelines and not other structured questionnaires, e.g. AUDIT-C.)
• addressing barriers,392, 393 for example, ensuring that there is a supportive organisational practice
infrastructure387, 394, 395 and adequate training for clinicians394–396 and practice nurses.381, 394, 397
8th edition 49
7.5 Physical activity

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
All adults should be advised to participate in 30 minutes of moderate activity on most, preferably all, days of the week (at
least 2.5 hours per week)398 (A) and to avoid prolonged sitting, which is a cardiovascular risk factor.399 While moderate
physical activity is recommended for health benefit, more vigorous exercise may confer additional cardiovascular
health and cancer prevention benefits if carried out for a minimum of 30 minutes three to four times a week.400 The
amount of physical activity can be accumulated over several bouts. The amount of activity for weight loss is greater. It
is recommended that at least 60 minutes of moderate-intensity physical activity (such as brisk walking) every day may
be required, in addition to reducing energy intake, in order to achieve measurable weight loss over a number of months
and prevent weight regain.401 Even without weight loss, physical activity can accrue health benefits.402
Table 7.5.1 Physical inactivity: identifying risk
Average risk Question regarding current level Every 2 years 403
• Those already performing moderate levels of activity of activity (II,A). (III,C)
for 30 minutes daily on at least 5 days of the week. Consider use of pedometer to
404
assess step count per day (III,C).
Increased risk
• Those not performing moderate levels of activity for Question regarding current level Every visit (IV,D) 405
30 minutes daily on at least 5 days of the week. of activity and readiness to be
• Others at higher risk include teenage girls, office more active (III,C).
workers, Aboriginal or Torres Strait Islander peoples, Provide brief advice and written
and people from low socioeconomic backgrounds physical activity materials (III,C).
and non-English speaking backgrounds.
Refer to an exercise or physical
• Those with a chronic condition or other CVD risk activity program: programs with
factors (see Section 8: Prevention of vascular and additional behaviour change
metabolic disease). support may be more beneficial
• Patients at high risk of CVD or diabetes (including (III,C).
impaired glucose tolerance).
Table 7.5.2 Physical inactivity: assessment and intervention
Assessment and Technique References
intervention
Determine level of • Moderate physical activity is associated with a moderate, noticeable increase in the 406
physical activity depth and rate of breathing while still being able to whistle or talk comfortably.
• Question regarding current level of activity and readiness to be more active. 407
• Consider use of pedometer to assess current number of steps per day over 408
1 week; 10 000 steps per day is regarded as sufficient although health benefits
also accrue at lower levels.
Brief interventions Interventions in general practice that have been shown to have short-term benefit in 407
to increase levels of changing behaviour related to physical activity include:
physical activity • patient screening to identify current level of activity (including use of a pedometer) and 404
readiness to be more active
• provision of brief advice or counselling on exercise
• supporting written materials and/or written prescription for exercise (e.g. Physical
Activity Lifescript).
• pedometer step target of 10 000 steps per day, or 2000 more than at baseline.
Physical activity program • Structured programs of physical activity education and exercise may be delivered as
individual or group program and over several sessions. The Heart Foundation is at http://
heartmoves.heartfoundation.org.au and some local councils have information on local
physical activity programs. Exercise physiologists are listed at www.essa.org.au
8th edition
8. Prevention of vascular and metabolic disease
CVDs occur in 18% of the population, with 6.9% of the population estimated to have disability associated with
them.168 They account for 36% of all deaths. Most of the risk of these conditions can be attributed to smoking,
raising BP, dyslipidaemia obesity, physical inactivity and poor diet.409 The majority of these can be prevented by
changing behavioural and physiological risk factors. The behavioural risk factors include smoking, poor nutrition,
hazardous alcohol consumption and physical inactivity as outlined in Section 7: Prevention of chronic disease. In
addition to these, depression, social isolation and lack of quality social support are risk factors for CHD.410
These risk factors are common in the Australian population: 90% of adults aged over 45 years have at least one
modifiable risk factor and two-thirds have three or more risk factors for CVD.411 Absolute CVD risk combines risk
factors in a calculation of the probability that an individual will develop a cardiovascular event (myocardial infarction,
stroke) or other vascular disease within a specified timeframe (usually 5 years).
Health inequity
Aboriginal and Torres Strait Islander peoples, people living in rural and remote areas and lower socioeconomic groups all have
an increased risk of cardiovascular disease.252
Both biological and behavioural risk factors play a part (see Section 7: Prevention of chronic disease for a discussion of the
relationship between behavioural risk factors and social disadvantage). Low income and education are generally associated with
worse biological risk factors for CVD, including BP, lipid profiles, waist circumference, fasting glucose and insulin levels. This is
only partly mediated by behavioural risk factors and is more consistently observed for women.412
Diabetes is three to four times more common in Aboriginal and Torres Strait Islander peoples and about twice as common in the
most disadvantaged compared to the most socioeconomically advantaged groups.413 Higher prevalence is found in people born
in North Africa, the Middle East, South-East Asia, the Pacific Islands and Southern and Eastern Europe. Little regional variation
occurs within Australia.
The incidence of end-stage renal disease (ESRD) among Aboriginal and Torres Strait Islander peoples varies from up to 30 times
the national incidence in some remote areas to around double in some urban areas.414–416 Factors that affect rates of ESRD in
the Aboriginal and Torres Strait Islander population include low birthweight, poor nutrition, infections such as scabies, smoking,
other behavioural risk factors and socioeconomic disadvantage.417–419 There is also a threefold variation within urban areas
among non-Indigenous Australians, with higher ESRD incidence in more disadvantaged areas.420
The role of socioeconomic disadvantage in preventive activities for CVD is complex. Preventive care may be more commonly
offered to low socioeconomic groups, but may be less likely to be followed up421 or it may be less comprehensive or
complete422 suggesting additional targeted strategies may be needed for these groups. There is evidence that men from
socioeconomically disadvantaged backgrounds may be less likely to be offered statins.423
8.1 Assessment of absolute cardiovascular risk

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
General
population
Aboriginal and
Torres Strait
Islander peoples
Absolute cardiovascular risk assessment should be conducted at least every 2 years in all adults aged 45 years
and older who are not known to have CVDs or to be at clinically determined high risk (B).424 This calculation requires
information on the patient’s age, sex, smoking status, total and HDL cholesterol, systolic blood pressure (SBP) and
if the patient is known to have diabetes or left ventricular hypertrophy (LVH).
8th edition 51
Table 8.1.1 Cardiovascular disease: identifying risk

Population group What should be How often? References
done?
Adults aged 45 years and older not known to have CVD Calculate absolute Every 2 years† 424
or not clinically determined to be at high risk cardiovascular risk* (IV,C)
45–74 years (II,B)
≥75 years (Practice Point)
Aboriginal and Torres Strait Islander peoples aged Assess absolute CVD Every 2 years (IV,C)
35 years and older not known to have CVD or not risk (may underestimate
clinically determined to be at high risk risk) (IV,C)
* Calculate risk using the Heart Foundation risk charts (Appendix 5) or online at www.cvdcheck.org.au Blood lipid results within 5 years can
be used in the calculation of absolute CVD risk, but BP should be measured at the time of assessment.
On-therapy measures of BP and cholesterol may underestimate absolute risk and thus recently recorded pre-treatment measures may
be more appropriate to use if available. An electrocardiograph (ECG) is not required to determine LVH if not previously known.
† Adults with any of the following do not require absolute CVD risk assessment using the Framingham Risk Equation because they are
already known to be at clinically determined high risk of CVD (IV,D):
• diabetes and age >60 years
• diabetes with microalbuminuria (>20 μg/min or urine albumin:creatinine ratio (UACR) >2.5 mg/mmol for males,
>3.5 mg/mmol for females)
• moderate or severe CKD (persistent proteinuria or estimated glomerular filtration rate
(eGFR) <45 mL/min/1.73 m2)
• previous diagnosis of FH
• SBP ≥180 mmHg or diastolic blood pressure (DBP) ≥110 mmHg
• serum total cholesterol >7.5 mmol/L
• Aboriginal or Torres Strait Islander peoples aged over 74 years (Practice Point).
Adults aged older than 74 years may have their absolute risk assessed with age entered as 74 years. This is likely to
underestimate 5-year risk but will give an estimate of minimum risk.425 Patients with a strong family history of CVD
(first-degree relatives) or obesity (BMI above 30 kg/m2 or more) may be at greater risk.310, 426, 427 Similarly patients with
depression and atrial fibrillation (AF) may be at increased risk.424
See Appendix 5 or www.cvdcheck.org.au
8.2 Blood pressure

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Blood pressure (BP) should be measured in all adults from age 18 years (A) at least every 2 years. BP should be
interpreted in the context of an absolute cardiovascular risk assessment after age 45 years (35 years of age for Aboriginal
and Torres Strait Islander peoples) (B). Secondary causes of hypertension and ‘white coat’ hypertension should be
considered.
8th edition
Table 8.2.1 Hypertension: identifying risk

Low absolute risk Provide lifestyle advice and BP every 2 years 424, 428–430
• <10% CVD risk education (I,B). (III,C)
Offer pharmacotherapy if BP
persistently over 160/100
mmHg
Moderate risk Provide intensive lifestyle advice BP every 6–12 310, 424,
• 10–15% absolute cardiovascular risk (II,B). months (III,C) 426–428, 431
Consider pharmacotherapy if
risk factors have not reduced
after 3–6 months of lifestyle
intervention.
Offer pharmacotherapy
simultaneously with lifestyle
intervention if BP persistently
over 160/100 mmHg or if family
history of premature CVD or
South Asian, Middle Eastern,
Maori, Aboriginal or Pacific
Islander descent (III,C).
High risk Provide intensive lifestyle advice BP every 6–12 424, 429
• >15% absolute cardiovascular risk (II,B) weeks (III,C)
• Clinically determined high risk: Commence pharmacotherapy
(simultaneously with lipid
– diabetes and age >60 years 432, 433
therapy unless contraindicated)
– diabetes with microalbuminuria (>20 μg/min
Treatment goal is BP
or UACR >2.5 mg/mmol for males,
≤140/90 mmHg in adults
>3.5 mg/mmol for females)
without CVD including those
– moderate or severe CKD (persistent with CKD (I,B–III,D)* (≤130/80 in
proteinuria or eGFR <45 mL/min/1.73 m2) people with diabetes or micro or
– previous diagnosis of FH macroalbuminuria (UACR >2.5
– SBP ≥180 mmHg or DBP ≥110 mmHg mg/mmol in males and >3.5
mg/mmol in females))
– serum total cholesterol >7.5 mmol/L
– Aboriginal and Torres Strait Islander peoples
aged over 74 years
High risk Lifestyle risk factor counselling Every 6 months 429

Existing CVD (previous event, symptomatic CVD), Pharmacotherapy to lower risk (III,C)
stroke or transient ischaemic attacks (TIAs) or (I,A)
CKD
* D recommendation for clinically determined high risk.
8th edition 53
Table 8.2.2 Hypertension: preventive interventions

Measure BP Measure BP on at least two separate occasions with a calibrated mercury 424, 429
sphygmomanometer, or automated device that is regularly calibrated against a mercury
sphygmomanometer. At the patient’s first BP assessment, measure BP on both arms.
Thereafter, use the arm with the higher reading. In patients who may have orthostatic
hypotension (e.g. the elderly, those with diabetes), measure BP in sitting position and repeat
after the patient has been standing for at least 2 minutes.
If possible, use ambulatory BP monitoring or self-measurement for patients with any of
the following:
• unusual variation between BP readings in the clinic
• suspected white coat hypertension
• hypertension that is resistant to drug treatment
• suspected hypotensive episodes (e.g. in elderly or diabetic patients)
Risk calculation should be performed using clinical BP measurements (as the algorithms
are based on these). Ambulatory BP readings are considered to be better predictors of
outcomes than clinic BP measurements, and therefore should be used to monitor BP
lowering therapy.
Lifestyle Lifestyle risk factors should be managed at all risk levels. 424, 429
modification All people, regardless of their absolute risk level, should be given dietary advice. Those at
low to moderate absolute risk of CVD should be given dietary and other lifestyle advice.
(See Section 7: Prevention of chronic disease)
Advise to aim for healthy targets:
• at least 30 minutes of moderate-intensity physical activity on most, if not all, days
• smoking cessation
• waist measurement <94 cm for men and <80 cm for women, BMI <25 kg/m2
• dietary salt restriction ≤4 g/day (65 mmol/day sodium)
• limit alcohol intake to ≤2 standard drinks per day for males and ≤1 standard drink per
day for females.
Medications BP treatment should aim to lower BP towards (while balancing risks and benefits): 424
• ≤140/90 for adults without CVD (including those with CKD)
• ≤130/80 for adults with diabetes or with micro- or macro-albuminuria (UACR >2.5 mg/
mmol for males, >3.5 mg/mmol for females).
Treatment may commence with an ACE inhibitor, angiotensin II antagonist, calcium
channel blocker or a low-dose thiazide or thiazide-like diuretic. A second or third agent
from a different class may be added to treat towards targets.
8.3 Cholesterol and other lipids

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
General
population
Aboriginal and
Torres Strait
Islander peoples
Adults should have their fasting blood lipids assessed starting at age 45 years, every 5 years (A for males, C for
females). Lipid levels should be interpreted in the context of an absolute cardiovascular risk assessment after age
45 years (35 years for Aboriginal and Torres Strait Islander peoples) (B). Aboriginal and Torres Strait Islander adults
should have fasting lipid tests performed every 5 years from age 35 years (B).
8th edition
Table 8.3.1 Cholesterol and lipids: identifying risk

Low risk Provide lifestyle advice (I,A). Repeat fasting 424
• Absolute CVD risk <10% lipids every
5 years*
Moderate risk Provide intensive lifestyle Repeat fasting 310, 424, 426,
• Absolute CVD risk 10–15% advice (II,B). lipids every 427
Consider pharmacotherapy 2 years
if not reaching target after
6 months (I,A) or if family
history of premature CVD,
or Aboriginal or Torres Strait
Islander, South Asian, Middle
Eastern, Maori or Pacific
Islander descent (II,C).
High risk Provide intensive lifestyle Every 12 months 424

• Absolute cardiovascular risk >15% advice (II,C). (III,C)
• Patient with the following clinically determined high- Commence cholesterol
risk factors: lowering therapy
(simultaneously with
– diabetes and age >60 years
antihypertensive unless
– diabetes with microalbuminuria (>20 µg/min or contraindicated) (II,C-III,D).†
UACR >2.5 mg/mmol for males, >3.5 mg/mmol for
females)
– CKD (persistent microalbuminuria or Stage 4 renal
failure eGFR <30 mL/min/1.73 m2) or Stage 3a
renal failure eGFR <45 mL/min/1.73 m2)
–p
revious diagnosis of FH
–S
BP ≥180 mmHg or DBP ≥110 mmHg
– s erum total cholesterol >7.5 mmol/L
–A
boriginal and Torres Strait Islander peoples aged
over 74 years
See Section 8.2: BP
High risk Lifestyle risk factor counselling Every 12 months 434

Existing CVD (previous event, symptomatic CVD) Pharmacotherapy to lower (III,C)
risk (I,A)
* Lipid blood test results within 5 years can be used to calculate absolute CVD risk every 2 years. Patients with diabetes,
cardiac disease, stroke, hypertension or kidney disease should have their lipids tested every 12 months (III,C).
† D recommendation for clinically determined high risk.
8th edition 55
Table 8.3.2 Cholesterol and lipids: preventive interventions

Fasting blood lipids Fasting total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides (TG). 435
If lipid levels are abnormal, a second confirmatory sample should be taken on a
separate occasion (as levels may vary between tests) before a definitive diagnosis is
made. 436, 437
Screening tests using capillary blood samples produce total cholesterol results that
are slightly lower than on venous blood. These may be used, providing they are
confirmed with full laboratory testing of venous blood for patients with elevated levels
and there is good follow-up.
In adults at low absolute risk of CVD, blood test results within 5 years may be used for
review of absolute cardiovascular risk unless there are reasons to the contrary.
Lifestyle Lifestyle risk factors should be managed at all risk levels. 424, 429
modification All people, regardless of their absolute risk level, should be given dietary advice
Those at low to moderate absolute risk of CVD should be given dietary and other
lifestyle advice (see Section 7: Prevention of chronic disease).
Advise to aim for healthy targets:
• at least 30 minutes of moderate-intensity physical activity on most, if not all, days
• smoking cessation
• waist measurement <94 cm for men and <80 cm for women, BMI <25 kg/m2
• dietary salt restriction ≤4 g/day (65 mmol/day sodium)
• limit alcohol intake to ≤2 standard drinks per day for men and ≤1 standard drink per
day for women.
Pharmacotherapy Lipid lowering therapy for primary prevention should (while balancing risks and 424
benefits) aim towards:
• Total cholesterol <4.0 mmol/L
• HDL-C ≥1.0 mmol/L
• LDL-C <2.0 mmol/L
• Non-HDL-C <2.5 mmol/L
• TG <2.0 mmol/L
Treatment should commence with a statin. If LDL-C levels are not sufficiently reduced
on maximally tolerated dose of a statin, add one of ezetimibe, bile acid binding
resin or nicotinic acid. These agents may be used as monotherapy if statins cannot
be tolerated at all. If TG levels remain elevated, consider use of one of fenofibrate,
nicotinic acid or fish oil.
8.4 Type 2 diabetes

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
General population
Aboriginal and Torres

Strait Islander peoples
Patients should be screened for diabetes every 3 years from age 40 years using AUSDRISK (B). Aboriginal and
Torres Strait Islander peoples should be screened from age 18 years. Those with a risk score of 12 or more should
be tested by fasting plasma glucose (C).
8th edition
Table 8.4.1 Type 2 diabetes: identifying risk

Who is at risk? What should How often? References
be done?
Increased risk AUSDRISK (III,B) Every 3 years 438
• Age >40 years (Appendix 4) (III,C)
• Aboriginal and Torres Strait Islander peoples
High risk Fasting blood Every 3 years 439, 440

• Any one of following risk factors: sugar (III,B) (III,C)
–– AUSDRISK score of 12 or more
–– all people with a history of a previous cardiovascular event
(acute myocardial infarction or stroke)
–– women with a history of gestational diabetes mellitus
–– women with polycystic ovary syndrome
–– patients on antipsychotic drugs
High risk Fasting blood Every 12 439

• Those with impaired glucose tolerance test or impaired fasting sugar (III,B) months (III,C)
glucose (not limited by age)
Table 8.4.2 Tests to detect diabetes

Test Technique References
Fasting blood sugar Measure plasma glucose levels on a fasting sample. 439
• <5.5 mmol/L: diabetes unlikely
• 5.5–6.9 mmol/L fasting: may need to perform an oral glucose tolerance test
• 7.0 mmol/L or more fasting (>11.1 non-fasting): diabetes likely, repeat fasting
blood sugar to confirm on a separate day.
The test should be performed on venous blood and tested in a laboratory to
confirm a diagnosis.
Oral glucose tolerance Before and 2 hours after a 75 gram oral glucose load is taken orally, the plasma 439
test glucose is measured. If this is greater than 11.1 mmol/L, diabetes is likely. If the 2
hour plasma glucose is between 7.8 and 11.0 mmol/L, there is impaired glucose
tolerance. If it is less than 7.8 mmol/L, diabetes is unlikely.
Diabetes risk Diabetes risk may be calculated using AUSDRISK. This calculates a score related 441
(AUSDRISK) to the risk of developing diabetes over a 5-year period (Appendix 4).
Glycated haemoglobin HbA1c may be used as a diagnostic test for diabetes. HbA1c of 6.5% is the 442
(HbA1c) diagnostic cut-off. However, this is not currently approved by the MBS as a test to 443
diagnose diabetes in Australia.
8th edition 57
Table 8.4.3 Type 2 diabetes: preventive interventions

Target group Intervention References
Pre-diabetes (impaired glucose • Increasing physical activity (e.g. 30 minutes brisk walking five 444–447
tolerance, impaired fasting glycaemia, times a week) and/or weight loss reduces risk of developing
gestational diabetes) and those with diabetes by 40–60% in those at high risk.
an elevated AUSDRISK score or • Give advice on healthy low fat diet (<30% kcal or kilojoules from
with other specific risk factors with fat and <10% from saturated fat; high fibre, low glycaemic index
negative screening test with cereals, legumes, vegetables and fruits), weight loss and
increased physical activity (see RACGP SNAP: A population
health guide to behavioural risk factors in general practice).
• Refer patients to a dietitian and a physical activity program.
• Provide pre-conception advice to women with a history of
gestational diabetes.
8.5 Stroke
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
GPs should be alert to symptoms of TIAs in those aged 45 years and older and assess early in order to prioritise
those needing urgent investigation and management. People at high risk should be questioned about symptoms of
TIA to determine appropriate action. Adults with AF should have their absolute cardiovascular risk assessed and be
treated accordingly. Patients with AF are at additional risk of thromboembolic disease and stroke.448
Table 8.5.1 Stroke: identifying risk

High absolute risk Question about symptoms of TIA. If TIA, stratify risk Every 12 424, 434,
• Either calculated >15% absolute of stroke and consider anticoagulation* (I,A). months (IV,C) 449–451 for
risk, clinical determined high risk or If AF, determine cause of AF and treat according to stroke/TIA
pre-existing CVD or cardiovascular and thromboembolic risk (II,B).
• Previous stroke (especially with Manage behavioural and physiological risk factors
coexistent AF or high grade actively. Treat with antihypertensive and lipid-
(70–99%) symptomatic carotid lowering medications unless contraindicated or
stenosis) clinically inappropriate (II,B).
• Previous TIA
Auscultation for carotid bruit Auscultating for carotid bruits in asymptomatic 452, 453
people is not recommended in the general adult 449
population as a screening tool for stroke risk.
454
Screening with duplex ultrasonography in this
population is not cost-effective (yields many false
positive results) coupled with the fact that the 449
overall benefit of surgery is at best small, hence
very careful selection of patients is needed to
justify surgery in those with severe (>60%) but
asymptomatic stenosis.†
However, the presence of a carotid bruit has been
shown to be associated with increased risk of
myocardial infarction and cardiovascular death, so
may be a useful prognostic marker when assessing
cardiovascular risk generally.
Screen patients with known asymptomatic carotid
artery stenosis for other treatable causes of stroke
and treat these intensively.
* Anticoagulation with warfarin should be considered in patients with documented ischaemic stroke or TIAs due to AF.
8th edition
† Antiplatelet therapy should be considered for non-cardioembolic stroke or TIA.
Table 8.5.2 Tests to detect stroke risk

Question Question patient or carer regarding symptoms of sudden onset of loss of focal neurological
about TIA function such as weakness or numbness of arms or legs, speech disturbance, double vision
ABCD2 tool or vertigo.
434
All patients with suspected TIA should have stroke risk assessment including the ABCD2 tool:
• Age: >60 years (1 point)
• BP: >140/90 mmHg (1 point)
• Clinical features: unilateral weakness (2 points), speech impairment without weakness (1
point)
• Duration: >60 min (2 points), 10–59 min (1 point)
• Diabetes (1 point)
Important additional information also required:
• Presence of AF, signs that might indicate carotid disease (e.g. anterior circulation signs) who
are candidates for carotid surgery or two or more TIAs within previous 7 days (crescendo
TIA)
For those deemed high risk (ABCD2 tool 4–7 and/or AF, potential carotid disease or
crescendo TIA): urgent brain and carotid imaging (‘urgent’ is considered immediately, but
certainly within 24 hours). If carotid territory symptoms, consider duplex ultrasound for
patients who are potential candidates for carotid revascularisation.
For those deemed high risk (ABCD2 tool 0–3 without AF, potential carotid disease or
crescendo TIA): CT brain (and carotid ultrasound where indicated) as soon as possible (i.e.
within 48–72 hours)
For further information about secondary prevention after stroke or TIA, see www.strokefoundation.com.au
See also Section 15: Screening tests of unproven benefit.
8.6 Kidney disease

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Those at high risk
Patients should be screened for kidney disease if they are at high risk (B).
Table 8.6.1 Kidney disease: identifying risk

High risk BP, ACR and eGFR (III,A) Every 1–2 years* 419, 455–462
• Smoking ≥40 years (IV,C) 440, 463–466
• Hypertension 419, 439, 463,
• Obesity 465, 467
• Family history of kidney disease If ACR positive, arrange two 468
further samples for urine 469
• Diabetes
ACR over 2 months (III,B)
• Aboriginal or Torres Strait Islander aged
>30 years
* 1 year for patients with hypertension or diabetes.
8th edition 59
Table 8.6.2 Tests to detect kidney disease

Albuminuria Spot, untimed collection of urine for calculation UACR, preferably on a first morning void. 463, 465
Note: dipstick urine test is not adequate to identify microalbuminuria.
Albumin:creatinine ratio (ACR)
Females Males
Normal <3.5 mg/mmol <2.5 mg/mmol
Microalbuminuria 3.5–35 mg/mmol 2.5–25 mg/mmol
Macroalbuminuria >35 mg/mmol >25 mg/mmol
GFR This is currently automatically reported with every test for serum creatinine using the 466, 468, 470
abbreviated modification of diet in renal disease formula (staging is based on both GFR
level and UACR (normoalbuminuria, microalbuminuria or macroalbuminuria):
• Stage 1 >90 mL/min/1.73 m2 with microalbuminuria, proteinuria or haematuria
• Stage 2 (mild) 60–89 mL/min/1.73 m2 with microalbuminuria, proteinuria or haematuria
• Stage 3a (mod) 45–59 mL/min/1.73 m2
• Stage 3b (mod) 30–44 mL/min/1.73 m2
• Stage 4 (severe) 15–29 mL/min/1.73 m2
• Stage 5 (end-stage) <15 mL/min/1.73 m2
Refer patients with stage 4 or 5 to renal unit or nephrologist, and consider referral at stage
3 or earlier if:
• persistent significant albuminuria (ACR ≥30 mg/mmol, approximately equivalent to
protein:creatinine ratio ≥50 mg/mmol, or urinary protein excretion ≥500 mg/24 hours,
• rapidly declining eGFR (average (of at least three readings) decline >5 mL/min/1.73 m2
in 6 months)
• CKD and hypertension that is hard to get to target despite at least three anti-hypertensive
agents
• unexplained anaemia (<100 g/L) with eGFR <60mL/min/1.73m2
See www.racgp.org.au/Content/NavigationMenu/ClinicalResources/RACGPGuidelines/
ChronicKidneyDiseaseCKDManagementinGeneralPractice/CKDManagement.pdf
The eGFR may be unreliable in the following situations:
• acute changes in renal function
• dialysis patients
• certain diets (e.g. vegetarian, high protein, recent ingestion of cooked meat)
• extremes of body size
• muscle diseases (may overestimate) or high muscle mass (may underestimate)
• children <18 years
• severe liver disease.
It has not been validated in all ethnic groups.
8th edition
9. Early detection of cancers
9.1 Skin cancer

General population screening for melanoma or non-melanoma skin cancer (NMSC) is not recommended as the
prerequisite (evidence to show this reduces death) is not available.471 Providing education that raises awareness of
early detection of skin cancer or its prevention is recommended.
Assess people opportunistically or when the patient is concerned (about skin lesions or their skin cancer risk) and
plan appropriate strategies for their level of risk. People generally should be encouraged to become familiar with
their skin, including skin not normally exposed to the sun, and be alert for new or changing skin lesions, particularly
people aged over 40 years.
9.1.1 Melanocytic skin cancer

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Advise on sun protection
and prevention
Screen increased and
high risk
Skin self-examination should be encouraged for high-risk individuals every 3 months (B).
All people, particularly children, should be advised to adopt protective measures when UV levels are 3 and above
(C). Sunscreen may prevent melanoma in adults,472 and generally minimising sun exposure may reduce the risk of
melanoma.472–477
Table 9.1.1.1 Melanocytic skin cancer: identifying risk

Who is at risk? What should be How often? References
done?
Average risk Primary preventive Opportunistically 471
Light skin without past history of risk advice (III,B)
Increased risk Primary preventive Opportunistically 471, 478

(Risk 2–5 times normal) advice and
examination of skin
• Family history of melanoma in first-degree relative
(III,B)
• Fair complexion, a tendency to burn rather than tan, the
presence of freckles, light eye colour, light or red hair colour
• Age over 30 years (over 50 years most at risk)
• Presence of solar lentigines
• Past history of NMSC (age <40 years higher risk)
• People with childhood high levels of UV exposure and
episodes of sunburn in childhood
High risk Preventive advice, Every 3–12 479

(Risk >6 times normal) Examination of skin months (Practice
(with or without Point)
• Those with multiple atypical or dysplastic naevi and who
photography) and
have a history of melanoma in themselves or in a first-
advice on self-
degree relative
examination (III,C)
8th edition 61
Table 9.1.1.2 Melanocytic skin cancer: preventive interventions

Sun protection All people (especially children aged ≤10 years) should be advised to adopt protective 471, 480
advice measures when UV levels are 3 and above. These measures include use of shade;
broad-brimmed, bucket or legionnaire-style hats; protective clothing; sunglasses; and
sun protection factor (SPF) 30+ sunscreens, (which need to be reapplied every 2 hours).
Times when the UV is forecast to reach 3 and above and sun protection is
recommended are available from the Bureau of Meteorology. ‘SunSmart’ applications
for smart phones or desktops provide real-time electronic alerts on recommended
sun protection times, maximum UV levels, and information on recommended
exposure for vitamin D. They are adjustable to specific geographic locations around
Australia at www.sunsmart.com.au
Skin examination Before examining the skin, it is worth asking about any new, or changes in old 471, 484–486
lesions. Characteristics of suspicious naevi include asymmetry, border irregularity,
variable colour (including a surrounding coloured halo) and diameter >6 mm elevation
(mnemonic ‘ABCD’). Naevi that stand out from the others (‘ugly duckling’) are also
suspicious.
Nodular melanomas (with a much worse prognosis) are characteristically elevated,
firm, growing over the past month (mnemonic ‘EFG’).
Excision biopsy or referral should be considered. Examination under surface
magnification (x 10) (after appropriate training) can assist in diagnosis.
Photography aids in monitoring skin lesions by detecting changes over time, and may
reduce the excision rate of benign lesions.481, 482
Full body skin examination has been shown in general and dermatology practice, with
and without dermatoscopy, to take on average 2–3 minutes.483
Self-examination People should be advised on the specific changes that suggest melanoma, be 478, 487
encouraged to become familiar with their skin, and be alert for new or changing skin
lesions. High-risk individuals should be encouraged to perform self-examination,
especially of naevi. Those at high risk can benefit from use of self-photography.
Implementation
GPs over-excise pigmented lesions in people who are younger (age <40 years), or female, in whom they excise
relatively more benign lesions.482 GPs should be more suspicious of skin lesions in men aged over 50 years.482
9.1.2 NMSC (basal cell and squamous cell carcinoma)

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Opportunistic
case finding
Prevention advice
High-risk individuals from age 40 years should be examined for NMSC opportunistically (B). Skin self-examination
should be encouraged for high-risk individuals (B). The most common preventable cause of NMSC is UV exposure.
All people, especially children, should be advised to use protective measures when UV levels are 3 or above (A).
Use of sunscreen helps prevent squamous cell skin cancer (B).488
8th edition
Table 9.1.2.1 NMSC: identifying risk

Average risk Preventive advice (III,B) Opportunistically 489
• Those with fair to lighter than olive
skin colour, under age 40 years
without any risk factors
Increased risk Preventive advice, education Opportunistically 489

• Fair complexion, a tendency to burn to present if changes occur in
rather than tan, the presence of a skin lesion, and examination
freckles, light eye colour, light or red of skin (III,B)
hair colour
• Family history of skin cancer
• Age over 40 years
• Male sex
• Presence of multiple solar keratoses
• People with high levels of UV
exposure such as outdoor workers
High risk Preventive advice, education If initial opportunistic assessment

• Fair complexion, a tendency to burn to present if changes occur indicates the need. Every 490
rather than tan, the presence of in a skin lesion, examination 12 months, or when patient
freckles, light eye colour, light or red of skin, and advice on self- develops new skin lesion
hair colour examination (III,B) (Practice Point)
• Age over 40 years
• Previous NMSC (up to 60% grow
another in 3 years)
• Past exposure to arsenic
• Immunosuppressed (e.g. post-renal
or heart transplant)
Table 9.1.2.2 Non-melanocytic skin cancer: preventive interventions

Sun protection All people (particularly children) should be advised to adopt protective measures when 491
advice UV levels are 3 or above, especially between the hours of 10 am and 3 pm. These
measures include use of shade; broad-brimmed, bucket or legionnaire-style hats;
protective clothing; sunglasses; and SPF 30+ sunscreens (which need to be reapplied
every 2 hours).
Skin examination Skin examination should be preceded by enquiry for relevant history (e.g. of lesions 482, 486
of concern to patient or recent appearance or change in any lesions in the past few
months or years). Examination should identify skin lumps, ulcers or scaly patches,
particularly growing, scarred or inflamed lesions. Incision, shave or excision biopsy for
histology (or referral) should be considered. There are many suitable means to treat
NMSC; these include the use of surgery, cryotherapy, curettage and cytotoxic and
immune modulating creams. Examination under magnification can assist in diagnosis.
Full body skin examination has been shown to take on average 2–3 minutes in general
and dermatology practice, with and without dermatoscopy.
Self-examination People should be advised to be alert for skin lesion changes. 489
8th edition 63
9.2 Cervical cancer

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Pap test screening is recommended every 2 years for women who have ever had sex and have an intact cervix,
commencing from age 18–20 years (or up to 2 years after first having sexual intercourse, whichever is later). These
recommendations are under review because evidence is challenging some of the following recommendations,492
and may change in the National Cervical Screening Program renewal. Currently, in 2012, this is in a consultation
process. Go to www.msac.gov.au/internet/msac/publishing.nsf/Content
Australia has the lowest mortality rate and the second lowest incidence of cervical cancer in the world. The success
of the cervical screening program is dependent upon the recruitment of women: 85% of women in Australia who
develop cervical cancer have either not had a Pap test or been inadequately screened in the past 10 years. Women
aged >50 years still represent an underscreened group. The introduction of the HPV vaccine as part of the National
Immunisation Program (NIP) 2007 may reduce the future incidence of cervical cancer, but is not a substitute for a
continuing screening program.
Table 9.2.1 Cervical cancer: identifying risk

Average risk Pap test (III–2,B) Women who have ever had sex and still have
• All women who have ever an intact cervix should undergo Pap test 493
been sexually active screening.
Routine screening with Pap tests should be
carried out every 2 years for women who have
no symptoms or history suggestive of cervical
pathology (Practice Point).
All women who have ever been sexually active
should start having Pap tests between age 18
and 20 years, or 1–2 years after first having
sexual intercourse, whichever is later.
Pap tests may cease at age 70 years for
women who have had two normal Pap tests
within the last 5 years. Women over age
70 years who have never had a Pap test, or
who request a Pap test, should be screened.
Women with female sex partners are also at
risk of developing cervical cancer and should
be screened as above.
HPV vaccination (B) For maximal effect the vaccination should be 47, 494
given prior to the onset of sexual activity. It has
no modifying effect on already acquired HPV
infections. It is available as part of the NIP for
girls in year 7.
8th edition

Increased risk Pap test (Practice Point) It is important to ensure the patient always
• Persistent infection with receives the results of her test. 495, 496
high-risk HPV types Low-grade squamous intraepithelial
is necessary for the lesions (LSIL)
development of cervical • A woman with a Pap test report of possible/
cancer. Other risk factors definite LSIL should have a repeat Pap test
include: in 12 months (Practice Point). If the repeat
–– immunosuppression test at 12 months shows LSIL (definite or
–– cigarette smoking possible) the woman should be referred for
colposcopy.
–– use of combined oral
contraception >5 years. • A woman aged 30 years or more with a
Pap test report of LSIL, without a history of
negative smears in the preceding
2–3 years, should be offered either
colposcopy or a repeat Pap smear at
6 months (Practice Point).
High-grade squamous intraepithelial lesion
(HSIL)
• Refer for colposcopic assessment and
targeted biopsy where indicated.
Glandular abnormality or adenocarcinoma
• Refer for colposcopy by an experienced
gynaecologist or gynaecological oncologist.
• If the woman is symptomatic or if she has
a clinically abnormal cervix, referral for
colposcopy is recommended.
Table 9.2.2 Tests to detect cervical cancer risk

Pap test A sample of the ectocervix – using an extended tip spatula – then the endocervix, using 497
a cytobrush, provides the best method of sampling and can be used in all age groups of
women. (The cytobrush is not recommended for use during pregnancy.) The cervical
broom can be used on its own in premenopausal women if it is possible to sample from
both sides of the transformation zone. In postmenopausal women the transformation zone
tends to be higher in the endocervical canal. The cervical cells should be placed onto a
glass slide and fixed with spray within 5 seconds. If the smear is reported as technically
unsatisfactory, it should not be repeated before 6 weeks. In postmenopausal women with
atrophic changes, it may be necessary to use vaginal oestrogen for 14–21 days prior to the
test. See also Section 15: Screening tests of unproven benefit regarding evidence related to
bimanual vaginal examination.
HPV testing As a primary screening tool:
• Current national guidelines do not support the use of HPV testing as a primary 493, 498, 499
screening tool for cervical cancer.
In triage of LSIL:
• The use of HPV testing in the triage of LSIL remains under investigation and is not 493, 500–502
currently recommended by the National Cervical Cancer Screening guidelines.
In follow-up of HSIL:
• In women treated for HSIL, cervical cytology plus HPV testing should be performed 12
months post-treatment and annually thereafter until both tests are negative on two
consecutive occasions, at which point women can return to the routine cervical
screening interval.
Liquid-based Liquid-based cytology can be used as an additional test to the conventional smear but 503, 504
cytology not as a substitute. Its addition may be useful when repeating an unsatisfactory smear, or
added if requested by the woman.
8th edition 65
Implementation
Strategy
Methods of encouraging women to undergo cervical screening include invitations, reminders, education, message
framing, counselling, risk-factor assessment, procedures and economic interventions. Evidence supports the use of
invitations and, to a lesser extent, educational materials. It is likely other methods are advantageous, but the evidence
is not as strong. Further research is required.505
9.3 Breast cancer

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
It is recommended that women aged 50–69 years attend the BreastScreen Australia Program every 2 years for
screening mammograms (A).
Women should be aware that a recommendation for clinical breast examination is not possible because there is
insufficient evidence that this offers benefits to women of any age (C).
However, it is recommended that all women, whether or not they undergo mammographic screening, are aware of
how their breasts normally look and feel, and promptly report any new or unusual changes (such as a lump, nipple
changes, nipple discharge, change in skin colour, or pain in a breast) to their GP.506
Table 9.3.1 Breast cancer: identifying risk

done?
Average or only slightly higher* risk Clarify risk at www. 507
(>95% of women) nbocc.org.au/fraboc
• No confirmed family history of breast cancer Mammogram Every 2 years from
age 50–69 years‡
• One first-degree relative diagnosed with breast cancer at
age 50 years or older Breast awareness Regular (Practice
• One second-degree relative diagnosed with breast cancer (I,A) Point)
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- or second-degree relatives diagnosed with
breast cancer, at age 50 years or older, but on different
sides (i.e. on each side) of the family
As a group, risk of breast cancer up to age 75 years is
between 1:11 and 1:8.
Moderately increased risk† Clarify risk at www. 507
(<4% of the female population) nbocc.org.au/fraboc
• One first-degree relative diagnosed with breast cancer Mammogram (III,C) At least every
before the age of 50 (without the additional features of the Breast awareness 2 years from age
potentially high-risk group) 50–69 years‡
Consider referral
• Two first-degree relatives, on the same side of the family, to or consultation Annual
diagnosed with breast cancer (without the additional with a family cancer mammograms
features of the potentially high-risk group) clinic for further from age 40 may
assessment and be recommended
• Two second-degree relatives, on the same side of the
management plan if the woman has
family, diagnosed with breast cancer, at least one before
a first-degree
age 50 years (without the additional features of the
relative <age 50
potentially high-risk group)
years diagnosed
As a group, the relative risk of breast cancer up to age 75 with breast cancer
years is between 1:8 and 1:4. (Practice Point)
8th edition

done?
Potentially high risk§ Clarify risk at www. Individualised 507
(<1% of the female population) nbocc.org.au/fraboc surveillance
Advise referral to a program. This may
• Women who are at potentially high risk of ovarian cancer
cancer specialist include regular
• Two first- or second-degree relatives on one side of the clinical breast
or family cancer
family diagnosed with breast or ovarian cancer plus one examination, and
clinic for risk
or more of the following features on the same side of the annual breast
assessment, possible
family: imaging with
genetic testing and
–– additional relative(s) with breast or ovarian cancer management plan mammography,
–– breast cancer diagnosed before age 40 years MRI or ultrasound
Ongoing surveillance
–– bilateral breast cancer strategies may (Practice Point)
–– breast and ovarian cancer in the same woman include regular clinical
breast examination,
–– Ashkenazi Jewish ancestry breast imaging with
–– breast cancer in a male relative. mammography,
• One first- or second-degree relative diagnosed with breast magnetic resonance
cancer at age 45 years or younger plus another first- or imaging (MRI) or
second-degree relative on the same side of the family with ultrasound and
sarcoma (bone/soft tissue) at age 45 years or younger consideration of
ovarian cancer risk
• Member of a family in which the presence of a high-risk
(III,C)
breast cancer gene mutation has been established
See the National Breast and Ovarian Cancer Centre
guidelines at www.nbocc.org.au/fraboc for further
information.
As a group, risk of breast cancer up to age 75 years is
between 1:2 and 1:4.
* About 1.5 times the population average.
† About 1.5–3 times the population average.
‡ Population-based screening using mammography is the best early detection method available for reducing deaths from breast
cancer.508 Evidence of the benefit is strongest for women aged 50–69 years. For all women there is a chance that mammography
will either miss breast cancer (false negative) or detect a change not caused by breast cancer (false positive). The chance of a false
negative or false positive result is higher in younger women because their breast tissue is denser, making it more difficult to detect
changes.
Women aged 40–49 years are eligible for free 2-yearly screening mammograms through BreastScreen Australia, although they are
not targeted by the program. In deciding whether to attend for screening mammography, women in this age group should balance
the potential benefits and downsides for them, considering the evidence that screening mammography is less effective for women
in this age group than for older women. Generally, breasts become less dense as women get older, particularly after menopause,
which is why mammograms become more effective as women get closer to age 50 years. Mammographic screening is not
recommended for women aged <40 years because the reduced accuracy of mammography produces a high risk of false positive
and false negative results.506
Women aged ≥70 years are eligible for free 2-yearly screening mammograms through BreastScreen Australia, although they
are not targeted by the program because there is limited evidence available from randomised control trials about the benefits of
screening them.509 Women in this age group should balance the potential benefits and downsides of screening, considering their
general health and whether they have other diseases or conditions.506
§ More than 3 times the population average. Individual risk may be higher or lower if genetic test results are known.
8th edition 67
Table 9.3.2 Breast cancer: clinical breast examination and breast awareness
Other tests Comment References
Clinical breast Clinical trials in Russia and China showed that population-based screening using clinical 506
examination breast examination did not reduce the number of deaths from breast cancer. New RCTs
trials are underway in India and Egypt.
Breast In Australia, despite our fully implemented mammographic screening program, most 506
awareness breast cancers are diagnosed after the woman develops symptoms, or by her doctor.
If women are aware of the normal look and feel of their breasts, and report unusual
symptoms, breast cancer might be detected earlier.
In the past, regular ‘breast self-examination’ (women examining their own breasts) was
promoted and taught. However, this is not supported by evidence of the size or stage of
tumours at diagnosis or in the number of deaths from breast cancer. Therefore, teaching
women breast self-examination is no longer recommended (I,B).
Implementation
Strategies
A systematic review of strategies for increasing the participation of women in community breast cancer screening
found five favourable active strategies: letter of invitation, mailed educational material, letter of invitation plus phone
call, phone call, and training activities plus direct reminders for the women.510
Physical activity during leisure time and at work is associated with a reduced risk of breast cancer,511 estimated as a
20–40% reduction in both premenopausal and postmenopausal women.512
9.4 Ovarian cancer

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Not recommended as a preventive activity
Routinely screening for ovarian cancer using blood tests for cancer antigen (CA) 125, or transabdominal or
transvaginal ultrasound provides no benefit. Three large trials have been started: the United Kingdom Collaborative
Trial of Ovarian Cancer Screening will report in 2014; a European equivalent was commenced in 2005 and has not
reported yet; and the United States Prostate Lung Colorectal and Ovarian trial reported in 2011 with no benefits
from CA125 or transvaginal ultrasound screening.513
Table 9.4.1 Ovarian cancer: identifying risk

done?
Lower risk No screening 514
• Those who have used the oral contraception, or
carried a pregnancy to term (risk of about half the
population average)
Higher risk No screening 515

• Family history of ovarian cancer, especially first-degree Consider increased
relatives and more than one relative (risk of about 3 frequency of screening
times the population average) for breast and CRC
• Presence of the breast cancer susceptibility gene 1 516
(BRCA1) or breast cancer susceptibility gene 2 (BRCA2)
8th edition
9.5 Oral cancer

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
There is insufficient evidence to recommend screening by visual inspection or by other screening methods.517, 518
Table 9.5.1 Oral cancer: identifying risk

done?
Average risk Education regarding Every 2 years 519
prevention (Practice (Practice Point)
Point)
Increased risk Opportunistic Every 12 months 519, 520

• Smokers aged >50 years, heavy drinkers, patients examination of the (Practice Point)
chewing tobacco or areca/betel nut mouth and lips
(Practice Point)
• Patients exposed to excessive amounts of sunlight
(at risk of lip cancer)
Table 9.5.2 Oral cancer: preventive care

Method Technique References
Education All patients should be advised about the hazards of smoking or chewing tobacco, 519
excessive alcohol consumption and sunlight exposure
Oral examination 1. Examination of the extra oral areas – neck, lips and facial areas – looking for lumps 521
and swellings
2. Inspection of the oral cavity – buccal mucosa, gums, tongue (lateral borders and
dorsum), floor of mouth and palate (looking for white or red patches, ulceration or
induration)
9.6 Colorectal cancer(CRC)

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
High risk 10 years prior to age of onset of affected family member
Organised screening by FOBT is recommended for the asymptomatic average risk population from age 50
years every 2 years (A) until age 75 years with repeated negative findings.522, 523 Increased risk is determined by
family history; this should include determining the number of relatives affected by CRC, side of family and age at
diagnosis. DRE is not recommended as a screening tool (D), (but is important in evaluating patients who present
with symptoms such as rectal bleeding).
A GP recommendation can positively influence participation in bowel cancer screening using FOBT.524–526 Regular
FOBT can reduce CRC mortality by up to 16%.527
8th edition 69
Table 9.6.1 CRC: identifying risk

done?
Category 1: Average or slightly increased risk FOBT (I,A) Every 2 years from age 50 years 491, 522, 527,
Asymptomatic people with: (Practice Point) 528
• no personal history of bowel cancer, colorectal
adenomas or ulcerative colitis and no confirmed
family history of CRC,
or
• one first- or second-degree relative with CRC
diagnosed at age 55 years or older
Category 2: Moderately increased risk Colonoscopy Every 5 years from age 50 years, 522, 529, 530
(1–2% of the population) Sigmoidoscopy plus or at an age 10 years younger
double-contrast than the age of first diagnosis
Asymptomatic people with:
barium enema or of CRC in the family, whichever
• one first-degree relative with CRC diagnosed comes first (Practice Point)
CT colonography
before age 55 years,
(performed by
or an experienced
• two first-degree or one first- and one second- operator) acceptable
degree relative/s on the same side of the if colonoscopy is
family with CRC diagnosed at any age (without contraindicated
potentially high-risk features as in Category 3) Consider offering FOBT In intervening years
(III,B)
Category 3: High risk (relative risk of ~4–20) Refer for genetic Those at risk for: 529, 530
(<1% of the population)* screening of affected • FAP (no APC mutation
relatives defined): every 12 months from
Asymptomatic people with:
Refer to bowel cancer age 12–15 years to age 30–35
• three or more first- or second-degree relatives
specialist to plan years and every 3 years after
on the same side of the family diagnosed with
appropriate surveillance age 35 yearsII
CRC (suspected Lynch syndrome, also known as
(III,B) • Lynch syndrome: 1–2 yearly
hereditary non-polyposis CRC or HNPCC) or other
Lynch syndrome-related cancers† FAP: flexible from age 25 years or 5 years
or sigmoidoscopy earlier than the youngest
or affected member of the
• two or more first- or second-degree relatives on family (whichever is earliest).
the same side of the family diagnosed with CRC, Colonoscopy in
Aspirin 100 mg/day is effective
including any of the following high-risk features: attenuated FAP‡
prophylaxis
–– multiple CRC in the one person
–– CRC before age 50 years
–– a family member who has or had Lynch
syndrome-related cancer
or
• at least one first- or second-degree relative
with CRC, with a large number of adenomas
throughout the large bowel (suspected familial
adenomatous polyposis: FAP)
or
• somebody in the family in whom the presence of a In intervening years
high-risk mutation in the adenomatous polyposis HNPCC:
coli (APC) or one of the mismatch repair genes – colonoscopy
has been identified
Members of proven FAP§ and Lynch syndrome
Consider offering FOBT (Practice Point)
families who are shown not to carry the family
(III,B)
mutation are no longer at high risk and revert to
the average-risk group and still require population-
based screening.
8th edition
* Age of starting screening varies in high-risk groups: age 25 years for those with Lynch syndrome or 5 years earlier than the earliest
age of onset in the family.
† Lynch syndrome criteria can be found at www.ncbi.nlm.nih.gov/pubmed/14970275 531
‡ Attenuated FAP is characterised by a significant risk for colon cancer but fewer colonic polyps (average of 30), more proximally
located polyps, and diagnosis of colon cancer at a later age. Patients with 10–100 adenomas have an attenuated form of FAP,
which can be due to APC mutation (dominantly inherited) or MUTYH bi-allelic mutations (recessive). In each case the CRC risk is
high.
§ FAP is an autosomal disorder caused by a germline mutation in the APC gene. APC mutation, as manifested by the development
of CRC, approaches 100% by the age of 50 years in untreated subjects. FAP, however, accounts for less than 1% of all CRC
cases. HNPCC, also known as Lynch syndrome, is due to an inherited mutation (abnormality) in a gene that normally repairs
the body’s DNA. Both disorders have an autosomal dominant mode of transmission within families and carry a very high risk for
cancer. As the HNPCC gene mutation is present in every cell in the body, other organs can also develop cancer. In untreated
FAP, mutation carriers have a lifetime risk for CRC close to 100%. In HNPCC, their risk for colorectal or other syndrome cancers is
70–90%.522 Aspirin at 600 mg/day reduced Lynch syndrome cancer incidence by 50–68% in the CAPP2 trial.532 Follow-up of the
low-dose aspirin RCTs.533, 534 suggests low-dose aspirin (100 mg/day) also reduces cancer incidence by half. A dose–response
RCT in Lynch syndrome is open for recruitment at www.CAPP3.org
II Bi-annual (6-monthly) or annual sigmoidoscopy for APC gene carriers of diagnosed FAP (colonoscopy in attenuated FAP).
Table 9.6.2 Test to detect CRC

FOBT screening Two main types of FOBT are available: guaiac and faecal immunochemical tests. 535, 536
Immunochemical tests are preferred as they have greater sensitivity and higher uptake535
(A). Two or three serial stools should be tested, depending on the type and brand of test
being used. Follow the manufacturer’s instructions. It is essential that any positive FOBT
(including just one of the samples) is appropriately investigated by diagnostic tests (such
people being at least 12 times more likely to have CRC than those with a negative test).
With guaiac tests, even if a subject fails to follow dietary restrictions, it is dangerous to
assume that a positive result is a result of dietary non-compliance.
Implementation
Strategy
Measures to increase screening in these groups include organised approaches such as employing recall and
reminders;536, 537 recommendations by the GP for the screening;537, 538 addressing capacity issues, including
convenience;537, 538 and minimising barriers such as cost.537–539 See the RACGP green book.
The National Bowel Cancer Screening Program commenced in 2006 targeting specific age groups. GPs are critical,
not just in maximising participation, but managing participants with a positive FOBT.540, 541
Participation is underrepresented by Aboriginal and Torres Strait Islander peoples,198 who have lower survival rates
from CRC.542, 543
8th edition 71
9.7 Testicular cancer

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
There is insufficient evidence to routinely screen for testicular cancer using clinical or self-examination.544, 545 Those
performing testicular self-examination are not more likely to detect early-stage tumours or have better survival than
those who do not (C).
Table 9.7.1 Testicular cancer: identifying risk

High risk Testicular examination Opportunistically 544, 546, 547
• Those with a history of cryptorchidism (relative risk (Practice Point) (Practice Point)
above average of 3.5–17), orchidopexy, testicular
atrophy, or previous testicular cancer (relative risk
25–28)
9.8 Prostate cancer

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Screening for prostate cancer is not recommended unless:
1. the man specifically asks for it; and
2. he is fully counselled on the pros and cons.
Routine screening for prostate cancer with DRE, PSA or transabdominal ultrasound is not recommended.548–550
DRE has poor ability to detect prostate disease.551 Yet some cancers missed by PSA testing alone are detected by
DRE,551 which is why those recommending screening advocate DRE as well as PSA.
The recommendation is contentious. Two large RCTs552, 553 found none or marginal benefit. However, analysis of
the data from one centre contributing to one of these554 showed an increased survival from prostate cancer (but
not mortality from any cause) beyond 10 years. Two recent systematic reviews concluded that screening is not
effective.555, 556
Even if we were to conclude there was a survival benefit (from current or future trial data), this survival would need to
be balanced against the harms of cancer overdetection and treatment.
GPs need not raise this issue, but if men ask about prostate screening they need to be fully informed of the potential
benefits, risks and uncertainties of prostate cancer testing.556 When a patient chooses screening, both PSA and
DRE should be performed.
8th edition
Table 9.8.1 Prostate cancer: identifying risk

done?
Average risk Respond to requests On demand 557–559
• The risk of developing prostate cancer increases with age for screening by (Practice Point)
and positive family history. However, because prostate informing patients of
cancer is normally slow growing, men older than age 75 risks and benefits of
years or with a life expectancy of less than 10 years are at screening (I,A)
reduced threat of dying from a diagnosis of prostate cancer.
• Men with uncomplicated lower urinary tract symptoms

(LUTS) do not appear to have an increased risk of prostate
cancer. The most common cause of LUTS is benign
prostate enlargement. Early prostate cancer often does not
have symptoms.
High risk Respond to requests On demand 558–560

• Men with one or more first-degree relatives diagnosed for screening by (Practice Point)
under age 65 years informing patients of
risks and benefits of
• Men with a first-degree relative with familial breast cancer
screening (Practice
(BRCA1 or BRCA2)
Point)
Table 9.8.2 Screening for prostate cancer

Not recommended Justification References
PSA screening The most common adverse effect of radical prostatectomy is erectile
dysfunction, which affects most men (it is less common in younger men, those 548–550, 555,
with a lower PSA, and when nerve-sparing surgical techniques are used). 561
Other complications are common as well, including urinary incontinence (which 562
is very common in the months after treatment, but returns to normal in 75–90%
men after 2 years, depending on treatment type), and to a lesser extent, urinary
irritation and bowel symptoms. General feelings of ‘vitality’ are lost in about
10% of men.
Both suicide and CVD increase enormously (8 and 11 times more, respectively) 563
in the week after men are given their diagnosis of prostate cancer.
Even diagnostic procedures following positive screening are harmful, with
Australian data showing that the risk of life-threatening sepsis needing intensive 564
care admission is not uncommon after biopsy.
Despite large trials, their meta-analysis suggests that prostate cancer screening
does not save lives. 555, 556
Implementation
Strategy
Patients who request testing should be informed about the risks and benefits of tests for prostate cancer, and
assisted to make their own decision.565 Written material, particularly decision aids, may be useful for this purpose:
see the RACGP green book and a free book providing a balanced presentation of facts566 at http://ses.library.usyd.
edu.au/bitstream/2123/6835/3/Let-sleeping-dogs-lie.pdf
Responding to the patient’s concerns and fulfilling medico-legal responsibilities are considerations in discussion with
patients.
8th edition 73
10. Psychosocial
GPs have an important role in the detection and management of mental illness, especially high-prevalence
conditions such as depression and anxiety. In the most recent Australian National Survey of Mental Health and
Wellbeing, the prevalence of any lifetime mental disorder was 45.5%, with a 12-month prevalence of 14.4% for
anxiety disorders and 6.2% for affective disorders.567 Patients, especially women, who experience underlying family
violence, may present with depression and anxiety.568
Health inequity
The national health survey identified that ‘the proportion of people who reported having mental problems increased as
levels of socioeconomic disadvantage increased. In 2007–08, 16% of people living in the most disadvantaged areas
had a mental or behavioural problem, compared with 11% of people living in the least disadvantaged areas’.569 The
likelihood of depression among low SES persons is almost double that of high SES persons (most marked for persistent
depression).570 Anxiety and affective disorders are more common in unemployed people and they are less likely to seek
help from their GP.571, 572 In patients with chronic disease, lower educational level and unemployment are predictive
of depression.573 Differences in the way depression is understood and presented may create barriers to accessing
effective depression care for patients from non-English speaking and culturally diverse backgrounds.574 Practices in
disadvantaged areas have a higher prevalence of depression to identify and manage in their patients.575
Being aware of this is important in the opportunistic screening for depression. Other general strategies to increase
screening in this group are outlined above and are discussed in the RACGP green book.
Suicide and attempted suicide are consistently associated with markers of SES disadvantage,576–579 including low SES,
limited educational achievement and homelessness,580–582 and are also more prevalent in Aboriginal and Torres Strait
Islander peoples.583 Refer to the National Guide to a Preventive Health Assessment for Aboriginal and Torres Strait
Islander people, second edition.
Postpartum depression is more common in women from culturally and linguistically diverse backgrounds and they are
less likely to receive help for this.584
10.1 Depression
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79+
While there is evidence that depression screening instruments have reasonable sensitivity and specificity, the
evidence for improved health outcomes and cost-effectiveness of screening for depression in primary care remains
unclear. There is evidence for routine screening for depression in the general adult population in the context of
staff-assisted support to the GP in providing depression care, case management and coordination (e.g. via practice
nurses) (B).585 There is insufficient evidence to recommend routine screening in adults or adolescents where this
level of feedback and management is not available (C).585 There is insufficient evidence to recommend screening in
children.586 Clinicians should maintain a high level of awareness for depressive symptoms in patients at high risk for
depression.
8th edition
Table 10.1.1 Depression: identifying risk

Average risk Be alert to possible Opportunistically 585
• Adult population aged 18 years and older depression, but do not
routinely screen unless staff-
assisted depression care
supports are in place (C).
Adolescents The benefits of screening At every encounter 586, 588

• Aged 12–18 years, particularly with: have not been established,
particularly where access to
–– parental depression
effective treatment and follow-
–– comorbid mental health or chronic up is not available.
medical conditions
Be alert for signs of depression
–– experienced a major negative life event in this age group (B).
Consider use of HEADSS 112, 587
assessment tool (see Section
3: Preventive activities in
children and young people)
Increased risk Recurrent screening may Opportunistically 585

• Family history of depression be more useful in people
deemed to be at higher risk of
• Other psychiatric disorders, including
depression (B)
substance misuse
• Chronic medical conditions
Maintain a high level of clinical
• Unemployment
awareness of those at high risk
• Low SES of depression.
• Older adults with significant life events
(e.g. illness, cognitive decline, bereavement
or institutional placement)
• All family members who have experienced
family violence
• Experience of child abuse
Table 10.1.2 Test to detect depression

Question Asking two simple questions may be as effective as longer instruments: 589
regarding ‘Over the past 2 weeks, have you felt down, depressed or hopeless?’ 590
mood and
and
anhedonia
‘Over the past 2 weeks, have you felt little interest or pleasure in doing things?’
Asking a patient if help is needed in addition to these two screening questions improves the
specificity of a GP diagnosis of depression (IV)
In adolescents, consider use of HEADSS assessment tool (see Section 3: Preventive
activities in children and young people).
In women in the perinatal period, the Edinburgh Postnatal Depression Scale (also known 591
as the EPDS) can be used to detect women requiring further assessment of possible
major depression (B in the postnatal period) at www.blackdoginstitute.org.au/docs/
CliniciansdownloadableEdinburgh.pdf or www.beyondblue.org.au/index.aspx?link_
id=103.885 112, 587
See also Section 10.3: Identification of intimate partner violence, as depression is a common
reason for presentation in those experiencing violence.
8th edition 75
10.2 Suicide
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Lack of evidence for routine screening with a screening instrument, but be alert for higher-risk individuals
and the possibility of suicide in those at higher risk
There is a lack of evidence for the routine screening of patients using a screening instrument (C). GPs should
be alert for higher-risk individuals and the possibility of suicide in those patients who are at higher risk. There is
evidence that detecting and treating depression has a role in suicide prevention.592, 593 For example, incidence of
suicide has decreased in older men and women in association with exposure to antidepressants.594, 595
Table 10.2.1 Suicide: identifying risk

Who is at risk? What should How often? References
be done?
Average risk No routine n/a 596–598
• General population screening for
suicide (III,C)
Increased risk Evaluate risk for When risk factors 52, 592, 595,
Attempted suicide is a higher risk in the following. suicide (III,C) present and with all 596
people aged 14–24
• Mental illness, especially mood disorders, alcohol and drug
years
abuse
• Previous suicide attempts or deliberate self-harm
• Male
• Young people and older people
• Those with a recent loss or other adverse event
• Patients with a family history of attempted or completed
suicide
• Aboriginal and Torres Strait Islander peoples
• Widowed
• Living alone or in prison
• Chronic and terminal medical illness.
Table 10.2.2 Tests to detect suicide risk

Evaluate the risk of suicide Assessment of risk involves enquiring into the extent of the person’s suicidal 112
in the presence of risk thinking and intent, including:
factors • suicidal thinking – If suicidal thinking is present, how frequent and
persistent is it?
• plan – If the person has a plan, how detailed and realistic is it?
• lethality – What method has the person chosen, and how lethal is it?
• means – Does the person have the means to carry out the method?
• past history – Has the person ever planned or attempted suicide?
• suicide of family member or peer – Has someone close to the person
attempted or completed suicide?
Consideration should also be given to:
• risk and protective factors
• mental state – hopelessness, despair, psychosis, agitation, shame, anger,
guilt, impulsivity
• substance use – current misuse of alcohol or other drugs
• strengths and supports – availability, willingness and capacity of supports.
Patients with suicidal ideation should be questioned regarding preparatory
actions (e.g. obtaining a weapon, making a plan, putting affairs in order, giving
away prized possessions, preparing a suicide note).
8th edition

Screening for psychological The HEADSS tool has questions that can assist in assessing suicide risk, for 587
distress with young people example:
• 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, e.g. unsafe sex)?
• 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?
• On a scale of 1 to 10, with 1 being the worst you feel and 10 being really
great and positive, how would you rate your mood today?
10.3 Identification of intimate partner violence

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Consider asking all pregnant adult and adolescent women about partner violence during antenatal care.599
There is insufficient evidence for screening the general population; however, there should be a low threshold for
asking about abuse, particularly when the GP suspects underlying psychosocial problems.599 Training GPs to
identify violence has resulted in increased identification and referral to services.600 There is some evidence for the
effectiveness of interventions in clinical practice to reduce partner violence.
Table 10.3.1 Intimate partner violence: identifying risk

done?
Increased risk Ask about partner Opportunistically 599
• Pregnant adult and adolescent women violence
• Women with:
–– symptoms of mental ill-health Ask about
relationship and
–– chronic unexplained physical symptoms
any abusive
–– unexplained injuries or controlling
–– frequent attendance behaviours
• Men who:
–– ask for help with anger
–– have marital problems
–– are ‘wife mandated’ to change their behaviour
–– have alcohol or other substance abuse problems
–– were abused or witnessed intimate partner violence as a
child
8th edition 77
Table 10.3.2 Tests to detect intimate partner violence

Ask about Victimised women stress the importance of a trusting patient–doctor relationship, 601
partner confidentiality, respectful and non-judgemental attitudes to achieving disclosure as well as
violence acceptance of non-disclosure and a supportive response. It is crucial for safety reasons
that any questions are asked privately, when the patient is alone – not when another family
member, adult or child over the age of 2 years is present. It is a clinician’s responsibility to ask
and support women regardless of their response. Asking about abuse may ‘plant a seed’ for
later action.
The collaborative group believed that GPs should ask women who are ‘symptomatic’ (e.g.
symptoms of mental ill-health, chronic unexplained, physical symptoms, unexplained injuries,
frequent attendance).
Questions and statements to make if you suspect domestic violence 599
• Has your partner ever physically threatened or hurt you?
• Is there a lot of tension in your relationship? How do you resolve arguments?
• Sometimes partners react strongly in arguments and use physical force. Is this happening
to you?
• Are you afraid of your partner?
• Violence is very common in the home. I ask a lot of my patients about abuse because
nobody should have to live in fear of their partners.
8th edition
11. Oral hygiene
Age <2 2–3 4–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 ≥ 65
Good oral hygiene helps to prevent dental caries and gingivitis and improves oral health. There is evidence that use
of fluoride in water, or topically, reduces caries in children.602
Table 11.1 Oral hygiene: identifying risk
Increased risk Examination of the mouth At least every 12 months 52
• Aboriginal and Torres Strait Islander peoples (IV,C) (More frequent dental check-
• Rural and remote populations Education regarding ups as determined by dentist) 491
prevention (I,B)
• Migrant groups (especially refugees)
Recommendation of 603
• Lower socioeconomic groups with difficulty
professional or home
accessing dental care
application of topical fluoride
• People with reduced saliva flow pastes, gels or mouth rinses
(e.g. head and neck radiation therapy, (I,A)
Sjögren syndrome, multiple drug therapy
including psychotropic medications)
Table 11.2 Oral hygiene: preventive interventions

Education • Advise about the hazards of snacks and drinks that contain high levels of carbohydrate and 52, 491, 602
acid, especially between meals.
• Advise against the use of baby bottles with any fluid apart from water at night.
• Advise patients to brush teeth twice daily with fluoride toothpaste. A pea-sized amount of low- 604, 605
fluoride toothpaste should be used before age 6 years. Encourage to spit not rinse.
• Encourage home use of high-fluoride toothpastes, gels or mouth rinses for those at high risk.
• Advise the use of sugar-free chewing gum for saliva stimulation. 606
• Advise the use of mouthguards for contact sports. 607
• Recommend regular dental check-ups.
Additional advice can be obtained from the findings of a national consensus workshop 608
conducted in 2011.
Oral • Inspect mouth for dental caries, stained, worn or broken teeth and inflamed or swollen gums.
examination • Xerostomia may present as dry and reddened gums and increased caries rate particularly
on root surfaces.
• ‘Lift the lip’ of children for early identification of oral problems (see also Section 3: Preventive 94, 95
activities in children and young people).
Fluoridation • Water fluoridation is beneficial at reducing dental caries. 602
• Approximately 76% of Australians now drink fluoridated water. Details regarding fluoride
levels in Australian water supplies and recommended dosages of fluoride are provided at
www.nhmrc.gov.au/_files_nhmrc/publications/attachments/eh41_1.pdf
Implementation
Health inequity
Oral disease is more prevalent among low socioeconomic groups. Significant financial barriers to accessing dental
care remain in Australia. People on low incomes are more likely to delay dental visits and less likely to receive
appropriate dental care. Private dental insurance is associated with higher rates of dental care, but insurance is less
common in low income groups or those in regional or remote location. People who hold healthcare cards are less
likely to receive preventive dental care and more likely to receive extractions when visiting the dentist.609, 610
8th edition 79
12. Glaucoma
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
The glaucomas are a group of relatively common optic neuropathies, in which there is pathological loss of retinal
ganglion cells, progressive loss of sight and associated alteration in the retinal nerve fibre layer and optic nerve head.
Evidence supports screening people at higher risk for glaucoma (A). GPs have an important role in identifying
those at increased risk for glaucoma and referring them for testing. There is no consensus on the recommended
frequency of screening for at-risk groups.611, 612
Table 12.1 Glaucoma: identifying risk

Increased risk Refer for ocular examination No consensus on 611, 612
• Family history of glaucoma (first-degree 5–10 years earlier than the age frequency
relatives) of onset of glaucoma in the
affected relative (A).
• Caucasian and Asian patients aged
≥50 years
• African descent aged ≥40 years
Higher risk Refer for examination 611, 612

• Patients aged >50 years with: of the optic nerve head
(ophthalmoscopy),
–– diabetes
measurement of intraocular
–– myopia pressure (tonometry) and
–– long-term steroid use assessment of visual fields
–– migraine and peripheral vasospasm (perimetry).*
–– abnormal BP
–– history of eye trauma
* This may be by ophthalmologist or optometrist.
Table 12.2 Glaucoma: preventive interventions

Patient education Educate patients about glaucoma and alert them to associated 611, 612
risk factors, with advice to attend regular full comprehensive eye
examinations.
Tonometry Schiotz tonometry has poor sensitivity and specificity for early
detection of glaucoma. Tonometry alone is an inadequate screening
tool, as it overestimates the prevalence of glaucoma.
Perimetry (visual fields) Not advisable in general practice as only automated perimetry is
sensitive for detecting loss of visual field due to glaucoma.
Assessment of eye structure Indirect ophthalmoscopy performed with a slit lamp is the examination 611, 612
(ophthalmoscopy) of choice.
8th edition
13. Urinary incontinence

Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
No evidence for screening general population
There is no evidence for screening in the general population. Case finding in those at higher risk (B).
Within the general population, up to 19% of children, 13% of men and 37% of women may be affected by some
form of urinary incontinence.613 While urinary incontinence is most common in women and increases with age,
bedwetting (enuresis) is common in children and 5.5% of children also report daytime wetting.614 In men, lower
urinary tract symptoms, including urinary incontinence, is associated with surgical or radiation treatment for prostate
cancer.615 Primary care professionals are in a position to take a more proactive approach to incontinence treatment
by screening for urinary symptoms in at-risk groups during routine appointments. There remains considerable
health decrement due to urinary incontinence in those not receiving help in a population readily accessible to
primary care services.616
Table 13.1 Urinary incontinence: identifying risk

Average risk There is no evidence to support n/a
screening (IV)
Higher risk Case finding (IV,B) Every 12 months 613

• Perinatal and postnatal women Ask about the occurrence of urinary
• Younger women who have had children incontinence
• Women who are overweight
• Men following treatment for prostate cancer
• People with respiratory conditions, diabetes, In residential aged care facilities,
stroke, heart conditions, recent surgery or residents are automatically
neurological disorders assessed
• Frail elderly people or long-term care
residents
8th edition 81
Table 13.2 Urinary incontinence: preventive interventions

Case finding Ask probing questions such as ‘Other people with … (state conditions of higher risk here) 617
… have had problems with bladder control. Have you had any problems with leaking
urine?’
Simple patient survey assessment tools have been shown to be valid and reliable (A). 618
The three incontinence questions questionnaire (Appendix 6) is a simple, quick and non-
invasive test with acceptable accuracy for classifying urge and stress incontinence and
may be appropriate for use in primary care settings (A).
Patients with urinary incontinence should be assessed to determine the diagnostic
category as well as underlying aetiology. This can usually be determined on the basis
of history, physical examination and urinary dipstick and culture if indicated. A post-void
residual may be required in the assessment of possible retention/overflow.
Assessment There are four common types of incontinence:

• Stress incontinence is the leaking of urine, which may occur during exercise,
coughing, sneezing, laughing, walking, lifting or playing sport. This is more common in
women, although it also occurs in men, especially after prostate surgery. Pregnancy,
childbirth and menopause are the main contributors.
• Urge incontinence is a sudden and strong need to urinate. It is often associated with 619
frequency and nocturia, and is often due to having an over-active or unstable bladder,
neurological conditions, constipation, enlarged prostate or history of poor bladder
habits.
• Mixed incontinence is a combination of both stress and urge incontinence and is
most common in older women.
• Overflow incontinence is a result of bladder outflow obstruction or injury. Symptoms
may be confused with stress incontinence.
Because treatments differ, urge incontinence should be distinguished from stress
incontinence (A). The patient’s diagnostic category can be reliably determined using the
three incontinence questions questionnaire (Appendix 6).
The Continence Foundation of Australia Helpline (telephone 1800 33 00 66) is available
5 days a week and is staffed by qualified continence advisers. Referral information is
available regarding physiotherapy, nurse continence advisors and residual urine testing.
8th edition
14. Osteoporosis
Age 0–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–79 ≥80
Women
Men
Review of fracture risk factors for women aged over 45 years and men aged over 50 years is recommended (C).
Those with increased risk should have bone density assessed (A).
Osteoporosis is a disease characterised by low bone mass and micro-architectural deterioration of bone tissue,
leading to bone fragility and increased fracture risk.620 It is diagnosed on the presence of a fragility fracture (fracture
from the equivalent of a fall from standing height or less, or a fracture that under normal circumstances would not
be expected in a healthy young man or woman). For epidemiological and clinical purposes, osteoporosis is defined
by BMD as a T-score of ≤–2.5. However, age, lifestyle factors, family history and some medications and diseases
all contribute to bone loss and increased risk of fragility fractures. Thus, the goal of prevention and treatment is to
reduce a person’s overall fracture risk (not just bone density maintenance).
Methods to estimate absolute fracture risk for osteoporotic fractures are available at:
• www.shef.ac.uk/FRAX
• garvan.org.au/promotions/bone-fracture-risk/calculator/
As bone densitometry is part of these estimates, BMD should be considered as part of the overall fracture risk
assessment (D). Risk estimation is imperfect, but the calculator’s predictive performance is similar to absolute
cardiovascular risk calculators.621 Risk factors (e.g. falls, glucocorticoid use, etc.) not included in one or other risk
algorithm require clinical judgement to modify the risk estimate.
To date, there are no RCTs directly evaluating screening effectiveness, harms and intervals, whether screening is
performed by bone density screening by dual-energy X-ray absorptiometry (DXA) or by estimating absolute fracture
risk. The place of absolute fracture risk assessment in the prevention and management of osteoporosis requires
further clarification as its effectiveness is yet to be tested.
8th edition 83
Table 14.1 Osteoporosis: identifying risk

Average risk Assessment for risk factors Every 12 months 620, 621
• Postmenopausal women (aged 45 years or older) (II,C) (Practice Point)
• Men aged 50 years or older Preventive advice (II,C)
Increased risk Bone mineral densitometry and At presentation 622, 623

• Age >60 years for men and >50 years for women management of risk factors and no more than
plus any of: (II,A) every 2 years.
Investigate for causes of Repeat when it is
–– family history of fragility fracture
secondary osteoporosis likely to change
–– smoking management (II,C)
if indicated by history,
–– high alcohol intake (>2–4 standard drinks per examination findings or BMD Where there is
day for men, less for women) result (Practice Point) a specific bone
–– vitamin D deficiency <60 nmol (screening for mineral wasting
vitamin D not indicated just for risk assessment) condition or
–– low body weight (BMI <20) medication,
consider more
–– recurrent falls frequent repeat
–– low levels of physical activity of DXA if likely to
–– immobility (to the extent that person cannot change treatment
leave their home or cannot do any housework) (Practice Point)
• Medical conditions and medications that may
cause secondary osteoporosis:
–– endocrine (e.g. hypogonadism, Cushing
syndrome, hyperparathyroidism,
hyperthyroidism)
–– inflammatory conditions (e.g. rheumatoid
arthritis)
–– malabsorption (e.g. coeliac)
–– CKD, chronic liver disease
–– drugs, especially corticosteroids (e.g. 7.5 mg x
3 months) used for immunosuppression
including as part of chronic anti-rejection therapy
in organ or bone marrow transplant, anti-
epileptic, aromatase inhibitors, anti-androgen,
excessive thyroxine, possibly selective serotonin
reuptake inhibitors (also known as SSRIs)
High risk of further fracture BMD and management of risk DXA at presentation 620
• Patients aged over 45 years who sustain a low factors (II,A) and no more than
trauma fracture Investigate for causes of every 2 years (II,B)
• Postmenopausal women, and men with a secondary osteoporosis Repeat only when
suspected vertebral fracture (loss of height >3 cm, if indicated by history, it is likely to change
kyphosis, back pain) examination findings or BMD management
result (Practice Point) (Practice Point)
Recommend that such Where there is
individuals are initiated on a specific bone
effective anti-osteoporosis mineral wasting
therapy unless there are condition or
specific contraindications medication,
consider more
frequent repeat of
DXA (Practice Point)
8th edition
Table 14.2 Osteoporosis: preventive interventions

Assessment of Take a thorough history, paying particular attention to the risk factors above plus:
risk factors • vertebral deformity (if within 5–10 years, this is equivalent risk as any other fragility
fracture)
• loss of height (>3 cm) and/or thoracic kyphosis (consider lateral spine X-ray for
vertebral deformity)
• premature menopause
• anorexia nervosa or amenorrhea for greater than 12 months before age 45 years
Preventive • Ensure adequate daily calcium intake: dietary calcium ((A) for prevention of bone loss,
actions (C) for fracture) 1200 mg/day. Exercise caution with supplements.*
• Encourage healthy lifestyle (e.g. smoking cessation and limiting alcohol and caffeine
intake) (D).
• Education and psychosocial support for risk factor modification (Practice Point)
• Falls reduction strategies: for fracture risk reduction (Practice Point)
• Encourage exercise: for prevention of bone loss (A) and fracture risk reduction
(Practice Point).
• Advise on safe sun exposure levels as a source of vitamin D (II,C).†
• Discuss absolute risk of fracture (Practice Point)
Bone mineral BMD should be measured by DXA scanning performed on two sites, preferably antero- 624
densitometry posterior spine and hip. Without bone-losing medical conditions (e.g. steroid use), it is
(BMD) unlikely to change significantly in less than 2 years (II,B) and DXA should generally be
repeated only when patient is at risk of reaching treatment thresholds (average decrease
in T-score is usually approx 0.1/year if no specific bone-losing medical conditions)
(Practice Point). Rate of bone loss tends to be slower in early older age (60+) than in
later old age (80+), and slower in men than women.
* Controversial level II evidence of increased risk of cardiovascular events with calcium supplements in postmenopausal women, not
seen in dietary studies.625–627
† Population screening for vitamin D deficiency is not recommended, but targeted testing of people who are at risk of osteoporosis
and who are at high risk of vitamin D deficiency should be considered. Vitamin D supplements could be considered in deficient
individuals if increasing sun exposure is contraindicated or not feasible or if deficiency is more than mild (i.e. <25 nmol/L) and so is
less likely to be corrected by safe sun exposure628 (Practice Point).
Other tests for bone density

A number of other X-ray and ultrasound tests have been shown to predict fractures, although not as well as DXA.
Moreover, intervention trials have been based on cases identified through DXA assessment, so their results cannot
readily be applied to individuals identified by other means.620, 621
Implementation
Several Australian studies have shown an evidence–practice gap, where the majority of people with a fragility fracture
tend to have their fracture treated, but not the underlying osteoporosis.629, 630 Those with a previous fragility fracture
have a very high risk of further fracture, and have greatest benefit from specific anti-osteoporosis treatment. Fracture
risk reductions with optimal therapy are substantial and treatment according to current guidelines is recommended
unless absolutely contraindicated. Optimal treatment includes ensuring adequate calcium intake and correcting
vitamin D deficiency.
There are inequities in the use of BMD measurement with relative underutilisation in people from rural and remote
locations and men.631
8th edition 85
15. Screening tests of unproven benefit
The following are not recommended as screening tests in low-risk general practice populations. These tests may
have value as diagnostic tests or as tests to monitor disease progression.
Table 15.1 Screening tests not recommended in low-risk general practice populations
Screening test Condition Reason not to use References for
further reading
Genetic profiling Genetic Limited evidence on the balance of benefits and harms, ethical 632, 633
disorders issues and uncertain utility
Vascular
Cardiac CT CHD No RCT evidence. RCTs of therapy show no effect on 634–636
coronary artery progression. May be of benefit in those at
intermediate risk of CHD
Serum homocysteine CHD Value as a risk factor for CHD is uncertain and published RCTs 636–638
show no evidence of benefit by lowering levels
Exercise ECG CHD Low yield and high false positive rate given low prevalence in 636, 639
asymptomatic population
High sensitivity CVD Some evidence of benefit (i.e. reduction in CRP linked with 636, 639–643
C-reactive protein reduction in major CVD events in one study, but not currently
(CRP) recommended as a screening test for CVD)
Ankle:brachial index Peripheral Longitudinal studies showing increased risk of clinical CVD if 640, 644, 645
(ABI) vascular low ABI, but there is variable reliability and low sensitivity of
disease assessment and no published RCT evidence showing benefit
of screening
Cancer
MRI Breast cancer Ongoing surveillance strategies for women at high risk of 506, 507, 646–648
breast cancer may include imaging with MRI. A Medicare
rebate is available for MRI scans for asymptomatic women
under 50 years at high risk of breast cancer
CA125/transvaginal Ovarian cancer There is no evidence to support the use of any test – including 649, 650
ultrasound pelvic examination, CA125, or other biomarkers, ultrasound
(including transvaginal ultrasound), or combination of tests –
for routine population-based screening for ovarian cancer.
CA125 is limited by poor sensitivity in early-stage disease and
low specificity. The specificity of transvaginal ultrasound is
low. The low prevalence of ovarian cancer means that even
screening tests that have very high sensitivity and specificity
have a low positive predictive value for disease detection
Virtual colonoscopy/ CRC Good sensitivity for lesions larger than 10 mm, but no 523, 651–655
CT colonography evidence of reduction of CRC incidence or mortality. Not
currently recommended
Whole body CT or Cancer Whole body imaging has not been shown to improve 656–661
MRI quality of life and/or decrease mortality. It is associated with
additional radiation exposure and a high number of false
positive results. There are no RCTs of whole body imaging to
detect cancer or CVD
8th edition
Screening test Condition Reason not to use References

Lung disease
Spirometry Chronic Assessment is unreliable and screening for COPD using 662–665
obstructive spirometry has no net benefit.
pulmonary
disease (COPD)
Endocrine
Thyroid function tests Thyroid Despite the relatively high incidence of subclinical hypothyroidism 666–669
dysfunction in older women (up to 17%), there is a lack of convincing data
from controlled trials that early treatment reduces lipid levels,
symptoms or the risk for CVD in patients with mild thyroid
dysfunction detected by screening.
Chronic disease prevention
Vitamin D Vitamin D High prevalence, variability in assessment and lack of 670–674
deficiency rigorous evidence of benefit of screening
Infection
MSU culture Asymptomatic Identifying and treating non-pregnant adults with 675
bacteriuria asymptomatic bacteriuria does not improve outcomes and
(elderly) may increase antibiotic resistance
Table 15.2 Screening tests of indeterminate value

Screening test Condition Reason not to use References
Women
Vitamin D Pregnancy Moderate prevalence and associated morbidity, but no 676–679
RCT evidence of benefit. There is debate about what is an
adequate level of vitamin D. High-risk groups for vitamin D
deficiency may benefit from screening and supplementation.
Vascular
Ultrasound Abdominal USPSTF recommend screening, but low yield as declining 680–682
aneurysm incidence and ethical issues of screening only one subgroup
(male smokers), and cost-effectiveness not clear
B-type natriuretic Congestive The evidence for screening for heart failure using BNP is mixed 683–686
peptide (BNP) cardiac failure despite its sensitivity and prognostic significance. It may be
useful in excluding the condition in suspected heart failure
Cancer
Chest CT Lung cancer Good sensitivity but poor specificity; one RCT underway in 687–689
smokers has preliminary results showing a 20% reduction
in mortality in the CT arm. Low-dose CT screening may
benefit individuals at an increased risk for lung cancer, but
uncertainty exists about the potential harms of screening
and the generalisability of results. Approximately 20% of
individuals in each round of screening had positive results
requiring some degree of follow-up, while approximately 1%
had lung cancer.
Positron emission Lung cancer Good sensitivity and specificity, but no RCT results 688
tomography –
computed tomography
(or PET CT scan)
Elderly
Visual acuity Visual No benefits of screening, even though impaired visual acuity 165, 690
impairment is common and effective treatments are available
8th edition 87
References
1. Britt H, Miller GC, Charles J, Henderson J, Bayram C, Pan Y, et al. General practice activity in Australia 2009–10. General
practice series no. 27. Cat. no. GEP 27. Canberra: AIHW. 2010
2. World Health Organization. Preventing chronic diseases. A vital investment. Geneva: WHO, 2005 [accessed 2012 June].
Available at www.who.int/chp/chronic_disease_report/full_report.pdf
3. Council of Australian Governments. Australian better health initiative: promoting good health, prevention and early intervention.
Canberra: COAG, 2007 [accessed 2012 June]. Available at www.health.gov.au/internet/main/publishing.nsf/Content/8F84093D
1e4FA53FcA25711100261015/$File/factsheet3.pdf
4. National Preventative Health Taskforce. Australia: the healthiest country by 2020. Discussion paper. Canberra: Commonwealth
of Australia, 2008
5. Commonwealth of Australia. Towards a National Primary Health Care Strategy: a discussion paper from the Australian
Government. Canberra: Department of Health and Ageing, 2008 [accessed 2012 June]. Available at www.health.gov.au/
internet/main/publishing.nsf/Content/D66FEE14F736A789CA2574E3001783C0/$File/DiscussionPaper.pdf
6. Australian Institute of Health and Welfare. Australia’s health 2012. Australia’s health series no. 13. Cat. no. AUS 156. Canberra:
AIHW, 2012
7. Vos T, Carter R, Barendregt J, Mihalopoulos C, Veerman JL, Magnus A, et al. Assessing cost-effectiveness in prevention (ACE–
Prevention): final report. Brisbane: University of Queensland, Melbourne: Deakin University, 2010
8. Mazza D, Shand LK, Warren N, Keleher H, Browning CJ, Bruce EJ. General practice and preventive health care: a view through
the eyes of community members. Med J Aust 2011;195(4):180–3
9. Australian Institute of Health and Welfare. Chronic diseases and associated risk factors in Australia. Canberra: AIHW, 2006
10. Morrison AS. Screening 2nd edn. In: Rothman KJ, Greenland S, eds. Modern epidemiology. Philadelphia: Lippincott-Raven,
1998
11. Wilson J, Jungner Y. Principles and practices of screening for disease. Geneva: WHO, 1968
12. World Health Organization. Screening for various cancers. Geneva: WHO, 2008. Available at www.who.int/cancer/detection/
variouscancer/en/
13. UK National Health Services. What is screening? London: UK National Screening Committee, 2004 [accessed 2012 June].
Available at www.nsc.nhs.uk/whatscreening/whatscreen_ind.htm
14. Royal Australian College of General Practitioners National Standing Committee Quality Care. Smoking, nutrition, alcohol
and physical activity (SNAP). A population health guide to behavioural risk factors in general practice. Melbourne: RACGP,
2004 [accessed 2012 May]. Available at www.racgp.org.au/Content/NavigationMenu/ClinicalResources/RACGPGuidelines/
SNAPapopulationhealthguidetobehaviouralriskfactorsingeneralpractice/SNAPguide2004.pdf
15. Aldrich R, Kemp L, Williams JS, Harris E, Simpson S, Wilson A, et al. Using socioeconomic evidence in clinical practice
guidelines. BMJ 2003;327(7426):1283–5
16. Bouleware LE, Barnes GJ, Wilson RF, Phillips K, Maynor K, Hwang C, et al. Systematic review: the value of the periodic health
evaluation. Ann Intern Med 2007;146:289–300
17. Dolan M, Simons-Morton D, Ramirez G, Frankowski R, Green L, Mains D. A meta-analysis of trials evaluating patient education
and counseling for three groups of preventive health behaviours. Patient Education and Counseling, 1997;32(3):157–73.
18. Wallace LS, Rogers ES, Roskos SE, Holiday DB, Weiss BD. Brief report: screening items to identify patients with limited health
literacy skills. J Gen Intern Med 2006;21(8):874–7
19. Trachtenberg F, Dugan E, Hall M. How patients’ trust relates to their involvement in medical care. J Fam Pract 2005;54(4):344–
52
20. Ellis S, Speroff T, Dittus R, Brown A, Pichert J, Elasy T. Diabetes patient education: a meta-analysis and meta-regression. Pat
Educ Couns 2004;52(1):97–105
21. Lewin S, Skea Z, Entwistle V, Zwarenstein M, Dick J. Interventions for providers to promote a patient-centred approach in
clinical consultations. Cochrane Database Syst Rev 2002;4:CD003267
22. Mead N, Bower P. Patient-centred consultations and outcomes in primary care. Patient Education and Counseling
2002;48(1):51–61
8th edition
23. Rao J, Weinberger M, Kroenke K. Visit-specific expectations and patient-centred outcomes: literature review. Arch Fam Med
2000;9(10):1149–55
24. Littell J, Girvin H. Stages of change: a critique. Behav Modif 2002;26(2):223–73
25. Schauffler H, Rodriguez T, Milstein A. Health education and patient satisfaction. J Fam Pract 1996;42(1):62–8
26. Ley P, ed. Patients’ understanding and recall in clinical communication failure. London: Academic Press, 1983
27. Steptoe A, Kerry S, Rink E, Hilton S. The impact of behavioral counseling on stage of change in fat intake, physical activity,
and cigarette smoking in adults at increased risk of coronary heart disease. Am J Public Health 2001;91(2):265–9
28. Branch L, Rabiner D. Rediscovering the patient’s role in receiving health promotion services. Med Care 2000;38(1):70–7
29. O’Connor AM, Bennett CL, Stacey D, Barry M, Col NF, Eden KB, et al. Decision aids for people facing health treatment or
screening decisions. Cochrane Database Syst Rev 2003;1;CD001431
30. Ofman J, Badamgarav E, Henning J, Knight K, Gano A, et al. Does disease management improve clinical and economic
outcomes in patients with chronic diseases? A systematic review. Am J Med 2004;117(3):182–92
31. Warsi A, Wang P, LaValley M, Avorn J, Solomon D. Self-management education programs in chronic disease: a systematic
review and methodologic critique of the literature. Arch Intern Med 2004;164(15):1641–9
32. Hibbard J. Engaging health care consumers to improve quality of care. Med Care 2003;41(1 Suppl):161–70
33. Joos S, Hickam D, Gordon G, Baker L. Effects of physician communication intervention on patient care outcomes. J Gen
Intern Med 1996;11(3):147–55
34. Bodenheimer T, Wagner E, Grumbach K. Improving primary care for patients with chronic illness. JAMA
2002;288(14):1775–9
35. Rosenstock I. The health belief model and preventative health behaviour. Health Education Monographs 1974;2:27–57
36. Cassidy C. Using the transtheoretical model to facilitate behaviour change in patients with chronic illness. J Am Acad Nurse
Pract 1999;11(7):281
37. Furler J, Mihalopoulos C, Lee P, Harris E, Powell Davies G, Naccarella L, et al. Action on Health Inequalities Through General
Practice: Discussion Paper. Melbourne and Sydney: Integration & Access SERU and Centre for Health Equity Training
Research and Evaluation, 1998
38. Commonwealth Department of Health and Aged Care. General practice in Australia: 2000. Canberra: DHAC, 2000
39. AGREE collaboration. Development and validation of an international appraisal instrument for assessing the quality of clinical
practice guidelines: the AGREE project. Qual Saf Health Care 2003;12:18–23
40. Harris MF, Bailey L, Snowdon T, Litt J, Smith JW, Joyner B, et al. Developing the guidelines for preventive care – two
decades of experience. Aust Fam Physician 2010;39(1–2):63–5
41. National Health and Medical Research Council. NHMRC additional levels of evidence and grades for recommendations for
developers of guidelines. Canberra: NHMRC, 2009
42. Johnson K, Posner SF, Biermann J, Cordero JF, Atrash HK, Parker CS, et al. Recommendations to improve preconception
health and health care. United States. MMWR Recomm Rep 2006;55(RR-6):1–23
43. Lumley J, Chamberlain C, Dowswell T, Oliver S, Oakley L, Watson L. Interventions for promoting smoking cessation during
pregnancy. Cochrane Database Syst Rev 2009;3:CD001055
44. National Health and Medical Research Council. Australian guidelines to reduce health risks from drinking alcohol. Canberra:
NHMRC, 2009
45. Lumley J, Watson L, Watson M, Bower C. Periconceptual supplementation with folate and/or multivitamins for preventing
neural tube defects. Cochrane Database Syst Rev 2001;3:CD001056
46. National Health and Medical Research Council. Iodine supplementation for pregnant and breastfeeding women. Canberra:
NHMRC, 2010 [accessed 2011 June]. Available at www.nhmrc.gov.au/_files_nhmrc/file/publications/synopses/new45_
statement.pdf
47. National Health and Medical Research Council. Australian immunisation handbook, 9th edn. Canberra: NHMRC, 2008.
48. Australian Drug Evaluation Committee. Medicines in Pregnancy Working Party, Therapeutic Goods Administration (Australia),
Australian Drug Evaluation Committee. Medicines in Pregnancy Working Party and Commonweath Department of Health
and Aged Care. Prescribing medicines in pregnancy: an Australian categorisation of risk of drug use in pregnancy 4th edn.
Canberra: Therapeutic Goods Administration, 1999
8th edition 89
49. Korenbrot CC, Steinberg A, Bender C, Newberry S. Preconception care: a systematic review. Matern Child Health J
2002;6(2):75–88
50. Gjerdingen DK, Fontaine P. Preconception health care: a critical task for family physicians. J Am Board Fam Pract 1991
4(4):237–50
51. de Jong-Potjer LC, Elsinga J, le Cessie S, van der Pal-de Bruin KM, Knuistingh Neven A, Buitendijk SE, et al. GP-initiated
preconception counselling in a randomised controlled trial does not induce anxiety. BMC Family Practice 2006;7:66
52. US Preventive Services Task Force. Guide to clinical preventive services 2nd edn. Washington, DC: Office of Disease
Prevention and Health Promotion, 2004
53. Wilson RD, Johnson JA, Wyatt P, Allen V, Gagnon A, Langlois S, et al. Pre-conceptional vitamin/folic acid supplementation
2007: the use of folic acid in combination with a multivitamin supplement for the prevention of neural tube defects and
other congenital anomalies. J Obstet Gynaecol Can 2007;29(12):1003–26
54. National Collaborating Centre for Women’s and Children’s Health. Diabetes in pregnancy: management of diabetes and its
complications from preconception to the postnatal period. London: NICE, 2008
55. Zwar N, Richmond R, Borland R, Peters M, Litt J, Bell J, et al. Supporting smoking cessation: a guide for health
professionals. South Melbourne: RACGP, 2011
56. Conde-Agudelo A, Rosas-Bermúdez A, Kafury-Goeta AC. Birth spacing and risk of adverse perinatal outcomes: a meta-
analysis. JAMA 2006;295:1809–23
57. Australian Institute of Health and Welfare. Mandatory folic acid and iodine fortification in Australia and New Zealand:
baseline report for monitoring. Report no. PHE 139. Canberra: AIHW, 2011
58. World Health Organization. Familial hypercholesterolaemia. Report of a second WHO consultation. Geneva: WHO, 1999
59. Watts GF, Sullivan DR, Poplawski N, van Bockxmeer F, Hamilton-Craig I, Clifton PM, et al. Familial hypercholesterolaemia:
a model of care for Australasia. Atheroscler Suppl 2011;12(2):221–63
60. The Cardiac Society of Australia and New Zealand. Guidelines for the diagnosis and management of familial
hypercholesterolaemia. CSANZ, 2010 [accessed 2012 April]. Available at www.csanz.edu.au/LinkClick.aspx?fileticket=EOv
Avk2jApc%3d&tabid=148
61. Lees C, Smythe R. Antenatal screening for cystic fibrosis (protocol for a Cochrane Review). Oxford: The Cochrane Library,
2000
62. Merelle M, Dankert-Roelse JE, Dezateux C, Lees CM, Nagelkerke AF, Southern KW. Newborn screening for cystic fibrosis.
Cochrane Database Syst Rev 2001;3:CD001402
63. Genetics Education in Medicine Consortium. Genetics in family medicine: the Australian handbook for general
practitioners. Canberra: Biotechnology Australia, 2008 [accessed 2008]. Available at www.nhmrc.gov.au/_files_nhmrc/file/
your_health/egenetics/genetics_in_family_mdicine.pdf
64. Facher J, Robin N. Genetic counselling in primary care. What questions are patients likely to ask, and how should they be
answered. Postgrad Med 2000;107(3):59–66
65. Dick P. Periodic health examination, 1996 update. 1. Prenatal screening for and diagnosis of Down syndrome. Canadian
Task Force on the Periodic Health Examination. CMAJ 1996;154(4):465–79
66. American College of Obstetricians and Gynecologists. Screening for foetal chromosomal abnormalities. Washington, DC:
ACOG, 2007
67. Centre for Genetic Education. Screening and testing during pregnancy. Sydney: NSW Department of Health, 2011 [accessed
2012 April]. Available at www.genetics.edu.au/Information/Genetics-Fact-Sheets/Prenatal-Testing-Overview-FS17/view
68. Emery J, Barlow-Stewart J, Metcalfe SA, Sullivan D. Genetics and preventive health care. Aust Fam Physician
2007;36(10):808–11
69. Powell LW, Dixon JL, Ramm GA, Purdie DM. Screening for hemochromatosis in asymptomatic subjects with or without a
family history. Arch Intern Med 2006;166(3):294–303
70. Bacon BR, Adams PC, Kowdley KV, Powell LW, Tavill AS. Diagnosis and management of hemochromatosis: 2011 practice
guideline by the American Association for the Study of Liver Diseases. Hepatology 2011;54(1):328–43
71. Pagon RA, Bird TD, Dolan CR, Stephens K and Adam MP, eds. Gene reviews. Seattle: University of Washington, 2010
72. Jean Hailes Foundation. Menopause – premature (early menopause). Better Health Channel, 2003 [accessed
2008]. Available at www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Menopause_premature_early_
menopause?OpenDocument
8th edition
73. Cohen J, Lennox N. Fragile X syndrome. In: Lennox N, Diggens J, eds. Management guidelines: people with
developmental and intellectual disabilities. West Melbourne: Therapeutic Guidelines Ltd, 1999
74. Mefford HC, Batshaw ML, Hoffman EP. Genomics, intellectual disability, and autism. N Engl J Med 2012;366(8):733–43
75. Laml T, Preyer O, Umek W, Hengstschlager M. Genetic disorders in premature ovarian failure. Hum Reprod Update
2002;8(5):483–91
76. Jacquemont S, Hagerman RJ, Leehey MA, Hall DA. Penetrance of the fragile X-associated tremor/ataxia syndrome in a
premutation carrier population. JAMA 2004;291(4):460–9
77. Centre for Community Child Health. Early childhood and the lifecourse. Melbourne: Royal Children’s Hospital, 2006
[accessed 2012 June]. Available at www.rch.org.au/emplibrary/ccch/PB1_Earlychood_lifecourse.pdf
78. Marmot M. Fair society, healthy lives. The Marmot Review, 2010 [accessed 2011 August]. Available at www.
instituteofhealthequity.org/projects/fair-society-healthy-lives-the-marmot-review
79. Hayes A. The ‘two worlds’ of Australian childhoods: current research insights into early opportunities, challenges and life
chances. National Investment for the Early Years/Centre for Community Child Health Conference 28 July 2011. Melbourne:
Royal Children’s Hospital, 2011
80. Patton GC, Viner R. Pubertal transitions in health. Lancet 2007;369:1130–9
81. Tylee A, Haller DM, Graham T, Churchill R, Sanci LA. Youth-friendly primary-care services: how are we doing and what
more needs to be done? Lancet 2007;369(9572):1565–73
82. Kuhlthau KA, Bloom S, Van Cleave J, Knapp AA, Romm D, Klatka K, et al. Evidence for family-centered care for children
with special health care needs: a systematic review. Acad Pediatr 2011;11(2):136–43
83. Long WE, Bauchner H, Sege RD, Cabral HJ, Garg A. The value of the medical home for children without special health
care needs. Pediatrics 2012;129(1):87–98
84. National Public Health Partnership. Healthy children – strengthening promotion and prevention across Australia:
development of the Aboriginal and Torres Strait Islander component of the National Public Health Action Plan for Children,
2005–2008: a background paper. Melbourne: NPHP, 2004
85. National Health and Medical Research Council. Child health screening and surveillance: a critical review of the evidence.
Canberra: NHMRC, 2002
86. National Health and Medical Research Council. Dietary guidelines for children and adolescents in Australia. Incorporating
the infant feeding guidelines for health workers. Canberra: NHMRC, 2003
87. NSW Health. My first health record. Sydney: NSW Health, 2008 [accessed 2012 June]. Available at www.health.nsw.gov.
au/pubs/2008/pdf/child_personal_health_record.pdf
88. The Royal Australian and New Zealand College of Psychiatrists. Report from the Faculty of Child and Adolescent
Psychiatry. Prevention and early interventionof mental illness in infants, children and adolescents: planning strategies for
Australia and New Zealand. Melbourne: RANZCP, 2010
89. The Australasian Society of Clinical Immunology and Allergy. Infant feeding advice. Balgowlah, NSW: ASCIA, 2010
[accessed 2011 May]. Available at www.allergy.org.au/images/stories/aer/infobulletins/2010pdf/ascia_infant_feeding_
advice_2010.pdf
90. Sanders MR, Ralph A, Thompson R, Sofronoff K, Gardiner P, Bidwell K, et al. Every family: a public health approach to
promoting children’s wellbeing. Final report. Brisbane: University of Queensland, 2007
91. Australian Government Department of Health and Ageing. Australia’s physical activity recommendations for children and
young people. Canberra: AGDHA, 2007 [accessed 2012 June]. Available at www.health.gov.au/internet/main/publishing.
nsf/Content/health-pubhlth-strateg-active-recommend.htm
92. Clamp M, Kendrick D. A randomized controlled trial of general practitioner safety advice for families with children under 5
years. BMJ 1998;316:1576–9
93. Kendrick D. Preventing injuries in children: cluster randomized controlled trial in primary care. BMJ 1999;318:980–3
94. NSW Health. Early childhood oral health guidelines for child health professionals, 2nd edn. Sydney: NSW Health, 2009
[accessed 2011 May]. Available at www.health.nsw.gov.au/policies/gl/2009/pdf/GL2009_017.pdf
95. Rogers JG. Evidence-based oral health promotion resource. Melbourne: Prevention and Population Health Branch,
Department of Health, 2011
96. Li M, Waite KV, Ma G, Eastman CJ. Declining iodine content of milk and re-emergence of iodine deficiency in Australia.
Med J Aust 2006;184(6):307
8th edition 91
97. National Institute for Health and Clinical Excellence. Improving the nutrition of pregnant and breastfeeding mothers and
children in low-income households. London: NICE, 2011
98. US Preventive Services Task Force. Screening for visual impairment in children ages 1 to 5 years: topic page. Rockville,
MD: USPSTF, 2011 [accessed 2012 June]. Available at www.uspreventiveservicestaskforce.org/uspstf/uspsvsch.htm
99. Australian Department of Health and Ageing. MBS Online – Medicare Benefits Schedule. Medicare item number 701.
Canberra: AGDHA [accessed 2012 June]. Available at www9.health.gov.au//mbs/search.cfm?q=701&sopt=S
Canberra: AGDHA [accessed 2012 June]. Available at www9.health.gov.au/mbs/search.cfm?q=703&sopt=S
103. Barton M. Screening for obesity in children and adolescents: US Preventive Services Task Force recommendation
statement. Pediatrics 2010;125(2):361–7
104. National Institute of Clinical Studies. CG43 obesity: guidance on the prevention, identification, assessment and
management of overweight and obesity in adults and children. London: NICE, 2006
105. US Preventive Services Task Force. Screening for major depressive disorder in children and adolescents: topic page.
Rockville, MD: USPSTF, 2009 [accessed 2012 June]. Available at www.uspreventiveservicestaskforce.org/uspstf/
uspschdepr.htm
106. Brookes-Gunn J, Berlin LJ, Fuligni AS. Early childhood intervention programs: what about the family? In: Shonkoff JP,
Meisels SJ, eds. Handbook of early childhood intervention 2nd edn. New York: Cambridge University Press, 2000:549–88
107. Glascoe FP. If you don’t ask … parents may not tell: noticing problems vs expressing concerns (Letter). Arch Pediatr
Adolesc Med 2006;160:220
108. beyondblue. Clinical practice guidelines for depression and related disorders – anxiety, bipolar disorder and puerperal
psychosis – in the perinatal period. A guideline for primary care health professionals. Melbourne: beyondblue, 2011
109. Milgrom J, Ericksen J, McCarthy RM, Gemmill AW. Stressful impact of depression on early mother–infant relations. Stress
and Health 2006;22:229–38
110. Bakermans-Kranenburg MJ, van IJzendoorn MH, Juffer F. Less is more: meta-analyses of sensitivity and attachment
interventions in early childhood. Psychol Bull 2003;129(2):195–215
111. Australian Infant, Child, Adolescent and Family Mental Health Association. Improving the mental health of infants,
children and adolescents in Australia. Position Paper of the Australian Infant, Child, Adolescent and Family Mental Health
Association Ltd. AICAFMHA, 2011 [accessed 2012 June]. Available at www.youth.wa.gov.au/MS/LMSfiles/aicafmha_pos_
paper_final.pdf
112. McDermott B, Baigent M, Chanen A, Fraser L, Graetz B, Hayman N, et al; beyondblue Expert Working Committee (2010)
Clinical practice guidelines: Depression in adolescents and young adults. Melbourne: beyondblue: the national depression
initiative
113. McNeill YL, Gillies ML, Wood SF. Fifteen year olds at risk of parasuicide or suicide: how can we identify them in general
practice? Fam Pract 2002;19(5):461–5
114. Dowell AC, Ochera JJ, Hilton SR, Bland JM, Harris T, Jones DR, et al. Prevention in practice: results of 2-year follow-up of
routine health promotion interventions in general practice. Fam Pract 1996;13(4):357–62
115. Imperial Cancer Research Fund OXCHECK Study Group. Effectiveness of health checks conducted by nurses in primary
care: final results of the OXCHECK study. BMJ 1995;310(6987):1099–104
116. Spurling GKP, Hayman NE, Cooney AL. Adult health checks for Indigenous Australians: the first year’s experience from the
Inala Indigenous Health Service. Med J Aust 2009;190:562–4
117. Eriksson MK, Franks PW, Eliasson M. A 3-year randomized trial of lifestyle intervention for cardiovascular risk reduction in
the primary care setting: the Swedish Björknäs study. PLoS one 2009;4(4):e5195
118. Engberg M, Christensen B, Karlsmose B, Lous J, Lauritzen T. General health screenings to improve cardiovascular risk
profiles: a randomized controlled trial in general practice with 5-year follow-up. J Fam Pract 2002;51(6):546–52
119. Family Heart Study Group. Randomised controlled trial evaluating cardiovascular screening and intervention in general
practice: principal results of British family heart study. BMJ 1994;308(6924):313–20
8th edition
120. Raftery JP, Yao GL, Murchie P, Campbell NC, Ritchie LD. Cost effectiveness of nurse led secondary prevention clinics for
coronary heart disease in primary care: follow up of a randomised controlled trial. BMJ 2005;330(7493):707
121. Goldstein M, Witlock E, DePue J. Multiple behavioural risk factor interventions in primary care. Am J Prev Med
2004;27(2S):61–79
122. Royal Australian College of General Practitioners. Putting prevention into practice. Guidelines for the implementation of
prevention in the general practice setting. Melbourne: RACGP, 2006
123. Australian Government Department of Health and Ageing. The carer experience: an essential guide for carers of people
with dementia. Canberra: AGDHA, 2002
124. Argimon J, Limon E, Vila J, Cabezas C. Health-related quality of life in carers of patients with dementia. Fam Pract
2004;21(4):454–7
125. Mafullul Y. Burden of informal carers of mentally infirm elderly in Lancashire. East Afr Med J 2002;79(6):291–8.
126. Smith L, Norrie J, Kerr SM, Lawrence IM. Impact and influence on caregiver outcomes at one year post-stroke.
Cerebrovasc Dis 2004;18(2):145–53
127. Hare P. Keeping carers healthy: the role of community nurses and colleagues. Br J Community Nurs 2004;9(4):155–9
128. Bruce D, Paley G, Underwood PJ, Roberts D. Communication problems between dementia carers and general
practitioners: effect on access to community support services. Med J Aust 2002;177:186–8
129. Australian Bureau of Statistics. Disability, ageing and carers, Australia: summary of findings. Canberra: ABS, 2009
[accessed 2012 June]. Available at www.abs.gov.au/ausstats/abs@.nsf/Latestproducts/4430.0Main%20Features22009?op
endocument&tabname=Summary&prodno=4430.0&issue=2009&num=&view=
130. Droes R, Breebaart E, Meiland FJM, van Tilburg W. Effect of meeting centres support program on feelings of competence
of family carers and delay of institutionalization of people with dementia. Aging Ment Health 2004;8(3):2001–11
131. Marriott A, Donaldson C, Tarrier N, Burns A. Effectiveness of cognitive-behavioural family intervention in reducing the
burden of care in carers of patients with Alzheimer’s disease. Brit J Psych 2000;176:557–62
132. Jano E, Aparasu RR. Healthcare outcomes associated with beers’ criteria: a systematic review. Ann Pharmacother
2007;41(3):438–47
133. Easton K, Morgan T, Williamson M. Medication safety in the community: a review of the literature. Sydney: National
Prescribing Service, 2009
134. Holland R, Smith R, Harvey I. Where now for pharmacist led medication review? J Epidemiol Community Health
2006;60(2):92–3
135. Jefferson T, Di Pietrantonj C, Al-Ansary LA, Ferroni E, Thorning S, Thomas RE. Vaccines for preventing influenza in the
elderly. Cochrane Database Syst Rev 2010;7:CD004876
136. Moberley S, Holden J, Tatham DP, Andrews RM. Vaccines for preventing pneumococcal infection in adults. Cochrane
Database Syst Rev 2008;1:CD000422
137. Harpaz R, Ortega-Sanchez IR, Seward JF. Prevention of herpes zoster: recommendations of the Advisory Committee on
Immunization Practices (ACIP). MMWR Recomm Rep 2008;57(RR–5):1–30; quiz CE2–4
138. Health Education Authority. Physical activity and the prevention and management of falls and accidents among older
people. A framework for practice. London: Health Education Authority, 1999
139. Panel on Prevention of Falls in Older Persons, American Geriatrics Society, British Geriatrics Society. Summary of the
updated American Geriatrics Society/British Geriatrics Society clinical practice guideline for prevention of falls in older
persons. J Am Geriatr Soc 2011;59(1):148–57
140. National Falls Prevention for Older People Initiative. An analysis of research on preventing falls and falls injury in older
people: community, residential care and hospital settings. Canberra: AGDHA, 2004
141. Nelson ME, Rejeski WJ, Blair SN, Duncan PW, Judge JO, King AC, et al. Physical activity and public health in older adults:
recommendation from the American College of Sports Medicine and the American Heart Association. Med Sci Sports
Exerc 2007;39(8):1435–45
142. Gillespie L, Gillespie WJ, Robertson MC, Lamb SE. Interventions for preventing falls in elderly people. Cochrane Database
Syst Rev 2003;4:CD000340
143. Chang JT, Morton SC, Rubenstein LZ, Mojica WA, Maglione M, Suttorp MJ, et al. Interventions for the prevention of falls in
older adults: systematic review and meta-analysis of randomised clinical trials. BMJ 2004;328(7441):680
8th edition 93
144. Bischoff-Ferrari HA, Dawson-Hughes B, Willett WC, Staehelin HB, Bazemore MG, Zee RY, et al. Effect of vitamin D on falls:
a meta-analysis. JAMA 2004;291(16):1999–2006
145. Coleman AL, Stone K, Ewing SK, Nevitt M, Cummings S, Cauley JA, et al. Higher risk of multiple falls among elderly
women who lose visual acuity. Ophthalmology 2004;111(5):857–62
146. Hodge W, Horsley T, Albiani D, Baryla J, Belliveau M, Buhrmann R, et al. The consequences of waiting for cataract surgery:
a systematic review. CMAJ 2007;176(9):1285–90
147. Weiner D, Tighiouart H, Amin MG, Stark PC. 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
148. American Geriatric Society, British Geriatrics Society, American Academy of Orthopedic Surgeons Panel on Falls
Prevention. Guideline for the prevention of falls in older persons. J Am Geriatr Soc 2001;49(5):664–72
149. Podsiadlo D, Richardson S. The timed ‘Up & Go’: a test of basic functional mobility for frail elderly persons. J Am Geriatr
Soc 1991;39(2):142–8
150. National Institute for Clinical Excellence. Clinical practice guideline for the assessment and prevention of falls in older
people. London: NICE, 2004
151. Scott V, Votova K, Scanlan A, Close J. Multifactorial and functional mobility assessment tools for fall risk among older
adults in community, home-support, long-term and acute care settings. Age Ageing 2007;36(2):130–9
152. Thrane G, Joakimsen RM, Thornquist E. The association between timed up and go test and history of falls: the Tromso
study. BMC Geriatr 2007;7:1
153. Tiedemann A, Shimada H, Sherrington C, Murray S, Lord S. The comparative ability of eight functional mobility tests for
predicting falls in community-dwelling older people. Age Ageing 2008;37(4):430–5
154. Tiedemann A, Lord SR, Sherrington C. The development and validation of a brief performance-based fall risk assessment
tool for use in primary care. J Gerontol A Biol Sci Med Sci 2010;65(8):896–903
155. Zijlstra GA, van Haastregt JC, van Rossum E, van Eijk JT, Yardley L, Kempen GI. Interventions to reduce fear of falling in
community-living older people: a systematic review. J Am Geriatr Soc 2007;55(4):603–15
156. Wyman JF, Croghan CF, Nachreiner NM, Gross CR, Stock HH, Talley K, et al. Effectiveness of education and individualized
counseling in reducing environmental hazards in the homes of community-dwelling older women. J Am Geriatr Soc
2007;55(10):1548–56
157. Borschmann K, Moore K, Russell M, Ledgerwood K, Renehan E, Lin X, et al. Overcoming barriers to physical activity
among culturally and linguistically diverse older adults: a randomised controlled trial. Australas J Ageing 2010;29(2):77–80
158. Australian Commission on Safety and Quality in Health Care. Preventing falls and harm from falls in older people: best
practice guidelines for Australian hospitals, residential aged care facilities and community care. Darlinghurst, NSW:
ACSQHC, 2009
159. Cameron ID, Murray GR, Gillespie LD, Robertson MC, Hill KD, Cumming RG, et al. Interventions for preventing falls in older
people in nursing care facilities and hospitals. Cochrane Database Syst Rev 2010;1:CD005465
160. Gillespie LD, Robertson MC, Gillespie WJ, Lamb SE, Gates S, Cumming RG, et al. Interventions for preventing falls in older
people living in the community. Cochrane Database Syst Rev 2009;2:CD007146
161. US Preventive Services Task Force. Prevention of falls in community-dwelling older adults. Rockville, MD: USPSTF, 2012
[accessed 2012 June]. Available at www.uspreventiveservicestaskforce.org/uspstf/uspsfalls.htm
162. Sherrington C, Whitney J, Lord S, Herbert R, Cumming R, Close J. Effective exercise for the prevention of falls: a
systematic review and meta-analysis. J Am Geriatr Soc 2008;56,(12):2234–43
163. Tiedemann A, Sherrington C, Close JC, Lord SR. Exercise and Sports Science Australia position statement on exercise
and falls prevention in older people. J Sci Med Sport 2011;14(6):489–95
164. Nowson CA, McGrath JJ, Ebeling PR, Haikerwal A, Daly RM, Sanders KM, et al. Vitamin D and health in adults in Australia
and New Zealand: a position statement. Med J Aust 2012;196(11):686–7
165. Smeeth L, Iliffe S. Community screening for visual impairment in the elderly. Update of Cochrane Database Syst Rev 2000
(2). Cochrane Database Syst Rev 2006;3:CD001054
166. Austroads. Assessing fitness to drive for commercial and private vehicle drivers: medical standards for licensing and
clinical management guidelines. Austroads, 2012 [accessed July 2012]. Available at www.austroads.com.au/images/
stories/AFTD_reduced_for_web.pdf
167. Taylor H, Keeffe J. Updates in medicine: Ophthalmology. Med J Aust 2002;176(1):29

8th edition
168. Australian Institute of Health and Welfare. Australia’s health 2006. Cat. no. AUS 73. Canberra: AIHW, 2006
169. US Preventive Services Task Force. Screening for hearing loss in older adults. Rockville, MD: USPSTF, 2011 [accessed
2012 July]. Available at www.uspreventiveservicestaskforce.org/uspstf/uspshear.htm#top
170. Patterson C. Screening for visual impairment in the elderly. Canadian Task Force on the periodic health examination
Canadian guide to clinical preventive health care. Ottawa: Health Canada, 1994: 932–42
171. Patterson C. Prevention of hearing impairment and disability in the elderly. Canadian Task Force on the periodic health
examination Canadian guide to clinical preventive health care. Ottawa: Health Canada, 1994: 954–63
172. The Royal Australian College of General Practitioners, NSW Health. Care of patients with dementia in general practice:
guidelines. Sydney: NSW Department of Health 2003
173. Boustani M, Peterson B, Hanson L, et al. Screening for dementia in primary care: A summary of the evidence for the US
Preventive Services Task Force. Ann Intern Med 2003;138:927–37
174. National Collaborating Centre for Mental Health. Dementia: A NICE–SCIE Guideline on supporting people with dementia
and their carers in health and social care. London: NICE 2007
175. Gao S, Hendrie HC, Hall KS, Hui S. The relationship between age, sex and the incidence of dementia and Alzheimer
disease: a metaanalysis. Arch Gen Psychiatry 1998;55:809–15
176. Lautenschlager NT, Cupples LA, Rao VS, Auerbach SA, Becker R, Burke J, et al. Risk of dementia among relatives of
Alzheimer’s disease patients in the MIRAGE study: what is in store for the oldest old? Neurology 1996;46:641–50
177. Lenoir H, Dufouil C, Auriacombe S, Lacombe JM, Dartigues JF, Ritchie K, et al. Depression history, depressive
symptoms, and incident dementia: the 3C Study. J Alzheimers Dis 2011;26(1):27–38
178. Fleminger S, Oliver DL, Lovestone S, Rabe-Hesketh S, Giora A. Head injury as a risk factor for Alzheimer’s disease: the
evidence ten years on; a partial replication. J Neurol Neurosurg Psychiatry 2003;74:857–62
179. Peila R, White LR, Petrovich H, Masaki K, Ross GW, Havlik RJ, et al. Joint effect of the APOE gene and midlife systolic
blood pressure on late-life cognitive impairment: the Honolulu-Asia aging study. Stroke 2001;32:2882–9
180. Razay G, Williams J, King E, Smith AD, Wilcock G. Blood pressure, dementia and Alzheimer’s disease: the OPTIMA
longitudinal study. Dement Geriatr Cogn Disord 2009;28:70–4
181. Stewart R, Asonganyi B, Sherwood R. Plasma homocysteine and cognitive impairment in an older British African-
Caribbean population. J Am Geriatr Soc 2002;50(7):1227–32
182. White L, Launer L. Relevance of cardiovascular risk factors and schemic cerebrovascular disease to the pathogenesis
of Alzheimer disease: a review of accrued findings from the Honolulu-Asia Aging Study. Alzheimer Dis Assoc Disord
2006;20:S79–83
183. Farooki A. Central obesity and increased risk of dementia more than three decades later. Neurology 2009;72:1030–1
184. Helzner EP, Luchsinger JA, Scarmeas N, Cosentino S, Brickman AM, Glymour MM, et al. Contribution of vascular risk
factors to the progression in Alzheimer disease. Arch Neurol 2009;66:343–8
185. University of New South Wales as represented by the Dementia Collaborative Research Centre – Assessment and Better
Care 2011. 14 Essentials for good dementia care in general practice. NSW: The University of New South Wales, 2011
186. Brodaty H, Pond D, Kemp NM, Luscombe GS, Harding L. The GPCOG: a new screening test for dementia designed for
general practice. J Am Geriatr Soc 2002;50(3):530–4
187. DeLepeleire J, Heyrman J, Baro F, Buntinx F. A combination of tests for the diagnosis of dementia had significant
diagnostic value. J Clin Epidemiol 2005;58(3):217–25
188. Kirby M, Denihan A, Bruce I, Coakley D, Lawlor BA. The clock drawing test in primary care: sensitivity in dementia
detection and specificity against normal and depressed elderly. Int J Geriatr Psychiatry 2001;16(10):935–40
189. Storey J, Rowland JTJ, Conforti DA, Dickson HG. The Rowland Universal Dementia Assessment Scale (RUDAS): a
multicultural cognitive assessment scale. Int Psychogeriatr 2004;16(1):13–31
190. Barber B, Ames D, Ellis K, Martins R, Masters C, Szoeke C. Lifestyle and late life cognitive health: sufficient evidence to
act now? Int Psychogeriatr 2012;24(5):683–8
191. Legislative Council of Western Australia. Report of the Select Committee on Immunisation and Vaccination Rates in
Children. Perth: LCWA, 1999
192. Australian Bureau of Statistics. 1989/90 National Health Survey. Canberra: ABS, 1996
8th edition 95
193. Bell J, Whitehead P, Chey T, Smith W, Capon AG. The epidemiology of incomplete childhood immunisation: an analysis of
reported immunisation status in western Sydney. J Paediatr Child Health 1993;29(5):384–8
194. Herceg A, Daley C, Schubert P, Hall R. A population based survey of immunisation coverage in two year old children. Aust
J Public Health 1995;19(5):465–70
195. Jones K, Fasher B, Hanson B, Burgess M, Isaacs D. Immunisation status of casualty attenders: risk factors for non-
compliance and attitudes to ‘on the spot’ immunisation. J Paediatr Child Health 1993;29(5):384–8
196. Australian Bureau of Statistics. Children’s immunisation Australia April 1995. Canberra: ABS, 1996
197. Skinner J, March L, Simpson J. A retrospective cohort study of childhood immunisation status in Northern Sydney. Aust J
Public Health 1995;19(1):58–63
198. Australian Institute of Health and Welfare. The health and welfare of Australia’s Aboriginal and Torres Strait Islander
peopless. Canberra: AIHW, 2008
199. Gracey M, King M. Indigenous health part 1: determinants and disease patterns. Lancet 2009;374(9683):65–75
200. Dower J, Donald M, Begum N, Vlack S, Ozolins I. Patterns and determinants of influenza and pneumococcal immunisation
among adults with chronic disease living in Queensland, Australia. Vaccine 2011;29(16):3031–7
201. Pavlin NL, Parker R, Fairley CK, Gunn JM, Hocking J. Take the sex out of STI screening! Views of young women on
implementing chlamydia screening in general practice. BMC Infect Dis 2008;8:62
202. Preswell N, Barton D. Taking a sexual history. Aust Fam Physician 2000;29(5):533–9
203. Guy RJ, Ali H, Liu B, Hocking J, Donovan B, Kaldor J. Genital chlamydia infection in young people: a review of the
evidence. Sydney: The Kirby Institute, University of New South Wales, 2011
204. Hocking J, Fairley C. Need for screening for genital chlamydia trachomatis infection in Australia. Aust N Z J Public Health
2003;27(1):80–1
205. Meyers D, Wolff T, Gregory K, Marion L. USPSTF recommendations for STI screening. Am Fam Physician 2008;77(6):819–
24
206. Cook RL, Hutchison SL, Ostergaard L. Systematic review: noninvasive testing for Chlamydia trachomatis and Neisseria
gonorrhoeae. Ann Intern Med 2005;142(11):914–25
207. Bourne C, Edwards B, Shaw M, Gowers A, Rodgers C, Ferson M. Sexually transmitted infections: testing guidelines for
men who have sex with men. Sexual Health 2008;5:189–91
208. Cheney K, Wray L. Chlamydia and associated factors in an under 20s antenatal population. Aust N Z J Obstet Gynaecol
2008;48(1):40–3
209. Chen MY, Fairley CK, De Guingand D, Hocking J, Tabrizi S, Wallace EM, et al. Screening pregnant women for chlamydia:
what are the predictors of infection? Sex Transm Infect 2009;85(1):31–5
210. Kong FY, Guy RJ, Hocking JS, Merritt T, Pirotta M, Heal C, et al. Australian general practitioner chlamydia testing rates
among young people. Med J Aust 2011;194(5):249–52
211. Hayman N. Chlamydia PCR screening in an Indigenous health general practice clinic in Brisbane 2002–3. Brisbane: 2004
212. Low N, McCarthy A, Macleod J, Salisbury C. Epidemiological, social, diagnostic and economic evaluation of population
screening for genital chlamydial infection. Health Technol Assess 2007;11(8):1–165
213. Queensland Health. Indigenous sexual health service report for Brisbane Southside. Brisbane: Communicable Diseases
Unit, 2004
214. Heal C, Jones B, Veitch C, Lamb S, Hodgens S. Screening for chlamydia in general practice. Aust Fam Physician
2002;31(8):779–82
215. Scholes D, Stergachis A, Heidrich FE, Andrilla H. Prevention of pelvic inflammatory disease by screening for cervical
chlamydial infection. N Engl J Med 1996;334(21):1362–6
216. Uddin RN, Ryder N, McNulty AM, Wray L, Donovan B. Trichomonas vaginalis infection among women in a low prevalence
setting. Sex Health 2011;8(1):65–8
217. STIs in Gay Men Action Group (STIGMA). Sexually transmitted infection testing guidelines for men who have sex with men
2010. Sydney: STIGMA, 2010 [accessed 2011 June 6]. Available at www.stigma.net.au/resources/STIGMA_MSM_Testing_
Guidelines_2010.pdf
218. Whiley DM, Garland SM, Harnett G, Lum G, Smith DW, Tabrizi SN, et al. Exploring ‘best practice’ for nucleic acid detection
of Neisseria gonorrhoeae. Sex Health 2008;5(1):17–23
8th edition
219. Australasian Society for HIV Medicine. HIV, viral hepatitis and STIs: a guide for primary care. Sydney: ASHM, 2008
220. Guy R, Wand H, Franklin N, Fairley CK, Chen MY, O’Connor CC, et al. Re-testing for chlamydia at sexual health services in
Australia, 2004–08. Sex Health 2011;8(2):242–7
221. Whittington WL, Kent C, Kissinger P, Oh MK. Determinants of persistent and recurrent Chlamydia trachomatis infection in
young women: results of a multicenter cohort study. Sex Transm Dis 2001;28(2):117–23
222. Orr DP, Johnston K, Brizendine E, Katz B. Subsequent sexually transmitted infection in urban adolescents and young
adults. Arch Pediatr Adolesc Med 2001;155(8):947–53
223. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines. MMWR 2006;55:38–40
224. Watson E, Templeton A, Russell I, Paavonen J. The accuracy and efficacy of screening tests for Chlamydia trachomatis: a
systematic review. J Med Microbiol 2002;51(12):1021–31
225. Ministry of Health. Draft chlamydia management guidelines. Wellington: Ministry of Health, 2008
226. The Kirby Institute. HIV, viral hepatitis and sexually transmissible infections in Australia: Annual Surveillance Report 2011.
Sydney, NSW: The Kirby Institute, the University of New South Wales, 2011
227. Atkins D. First new screening recommendations from the third US Preventive Services Task Force. BMJ 2003;327:21–4
228. Trelle S, Shang A, Nartey L, Cassel J, Low N. Improved effectiveness of partner notification for patients with sexually
transmitted infections: systematic review. BMJ 2007;334(7589):354
229. Burnet Insitute. Partner notification of sexually transmitted infections in New South Wales: an informed literature review.
Melbourne: Centre for Population Health, 2010 [accessed 2011 June]. Available at www.stipu.nsw.gov.au/content/
Document/Contact_Tracing_Literature.pdf
230. Honey E, Augood C, Templeton A, Russell I, Paavonen J, Mardh PA, et al. Cost effectiveness of screening for chlamydia
trachomatis: a review of published studies. Sex Transm Infect 2002;78(6):406–12
231. Britt H, Miller GC, Charles J, Bayram C, Valenti L, Pan Y, et al. General practice activity in Australia 1990–00 to 2008–09:
10 year data tables. Cat. no. GEP 26. Canberra: AIHW, 2009
232. Ezzati M, Lopez AD, Rodgers A, Vander Hoom S. Selected major risk factors and global and regional burden of disease.
Lancet 2002;360(9343):1347–60
233. Weingarten M, Matalon A. The ethics of basing community prevention in general practice. J Med Ethics 2010;36(3):138–41
234. Fleming P, Godwin M. Lifestyle interventions in primary care: systematic review of randomized controlled trials. Can Fam
Physician 2008;54(12):1706–13
235. Ebrahim S, Beswick A, Burke M, Davey Smith G. Multiple risk factor interventions for primary prevention of coronary heart
disease. Cochrane Database Syst Rev 2006;4:CD001561
236. van Schayck OC, Pinnock H, Ostrem A, Litt J, Tomlins R, Williams S, et al. IPCRG Consensus statement: tackling the
smoking epidemic – practical guidance for primary care. Prim Care Respir J 2008;17(3):185–93
237. Fiore M, Jaen CR, Baker TB, Bailey WC, Benowitz N, Curry SJ, et al. Treating tobacco use and dependence: 2008 Update.
Rockville, MD: U.S. Department of Health and Human Services. Public Health Service. 2008
238. Kaner E, Bland M, Cassidy P, Coulton S, Deluca P, Drummond C, et al. Screening and brief interventions for hazardous
and harmful alcohol use in primary care: a cluster randomised controlled trial protocol. BMC Public Health 2009;9:287
239. Greaves CJ, Sheppard KE, Abraham C, Hardeman W, Roden M, Evans PH, et al. Systematic review of reviews of
intervention components associated with increased effectiveness in dietary and physical activity interventions. BMC Public
Health 2011;11(1):119
240. Conn VS, Hafdahl AR, Mehr DR. Interventions to increase physical activity among healthy adults: meta-analysis of
outcomes. Am J Public Health 2011;101(4):751–8
241. Foster C, Hillsdon M, Thorogood M. Interventions for promoting physical activity. Cochrane Database Syst Rev
2009;1:CD003180
242. Sargent GM, Pilotto LS, BaurLA. Components of primary care interventions to treat childhood overweight and obesity: a
systematic review of effect. Obes Rev 2010;12(5):e219–e35
243. NSW Refugee Health Service. Managing survivors of torture and refugee trauma: guidelines for general practitioners.
Sydney: NSW Refugee Health Service, 2000
244. The Royal Australian College of General Practitioners. Putting prevention into practice. Guidelines for the implementation of
prevention in the general practice setting 2nd edn. Melbourne: RACGP, 2006
8th edition 97
245. Dosh SA, Holtrap JS, Torres T, Arnold AK, Bauman J, White LL. Changing organizational constructs into function tools: an
assessment of the 5As in primary care practices. Ann Fam Med 2005;3(Suppl 2):S50–2
246. Hung DY, Shelley DR. Multilevel analysis of the chronic care model and the 5A services for treating tobacco use in urban
primary care clinics. Health Serv Res 2009;44(1):103–27
247. Trinite T, Loveland-Cherry C, Marion L. The US Preventive Services Task Force: an evidence-based prevention resource for
nurse practitioners. J Am Acad Nurse Pract 2009;21(6):301–6
248. US Preventive Services Task Force. Guide to clinical preventive services, 2nd edn. Alexandria, VA: Williams & Wilkins, 1996
249. Glascow R, Goldstein MG, Ockene JK, Pronk NP. Translating what we have learned into practice: principles and
hypotheses for interventions addressing multiple behaviors in primary care. Am J Prev Med 2009;27(2 Suppl):88–101
250. Li R, Zhang P, Barker LE, Chowdhury FM, Zhang X. Cost-effectiveness of interventions to prevent and control diabetes
mellitus: a systematic review. Diabetes Care 2010;33(8):1872–94
251. Boulware LE, Marinopoulos S, Phillips KA, Hwang CW, Maynor K, Merenstein D, et al. Systematic review: the value of the
periodic health evaluation. Ann Intern Med 2007;146(4):289–300
252. Australian Institute of Health and Welfare. Cardiovascular disease: Australian facts 2011. Canberra: AIHW, 2011
253. DiGiacomo M, Davidson PM, Abbott PA, Davison J, Moore L, Thompson SC. Smoking cessation in indigenous populations
of Australia, New Zealand, Canada, and the United States: elements of effective interventions. Int J Env Res Public Health
2011;8(2):388–410
254. Australian Bureau of Statistics. 4704.0 The health and welfare of Australia’s Aboriginal and Torres Strait Islander peopless.
Canberra: ABS, 2010
255. Bowden JA, Miller CL, Hiller JA. Smoking and mental illness: a population study in South Australia. Aust NZ J Psychiatry
2011;45(4):325–31
256. Australian Bureau of Statistics. 4842.0.55.001 Overweight and obesity in adults in Australia: A snapshot, 2007–08.
Canberra: ABS, 2011
258. Brimblecombe JK, O’Dea K. The role of energy cost in food choices for an Aboriginal population in northern Australia. Med
J Aust 2009;190(10):549–51
259. National Health and Medical Research Council. Nutrition in Aboriginal and Torres Strait Islander peopless. Canberra:
NHMRC, 2000
260. Queensland Health. The 2006 Healthy Food Access Basket Survey. Brisbane: Queensland Health, 2006
261. Australian Institute of Health and Welfare. Australia’s health. Canberra: AIHW, 2004
262. Jenum AK, Anderssen SA, Birkeland KI, Holme I, Graff-Iversen S, Lorentzen C, et al. Promoting physical activity in a
low-income multiethnic district: effects of a community intervention study to reduce risk factors for type 2 diabetes and
cardiovascular disease: a community intervention reducing inactivity. Diabetes Care 2006;29(7):1605–12
263. Dudley DA, Okely AD, Pearson P, Peat J. Engaging adolescent girls from linguistically diverse and low income backgrounds
in school sport: a pilot randomised controlled trial. J Sci Med Sport 2010;13(2):217–24
264. National Aboriginal Community Controlled Health Organisation. National guide to a preventive health assessment in
Aboriginal and Torres Strait Islander peoples. Melbourne: NACCHO, 2005
265. Roxburgh A, Degenhardt L. Characteristics of drug-related hospital separations in Australia. Drug Alcohol Depend
2008;92(1–3):149–55
266. Hoolahan B, Kelly B, Stain HJ, Killen D. Co-morbid drug and alcohol and mental health issues in a rural New South Wales
Area Health Service. Aust J Rural Health 2006;14(4):148–53
267. Stockdale SE, Klap R, Belin TR. Longitudinal patterns of alcohol, drug, and mental health need and care in a national
sample of US adults. Psychiatr Serv 2006;57(1):93–9
268. Najman JM, Williams GM, Room R. Increasing socioeconomic inequalities in male cirrhosis of the liver mortality: Australia
1981–2002. Drug Alcohol Rev 2007;26(3):273–8
269. Wilson M, Stearne A, Gray D, Saggers S. The harmful use of alcohol amongst Indigenous Australians. Perth: Australian
Indigenous HealthInfoNet, 2010
270. Harper S, Lynch J. Trends in socioeconomic inequalities in adult health behaviors among US states, 1990–2004. Public
Health Rep 2007;122(2):177–89
8th edition
271. Room R. Stigma, social inequality and alcohol and drug use. Drug Alcohol Rev 2005;24(2):143–55
272. Luoma JB, Twohig MP, Hayes SC. An investigation of stigma in individuals receiving treatment for substance abuse. Addict
Behav 2007;32(7):1331–46
273. van Schayck O, Pinnock H, Ostrem O, Buffels J, Giannopoulos D, Henrichsen S, et al. Tackling the smoking epidemic:
practical guidance for primary care. Prim Care Respir J 2008;17(3):185–93
274. Ministry of Health. New Zealand smoking cessation guidelines. Wellington: Ministry of Health, 2007
275. Stead LF, Perera R, Bullen C, Mant D, Lancaster T. Nicotine replacement therapy for smoking cessation. Cochrane
276. Cahill K, Stead LF, Lancaster T. Nicotine receptor partial agonists for smoking cessation. Cochrane Database Syst Rev
2011;2:CD006103
277. Stead LF, Perera R, Lancaster T. A systematic review of interventions for smokers who contact quitlines. Tob Control
2007;16(Suppl 1):i3–i8
278. Coleman T, Agboola S, Leonardi-Bee J, Taylor M, McEwen A, McNeill A. Relapse prevention in UK Stop Smoking Services:
current practice, systematic reviews of effectiveness and cost-effectiveness analysis. Health Technol Assess 2010;14(49)1–
152, iii-iv
279. Baker A, Ivers RG, Bowman J, Butler T, Kay-Lambkin FJ, Wye P, et al. Where there’s smoke, there’s fire: high prevalence of
smoking among some sub-populations and recommendations for intervention. Drug Alcohol Rev 2006;25(1):85–96
280. Ivers R. A review of tobacco interventions for Indigenous Australians. Aust NZ J Public Health 2003;27(3):294–9
281. Morissette SB, Tull MT, Gulliver SB, Kamholz BW, Zimering RT. Anxiety, anxiety disorders, tobacco use, and nicotine: a
critical review of interrelationships. Psychol Bull 2007;133(2):245–72
282. Ranney L, Melvin C, Lux L, McClain E, Lohr KN. Systematic review: smoking cessation intervention strategies for adults
and adults in special populations. Ann Intern Med 2006;145(11):845–56
283. Solberg L, Boyle R, Davidson G, Magnan S. Patient satisfaction and discussion of smoking cessation during clinical visits.
Mayo Clin Proc 2001;76(2):138
284. Young J, Ward J. Implementing guidelines for smoking cessation: advice in Australian general practice: opinions, current
practices, readiness to change and perceived barriers. Fam Pract 2001;18(1):14–20
285. Litt J, Rigby K. Literature review for the pregnancy Lifescript prescriptions: smoking. Adelaide: Flinders University, 2011
286. Sciamanna C, Novak S, Houston T, Gramling R, Marcus B. Visit satisfaction and tailored health behavior communications
in primary care. Am J Prev Med 2004;26(5):426–30
287. Okoli CT, Khara M, Procyshyn RM. Smoking cessation interventions among individuals in methadone maintenance: a brief
review. J Subst Abuse Treat 2010;38(2):191–9
288. Litt J, Pilotto L, Young R, Ruffin R, Wade T, Grbich C, et al. GPs Assisting Smokers Program (GASP II): report for the six
month post intervention period. Adelaide: Flinders University, 2005
289. Miller WR, Rollnick S. Ten things that motivational interviewing is not. Behav Cogn Psychother 2009;37(2):129–40
290. Australian Bureau of Statistics. 4719.0 Overweight and obesity in adults, Australia, 2004–05. Canberra: ABS, 2008
291. Stead M, Angus K, Holme I. Factors influencing European GPs’ engagement in smoking cessation: a multi-country
literature review. Br J Gen Pract 2009;59(566):682–90
292. Steptoe A, Perkins-Porras L, McKay C, Rink E, Hilton S, Cappuccio FB. Behavioural counselling to increase consumption
of fruit and vegetables in low–income adults: randomised trial. BMJ 2003;326(7394):855–7
293. Turrell G, Stanley L, de Looper M, Oldenburg B. Health inequalities in Australia: Morbidity, health behaviours, risk factors
and health service use. Cat. no. PHE 72. Canberra: AIHW, 2006
294. Borland R, Balmford J, Bishop N, Segan C. In-practice management versus quitline referral for enhancing smoking
cessation in general practice: a cluster randomized trial. Fam Pract 2008;25(5):382–9
295. Ferketich AK, Khan Y, Wewers ME. Are physicians asking about tobacco use and assisting with cessation? Results from
the 2001–2004 National Ambulatory Medical Care Survey (NAMCS). Prev Med 2006;43(6):472–6
296. Doran CM, Valenti L, Robinson M, Britt H. Smoking status of Australian general practice patients and their attempts to quit.
Addict Behav 2006;31(5):758–66
8th edition 99
297. Madson MB, Loignon AC, Lane C. Training in motivational interviewing: a systematic review. J Subst Abuse Treat
2009;36(1):101–9
298. Cahill K, Lancaster T, Green N. Stage-based interventions for smoking cessation. Cochrane Database Syst Rev
2010;11:CD004492
299. Hughes JR, Keely JP, Fagerstrom KO, Callas PW. Intentions to quit smoking change over short periods of time. Addict Behav
2005;30(4):653–62
300. National Institute for Health and Clinical Excellence. Brief interventions and referral for smoking cessation in primary care and
other settings. London: NICE, 2006
301. Prochaska J, Velicer W, Redding C, Rossi J, Goldstein M, DePue J, et al. Stage-based expert systems to guide a population
of primary care patients to quit smoking, eat healthier, prevent skin cancer, and receive regular mammograms. Prev Med
2005;41(2):406–16
302. Mendelsohn C, Richmond R. Smokescreen for the 1990s. A new approach to smoking cessation. Aust Fam Physician
1994;23(5):841–8
303. Businelle MS, Kendzor DE, Reitzel LR, Costello TJ, Cofta-Woerpel L, Li Y, et al. Mechanisms linking socioeconomic status to
smoking cessation: a structural equation modeling approach. Health Psychol 2010;29(3):262–73
304. Murray RL, Bauld L, Hackshaw LE, McNeil A. Improving access to smoking cessation services for disadvantaged groups: a
systematic review. J Pub Health 2009;31(2):258–77
305. Michie S, Jochelson K, Markham WA, Bridle C. Low-income groups and behaviour change interventions: a review of
intervention content and effectiveness. London: King’s Fund, 2008
306. Solberg LI. Improving medical practice: a conceptual framework. Ann Fam Med 2007;5(3):251–6
307. Anderson P, Jane-Llopis E. How can we increase the involvement of primary health care in the treatment of tobacco
dependence? A meta-analysis. Addiction 2004;99(3):299–312
308. National Health and Medical Research Council. Clinical practice guidelines for the management of overweight and obesity in
adults. Canberra: NHMRC, 2003
309. Pouliot MC, Despres JP, Lemieux S, Moorjani S, Bouchard C, Tremblay A, et al. Waist circumference and abdominal sagittal
diameter: best simple anthropometric indexes of abdominal visceral adipose tissue accumulation and related cardiovascular
risk in men and women. Am J Cardiol 1994;73(7):460–8
310. Welborn TA, Dhaliwal SS, Bennett SA. Waist–hip ratio is the dominant risk factor predicting cardiovascular death in Australia.
Med J Aust 2003;179(11/12):580–5
311. National Health and Medical Research Council. Overweight and obesity in adults – a guide for general practitioners. Canberra:
NHMRC, 2003 [accessed 2012 May]. Available at www.nhmrc.gov.au/nics/nics-programs/clinical-practice-guidelines-
management-overweight-and-obesity-adults-children-an
312. National Heart Foundation of Australia. Management of overweight and obesity in adults. NSW: NSW Health, 2007
313. Witham MD, Avenell A. Interventions to achieve long-term weight loss in obese older people: a systematic review and meta-
analysis. Age Ageing 2010;39:176–184
314. Groeneveld IF, Proper KI, van der Beek AJ, van Mechelen W. Sustained body weight reduction by an individual-based lifestyle
intervention for workers in the construction industry at risk for cardiovascular disease: results of a randomized controlled trial.
Prev Med 2010;51(3–4):240–6
315. Uusitupa M, Peltonen M, Lindstrom J, Aunola S, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, et al. Ten-year mortality and
cardiovascular morbidity in the Finnish Diabetes Prevention Study – secondary analysis of the randomized trial. PLoS One
2009;4(5):e5656
316. Pollard C, Lewis J, Woods L, Beurle D. National Obesity Taskforce – Aboriginal and Torres Strait Islander workshop, 10–11
September 2003. Adelaide: National Obesity Taskforce, 2003
317. Wadden TA, Volger S, Sarwer DB, Vetter ML, Tsai AG, Berkowitz RI, et al. A two-year randomised trial of obesity treatment in
primary care practice. N Engl J Med 2011;365(21):1969–79
318. Jebb SA, Ahern AL, Olson AD, Aston LM, Holzapfel C, Stoll J, et al. Primary care referral to a commercial provider for weight
loss treatment versus standard care: a randomised controlled trial. Lancet 2011;3378(9801):1485–92
319. World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO consultation. WHO Tech
Rep Ser 2000;894(3):i–xii,1–253
8th edition
320. Seo DC, Sa J. A meta-analysis of psycho-behavioral obesity interventions among US multiethnic and minority adults. Prev
Med 2008;47(6):573–82
321. Shaw K, Gennat H, O’Rourke P, Del Mar C. Exercise for overweight or obesity. Cochrane Database Syst Rev
2006;4:CD003817
322. Horvath K, Jeitler K, Siering U, Stich AK, Skipka G, Gratzer TW, et al. Long-term effects of weight-reducing interventions in
hypertensive patients: systematic review and meta-analysis. Arch Intern Med 2008;168(6):571–80
323. Neovius M, Johansson K, Rossner S. Head-to-head studies evaluating efficacy of pharmaco-therapy for obesity: a
systematic review and meta-analysis. Obes Rev 2008;9(5):420–7
324. Knowler WC, Fowler SE, Hamman RF, Christophi CA, Hoffman HJ, Brenneman AT, et al. 10–year follow-up of diabetes
incidence and weight loss in the Diabetes Prevention Program Outcomes Study. Lancet 2009;374(9702):1677–86
325. Padwal R, Klarenbach S, Wiebe N, Birch D, Karmali S, Manns B, et al. Bariatric surgery: a systematic review and network
meta-analysis of randomized trials. Obes Rev 2011;12(8):602–21
326. Picot J, Jones J, Colquitt JL, Gospodarevskaya E, Loveman E, Baxter L, et al. The clinical effectiveness and cost-
effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation. Health Technol
Assess 2009;13(41):1–190
327. Scottish Intercollegiate Guidelines Network. 115 Management of obesity: a national clinical guidelines. Edinburgh: SIGN, 2010
328. Dixon JB, Zimmet P, Albert G, Mbanya GB, Rubino F. Bariatric surgery for diabetes: the International Diabetes Federation
takes a position. J Diabetes 2011;3(4):261–4
329. Zimmet P, Dixon J. Bariatric interventions for obese type 2 diabetes: the ‘doctor’s dilemma’. Baker IDI Perspectives
2011;005
330. Crawford D, Jeffery R, eds. Obesity prevention and public health. Oxford: Oxford University Press, 2005
331. Australian Institute of Health and Welfare. Heart stroke and vascular diseases – Australian facts. Canberra: AIHW, 2004
333. World Health Organization. Diet, nutrition and the prevention of chronic diseases: report of a joint WHO/FAO expert
consultation. Geneva: WHO, 2003
334. National Health and Medical Research Council. Food for health: dietary guidelines for Australian adults. Canberra: NHMRC,
2003 [accessed 2008]. Available at www.nhmrc.gov.au/_files_nhmrc/publications/attachments/n33.pdf
335. Pignone MA, Ammerman A, Fernandez L, Orleans CT, Pender N, Woolf S, et al. Counselling to promote a healthy diet in
adults. A summary of the evidence for the US Preventive Services Task Force. Am J Prev Med 2003;24(1):75–92
336. National Health and Medical Research Council. Dietary guidelines for children and adolescents in Australia: a guide to
healthy eating. Canberra: NHMRC, 2003
337. Ammerman A, Lindquist C, Lohr K, Hersey J. The efficacy of behavioral interventions to modify dietary fat and fruit and
vegetable intake: a review of the evidence. Prev Med 2002;35(1):25–41
338. Hooper L, Summerbell CD, Thompson R, Sills D, Roberts FG, Moore HJ, et al. Reduced or modified dietary fat for
preventing cardiovascular disease. Cochrane Database Syst Rev 2012;5:CD002137
339. US Preventive Services Task Force. Behavioral counseling in primary care to promote a healthy diet: recommendations and
rationale. Am Fam Physician 2003;67(12):2573–6
340. Brunner EJ, Rees K, Ward K, Burke M, Thorogood M. Dietary advice for reducing cardiovascular risk. Cochrane Database
Syst Rev 2007;4:CD002128
341. Thompson RL, Summerbell CD, Hooper L, Higgins JPT, Little PS, Talbot D, et al. Dietary advice given by a dietitian
versus other health professional or self-help resources to reduce blood cholesterol. Cochrane Database Syst Rev
2007;3:CD001366
342. World Cancer Research Fund, American Institute for Cancer Research. Food, nutrition, physical activity, and the prevention
of cancer: a global perspective. Washington DC: AICR, 2007
343. He FJ, Nowson CA, MacGregor GA. Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet
2006;367(9507):320–6
344. He FJ, Nowson CA, Lucas M, MacGregor GA. Increased consumption of fruit and vegetables is related to a reduced risk of
coronary heart disease: meta-analysis of cohort studies. J Hum Hypertens 2007;21(9):717–28
8th edition 101
345. National Heart Foundation of Australia. Position statement: fish, fish oils, n-3 polyunsaturated fatty acids and cardiovascular
health. Heart Foundation, 2008 [accessed July 2012]. Available at www.heartfoundation.org.au/SiteCollectionDocuments/Fish-
FishOils-position-statement.pdf
346. He K, Song Y, Daviglus ML, Liu K, Van Horn L, Dyer AR, et al. Accumulated evidence on fish consumption and coronary heart
disease mortality: a meta-analysis of cohort studies. Circulation 2004;109(22):2705–11
347. Hooper L, Bartlett C, Davey SG, Ebrahim S. Advice to reduce dietary salt for prevention of cardiovascular disease. Cochrane
348. Kaner EFS, Dickinson HO, Beyer F, Pienaar E, Schlesinger C, Campbell F, et al. The effectiveness of brief alcohol interventions in
primary care settings: a systematic review. Drug Alcohol Rev 2009;28(3):301–23
349. Smedslund G, Berg RC, Hammerstrom KT, Steiro A, Leiknes KA, Dahl HM, et al. Motivational interviewing for substance abuse.
350. Apodaca TR, Longabaugh R. Mechanisms of change in motivational interviewing: a review and preliminary evaluation of the
evidence. Addiction 2009;104(5):705–15
351. Lundahl B, Burke BL. The effectiveness and applicability of motivational interviewing: a practice-friendly review of four meta-
analyses. J Clin Psychol 2009;65(11):1232–45
352. Pluijm SM, Smit JH, Tromp EAM, Stel VS. A risk profile for identifying community-dwelling elderly with a high risk of recurrent
falling: results of a 3-year prospective study. Osteoporos Int 2006;17(3):417–25
353. Fletcher PC, Hirdes JP. Risk factor for accidental injuries within senior citizens’ homes: analysis of the Canadian Survey on
Ageing and Independence. J Gerontol Nurs 2005;31(2):49–57
354. Aira M, Hartikainen S, Sulkava R. Community prevalence of alcohol use and concomitant use of medication–a source of
possible risk in the elderly aged 75 and older? Int J Geriatr Psychiatry 2005;20(7):680–5
355. Foxcroft D, Ireland D, Lister-Sharp DJ, Lowe G. Longer-term primary prevention for alcohol misuse in young people: Cochrane
systematic review. Int J Epidemiol 2005;34(4):758–9
356. Whitlock E, Polen MR, Green CA. Behavioral counseling interventions in primary care to reduce risky/harmful alcohol use by
adults: a summary of the evidence for the US Preventive Services Taskforce. Ann Int Med 2004;140(7):557–68
357. Ballesteros J, Gonzales-Pinto A, Querejeta I. Brief interventions for hazardous drinkers delivered in primary care are equally
effective in men and women. Addiction 2004;99(1):103–8
358. Ballesteros J, Duffy JC, Querejeta I. Efficacy of brief interventions for hazardous drinkers in primary care: a systematic review
and meta-analysis. Alcohol Clin Exp Res 2004;28(4):608–18
359. Fell JC, Voas RB. The effectiveness of reducing illegal blood alcohol concentration (BAC) limits for driving: evidence for lowering
the limit to .05 BAC. J Safety Res 2006;37(3):233–43
360. Taylor B, Irving HM, Kanteres F, Room R. The more you drink, the harder you fall: a systematic review and meta-analysis of how
acute alcohol consumption and injury or collision risk increase together. Drug Alcohol Depend 2010;110(1-2):108–16
361. Lunetta P, Smith GS, Penttila A. Unintentional drowning in Finland 1970–2000: a population-based study. Int J Epidemiol
2004;33(5):1053–63
362. Driscoll TR, Harrison JE, Steenkamp M. Alcohol and drowning in Australia. Inj Control Saf Promot 2004;11(3):175–81
363. Kaye S, Darke S. Non-fatal cocaine overdose among injecting and non-injecting cocaine users in Sydney, Australia. Addiction
2004;99(10):1315–22
364. O’Kane CJ, Tutt DC, Bauer LA. Cannabis and driving: a new perspective. Emerg Med (Fremantle) 2002;14(3):296–303
365. Rehm J, Baliunas D, Borges GLG, Graham K. The relation between different dimensions of alcohol consumption and burden of
disease: an overview. Addiction 2010;105(5):817–43
366. Odendaal HJ, Steyn DW, Elliott A, Burd L. Combined effects of cigarette smoking and alcohol consumption on perinatal
outcome. Gynecol Obstet Invest 2009;67(1):1–8
367. Rajendram R, Lewison G, Preedy V. Worldwide alcohol-related research and the disease burden. Alcohol Res Health 2006;41(1):99–106
368. Sullivan LE, Fiellin DA, O’Connor PG. The prevalence and impact of alcohol problems in major depression: a systematic review.
Am J Med 2005;118(4):330–41
369. Morris EP, Stewart SH, Ham LS. The relationship between social anxiety disorder and alcohol use disorders: a critical review.
Clin Psychol Rev 2005;25(6):734–60
8th edition
370. Abrams K, Kushner M, Lisdahl Medina K. The pharmacologic and expectancy effects of alcohol on social anxiety in individuals with
social phobia. Drug Alcohol Depend 2001;64(2):219–31
371. Moore AA, Whiteman EJ, Ward KT. Risks of combined alcohol/medication use in older adults. Am J Geriatr Pharmacother
2007;5(1):64–74
372. Weathermon R, Crabb DW. Alcohol and medication interactions. Alcohol Res Health 1999;23(1):40–54
373. Cuijpers P, Riper H, Lemmers L. The effects on mortality of brief interventions for problem drinking: a meta-analysis. Addiction
2004;99(7):839–45
374. Kaner EF, Dickinson HO, Beyer FR. Effectiveness of brief alcohol interventions in primary care populations. Cochrane Database
Syst Rev 2007;2:CD004148
375. Bertholet N, Daeppen JB, Wietlisbach V. Reduction of alcohol consumption by brief alcohol intervention in primary care: systematic
review and meta-analysis. Arch Intern Med 2005;165(9):986–95
376. Mulvihill C, Taylor L, Thom B. Prevention and reduction of alcohol misuse: evidence briefing. London: Health Development Agency, 2005
377. Babor T, Higgins-Biddle J. Alcohol screening and brief intervention: dissemination strategies for medical practice and public health.
Addiction 2000;95(5):677–86
378. Poikolainen K. Effectiveness of brief interventions to reduce alcohol intake in primary health care populations: a meta-analysis. Prev
Med 1999;28(5):503–9
379. Teesson M, Baillie A, Lynskey M, Manor B. Substance use, dependence and treatment seeking in the United States and Australia:
a cross-national comparison. Drug Alcohol Depend 2006;81(2):149–55
380. Litt J, Egger G. Understanding addictions: tackling smoking and hazardous drinking. In: Egger G, Binns A, Rossner S, eds.
Lifestyle medicine. Sydney: McGraw Hill, 2007
381. Roche A, Freeman T. Brief Interventions: good in theory but weak in practice. Drug Alcohol Rev 2004;23:11–8
382. Aira M, Kauhanen J, Larivaara P. Factors influencing inquiry about patients’ alcohol consumption by primary health care physicians:
qualitative semi-structured interview study. Fam Pract 2003;20(3):270–5
383. Miller NS, Sheppard LM, Colenda CC. Why physicians are unprepared to treat patients who have alcohol- and drug-related
disorders. Acad Med 2001;76(5):410–8
384. Kaner EF, Heather N, Brodie J. Patient and practitioner characteristics predict brief alcohol intervention in primary care. Br J Gen
Pract 2001;512(471):822–7
385. Litt J, Egger G. Understanding addictions: Tackling smoking and hazardous drinking. In: Egger G, Binns A, Rossner S, eds.
Lifestyle medicine. Sydney: McGraw Hill, 2010
386. Raistrick D, Heather N, Godfrey C. Review of the effectiveness of treatment for alcohol problems. London: National Treatment
Agency for Substance Misuse, 2006
387. Litt JC. Exploration of the delivery of prevention in the general practice setting. Department of General Practice. Adelaide: PhD
thesis, Flinders University, 2007
388. Kypri K, Stephenson S, Langley J, Cashell-Smith M, Saunders J, Russell D. Computerised screening for hazardous drinking in
primary care. N Z Med J 2005;118(1224):U1703
389. Bonevski B, Sanson-Fisher RW. Randomised controlled trial of a computer strategy to increase general practitioner preventive
care. Prev Med 1999;29(6):478–86
390. Berner MM, Kriston L, Bentele M. The alcohol use disorders identification test for detecting at-risk drinking: a systematic review
and meta-analysis. J Stud Alcohol Drugs 2007;68(3):461–73
391. Selin KH. Alcohol Use Disorder Identification Test (AUDIT): what does it screen? Performance of the AUDIT against four different
criteria in a Swedish population sample. Subst Use Misuse 2006;41(14):1881–99
392. Anderson P. Overview of interventions to enhance primary-care provider management of patients with substance-use disorders.
Drug Alcohol Rev 2009;28(5):567–74
393. Yoast RA, Wilford BB, Hayashi SW. Encouraging physicians to screen for and intervene in substance use disorders: obstacles and
strategies for change. J Addict Dis 2008;27(3):77–97
394. Babor T, Higgins-Biddle J. Alcohol screening and brief intervention: dissemination strategies for medical practice and public health.
Addiction 2005;95(5):677–86
395. Anderson P, Laurant M, Kaner E. Engaging general practitioners in the management of hazardous and harmful alcohol
consumption: results of a meta-analysis. J Stud Alcohol Drugs 2004;65(2):191–9
8th edition 103
396. Vogt F, Hall S, Marteau TM. General practitioners’ and family physicians’ negative beliefs and attitudes towards discussing
smoking cessation with patients: a systematic review. Addiction 2005;100(10):1423–31
397. Kaner E, Lock C, Heather N, McNamee P. Promoting brief alcohol intervention by nurses in primary care: a cluster
randomised controlled trial. Pat Educ Counsel 2003;51(3):277–84
398. Woodcock J, Franco OH, Orsini N, Roberts I. Non-vigorous physical activity and all-cause mortality: systematic review and
meta-analysis of cohort studies. Int J Epidemiol 2010;40(1):121–38
399. Katzmarzyk PT, Church TS, Craig CL, Bouchard C. Sitting time and mortality from all causes, cardiovascular disease, and
cancer. Med Sci Sports Exerc 2009;41(5):998–1005
400. Lollgen H, Bockenhoff A, Knapp G. Physical activity and all-cause mortality: an updated meta-analysis with different
intensity categories. Int J Sports Med 2009;30(3):213–24
401. National Physical Activity Program Committee, National Heart Foundation of Australia. Physical activity and
energy balance. Heart Foundation, 2007 [accessed 2008 July]. Available at www.heartfoundation.org.au/
SiteCollectionDocuments/physical-activity-and-energy-balance.pdf
402. Shaw K, Gennat H, O’Rourke P, Del Mar C. Exercise for overweight or obesity. Cochrane Database Syst Rev
2006;4:CD003817
403. Department of Health and Ageing (1999) National Physical Activity Guidelines for Australians, Canberra. National physical
activity guidelines for Australians. Canberra: DHAC, 1999
404. Bravata DM, Smith-Spangler C, Sundaram V, Gienger AL, Lin N, Lewis R, et al. Using pedometers to increase physical
activity and improve health. JAMA 2007;298(19):2296–304
405. 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
406. Briffa T, Maiorana A, Allan R. National Heart Foundation of Australia physical activity recommendations for people with
cardiovascular disease. Heart Foundation, 2006
407. The Royal Australian College of General Practitioners. Smoking, Nutrition, Alcohol and Physical (SNAP) activity: a
population health guide to behavioural risk factors for general practices. Melbourne: RACGP, 2004
408. Winzenberg T, Shaw K. Screening for physical inactivity in general practice – a test of diagnostic accuracy. Aust Fam
Physician 2011;40(1–2):57–61
409. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Effect of potentially modifiable risk factors associated
with myocardial infarction in 52 countries (the INTERHEART study): case control sudy. Lancet 2004;364(9438):937–52
410. Bunker S, Colquhoun D, Esler M. Hickie IB, Hunt D, Jelinek VM ‘Stress’ and coronary heart disease: psychosocial risk
factors. National Heart Foundation of Australia position statement update. Med J Aust 2003;178(6):272–6
411. Australian Institute of Health and Welfare. Health determinants, the key to preventing chronic disease. Cat. no. PHE 157.
Canberra: AIHW, 2011
412. Kavanagh A, Bentley RJ, Turrell G, Shaw J, Dunstan D, Subramanian SV. Socioeconomic position, gender, health
behaviours and biomarkers of cardiovascular disease and diabetes. Soc Sci Med 2010;71(6):1150–60
413. Australian Institute of Health and Welfare. Diabetes: Australian facts 2008. Canberra: AIHW, 2008
414. Cass A, Devitt J, Preece C, Cunningham J, Anderson K, Snelling P, et al. Barriers to access by Indigenous Australians to
kidney transplantation: the IMPAKT study. Nephrology 2004;Dec 9(Suppl 4):S144–6
415. Cass A, Cunningham J, Wang Z, Hoy W. Regional variation in the incidence of end-stage renal disease in Indigenous
Australians. Med J Aust 2001;175(1):24–7
416. Australian Institute of Health and Welfare. An overview of chronic kidney disease in Australia, 2009. Canberra: AIHW, 2009
417. 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;58(4):767–85
418. Hoy W, Rees M, Kile E, Mathews J, McCredie D, Pugsley D. Low et al. Birthweight and renal disease in Australian
aborigines. Lancet 1998;352(9143):1826-7
419. Hoy W, Mathews J, McCredie D, Pugsley D, Hayhurst B, Rees M, et al. The multidimensional nature of renal disease: rates
and associations of albuminuria in an Australian Aboriginal community. Kidney Int 1998;54(4):1296–304
420. Cass A, Cunningham J, Wang Z, Hoy W. Social disadvantage and variation in the incidence of end-stage renal disease in
Australian capital cities. Aust N Z J Public Health 2001;25(4):322–6
8th edition
421. Wiggers J, Sanson-Fisher R. Practitioner provision of preventive care in general practice consultations: association with
patient education and occupational status. Soc Sci Med 1997;44(2):137–46
422. Harris M. The role of primary health care in preventing the onset of chronic disease, with a particular focus on the lifestyle
risk factors of obesity, tobacco and alcohol. Commisioned Paper for the National Preventive Task Force. Sydney: Centre
for Primary Health Care and Equity, UNSW, 2008
423. Stocks N, Ryan P, McElroy H, Allan J. Statin prescribing in Australia: socioeconomic and sex differences. A cross sectional
study. Med J Aust 2004;180(5):229–31
424. National Vascular Disease Prevention Alliance. Guidelines for the management of absolute cardiovascular disease risk.
Heart Foundation, 2012
425. National Vascular Disease Prevention Alliance. Guidelines for the assessment of absolute cardiovascular disease risk.
2009. Heart Foundation, 2009
426. van Dis I, Kromhout D, Geleijnse JM, Boer JM, Verschuren WM. Body mass index and waist circumference predict both
10-year nonfatal and fatal cardiovascular disease risk: study conducted in 20,000 Dutch men and women aged 20–65
years. Eur J Cardiovasc Prev Rehabil 2009;16(6):729–34
427. Levy PJ, Jackson SA, McCoy TP, Ferrario CM. Clinical characteristics of patients with premature lower extremity
atherosclerosis associated with familial early cardiovascular disease and/or cancer. Int Angiol 2006;25(3):304–9
428. US Preventive Services Task Force. Screening for high blood pressure: US Preventive Services Task Force reaffirmation
recommendation statement. Ann Intern Med 2007;147(11):783–6
429. National Heart Foundation of Australia (National Blood Pressure and Vascular Disease Advisory Committee).Guide to
management of hypertension 2008. Updated December 2010. Heart Foundation, 2010
430. Vasan RS, Larson MG, Leip EP, Kannel WB, Levy D. Assessment of frequency of progression to hypertension in non-
hypertensive participants in the Framingham Heart Study: a cohort study. Lancet 2001;358(9294):1682–6
431. Australian Institute of Health and Welfare. The health and welfare of Australia’s Aboriginal and Torres Strait Islander
peopless. Canberra: AIHW, 2001
432. Go A, Chertow G, Fan D, McCulloch C, Hsu C-y. Chronic kidney disease and the risks of death, cardiovascular events, and
hospitalization. N Engl J Med 2004;351(13):1296–305
433. Culleton B, Larson M, Wilson P, Evans J, Parfrey P, Levy D. Cardiovascular disease and mortality in a community-based
cohort with mild renal insufficiency. Kidney Int 1999;56(6):2214–9
434. National Stroke Foundation. Clinical guidelines for stroke management. Melbourne: NSF, 2010
435. National Heart Foundation of Australia, The Cardiac Society of Australia and New Zealand. Position statement on lipid
management 2005. Heart Lung Circ 2005;14(4):275–91
436. Bachorik PS, Cloey TA, Finney CA, Lowry DR, Becker DM. Lipoprotein-cholesterol analysis during screening: accuracy
and reliability. Ann Intern Med 1991;114(9):741–7
437. Bradford RH, Bachorik PS, Roberts K, Williams OD, Gotto AM Jr. Blood cholesterol screening in several environments
using a portable, dry-chemistry analyzer and fingerstick blood samples. Lipid Research Clinics Cholesterol Screening
Study Group. Am J Cardiol 1990;65(1):6–13
438. National Health and Medical Research Council. National evidence based guidelines for case detection and diagnosis of
type 2 diabetes. Canberra: NHMRC, 2009
439. 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: NHMRC, 2005
440. Iseki K, Ikemiya Y, Iseki C, Takishita S. Proteinuria and the risk of developing end-stage renal disease. Kidney Int
2003;63(4):1468–74
441. International Diabetes Institute. The Australian type 2 diabetes risk assessment tool. Canberra: AGDHA, 2008
442. Lee TJ, Safranek S. FPIN’s clinical inquiries. A1C testing in the diagnosis of diabetes mellitus. Am Fam Physician
2006;71(1):143–4
443. Bennett CM, Guo M, Dharmage SC. HbA(1c) as a screening tool for detection of type 2 diabetes: a systematic review.
Diabet Med 2007;24(4):333–43
444. Williamson DF, Vinicor F, Bowman BA. Primary prevention of type 2 diabetes mellitus by lifestyle intervention: implications
for health policy. Ann Intern Med 2004;140(11):951–7
8th edition 105
445. Knowler WC, Barrett-Connor E, Fowler S, 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(6):393–403
446. Pan X, Li G, Hu Y, Wang J, Yang W, An Z, et al. Effects of diet and exercise in preventing NIDDM in people with impaired
glucose tolerence: the Da Qing IGT and Diabetes Study. Diabetes Care 1997;20(4):537–44
447. Tuomilehto J, Lindstrom J, Eriksson J, Valle T, Hamalaninen H, Ilanne-Parikka P, et al. Prevention of type 2 diabetes
melllitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001;344(18):1343–11350
448. Wolf PA, Abbot RD, Kannel WB. Atrial fibrillation as an independent risk facor for stroke: the Framingham study. Stroke
1991;22(8):983–8
449. Goldstein LB, Adams R, Alberts MJ, Appel LT, Brass LM, Bushnell CD, et al. Primary prevention of ischemic stroke:
a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the
Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical
Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research
Interdisciplinary Working Group. Circulation 2006;113(24):e873–923
450. National Heart Foundation. National Heart Foundation position statement on Non-valvular atrial fibrillation and stroke
prevention. Med J Aust 2001;174:234–348
451. Scottish Intercollegiate Guidelines Network. SIGN 108 Management of patients with stroke or TIA: assessment,
investigation, immediate management and secondary prevention. A national clinical guideline. Edinburgh: SIGN, 2008
452. Floriani M, Giulini SM, Bonardelli S, Portolani N. Value and limites of ‘critical auscultation’ of neck bruits. Angiology
1988;39(11):967–72
453. Sauve J, Thorpe KE, Sackett DL, Taylor W. Can bruits distinguish high-grade from moderate symptomatic carotid
stenosis? The North American Symptomatic Carotid Endarterectomy Trial. Ann Intern Med 1994;120(8):633–7
454. Pickett CA, Jackson JL, Hemann BA, Atwood JE. Carotid bruit as a prognostic indicator of cardiovascular death and
myocardial infarction: a meta-analysis. Lancet 2008;371(9624):1587–94
455. Wang Y, Chen X, Song Y, Caballero B, Cheskin LJ. Association between obesity and kidney disease: a systematic review
and meta-analysis. Kidney Int 2008;73(1):19–33
456. Chadban S, Briganti EM, Kerr PG, Dunstan DW. Prevalence of kidney damage in Australian adults: the AusDiab kidney
study. J Am Soc Nephrol 2003;14(7 Supp 2):S131–S8
457. Johnson D. Evidence-based guide to slowing the progression of early renal insufficiency. Intern Med J 2004;34(1–2):50–7
458. Fox C, Larson MG, Leip EP, Culleton B, Wilson PWF. Predictors of new-onset kidney disease in a community-based
population. JAMA 2004;29(7)1:844–50
459. Angelantonio ED, 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;341:4986
460. Hallan SI, Dahl K, Oien CM, Grootendorst DC, Aasberg A, Holmen J, et al. Screening strategies for chronic kidney
disease in the general population: follow-up of cross sectional health survey. BMJ 2006;333(7577):1047
461. Astor BC, Hallan SI, Miller ER, Yeung E, Coresh J. Glomerular filtration rate, albuminuria, and risk of cardiovascular and
all-cause mortality in the US population. Am J Epidemiol 2008;167(10):1226–34
462. Crowe E, Halpin D, Stevens P. Early identification and management of chronic kidney disease: summary of NICE
guidance. BMJ 2008;337:a1530
463. Eknoyan G, Hostetter T, Bakris GL, Hebert L, Levey AS, Parving HH, et al. Proteinuria and other markers of chronic
kidney disease: a position statement of the National Kidney Foundation (NKF) and the National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK). Am J Kidney Dis 2003;42(4):617–22
464. Bleyer A, Shemanski LR, Burke GL, Hansen KJ. Tobacco, hypertension, and vascular disease: risk factors for renal
functional decline in an older population. Kidney Int 2000;57(5):2072–9
465. Methven S, MacGregor MS, Traynor JP, Hair M, O’Reilly DS, Deighan CJ. Comparison of urinary albumin and urinary total
protein as predictors of patient outcomes in CKD. Am J Kidney Dis 2010;57(1):21–8
466. Levey AS, Coresh J, Balk E, Kausz AT, Levin A. National Kidney Foundation practice guidelines for chronic kidney
disease: evaluation, classification, and stratification. Ann Intern Med 2003;139(2):137–47
467. Scottish Intercollegiate Guidelines Network. SIGN103. Diagnosis and management of chronic kidney disease: a national
clinical guideline, Edinburgh: SIGN, 2008
468. Kidney Health Australia. Chronic kidney disease (CKD) management in general practice. Melbourne: KHA, 2007
8th edition
469. Kidney Health Australia. National Chronic Kidney Disease Strategy. Melbourne: KHA, 2006
470. Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF 3rd, Feldman HI, et al. A new equation to estimate glomerular
filtration rate. Ann Intern Med 2009;150(9):604–12
471. Australian Cancer Network Melanoma Guidelines Revision Working Party. Clinical Practice Guidelines for the
Management of Melanoma in Australian and New Zealand. Wellington: New Zealand Guidelines Group, Sydney and New
Zealand Guidelines Group, Wellington, 2008
472. Green AC, Williams GM, Logan V, Strutton GM. Reduced melanoma after regular sunscreen use: randomised trial follow-
up. J Clin Oncol 2011;29(3):257–63
473. Gefeller O, Pfahlberg A. Sunscreen use and melanoma: a case of evidence-based prevention? Photodermatol
Photoimmunol Photomed 2002;18(3):153–6
474. Marks R. Photoprotection and prevention of melanoma. Eur J Dermatol 1999;9(5):406–12
475. Azizi E, Iscovich J, Pavlotsky F, Shafir R, Luria I, Federenko L, et al. Use of sunscreen is linked with elevated naevi counts
in Israeli school children and adolescents. Melanoma Res 2000;10(5):491–8
476. English DR, Milne E, Simpson JA. Sun protection and the development of melanocytic nevi in children. Cancer Epidemiol
Biomarkers Prev 2005;14(12):2873–6
477. Goldenhersh MA. Increased melanoma after regular sunscreen use? J Clin Oncol 2011;29(18):e557–8
478. MacKie R, McHenry P, Hole D. Accelerated detection with prospective surveillance for cutaneous malignant melanoma in
high-risk groups. Lancet 1993;341(8861):1618–20
479. New Zealand Dermatological Society. New Zealand guidelines on the general management of malignant melanoma. NZDS, 2004
480. Baade PD, Balanda KP, Stanton WR, Lowe JB, Del Mar CB. Community perceptions of suspicious pigmented skin
lesions: are they accurate when compared to general practitioners? Cancer Detect Prev 2005;29(3):267–75
481. Hanrahan P, D’Este CA, Menzies SW, Plummer T, Hersey P. A randomised trial of skin photography as an aid to screening
skin lesions in older males. J Med Screening 2002;9(3):128–32
482. English D, Del Mar C, Burton R. Factors influencing the number needed to excise: excision rates of pigmented lesions by
general practitioners. Med J Aust 2004;180(1):16–9
483. Smith W. Skin cancer in Australia and the case for screening in general practice. Brisbane: University of Queensland, 2003
484. Kelly J, Chamberlain AJ, Staples MP, McAvoy B. Nodular melanoma. No longer as simple as ABC. Aust Fam Physician
2003;32(9):706–9
485. Scope A, Dusza SW, Halpern AC, Rabinovitz H. The ‘ugly duckling’ sign: agreement between observers. Arch Dermatol
2008;144(1):58–64
486. Zalaudek I, Kittler H, Marghoob AA, Balato A. Time required for a complete skin examination with and without
dermoscopy: a prospective, randomized multicenter study. Arch Dermatol 2008;144(4):509–13
487. Kanzler M, Mraz-Gernhard S. Primary cutaneous malignant melanoma and its precursor lesions: diagnostic and
therapeutic overview. J Am Acad Dermatol 2001;45(2):260–76
488. Green A, Williams G, Neale R, Hart V, Leslie D, Parsons P, et al. Daily sunscreen application and betacarotene
supplementation in prevention of basal-cell and squamous-cell carcinomas of the skin: a randomised controlled trial.
Lancet 1999;354(9180):723–9
489. National Health and Medical Research Council. Clinical practice guidelines non-melanoma skin cancer: Guidelines for
treatment and management in Australia. Canberra: NHMRC, 2002
490. Czarnecki D, Mar A, Staples M, Giles G, Meehan C. The development of non-melanocytic skin cancers in people with a
history of skin cancer. Dermatology 1994;189(4):364–7
491. Canadian Task Force on Periodic Health Examination. The Canadian guide to clinical preventive health care. Ottawa:
CTFPHE, 2000
492. Sasieni P, Castanon A, Cuzic J. Effectiveness of cervical screening with age: population based case-control study of
prospectively recorded data. BMJ 2009;339:b2968
493. National Health and Medical Research Council. Screening to prevent cervical cancer: Guidelines for the management of
asymptomatic women with screen detected abnormalities. Canberra: NHMRC, 2005
494. Skinner SR, Garland SM, Stanley MA, Pitts M, Quinn MA. Human papillomavirus vaccination for the prevention of cervical
neoplasia: is it appropriate to vaccinate women older than 26? Med J Aust 2008;188(4):238–42
8th edition 107
495. EUROGIN. Conclusions: cervical cancer control, priorities and new directions: international charter. France: EUROGIN, 2003
496. Monsonego J, Bosch FX, Coursaget P, Cox JT, Franco E, Frazer I, et al. Cervical cancer control, priorities and new directions. Int
J Cancer 2004;108(3):329–33
497. Buntinx F, Brouwers M. Relation between sampling device and detection of abnormality in cervical smears: a meta-analysis of
randomised and quasi-randomised studies. BMJ 1996;313(7068):1285–90
498. Mayrand MH, Duarte-Franco E, Rodrigues I, Walter SD, Hanley J, Ferenczy A, et al. Canadian Cervical Cancer Screening
Trial Study Group. Human papillomavirus DNA versus papanicolaou screening tests for cervical cancer. N Engl Med J
2007;357(16):1579–88
499. Koliopoulos G, Arbyn M, Martin-Hirsch P, Kyrgiou M, Prendiville W, Paraskevaidis E. Diagnostic accuracy of human papillomavirus
testing in primary cervical screening: a systematic review and meta-analysis of non-randomized studies. Gynecol Oncol
2007;104(1):232–46
500. Safaeian M, Solomon D, Wacholder S, Schiffman M, Castle P. Risk of precancer and follow-up management strategies for women
with human papillomavirus-negative atypical squamous cells of undetermined significance. Obstet Gynecol 2007;109(6):1325–31
501. Arbyn M, Buntinx F, Van Ranst M, Paraskevaidis E, Martin-Hirsch P, Dillner J. Virologic versus cytologic triage of women
with equivocal Pap smears: a meta-analysis of the accuracy to detect high-grade intraepithelial neoplasia. J Natl Cancer Inst
2004;96(4):280–93
502. Arbyn M, Paraskevaidis E, Martin-Hirsch P, Prendiville W, Dillner J. Clinical utility of HPV-DNA detection: triage of minor cervical
lesions, follow-up of women treated for high-grade CIN: an update of pooled evidence. Gynecol Oncol 2005;99(3 Suppl 1):S7–11
503. Davey E, Barratt A, Irwig L, Chan SF, Macaskill P, Mannes P, et al. Effect of study design and quality on unsatisfactory rates,
cytology classifications, and accuracy in liquid-based versus conventional cervical cytology: a systematic review. Lancet
2006;367(9505):122–32
504. Ronco G, Cuzick J, Pierotti P, Cariaggi MP, Dalla Palma P, Naldoni C, et al. Accuracy of liquid based versus conventional cytology:
overall results of new technologies for cervical cancer screening: randomised controlled trial. BMJ 2007;335(7609):28
505. Everett T, Bryant A, Griffin MF, Martin-Hirsch PPL, Forbes CA, Jepson RG. Interventions targeted at women to encourage the
uptake of cervical screening. Cochrane Database Syst Rev 2011;5:CD002834
506. National Breast and Ovarian Cancer Centre. Early detection of breast cancer – NBOCC Position statement. Sydney: NBOCC,
2009 [accessed 2012 May]. Available at www.nbocc.org.au/our-organisation/position-statements/early-detection-of-breast-
cancer
507. National Breast and Ovarian Cancer Centre. Advice about familial aspects of breast and epithelial ovarian cancer: a guide for
health professionals. Sydney: NBOCC, 2010 [accessed 2012 May]. Available at www.nbocc.org.au/view-document-details/bog-
advice-about-familial-aspects-of-breast-cancer-and-epithelial-ovarian-cancer
508. Nelson HD, Tyne K, Naik A, Bougatsos C, Chan BK, Humphrey L. Screening for breast cancer: An update for the US Preventive
Services Task Force. Ann Intern Med 2009;151(10):727–37
509. Australian Government Department of Health and Ageing. BreastScreen Australia evaluation final report. Canberra: AGDHA, 2009
510. Bonfill X, Marzo M, Pladevall M, Marti J, Emparanza JI. Strategies for increasing the participation of women in community breast
cancer screening. Cochrane Database Syst Rev 2001;1:CD002943
511. Thune I, Brenn T, Lund E, Gaard M. Physical activity and the risk of breast cancer. N Engl J Med 1997;336(18):1269–75
512. International Agency for Research on Cancer. Weight control and physical activity. Lyon: IARC, 2002
513. Buys SS, Partridge E, Black A, Johnson CC, Lamerato L, Isaacs C, et al. Effect of screening on ovarian cancer mortality: the
Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Randomized Controlled Trial. JAMA 2011;305(22):2295–303
514. Whittemore AS, Harris R, Itnyre J. Characteristics relating to ovarian cancer risk: collaborative analysis of 12 US case-
control studies. II. Invasive epithelial ovarian cancers in white women. Collaborative Ovarian Cancer Group. Am J Epidemiol
1992;136(10):1184–203
515. Kerlikowske K, Brown JS, Grady DG. Should women with familial ovarian cancer undergo prophylactic oophorectomy? Obstet
Gynecol 1992;80(4):700–7
516. Ford D, Easton DF. The genetics of breast and ovarian cancer. Br J Cancer 1995;72(4):805–12
517. Brocklehurst P, Kujan O, Glenny AM, Oliver R, Sloan P, Ogden G, et al. Screening programmes for the early detection and
prevention of oral cancer. Cochrane Database Syst Rev 2010;11:CD004150
518. National Cancer Institute. Oral cancer screening. Bethesda, MD: US National Institutes of Health, 2012 [accessed 2012 June].
Available at cancer.gov/cancertopics/pdq/screening/oral/HealthProfessional
8th edition
519. Smith RA, Cokkinides V, Brooks D, Saslow D, Brawley OW. Cancer screening in the United States, 2011: a review of
current American Cancer Society guidelines and issues in cancer screening. CA Cancer J Clin 2011;61(1):8–30
520. US Preventive Services Task Force. Screening for oral cancer: recommendation statement. Rockville, MD: Agency
for Healthcare Research and Quality, 2004 [accessed 2012 June]. Available at www.uspreventiveservicestaskforce.
org/3rduspstf/oralcan/oralcanup.htm
521. Sugerman P, Savage N. Current concepts in oral cancer. Aust Dent J 1999;44(3):147–56
522. Australian Cancer Network Colorectal Cancer Guidelines Revision Committee. Guidelines for the prevention, early
detection and management of colorectal cancer. Sydney: Cancer Council Australia and Australian Cancer Network, 2005
523. Zauber AG, Lansdorp-Vogelaar I, Knudsen AB, Wilschut J. Evaluating test strategies for colorectal cancer screening –
age to begin, age to stop, and timing of screening intervals: a decision analysis of colorectal cancer screening for the US
Preventive Services Task Force from the Cancer Intervention and Surveillance Modeling Network (CISNET). Rockville,
MD: Agency for Healthcare Research and Quality, 2009
524. Cole SR, Young GP, Byrne D, Guy JR, Morcom J. Participation in screening for colorectal cancer based on a faecal occult
blood test is improved by endorsement from the primary care practitioner. J Med Screening 2002;9(4):147–52
525. Salked GP, Solomon MJ, Short L, Ward J. Measuring the attributes that influence consumer attitudes to colorectal cancer
screening. A N Z J Surgery 2003;73(3):128–32
526. Klabunde CN, Lanier D, Breslau ES, Zapka JG, Fletcher RH, Ransohoff DF, et al. Improving colorectal cancer screening in
primary care practice: innovative strategies and future directions. J Gen Intern Med 2007;22(8):1195–205
527. Hewitson P, Glasziou PP, Irwig L, Towler B, Watson E. Screening for colorectal cancer using the faecal occult blood test,
Hemoccult. Cochrane Database Syst Rev 2007;1:CD001216
528. National Cancer Institute. Colorectal cancer screening. US National Institutes of Health, 2012 [accessed 2012 June].
Available at www.cancer.gov/cancertopics/pdq/screening/colorectal/HealthProfessional/page4
529. Australian Cancer Network. Familial aspects of bowel cancer: a guide for health professionals. Canberra: NHMRC, 2002
530. National Cancer Institute. Genetics of colorectal cancer. US National Institutes of Health, 2012 [accessed 2012 June].
Available at www.cancer.gov/cancertopics/pdq/genetics/colorectal/HealthProfessional/page1
531. Umar A, Boland CR, Terdiman JP, Syngal S, de la Chapelle A, Ruschoff J, et al. Revised Bethesda Guidelines
for hereditary nonpolyposis colorectal cancer (Lynch syndrome) and microsatellite instability. J Natl Cancer Inst
2004;96(4):261–8
532. Burn J, Gerdes AM, Macrae F, Mecklin JP, Moeslein G, Oschwang M, et al. Long-term effect of aspirin on cancer
risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial. Lancet
2011;378(9809):2081–7
533. Rothwell PM, Fowkes PG, Belch JP, Ogawa H, Warlow CP, Meade TW. Effect of daily aspirin on long-term risk of death
due to cancer – analysis of individual patient data from randomised trials. Lancet 2011;377(9759):31–41
534. Rothwell PM, Wilson M, Elwin CE, Norrving B, Algra A, Warlow CP, et al. Long-term effect of aspirin on colorectal cancer
incidence and mortality: 20 year follow up of 5 randomized controlled trials. Lancet 2010;376(9754):1741–50
535. van Dam L, Kuipers EJ, van Leerdama ME. Performance improvements of stool-based screening tests. Best Pract Res
Clin Gastroenterol 2010;24(4):479–92
536. Holden DJ, Jonas DE, Porterfield DS, Reuland D, Harris R. Systematic review: enhancing the use and quality of colorectal
cancer screening. Ann Intern Med 2010;152(10):668–76
537. Steinwachs D, Allen JD, Barlow WE, Duncan RP, Egede LE, Friedman LS, et al. National Institutes of Health state-
of-the-science conference statement: enhancing use and quality of colorectal cancer screening. Ann Intern Med
2010;152(10):663–7
538. Zapka J, Taplin SH, Price RA, Cranos C, Yabroff R. Factors in quality care--the case of follow-up to abnormal cancer
screening tests--problems in the steps and interfaces of care. J Natl Cancer Inst Monogr. 2010;2010(40):58–71
539. Senore C, Malila N, Minozzi S, Armarolia P. How to enhance physician and public acceptance and utilisation of colon
cancer screening recommendations. Best Pract Res Clin Gastroenterol 2010;24(4):509–20
8th edition 109
540. Australian Government Department of Health and Ageing. National Bowel Cancer Screening Program. Canberra: AGDHA,
2012 [accessed 2012 June]. Available at www.cancerscreening.gov.au/internet/screening/publishing.nsf/Content/bowel-about
541. Pignone MP, Flitcroft KL, Howard K, Trevena LJ, Salkeld GP, St John DJB. Costs and cost-effectiveness of full
implementation of a biennial faecal occult blood test screening program for bowel cancer in Australia. Med J Aust
2011;194(4):180–5
542. Condon JR, Barnes T, Cunningham J, Armstrong B. Long-term trends in cancer mortality for Indigenous Australians in
the Northern Territory. Med J Aust 2004;180(10):504–7
543. Valery PC, Coory M, Stirling J, Green AC. Cancer diagnosis, treatment, and survival in Indigenous and non-Indigenous
Australians: a matched cohort study. Lancet 2006;367(9525):1842–8
544. US Preventive Services Task Force. Screening for testicular cancer: recommendation statement. Rockville, MD: Agency
for Healthcare Research and Quality, 2011
545. Elford RW. Screening for testicular cancer. Canadian Task Force on the Periodic Health Examination Canadian Guide to
Clinical Preventive Health Care. Ottawa: Health Canada, 1994
546. Dieckmann KP, Pichlmeier U. Clinical epidemiology of testicular germ cell tumors. World J Urol 2004;22(1):2–14
547. National Cancer Institute. Testicular cancer screening. Bethesda, MD: National Institutes of Health, 2012 [accessed 2012
June]. Available at www.cancer.gov/cancertopics/pdq/screening/testicular/Patient/page3
548. US Preventive Services Task Force. Screening for prostate cancer: US Preventive Services Task Force Recommendation
Statement. Ann Intern Med 2008;149(3):185–91
549. Lim LS, Sherin K, ACPM Prevention Practice Committee. Screening for prostate cancer in US men: ACPM position
statement on preventive practice. Am J Prev Med 2008;34(2):164–70
550. Ilic D, O’Connor D, Green S, Wilt T. Screening for prostate cancer. Cochrane Database Syst Rev 2006;3:CD004720
551. Coley CM, Barry MJ, Fleming C, Mulley AG. Early detection of prostate cancer. Part I: Prior probability and effectiveness
of tests. Ann Intern Med 1997;126(5):394–406
552. Andriole GL, Crawford ED, Grubb RL, 3rd, Buys SS, Chia D, Church TR, et al. Mortality results from a randomized
prostate-cancer screening trial. New Engl J Med 2009;360(13):1310–9
553. Schroder FH, Hugosson J, Roobol MJ, Tammela TLJ, Ciatto S, Nelen V, et al. Screening and prostate-cancer mortality in
a randomized European study. New Engl J Med 2009;360(13):1320–8
554. Hugosson J, Carlsson S, Aus G, Bergdahl S, Khatami A, Lodding P, et al. Mortality results from the Göteborg randomised
population-based prostate-cancer screening trial. Lancet Oncol 2010;11(8):725–32
555. Ilic D, O’Connor D, Green S, Wilt TJ. Screening for prostate cancer: an updated Cochrane systematic review. BJU Int
2011;107(6):882–91
556. Djulbegovic M, Beyth RJ, Neuberger MM, Stoffs TL, Vieweg J, Djulbegovic B, et al. Screening for prostate cancer:
systematic review and meta-analysis of randomised controlled trials. BMJ (Clinical Research Ed) 2010;341:c4543
557. National Health and Medical Research Council. Clinical practice guidelines for the management of uncomplicated lower
urinary tract symptoms in men. Canberra: NHMRC, 1997
558. Bruner DW, Moore D, Parlanti A, Dorgan J, Engstron P. Relative risk of prostate cancer for men with affected relatives:
systematic review and meta-analysis. Int J Cancer 2003;107(5):797–803
559. Johns LE, Houlston RS. A systematic review and meta-analysis of familial prostate cancer risk. BJU Int 2003;91(9):789–94
560. Zeegers MP, 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
561. Alemozaffar M, Regan MM, Cooperberg MR, Wei JT, Michalski JM, Sandler HM, et al. Prediction of erectile function
following treatment for prostate cancer. JAMA 2011;306(11):1204–14
562. Sanda MG, Dunn RL, Michalski J, Sandler HM, Northouse L, Hembroff L, et al. Quality of life and satisfaction with
outcome among prostate-cancer survivors. N Engl J Med 2008;358(12):1250–61
563. Fall K, Fang F, Mucci LA, Ye W, Andrén O, Johansson J-E, et al. Immediate risk for cardiovascular events and suicide
following a prostate cancer diagnosis: prospective cohort study. PLoS Med 2009;6(12):e1000197
564. Bowden FJ, Roberts J, Collignon PJ. Prostate cancer screening and bacteraemia (letter). Med J Aust 2008;188(1):60
565. Gattellari M, Ward J. Does evidence-based information about screening for prostate cancer enhance consumer decision-
making? A randomised controlled trial. J Med Screen 2003;10(1):27–39
8th edition
566. Chapman S, Barratt A, Stockler M. Let sleeping dogs lie? What men should know before getting tested for prostate cancer.
Sydney: Sydney University Press, 2010 [accessed 2012 June]. Available at ses.library.usyd.edu.au/bitstream/2123/6835/3/Let-
sleeping-dogs-lie.pdf
567. Slade T, Johnston A, Oakley Browne MA, Andrews G, Whiteford H. 2007 National Survey of Mental Health and Wellbeing:
methods and key findings. Aust N Z J Psychiatry 2009;43(7):594–605
568. Campbell J, Laughon K, Woods A. Impact of intimate partner abuse on physical and mental health: how does it present in
clinical practice? In: Roberts G, Hegarty K, Feder G, eds. Intimate partner abuse and health professionals: new approaches to
domestic violence. London: Elsevier, 2006:43–60
569. Australian Bureau of Statistics. 4102.0 Health and socioeconomic disadvantage. Canberra: ABS, 2010
570. Lorant V, Deliege D, Eaton W, Robert A. Socioeconomic inequalities in depression: a meta-analysis. Am J Epidemiol
2003;157(2):98–112
571. Harris MF, Harris E, Shortus TD. How do we manage patients who become unemployed? Med J Aust 2010;192(2):98–101
572. Comino E, Harris E, Chey T, Manicavasagar V. Relationship between mental health disorders and unemployment status in
Australian adults. Aust N Z J Psychiatry 2003;37(2):230–5
573. Averill P, Novy DM, Nelson DV, Berry LA. Correlates of depression in chronic pain patients: a comprehensive examination. Pain
1996;65(1):93–100
574. Furler J, Kokanovic R, Dowrick C, Newton D, Gunn J, May C. Managing depression among ethnic communities: a qualitative
study. Ann Fam Med 2010;8(3):231–6
575. Ostler K, Thompson C, Kinmonth ALK, Peveler RC. Influence of socio-economic deprivation on the prevalence and outcome
of depression in primary care: the Hampshire Depression Project. Brit J Psych 2001;178(1):12–7
576. Lynch J, Smith GD, Harper SAM, Hillemeier H. Is income inequality a determinant of population health? Part 2. US national
and regional trends in income inequality and age- and cause-specific mortality. Milbank Quarterly 2004;82(2):355–400
577. Neeleman J. Beyond risk theory: suicidal behavior in its social and epidemiological context. Crisis 2002;23(3):114–20
578. Welch S. A review of the literature on the epidemiology of parasuicide in the general population. Psychiatric Services
2001;52(3):368–75
579. Stack S. Suicide: a 15-year review of the sociological literature. Part I: Cultural and economic factors. Suicide & Life-
Threatening Behavior 2000;32(2):145–62
580. Beautrais A. Risk factors for suicide and attempted suicide among young people. A literature review prepared for the NHMRC.
Canberra: AGPS 1998
581. Cantor C. The epidemiology of suicide and attempted suicide among young Australians. A literature review prepared for the
NHMRC. Canberra: AGPS 1998
582. Beautrais A, Joyce P, Mulder R. Unemployment and serious suicide attempts. Psychological Medicine 1998;28(1):209–18
583. Hunter E, Harvey D. Indigenous suicide in Australia, New Zealand, Canada, and the United States. Emerg Med 2002;14(1):14–23
584. Lansakara N, Brown SJ, Gartland D. Birth outcomes, postpartum health and primary care contacts of immigrant mothers in
an Australian nulliparous pregnancy cohort study. Matern Child Health J 2010;14(5):807–16
585. US Preventive Services Task Force. Screening for depression in adults, topic page. Rockville, MD: USPSTF, 2009 [accessed
2012 June]. Available at www.uspreventiveservicestaskforce.org/uspstf/uspsaddepr.htm
586. US Preventive Services Task Force. Screening and treatment for major depressive disorder in children and adolescents:
clinical summary. Rockville, MD: USPSTF, 2009 [accessed 2012 June]. Available at www.uspreventiveservicestaskforce.org/
uspstf09/depression/chdeprsum.htm
587. Chown, P, Kang M, Sanci L, Newnham V, Bennett DL. Adolescent health: enhancing the skills of general practitioners in
caring for young people from culturally diverse backgrounds, GP Resource Kit 2nd edn. Westmead: NSW Centre for the
Advancement of Adolescent Health, 2008
588. Sanci L, Lewis D, Patton G. Detecting emotional disorder in young people in primary care. Curr Opin Psychiatry
2010;23(4):318–23
589. National Collaborating Centre for Mental Health. Depression: the treatment and management of depression in adults. NICE
clinical guideline 90. London: NICE, 2009
590. Arroll B, Goodyear-Smith F, Kerse N, Fishman T. Effect of the addition of a ‘help’ question to two screening questions on
specificity for diagnosis of depression in general practice: diagnostic validity study. BMJ 2005;331(7521):884
8th edition 111
591. Austin M-P, Highet N, Guidelines Expert Advisory Committee. Clinical practice guidelines for depression and related
disorders – anxiety, bipolar disorder and puerperal psychosis – in the perinatal period. A guideline for primary care health
professionals. Melbourne: beyondblue, 2011
592. Gaynes BN, West SL, Ford CA, Frame P, Klein J, Lohr KN. 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
593. Goldney RD. Suicide prevention: a pragmatic review of recent studies. Crisis 2005;26(3):128–40
594. Hall W, Mant A, Mitchell PB, Rendle VA, Hickie IB. Association between antidepressant prescribing and suicide in
Australia, 1991–2000 trend analysis. BMJ 2003;326(7397):1008–12
595. O’Connor EA, Whitlock EP, Beil TL, Gaynes BN. Screening for depression in adults: US Preventive Services Task Force
Recommendation Statement. Ann Intern Med 2009;151(11):793–803
596. McNamee J, Offord D. Prevention of suicide. The Canadian guide to clinical preventive health care. Ottawa: Health
Canada, 1994
597. US Preventive Services Task Force. Screening for suicide risk, Topic page. Rockville, MD: Agency for Healthcare
Research and Quality, 2004
598. Goldney RD. Suicide prevention. Oxford: Oxford University Press, 2008
599. The Royal Australian College of General Practitioners. Abuse and violence: working with our patients in general practice,
3rd edn. Mebourne: RACGP, 2008
600. Feder G, Davies RA, Baird K, Dunne D, Eldridge S, Griffiths C, et al. Identification and Referral to Improve Safety (IRIS)
of women experiencing domestic violence with primary care training and support programme: a cluster randomised
controlled trial. Lancet 2011;378(9805):1788–95
601. Victorian Government Department of Justice. Management of the whole family when intimate partner violence is present:
guidelines for primary care physicians. Melbourne: Victorian Government Department of Justice, 2006 [accessed 2008].
Available at www.racgp.org.au/guidelines/intimatepartnerabuse
602. National Health and Medical Research Council. A systematic review of the efficacy and safety of fluoridation. Canberra:
NHMRC, 2007
603. National Health and Medical Research Council. Review of water fluoridation and fluoride intake from discretionary fluoride
supplements. Canberra: NHMRC, 1999
604. 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
605. Walsh T, Worthington HV, Glenny A-M, Appelbe P, Marinho VCC, Shi X. Fluoride toothpastes of different concentrations
for preventing dental caries in children and adolescents. Cochrane Database Syst Rev 2010;1:CD007868
606. Marinho VCC, Higgins JPT, Logan S, Sheiham A. Fluoride gels for preventing dental caries in children and adolescents.
607. Nordblan A. Smart Habit Xylitol Campaign: a new approach in oral health promotion. Comm Dental Health 1995;12(4):230–4
608. National Oral Health Promotion Clearing House. Oral health messages for the Australian public. Findings of a national
consensus workshop. Aust Dent J 2011;56(3):331–5
609. Australian Institute of Health and Welfare. Oral health and dental care in Australia: key facts and figures 2011. Cat. no.
DEN 214. Canberra: AIHW, 2011
610. AIHW Dental Statistics and Research Unit. Research report no. 9. Social determinants of oral health. Canberra: AIHW,
2003
611. National Health and Medical Research Council. A guide to glaucoma for primary health care providers – a companion
document to NHMRC Guidelines for the screening, prognosis, diagnosis, management and prevention of glaucoma.
Canberra: NHMRC, 2010
612. National Health and Medical Research Council. Guidelines for the screening, prognosis, diagnosis, management and
prevention of glaucoma. Canberra: NHMRC, 2010
613. Continence Foundation of Australia. What is incontinence: key statistics. CFA, 2011 [accessed 2011 May]. Available at
www.continence.org.au/pages/key-statistics.html
614. Bower W, ed. An epidemiological study of enuresis in Australian children. Sydney: Wells Medical, 1995
615. Parsons BA, Evans S, Wright M. Prostate cancer and urinary incontinence. Maturitas 2009;63(4):323–8
8th edition
616. Shawa C, Gupta RD, Bushnell DM, Passassa R, Abrams P, Wagg A. The extent and severity of urinary incontinence amongst
women in UK GP waiting rooms. Fam Pract 2006;23(5):497–506
617. Martin JL, Williams KS, Sutton AJ, Abrams KR, Assassa RP. Systematic review and meta-analysis of methods of diagnostic
assessment for urinary incontinence. Neurourol Urodyn 2006;25(7):674–83
618. Brown J, Bradley C, Subak L, Richter H, Kraus S, Brubaker L. The sensitivity and specificity of a simple test to distinguish
between urge and stress incontinence. Ann Intern Med 2006;144(10):715–23
619. Staskin D, Kelleher C, Avery K, Bosch R, Cotterill N, Coyne K, et al., editors. Committee 5: Initial assessment of incontinence.
Proceedings of the fourth international consultation on incontinence, 2009. Paris: France Health Publication Ltd, 2009
620. National Health and Medical Research Council. Clinical practice guideline for the prevention and treatment of osteoporosis in
postmenopausal women and older men. Melbourne: RACGP, 2010
621. Nelson HD, Haney EM, Chou R, Dana T, Fu R, Bougatsos C. Screening for osteoporosis: systematic review to update the
2002 US Preventive Services Task Force Recommendation. Evidence syntheses no. 77. Rockville, MD: Agency for Healthcare
Research and Quality, 2010
622. US Preventive Services Task Force. Screening for osteoporosis: clinical summary of US Preventive Services Task Force
Recommendation. Rockville, MD: Agency for Healthcare Research and Quality, 2011
623. Nakamura T, Tsujimoto M, Hamaya E, Sowa H, Chen P. Consistency of fracture risk reduction in Japanese and Caucasian
osteoporosis patients treated with teriparatide: a meta-analysis. J Bone Miner Metab 2012;30(3):321–5
624. Frost SA, Nguyen ND, Center JR, Eisman JA, Nguyen TV. Timing of repeat BMD measurements: Development of an absolute
risk-based prognostic model. J Bone Miner Res 2009;24(11):1800–7
625. Bolland MJ, Barber PA, Doughty RN, Mason B, Horne A, Ames R, et al. Vascular events in healthy older women receiving
calcium supplementation: randomised controlled trial. BMJ 2008;336(7638):262–6
626. Bolland MJ. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta analysis. BMJ
2010;341:3691
627. Lewis JR, Calver J, Zhu K, Flicker L, Prince RL. Response to ‘calcium supplements and cardiovascular risk’. J Bone Miner Res
2011;26(4):900–1
628. Winzenberg T, van der Mei I, Mason RS, Nowson C, Jones G. Vitamin D and the musculoskeletal health of older adults. Aust
Fam Physician 2012;41(3):92–9
629. National Institute of Clinical Studies. Evidence – practice gaps report. Melbourne: NICS, 2005
630. Barrack CM, McGirr EE, Fuller JD, Foster NM, Ewald DP. Secondary prevention of osteoporosis post minimal trauma fracture
in an Australian regional and rural population. Aust J Rural Health 2009;17(6):310–5
631. Ewald DP, Eisman JA, Ewald BD, Winzenberg TM, Seibel MJ, Ebeling PR, et al. Population rates of bone densitometry use in
Australia, 2001–2005, by sex and rural versus urban location. Med J Aust 2009;190(3):126–8
632. Udesky L. The ethics of direct-to-consumer genetic testing. Lancet 2010;376(9750):1377–8
633. Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group. Recommendations from the
EGAPP Working Group: genomic profiling to assess cardiovascular risk to improve cardiovascular health. Genet Med
2010;12(12):839–43
634. Taylor AJ. CCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 appropriate use criteria for cardiac computed
tomography. J Am Coll Cardiol 2010;56(22):1864–94
635. McEvoy JW, Blaha MJ, DeFilippis AP. Coronary artery calcium progression: an important clinical measurement? A review of
published reports. J Am Coll Cardiol 2010;56(20):1613–22
636. US Preventive Services Task Force. Using nontraditional risk factors in coronary heart disease risk assessment: US Preventive
Services Task Force recommendation statement. Ann Intern Med 2009;151(7):474–82
637. Loland KH, Bleie Ø, Blix AJ, Strand E. Effect of homocysteine-lowering B vitamin treatment on angiographic progression of coronary
artery disease: a Western Norway B Vitamin Intervention Trial (WENBIT) substudy. Am J Cardiol 2010;105(11):1577–84
638. Potter K, Lenzo N, Eikelboom JW. Effect of long-term homocysteine reduction with B vitamins on arterial wall inflammation
assessed by fluorodeoxyglucose positron emission tomography: a randomised double-blind, placebo-controlled trial.
Cerebrovasc Dis 2009;27(3):259–65
639. Lim LS, Haq N, Mahmood S. Atherosclerotic cardiovascular disease screening in adults: American College Of Preventive
Medicine position statement on preventive practice. Am J Prev Med 2011;40(3):381.e1–10
8th edition 113
640. Helfand M, Buckley DI, Freeman M, Fu R. 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
641. Genest J, McPherson R, Frohlich J. Canadian Cardiovascular Society/Canadian guidelines for the diagnosis and treatment of
dyslipidemia and 2 prevention of cardiovascular disease in the adult – 2009 recommendations. Can J Cardiol 2009;25(10):567–79
642. Buckley DI, Fu R, Freeman F, Rogers K. C-reactive protein as a risk factor for coronary heart disease: a systematic review and
meta-analyses for the US Preventive Services Task Force. Ann Intern Med 2009;151(7):483–95
643. Kones R. The Jupiter study, CRP screening, and aggressive statin therapy – implications for the primary prevention of
cardiovascular disease. Ther Adv Cardiovasc Dis 2009;3(4):309–15
644. Grondal N, Søgaard R, Henneberg EW. The Viborg Vascular (VIVA) screening trial of 65–74 year old men in the central region
of Denmark: study protocol. Trials 2010;11:67
645. Fowkes FG, Jamrozik K. Ankle brachial index combined with Framingham Risk Score to predict cardiovascular events and
mortality: a meta-analysis. JAMA 2008;300(2):197–208
646. National Breast Cancer Centre. Magnetic resonance imaging for the early detection of breast cancer in women at high risk: a
systematic review of the evidence. Sydney: NBCC, 2006 [accessed 2012 May]. Available at canceraustralia.nbocc.org.au/view-
document-details/mri-magnetic-resonance-imaging-for-early-breast-cancer-detection-in-women-at-high-risk-review
647. US Preventive Services Task Force. Screening for breast cancer: US Preventive Services Task Force recommendation
statement. Ann Intern Med 2009;151(10):716–26, W–236
648. Australian Department of Health and Ageing MBS Online – Medicare Benefits Schedule. [accessed 2012 June]. Available at
www9.health.gov.au/mbs/search.cfm?q=63464&sopt=I
649. Schorge JO, Modesitt SC, Coleman RL, Cohn DE, Kauff ND, Duska LR, et al. SGO White Paper on ovarian cancer: etiology,
screening and surveillance. Gynecol Oncol 2010;119(1):7–17
650. National Breast and Ovarian Cancer Centre. Population screening and early detection of ovarian cancer in asymptomatic
women – NBOCC Position statement. NBOCC, 2009 Available at canceraustralia.nbocc.org.au/our-organisation/position-
statements/population-screening-and-early-detection [accessed 2012 May].
651. Philip AK, Lubner MG, Harms B. Computed tomographic colonography. Surg Clin North Am 2011;91(1):127–39
652. Weizman AV, Nguyen GC. Colon cancer screening in 2010: an up-date. Minerva Gastroenterol Dietol 2010;56(2):181–8
653. Pox CP, Schmiegel W. Role of CT colonography in colorectal cancer screening: risks and benefits. Gut 2010;59(5):692–700
654. Laghi A, Lafrate F, Rengo M. Colorectal cancer screening: the role of CT colonography. World J Gastroenterol
2010;16(32):3987–94
655. Lieberman DA. Clinical practice. Screening for colorectal cancer. N Engl J Med 2009;361(12):1179–87
656. Weltermann B, Hermann M, Gesenhues S. Diagnostic screening for cancer and coronary heart disease with radiological and
nuclear imaging techniques: early diagnosis at any price? Dtsch Med Wochenschr 2010;135(16):813–8
657. Canadian Health Services Research Foundation. Myth: whole-body screening is an effective way to detect hidden cancers. J
Health Serv Res Policy 2010;15(2):118–9
658. Ladd SC. Whole-body MRI as a screening tool? Eur J Radiol 2009;70(3):452–62
659. Fayngersh V, Passero M. Estimating radiation risk from computed tomography scanning. Lung 2009;187(3):143–48
660. Schoder H, Gonen M. Screening for cancer with PET and PET/CT: potential and limitations. J Nucl Med 2007;48 (Suppl 1):S4–18
661. Anderiesz C, Elwood JM, McAvoy BR. Whole-body computed tomography screening: looking for trouble? Med J Aust
2004;181(6):295–6
662. O’Reilly J, Rudolf M. What’s nice about the new NICE guideline? Thorax 2011;66(2):93–6
663. COPD guidelines committee. The COPD-X Plan: Australian and New Zealand Guidelines for the management of chronic obstructive
pulmonary disease. Canberra: Australian Lung Foundation and the Thoracic Society of Australia and New Zealand, 2011
664. US Preventive Services Task Force. Screening for chronic obstructive pulmonary disease using spirometry: recommendation
statement. Am Fam Physician 2009;80(8):853
665. O’Donnell DE, Hernandez P, Kaplan A. Canadian Thoracic Society recommendations for management of chronic obstructive
pulmonary disease – 2008 update – highlights for primary care. Can Respir J 2008;15(Suppl A):A1–8
666. Gopinath B, Wang JJ, Kifley A. Five-year incidence and progression of thyroid dysfunction in an older population. Intern Med J
2010;40(9):642–9
8th edition
667. Ochs N, Auer R, Bauer DC. Meta-analysis: subclinical thyroid dysfunction and the risk for coronary heart disease and
mortality. Ann Intern Med 2008;148(11):832–45
668. Empson M, Flood V, Ma G. Prevalence of thyroid disease in an older Australian population. Intern Med J 2007;37(7):448–55
669. Helfand M. Screening for subclinical thyroid dysfunction in nonpregnant adults: a summary of the evidence for the US
Preventive Services Task Force. Ann Intern Med 2004;140(2):128–41
670. Bjelakovic G, Gluud LL, Nikolova D, Whitfield K, Wetterslev J, Simonetti RG, et al. Vitamin D supplementation for
prevention of mortality in adults. Cochrane Database Syst Rev 2011;7:CD007470
671. Chung M, Balk EM, Ip S, Lee J, Terasawa T, Raman G, et al. Systematic review to support the development of nutrient
reference intake values: challenges and solutions. Am J Clin Nutr 2010;92(2):273–6
672. Hanley DA, Cranney A, Jones G, Whiting SJ, Leslie WD. Vitamin D in adult health and disease: a review and guideline
statement from Osteoporosis Canada (summary). CMAJ 2010;182(12):1315–9
673. Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, et al. Evaluation, treatment,
and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab
2011;96(7):1911–30
674. Wang L, Manson JE, Song Y, Sesso HD. Systematic review: Vitamin D and calcium supplementation in prevention of
cardiovascular events. Ann Intern Med 2010;152(5):315–23
675. Lin K, Fajardo K. Screening for asymptomatic bacteriuria in adults: evidence for the U.S. Preventive Services Task Force
reaffirmation recommendation statement. Ann Intern Med 2008;149(1):W20–4
676. Ebeling PR. Routine screening for vitamin D deficiency in early pregnancy: past its due date? Med J Aust 2011;194(7):332–3
677. Dror DK, Allen LH. Vitamin D inadequacy in pregnancy: biology, outcomes, and interventions. Nutr Rev 2010;68(8):465–77
678. Lichtenstein AH. Nutrient supplements and cardiovascular disease: a heartbreaking story. J Lipid Res 2009;50
(Suppl):S429–33
679. Holmes VA, Barnes MS. Vitamin D deficiency and insufficiency in pregnant women: a longitudinal study. Br J Nutr
2009;102(6):876–81
680. Aggarwal S, Qamar A, Sharma V, Sharma A. Abdominal aortic aneurysm: a comprehensive review. Exp Clin Cardiol
2011;16(1):11–15
681. Ferket BS, Grootenboer N, Colkesen EB, Visser JJ, van Sambeek MR, Spronk S, et al. Systematic review of guidelines on
abdominal aortic aneurysm screening. J Vasc Surg 2012;55(5)1296–304
682. US Preventive Services Task Force. Screening for abdominal aortic aneurysm: recommendation statement. Ann Intern
Med 2005;142(3):198–202
683. Felker GM, Hasselblad V, Hernandez AF, O’Connor CM. Biomarker-guided therapy in chronic heart failure: a meta-
analysis of randomized controlled trials. Am Heart J 2009;158(3):422–30
684. Krum H, Jelinek MV, Stewart S, Sindone A, Atherton JJ. 2011 update to National Heart Foundation of Australia and
Cardiac Society of Australia and New Zealand Guidelines for the prevention, detection and management of chronic heart
failure in Australia, 2006. Med J Aust 2011;194(8):405–9
685. National Institute for Clinical Excellence. Chronic heart failure. National clinical guideline for diagnosis and management in
primary and secondary care. London: NICE, 2010
686. Porapakkham P, Zimmet H, Billah B, Krum H. B-type natriuretic peptide-guided heart failure therapy: a meta-analysis.
Arch Intern Med 2010;170(6):507–14
687. Mulshine JL, van Klaveren RJ. Lung cancer screening: what is the benefit and what do we do about it? Lung Cancer
2011;71(3):247–8
688. Baldwin DR. Imaging in lung cancer: recent advances in PET-CT and screening. Thorax 2011;66(4):275–7
689. Bach PB, Mirkin JN, Oliver TK, Azzoli CG, Berry DA, Brawley OW, et al. Benefits and harms of CT screening for lung
cancer: a systematic review. JAMA 2012:307(22):2418-29
690. Chou R, Dana T, Bougatsos C. Screening older adults for impaired visual acuity: a review of the evidence for the US
Preventive Services Task Force. Ann Intern Med 2009;151(1):44–58
8th edition 115
Appendix 1: Dutch Lipid Clinic Network Criteria for making

a diagnosis of Familial Hypercholesteroloemia (FH) in adults
Score
Family history
First-degree relative with known premature coronary and/or vascular disease (men <55 years, women <60 1
years)
or
First-degree relative with known LDL-cholesterol above the 95th percentile for age and sex
First-degree relative with tendinous xanthomata and/or arcus cornealis 2

or
Children aged less than 18 years with LDL-cholesterol above the 95th percentile for age and sex
Clinical history
Patient with premature coronary artery disease (ages as above) 2
Patient with premature cerebral or peripheral vascular disease (as above) 1
Physical examination
Tendinous xanthomata 6
Arcus cornealis prior to age 45 years 4
LDL-cholesterol (mmol/L)
LDL-C ≥8.5 8
LDL-C 6.5–8.4 5
LDL-C 5.0–6.4 3
LDL-C 4.0–4.9 1
DNA analysis: functional mutation in the LDLR, APOB or PCSK9 gene 8
STRATIFICATION Total score
Definite FH ≥8
Probable FH 6–7
Possible FH 3–5
Unlikely FH <3
8th edition
Modified UK Simon Broome criteria

1. DNA mutation
2. Tendon xanthomas in patient or first/second-degree relative
3. Family history MI <50 in second-degree or <60 in first-degree relative
4. Family history of cholesterol >7.5 in first- or second-degree relative
5. Cholesterol >7.5 (adult) or >6.7 (age <16 years)
6. LDL-C >4.9 (adult) or >4.0 (age <16 years)
Definite: (5 or 6) + 1
Probable: (5 or 6) + 2
Possible familial hypercholesteroloemia: (5 or 6) + (3 or 4)
Adapted from Watts GF, Sullivan DR, Poplawski N, van Bockxmeer F, Hamilton-Craig I, et al. Familial
Hypercholesterolaemia Australasia Network Consensus Group (Australian Atherosclerosis Society). Familial
hypercholesterolaemia: a model of care for Australasia. Atheroscler Suppl 2011;12(2):221–63
8th edition 117
Appendix 2: ‘Red flag’ early intervention referral guide
Reproduced with permission from Queensland Health. No further reproduction is allowed.
http://www.health.qld.gov.au/rch/professionals/brochures/red_flag.pdf
8th edition
Appendix 3: Audit-C (available for use in the public domain)
AUDIT-C – Overview
The AUDIT-C is a three-item alcohol screen that can help identify persons who are hazardous drinkers or have active alcohol
use disorders (including alcohol abuse or dependence). The AUDIT-C is a modified version of the 10-question
AUDIT instrument.
Clinical utility
The AUDIT-C is a brief alcohol screen that reliably identifies patients who are hazardous drinkers or have active alcohol use
disorders.
Scoring
The AUDIT-C is scored on a scale of 0–12.
Each AUDIT-C question has five answer choices. Points allocated are:
a = 0 points, b = 1 point, c = 2 points, d = 3 points, e = 4 points
• I n men a score of 4 or more is considered positive, optimal for identifying hazardous drinking or active alcohol use
disorders.
• In women a score of 3 or more is considered positive (same as above).
However, when the points are all from Questions 1 alone (questions 2 and 3 are zero), it can be assumed that the patient is
drinking below recommended limits and it is suggested that the provider review the patient’s alcohol intake over the past few
months to confirm accuracy.1
Generally, the higher the score, the more likely it is that the patient’s drinking is affecting their safety.
Psychometric properties
For identifying patients with heavy/hazardous drinking and/or active DSM alcohol abuse or dependence.
Men2 Women3
≥3 Sens: 0.95/Spec. 0.60 Sens: 0.66/Spec. 0.94
For identifying patients with active alcohol abuse or dependence:
Men2 Women3
1. B
radley KA, Bush KR, Epler AJ, et al. Two brief alcohol-screening tests from the Alcohol Use Disorders Identification Test (AUDIT): Validation in
a female veterans affairs patient population. Arch Internal Med April 2003;163:821–829
2. Frequently asked questions guide to using AUDIT-C can be found via the website: www.oqp.med.va.gov/general/uploads/FAQ%20AUDIT-C
3. B
ush K, Kivlahan DR, McDonell MB, et al. The AUDIT alcohol consumption questions (AUDIT-C): An effective brief screening test for problem
drinking. Arch Internal Med 1998(3):1789–95
www.thenationalcouncil.org/galleries/business-practice%20files/tool_auditc.pdf
8th edition 119
Audit-C Questionnaire
Patient name ____________________________________________________ Date of visit ______________
1. How often do you have a drink containing alcohol?
❍ a. Never
❍ b. Monthly or less
❍ c. 2–4 times a month
❍ d. 2–3 times a week
❍ e. 4 or more times a week
2. How many standard drinks containing alcohol do you have on a typical day?
❍ a. 1 or 2
❍ b. 3 or 4
❍ c. 4 or 6
❍ d. 7 to 9
❍ e. 10 or more
3. How often do you have six or more drinks on one occasion?
❍ a. Never
❍ b. Less than monthly
❍ c. Monthly
❍ d. Weekly
❍ e. Daily or almost daily
8th edition
Appendix 4:The Australian Type 2 Diabetes Risk

Assessment tool – AUSDRISK
The Australian Type 2 Diabetes Risk Assessment Tool was originally developed by the International Diabetes Institute on behalf
of the Commonwealth, State and Territory governments as part of the COAG reducing the risk of type 2 diabetes initiative.
The Australian Type 2 Diabetes

Risk Assessment Tool (AUSDRISK)
1. Your age group 8. How often do you eat vegetables or fruit?

Under 35 years  0 points Every day  0 points
35 – 44 years  2 points Not every day  1 point
45 – 54 years  4 points
9. On average, would you say you do at least 2.5 hours
55 – 64 years  6 points of physical activity per week (for example, 30 minutes
65 years or over  8 points a day on 5 or more days a week)?
2. Your gender Yes  0 points
No  2 points
Female  0 points
Male  3 points 10. Your waist measurement taken below the ribs
(usually at the level of the navel, and while standing)
3. Your ethnicity/country of birth:
3a. Are you of Aboriginal, Torres Strait Islander, Waist measurement (cm)
No  0 points For those of Asian or Aboriginal or Torres Strait

Yes  2 points Islander descent:
3b. Where were you born? Men Women

Australia  0 points Less than 90 cm Less than 80 cm  0 points
90 – 100 cm 80 – 90 cm  4 points
Asia (including the Indian sub-continent),
Middle East, North Africa, Southern Europe  2 points
More than 100 cm More than 90 cm  7 points
For all others:
Other  0 points
Men Women
4. Have either of your parents, or any of your brothers Less than 102 cm Less than 88 cm  0 points
or sisters been diagnosed with diabetes
102 – 110 cm 88 – 100 cm  4 points
(type 1 or type 2)?
More than 110 cm More than 100 cm  7 points
No  0 points
Yes  3 points
Add up your points
5. Have you ever been found to have high blood glucose
(sugar) (for example, in a health examination, Your risk of developing type 2 diabetes within 5 years*:
during an illness, during pregnancy)?
 5 or less: Low risk
No  0 points Approximately one person in every 100 will develop diabetes.
Yes  6 points
 6-11: Intermediate risk
6. Are you currently taking medication for high For scores of 6-8, approximately one person in every 50 will
blood pressure? develop diabetes. For scores of 9-11, approximately one person
in every 30 will develop diabetes.
No  0 points
Yes  2 points  12 or more: High risk
For scores of 12-15, approximately one person in every 14 will
7. Do you currently smoke cigarettes or any other develop diabetes. For scores of 16-19, approximately one person
tobacco products on a daily basis? in every 7 will develop diabetes. For scores of 20 and above,
approximately one person in every 3 will develop diabetes.
No  0 points
Yes  2 points *The overall score may overestimate the risk of diabetes in those aged less than 25 years.
If you scored 6-11 points in the AUSDRISK you may be at If you scored 12 points or more in the AUSDRISK you may have
increased risk of type 2 diabetes. Discuss your score and your undiagnosed type 2 diabetes or be at high risk of developing the
individual risk with your doctor. Improving your lifestyle may help disease. See your doctor about having a fasting blood glucose
reduce your risk of developing type 2 diabetes. test. Act now to prevent type 2 diabetes.
www.diabetesaustralia.com.au/PageFiles/937/AUSDRISK%20Web%2014%20July%2010.pdf
What is type 2 diabetes? What can you do to lower your risk of The Australian Type 2 Diabetes
Type 2 diabetes is a chronic (long-term) disease marked developing type 2 diabetes? Risk Assessment Tool (AUSDRISK)
by high levels of sugar in the blood. It occurs when the Your lifestyle choices can prevent or, at least, delay the onset
body does not produce enough insulin (a hormone released of type 2 diabetes. How do you score?
by the pancreas) or respond well enough to insulin.
You cannot change risk factors like age and your genetic
Type 2 diabetes is the most common form of diabetes.
background. You can do something about being overweight,
There are approximately 1 million people with type 2 diabetes
your waist measurement, how active you are, eating habits,
currently. This figure is expected to increase significantly in
or smoking.
Reproduced with permission. No further reproduction is permitted.

the coming years.
If there is type 2 diabetes in your family, you should be careful
People with diabetes have a higher risk of developing heart
not to put on weight. Reducing your waist measurement
disease, stroke, high blood pressure, circulation problems,
reduces your risk of type 2 diabetes.
lower limb amputations, nerve damage and damage to the
kidneys and eyes. By increasing your physical activity and improving your eating
habits you can lower your risk. Eat plenty of vegetables and
Risk factors high fibre cereal products every day and use a small amount
Many Australians, particularly those over 40, are at risk of of fats and oils. Monounsaturated oils, such as olive or
developing type 2 diabetes through lifestyle factors such canola oil, are the best choice.
as physical inactivity and poor nutrition. Family history of
You can have type 2 diabetes and not know it because there
diabetes and genetics also play a role in type 2 diabetes.
may be no obvious symptoms.
The Australian Type 2 Diabetes Risk Assessment Tool

was developed by the Baker IDI Heart and Diabetes
Institute on behalf of the Australian, State and Territory
Governments as part of the COAG initiative to reduce
the risk of type 2 diabetes
Current from: May 2010
6811 (1007)
121 8th edition
8th edition
Appendix 5: Australian cardiovascular risk charts

Figure 1. Australian cardiovascular risk charts
People without diabetes People

Women Men Women
Non-smoker Smoker Non-smoker Smoker Non-smoker Smoker
179 * 179 * 179 *
160 Age 160 160
140
65–74 140 140
Systolic blood pressure (mm Hg)

120 120 120
179 * 179 * 179 *

160 Age 160 160
140 55–64 140 140
120 120 120
179 * 179 * 179 *

160 Age 160 160
140 45–54 140 140
120 120 120
179 * 179 * Charts in this age 179 *

160 Age 160 bracket are for use in 160
140 35–44 140 Aboriginal and Torres 140
Strait Islander
120 120 120
populations only.
4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8
Total cholesterol:HDL ratio* Total cholesterol:HDL ratio* Total cholesterol:HDL ratio*
* In accordance with Australian guidelines, patients with systolic blood pressure ≥ 180 mm Hg, * In accordance with Australian guidelines, pa
or a total cholesterol of > 7.5 mmol/L, should be considered at increased absolute risk of CVD. or a total cholesterol of > 7.5 mmol/L, shou
Risk level for 5-year cardiovascular (CVD) risk Risk level for 5-year cardiovascular (CVD
High risk Moderate risk Low risk High risk Moderate risk
≥ 30% 10–15% 5–9% ≥ 30% 10–15 %

25–29% < 5% 25–29%
20–24% 20–24%
16–19% 16–19%
How to use the risk charts

1. Identify the table relating to the person’s diabetes status, 3. The colour of the cell that the person falls into
sex, smoking history and age. ‘Smoker’ is defined as provides their 5-year absolute cardiovascular risk
either current daily cigarette smoker or former smoker level (see legend above for risk category). For people
who has quit within the previous 12 months. The charts who fall exactly on a threshold between cells,
should be used for all adults aged 45–74 years (and use the cell corresponding to higher risk. The risk
all Aboriginal and Torres Strait Islander adults aged calculator may underestimate cardiovascular risk in
35 years and older) without known history of CVD or these groups:
already known to be at high risk.
• Aboriginal and Torres Strait Islander adults
2. Within the chart, choose the cell nearest to the
• adults with diabetes aged 60 years or less
person’s age, systolic blood pressure (SBP) and total
cholesterol (TC):HDL ratio. For example, the lower left • adults who are overweight or obese
cell contains all non-smokers without diabetes who • socioeconomically deprived groups.
are 35–44 years and have a TC:HDL ratio of less than
4.5 and a SBP of less than 130 mm Hg.
• SBP (mean of two readings on two occasions).
• Total cholesterol/high-density lipoprotein cholesterol
(HDL-C) ratio (ensure correct ratio is used).
Heart Foundation Guide to management of hypertension 2008 15
Reproduced with permission from the Heart Foundation. No further reproduction is permitted.
www.heartfoundation.org.au/SiteCollectionDocuments/aust-cardiovascular-risk-charts.pdf
8th edition 123
Figure 1. Australian cardiovascular risk charts (continued)
People with diabetes

Women Men
Non-smoker Smoker Non-smoker Smoker
179 * 179 * Adults over the age of
160 Age 160 60 with diabetes are
65–74 equivalent to high risk
140 140
(> 15%), regardless

120 120 of their calculated risk
level. Nevertheless,
179 * 179 * reductions in risk
160 Age 160 factors in this age
140 55–64 140 group can still lower
overall absolute risk.
120 120
179 * 179 *
160 Age 160
140 45–54 140
120 120
in this age 179 * 179 * Charts in this age

are for use in 160 Age 160 bracket are for use in
al and Torres 140 35–44 140 Aboriginal and Torres
Islander Strait Islander
120 120
tions only. populations only.
4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8
Total cholesterol:HDL ratio* Total cholesterol:HDL ratio*
* In accordance with Australian guidelines, patients with systolic blood pressure ≥ 180 mm Hg,
or a total cholesterol of > 7.5 mmol/L, should be considered at increased absolute risk of CVD.
Risk level for 5-year cardiovascular (CVD) risk

High risk Moderate risk Low risk
≥ 30% 10–15 % 5–9%

25–29% < 5%
20–24%
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.
CVD refers collectively to coronary heart disease (CHD), stroke and other vascular
disease including peripheral arterial disease and renovascular disease.
Charts are based on the NVDPA’s Guidelines for the assessment of absolute
cardiovascular disease risk and adapted with permission from New Zealand
Guidelines Group. New Zealand Cardiovascular Guidelines Handbook: A Summary
Resource for Primary Care Practitioners. Second edition. Wellington, NZ: 2009.
www.nzgg.org.nz.
16 Heart Foundation Guide to management of hypertension 2008
Reproduced with permission from the Heart Foundation. No further reproduction is permitted.
8th edition
Appendix 6: The three incontinence questions
1. During the last 3 months, have you leaked urine (even a small amount)?
Yes No >> questionnaire completed
2. During the last 3 months, did you leak urine
(check all that apply):
a. When you were performing some physical activity, such as coughing, sneezing, lifting or exercise?
b. When you had the urge or the feeling that you needed to empty your bladder, but you could not get to the
toilet fast enough?
c Without physical activity and without a sense of urgency?
3. During the last 3 months, did you leak urine most often:
(check only one)
a. When you are performing some physical activities such as coughing, sneezing and lifting or exercise?
b. When you had the urge or the feeling that you needed to empty your bladder but you could not get to the
toilet fast enough?
c. Without physical activity and without a sense of urgency?
d. About equally as often with physical activities as with a sense of urgency?
Response to question 3 Type of incontinence
a. Most often with physical activity Stress only or stress predominant
b. Most often with the urge to empty the bladder Urge only or urge predominant
c. Without physical activity or sense of urgency Other cause only or other cause predominant
d. About equally with physical activity and sense of urgency Mixed
Reference: Brown J, Bradley C, Subak L, Richter H, Kraus S, Brubaker L. The sensitivity and specificity of a simple test to distinguish
between urge and stress incontinence. Ann Intern Med 2006;144:715–23.
8th edition 125
Glossary
Screening
Screening: detection of unrecognised disease or condition in the general population by using reliable
tests, examinations or other procedures that can be applied rapidly
Opportunistic screening: detection of, or case finding of specific diseases that can be controlled better
when detected early in their natural history, particularly in individuals or groups who may be predisposed
to that disease, for example, those with particular risk factors
High risk individuals: those individuals who have risk factors that are likely to predispose them to
impending disease
High index of suspicion: level of awareness of clusters of risk factors such as lifestyle, socioeconomic,
personal medical history and family medical history, which may predispose individuals to disease.
Evidence
Good evidence: there is good quality evidence obtained from randomised clinical trials to support or
reject a recommendation
Fair evidence: evidence obtained from studies such as well designed pseudo-RCTs (alternate allocation
or some other method), comparative studies with concurrent controls and allocation not randomised
(cohort studies), case control studies, or interrupted time series with a control group or comparative
studies with historical control, two or more single arm studies, or interrupted time series without a
parallel control group
Poor evidence: evidence obtained from case series, either post- or pre-test and post-test, or opinions of
respected authorities based on clinical experience, descriptive studies or reports of expert committees
No evidence: exhaustive searches have revealed there are no studies that address recommendations in
general practice for the target disease or condition.
Prevention
Primary prevention: prevention of diseases or disorders in the general population by encouraging
community-wide measures such as good nutritional status, physical fitness, immunisation and making
the environment safe. Primary prevention maintains good health and reduces the likelihood of disease
occurring
Secondary prevention: detection of the early stages of disease before symptoms occur, and the prompt
and effective intervention to prevent disease progression
Tertiary prevention: prevention or minimisation of complications or disability associated with established
disease. Preventive measures are part of the treatment or management of the target disease or
condition.
Healthy Profession.
Healthy Australia.

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Guidelines for preventive

activities in general practice

Whilst the text is directed to health professionals possessing appropriate

Accordingly, The Royal Australian College of General Practitioners and its

First edition published 1989

Red book taskforce members

Professor Danielle Mazza

Abbreviations and acronyms

ALA Alpha-linolenic acid FAP Familial adenomatous polyposis

AMD Aged-related macular degeneration FH Familial hypercholesterolaemia

APC Adenomatous polyposis coli FOBT Faecal occult blood test

MMSE Mini-Mental State Examination

MRI Magnetic resonance imaging

MSM Men who have sex with men

MSU Midstream urine

MUKSB Modified UK Simon Broome criteria

NAAT Nucleic acid amplification test

NHMRC National Health and Medical Research Council

NIP National Immunisation Program

NIPS National Immunisation Program Schedule

NMSC Non-melanoma skin cancer

NTD Neural tube defect

PCR Polymerase chain reaction

PEDS Parents’ evaluation of developmental status

PND Postnatal depression

VZV Varicella Zoster Virus

WHO World Health Organization

8. Prevention of vascular and metabolic disease 50

The Australian experience

Preventive health activities

Screening versus case finding

II. Patient education and health literacy

Approaches to patient education

Table II.1 Stages of change model

Contemplation The person considers changing a specific behaviour

Determination The person makes a serious commitment to change

Action Change begins (these can be large or small changes)

Maintenance Change is sustained over a period of time

The complex needs and health problems of disadvantaged groups

III. Development of the red book

Scope and limitations of the red book

IV. How to use the red book

I Evidence obtained from a systematic review of level II studies

II Evidence obtained from a randomised controlled trial (RCT)

III–2 Evidence obtained from a comparative study with concurrent controls:

III–3 Evidence obtained from a comparative study without concurrent controls:

IV Case series with either post-test or pre-test/post-test outcomes

A Body of evidence can be trusted to guide practice

B Body of evidence can be trusted to guide practice in most situations

D Body of evidence is weak and recommendation must be applied with caution

V. What’s new in this 8th edition?

Table V.1 Key changes in the 8th edition

Glaucoma (Section 12) Updated recommendations in line with new NHMRC

Osteoporosis (Section 14) Details of risk factors have been refined.

1. Preventive activities prior to pregnancy

What does pre-conception care include?

General physical assessment

Folic acid supplementation

Healthy weight, nutrition and exercise

Smoking, alcohol and illegal drug cessation (as indicated)

Table 1.1 Pre-conception: preventive interventions

Pre-conception Address risk factors using Pregnancy Lifescripts

2. Genetic counselling and testing